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  1. How should cannabis or THC be taken to treat asthma? British Medical Association Acute doses of cannabis and THC exert a definitive bronchodilator effect on the small airways of the lungs. The mechanism of this effect is not known, but it appears to be different from that of other drugs used at present as bronchodilators for asthma. However, there have been very few studies on the bronchodilator effects of cannabinoids in asthmatic patients. All of these were studies carried out in the 1970s. Tashkin et al. studied 14 asthmatic volunteers and compared smoked cannabis (2%THC), oral THC (15mg) and the drug isoprenaline (0.5%). They found that smoked cannabis and oral THC produced significant bronchodilatation of at least two hours duration. The effect of smoked cannabis was nearly equivalent to the clinical dose of isoprenaline. Smoked cannabis was also capable of reversing experimentally induced bronchospasm in three asthmatic subjects. Williams et al. compared a THC aerosol containing 0.2 mg THC with a salbutamol aerosol (0.1 mg) in 10 asthmatic subjects. Both drugs significantly improved respiratory function. The onset of effect was more rapid with salbutamol, but the effects of both drugs were equivalent at one hour. Tashkin et al. compared several doses of THC aerosol (5-20mg) with a standard dose of isoprenaline in 11 normal volunteers and five asthmatic subjects. In the normal subjects and three of the asthmatics, the bronchodilator effect of THC was less than that of isoprenaline after five minutes, but significantly greater after one to three hours. source: http://www.budbuddie...elps/asthma.htm Asthma Asthma is the shortness of breath and wheezing caused by spasms of the bronchial tubes, overproduction of mucus, and swelling of the mucous membranes. Asthma kills more than 4,000 Americans each year.[1] Clinical research shows that THC acts as a bronchial dilator, clearing blocked air passageways and allowing free breathing.[2], [3] In one study, marijuana, “caused an immediate reversal of exercise-induced asthma and hyperinflation.”[4] Numerous cases of asthma have been treated successfully with both natural and synthetic THC. In one report, a young woman used marijuana with her doctor’s approval. Over the course of several years her attacks were almost completely cured with low doses of inhaled cannabis smoke.[5] Some asthmatics who have found relief through the use of synthetic THC often voice a preference for natural cannabis over Marinol. Marinol is said to be less effective than natural cannabis and has far greater psychoactive properties. Alternative methods of administration have been recommended by the Institute of Medicine [6] and other medical authorities. Plans for a noncombusting THC inhaler received attention for many years, yet designers have failed to produce a workable prototype.[7] “Experiments examining the antiasthmatic effects of THC or cannabis date mainly from the 1970s, and are acute studies. The effects of a marijuana cigarette (2 percent THC) or oral THC (15 mg), respectively approximately correspond to those obtained with therapeutic does of common bronchodilators drugs (salbutamol, isoprenaline). Following inhalation, the effect lasts about two hours. Since inhalation of cannabis products may irritate the mucous membranes, oral administration or another alternative delivery system would be preferable. Very few patients developed brochoconstriction after inhalation of THC.” [8] Related sections: Immune Responses, Muscle Spasms, Psychoactivity, Respiratory Disease, Smoking Methods, Stress Reduction. -------------------------------------------------------------------------------- [1] Grinspoon, “Marijuana and asthma.” The Forbidden Medicine Website, www.rxmarijuana.com [2] National Academy of Science, 1982 [3] “Therapeutic possibilities in cannabinoids,” Editorial, The Lancet, pp. 667-669, March 22, 1975 [4] Tashkin, Shapiro, Lee, and Harper, “Effects of smoked marijuana in experimentally induced asthma.” American Review of Respiratory Disease, Vol. 112, 1975 [5] Letters, High Times, No. 273, May, 1998 [6] Institute of Medicine, Marijuana and Medicine: Assessing the Science Base. Washington DC: National Academy Press, 1999 [7] Geiringer, “An overview of the human research studies on medical use of marijuana.” CANORML, 1994, www.norml.org/canorml/ [8] Grotenhermen, Russo. Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. New York: The Hawthorn Integrative Healing Press, 2002, Grotenhermen, “Review of Therapeutic Effects.” Chapter 11, p. 130 Acute effects of smoked marijuana and oral delta-9-tetrahydrocannabinol on specific airway conductance in asthmatic subjects American Review of Respiratory Disease, Volume 109, 1974, p. 420-428 By Donald P. Tashkin, Bertrand J. Shapiro, and Ira M. Frank SUMMARY: The acute effects of smoked 2 per cent natural marijuana (7 mg per kg) and 15 mg of oral delta-9-tetrahydrocannabinol (THC) on plethysmographically determined airway resistance (Raw) and specific airway conductance (SGaw) were compared with those of placebo in 10 subjects with stable bronchial asthma using a double-blind crossover technique. After smoked marijuana, SGaw increased immediately and remained significantly elevated (33 to 48 per cent above initial control values) for at least 2 hours, whereas Sgaw did not change after placebo. The peak bronchodilator effect of 1,250 mcg of isoproterenol was more pronounced than that of marijuana, but the effect of marijuana lasted longer. After ingestion of 15 mg of THC, SGaw was elevated significantly at 1 and 2 hours, and Raw was reduced significantly at 1 to 4 hours, whereas no changes were noted after placebo. These findings indicated that in the asthmatic subjects, both smoked marijuana and oral THC caused significant bronchodilation of at least 2 hours' duration. Introduction In the nineteenth century, one of the medicinal uses of marijuana was in the therapy of bronchial asthma (1); however, no definite evidence of its effectiveness as a bronchodilator was adduced until recent studies demonstrated significant airway dilatation in healthy young men after both the smoking of marijuana (2,3) and the ingestion of its principal psychoactive ingredient delta-9-tetrahydrocannabinol (THC) (3). Whether similar effects could be elicited in subjects with bronchospastic disease was of interest because the irritant effect of marijuana smoke, which is probably responsible for the symptoms of bronchitis attributed to heavy or chronic marijuana smoking (4,5), might outweigh the bronchodilator properties of delta-9-THC, thereby resulting in bronchospasm in patients with hyper-reactive airways. Consequently, the acute effects of both inhaled marijuana smoke and oral delta-9-THC on specific airway conductance (SGaw) were investigated in a group of patients with clinically stable bronchial asthma. Materials and Methods Subjects: Five men and 5 women (from 22 to 74 years of age) with a diagnosis of bronchial asthma according to the criteria established by the American Thoracic Society (6) were studied. Each subject had a clinical picture characterized by typical episodes of wheezing, cough, and dyspnea occurring either spontaneously or in response to exposure to inhaled allergens or nonspecific irritants, to emotional aspects, to respiratory tract infections, and/or to exercise, and relieved by bronchodilator medication. At the time of study, all subjects were clinically stable; asthmatic symptoms were absent in 4 subjects and chronic and of mild to moderate severity in the remainder. With the exception of 2 subjects (PF and JBon), who probably had pulmonary emphysema in addition to bronchospastic disease, there was no evidence of other significant medical illness by history, physical examination, complete blood count, blood chemistries (SMA-12), routine urinalysis, electrocardiogram, and chest radiograph. Significant psychiatric illness was excluded on the basis of interviews with one of the investigators and evaluation of performance on lthe Minnesota Multiphasic Personality Inventory. All subjects underwent screening pulmonary function studies, including spirometry using a 13.5-liter water spirometer (Warren E. Collins, Inc.), single-breath diffusing capacity for carbon monoxide (DLCO) (7), airway resistance (Raw), and thoracic gas volume (Vtg) using a 900-liter, variable-pressure body plethysmograph (8,9). To assess the degree of reversible airway obstruction, spirometry was performed both before and 10 minutes after inhalation of 0.25 ml of isoproterenol HCL (1:200) via a DeVilbiss nebulizer connected to a positive pressure breathing device powered by compressed air. The following technique was used to administer the isoproterenol aerosol. Subjects were instructed first to exhale to residual volume, then to inhale slowly from the nebulizer to total lung capacity during a period of approximately 10 seconds, and then to resume normal breathing for several seconds. These maneuvers were repeated until the bronchodilator solution in the nebulizer was consumed (usually after 4 to 5 deep breaths). In addition, Raw and Vtg were measured both 15 minutes before and immediately before inhalation of isoproterenol, and at 5, 15, 30, and 60 minutes after the bronchodilator. In all subjects, flows and/or SGaw (the ratio of the reciprocal of Raw to the simultaneously measured Vtg) increased more than 25% after isoproterenol inhalation, indicating the responsiveness of the airways to bronchodilator medication. Seven of the 10 subjects had smoked marijuana previously, but only sporadically (less than 1 cigarette per month). None admitted to the use of drugs other than those prescribed for bronchial asthma, and none was a tobacco cigarette smoker. No subject had used marijuana within 7 days before the present study. In addition, bronchodilator medication was withheld for at least 8 hours before the study. Experiments were carried out with each subject on 4 separate days beginning at 10 A.M., with at least 48 hours intervening between each study session. The subjects were informed that they would be randomly receiving marijuana or placebo. Smoked marijuana: During 2 of the 4 experimental sessions, subjects smoked 7 mg per kg of body weight of natural marijuana preparation containing either 0.0 % delta-9-THC, serving as a placebo control, or 2.0 % delta-9-THC according to a random, double-blind crossover design; however, because of the potent psychotropic effects of marijuana, it was recognized that the subjects probably had little difficulty in identifying the marijuana. The THC content of the experimental preparation had previously been assayed by gas-liquid chromatography. The 0 % preparation was obtained by extraction of the active cannabinoids from the natural material until assays for cannabinol, cannabidiol, delta-8-THC, and delta-9-THC were all 0.0 %. A uniform smoking technique was used in an effort to standardize the amount of volatilized delta-9-THC delivered in the inhaled material. Subjects inhaled the cigarette deeply for 2 to 4 seconds, held their breath for 15 seconds, resumed normal breathing for approximately 5 seconds, and then repeated these maneuvers until the cigarette was consumed, during a period of approximately 10 minutes. The cigarette butt, or "roach," was held with forceps to permit nearly complete consumption of the "roach," where the volatilized cannabinoids are concentrated. The following characteristics were measured 15 minutes before and immediately before marijuana or placebo was smoked (initial control period) and immediately, 5, 10, 15, 30, 60, 90, 120, and 180 minutes after completion of smoking: Raw, Vtg, respiratory rate, heart rate (determined from the electro-cardiogram), and systolic and diastolic blood pressures. In addition, to provide a rough assessment of the degree of intoxication; at each interval after the smoking of marijuana and placebo, the 7 subjects who had had prior experience with Cannabis were asked to estimate how "high" they felt on a scale of zero to 7 in which 7 represented the "highest" they had ever felt after smoking marijuana. Oral delta-9-THC: During the remaining 2 study days, after an overnight fast, according to a random double-blind design subjects ingested either placebo or 15 mg of synthetic delta-9-THC dissolved in sesame oil and contained in identical-gelatin capsules. Again, as in the smoked marijuana experiments, the subjects were probably able to identify the delta-9-THC because of the marked psychotropic effect. Measurements of the same characteristics as those determined in the smoking studies and scoring of subjective degrees of intoxication were carried out 30 minutes before and immediately before oral administration of the drug (initial control Period) and 30, 60, 90. 120. 180, 240, 300, and 360 minutes after ingestion. The order of the smoking and oral experiments was randomized among the study subjects. All natural marijuana and synthetic THC preparations were obtained from the National Institutes of Mental Health, under whose direction all extraction, blending, assay, and synthetic procedures had previously been performed. Results From each set of measurements of Raw and Vtg, SGaw was calculated to correct for changes in Raw secondary to changes in lung volume (10). For each subject at each time interval after inhalation of isoproterenol or the smoking or ingestion of the test agent, per cent change in each of the measured characteristics was calculated from the average of the 2 control values. Individual per cent changes were averaged for each inhaled or ingested agent separately for all subjects at each time interval for each type of experimental preparation. Using the Student t test, significance of the differences between means was determined for (1) the average per cent change in each characteristic for each experimental preparation compared with initial control values, (2) the per cent changes that followed smoked marijuana and oral THC compared with placebo using paired observations, (3) the differences between the mean scores from zero for the levels of "high" after smoked marijuana and oral delta-9-THC. Physical characteristics and the results of the baseline pulmonary function studies for each subject are indicated in table 1. Although baseline forced expiratory volume in 1 second (FEV1) was greater than 80 % of the predicted value in 3 asymptomatic subjects (MA, SC, GT), in 2 of the latter SGaw was more than 2 standard deviations below the mean predicted value for this laboratory, and in the third subject, SGaw increased 87 % after isoproterenol inhalation, indicting the presence of reversible bronchospasm. There, symptoms and/or functional abnormalities were present in all subjects. Average initial control values for the measured characteristics during each experimental session are indicated in table 2. There were no significant differences between the mean baseline values obtained on separate days. Smoking studies: The average per cent changes in SGaw and Vtg after smoked marijuana, smoked placebo marijuana, and inhaled isoproterenol are shown in figures 1 and 2. After placebo, neither SGaw nor Vtg changed significantly. After 2 per cent marijuana, average SGaw increased immediately and remained elevated (33 to 48 per cent more than initial control values) for at least 2 hours. These increases were significant (P<0.05) compared both with control values and with placebo values. The Vtg decreased slightly (4 to 13 per cent) but significantly (P<0.05) compared with baseline and/or marijuana. Changes in Raw after marijuana generally paralleled the changes in SGaw but were of lesser magnitude because of the associated decreases in Vtg. For comparison with the changes that followed marijuana smoking, average per cent changes in SGaw and Vtg after inhalation of 1,250 mcg of isoproterenol are also shown in figures 1 and 2. During the first 15 minutes after inhalation of isoproterenol, SGaw increased to levels greater than those observed after 2 per cent marijuana. By 60 minutes after isoproterenol, SGaw was elevated only slightly, and was significantly less than the SGaw after marijuana (P<0.05). During the first 30 minutes after isoproterenol inhalation, Vtg was significantly reduced, to a degee similar to that noted after marijuana. By 60 minutes after isoproterenol, Vtg had essentially returned to normal. The average percentage changes in heart rate after smoking of marijuana or placebo and after inhalation of isoproterenol are shown in figure 3. Pulse rate decreased gradually after placebo to levels that were slightly but significantly below baseline values after 30 to 120 minutes. After 2 per cent marijuana, pulse rate increased immediately and remained elevated for 30 minutes by amounts (7 to 22 Per cent) that were significantly different from the changes that followed placebo (P<0.05). Therafter, pulse rate decreased to levels that, at 90 and 120 minutes, were significantly below initial control values (P<0.05) but were not significantly different from the changes that followed placebo. Pulse rate increased after isoproterenol, but the increase was not significant at P<0.05. No significant change in systolic or diastolic blood pressure or in respiratory rate was observed after placebo, marijuana, or isoproterenol. All subjects admitted to a definite feeling of intoxication after smoking marijuana, whereas all but one subject had either no change or minimal change in state of consciousness after placebo. The latter subject (PF), who had not had any previous exposure to Cannabis, felt sleepy, lightheaded, and jittery after both marijuana and placebo. The scores for subjective degree of "high" after marijuana revealed a maximal feeling of intoxication during the 5-minute period immediately after completion of smoking, with a gradual decline thereafter (figure 4). By 2 hours, the magnitude of the "high" was approximately one-third of the peak level, and by 3 hours, the "high" had essentially dissipated. Oral studies: The results of the oral studies are shown in figures 5 and 6. The SGaw increased modestly (14 to 19 per cent) but significantly (P<0.05) at 60 to 120 minutes after ingestion of 15 mg of delta-9-THC, whereas the placebo was not associated with any significant changes. The Vtg did not change significantly after either placebo or THC. As noted with smoked marijuana, decreases in Raw after oral THC paralleled the increases in SGaw, except that Raw was still significantly reduced (-10.2 + 3.6 and -12.9 + 3.3, with P<0.05) at 3 and 4 hours, respectively. No alteration in respiratory rate, pulse rate, or systolic or diastolic pressure was observed after oral delta-9-THC or placebo. A subjective "high" was first experienced 1 hour after ingestion of THC, reached a peak at 2 to 3 hours, then declined gradually, and was gone by 6 hours (figure 4). The placebo preparation was not associated with any significant change in consciousness. Discussion The significant increases in SGaw after the smoking of marijuana compared with placebo suggested that inhaled marijuana caused airway dilatation in asthmatic subjects and was consistent with findings previously reported in persons without airway disease (2, 3). The dilatation was not due to an increase in lung volume (10), because Vtg decreased significantly in paralled with the increase in SGaw. The observed decrese in Vtg was consistent with a reduction in air trapping secondary to the decrease in bronchomotor tone. Also, the volume history of the lung, i.e., the deep, sustained inhalation breathing pattern, did not explain the increase in SGaw that followed marijuana smoking compared to placebo smoking, because the breathing patterns were similar. Because there was a significant correlation between the individual increases in SGaw after marijuana and the magnitude of the subjective "high" (r= 0.52; P< 0.01), the possibility that the observed bronchodilatation was causally related either to the psychologic effects of marijuana or to other effects of Cannabis on the central nervous system deserves consideration. Despite the significant correlation between the degree of marijuana-induced bronchodilatation and the level of intoxication, the time sequences for these changes were somewhat different, in that the bronchodilator effect at 2 hours was similar in magnitude to that noted immediately after smoking (figure 1), whereas by 2 hours the "high" had decreased to less than one half of the level experienced immediately after smoking (figure 4); however, these temporal differences did not exclude the possibility that the emotional changes experienced soon after smoking triggered a chain of reactions that eventuated in a relaxation of bronchomotor tone of longer duration than the initiating emotional stimulus. A cause-and-effect relationship between the psychologic and bronchial effects of marijuana is consistent with the common clinical observation that asthmatic attacks can be triggered by emotional factors and by the demonstrated effectiveness of suggestion (13) and behavior therapy (14) in the relief or prevention of bronchospasm. On the other hand, the fact that significant bronchodilatation after 2 per cent marijuana has also been noted in nonasthmatic persons suggests that the dilator effect observed in our asthmatic subjects was probably at least not predominantly of psychogenic origin, because there is no evidence that bronchomotor tone in normal man is influenced significantly by emotional factors. Moreover, although 3 of our subjects who had had no previous exposure to Cannabis experienced a less euphoric "high" than the others there was no difference in the degree of bronchodilatation observed between these persons and those who had smoked marijuana previously, suggesting that the pleasure associated with the "high" was probably not related to the relaxant effect on the airways. Although the mechanism whereby marijuana decreases bronchomotor tone has not been studied in asthmatic patients, previous work in this laboratory in normal subjects suggested that the bronchodilator effect is mediated neither by stimulation of B-adrenergic receptors nor by an atropine-like effect (15). These results make it appear unlikely that in normal persons the bronchodilator effect of marijuana is mediated by its effects on lthe central nervous system, and favor, instead, a direct effect of the drug on bronchial smooth muscle. This may also be true in asthmatic patients. The fact that the smoking of placebo marijuana did not cause a significant decrease in SGaw ;was surprising because the inhalation of particulate matter in the smoke was expected to cause reflex bronchoconstriction by analogy with tobacco cigarette smoking (16), particularly in asthmatic subjects, whose airways are more reactive to nonspecific irritants than those of subjects without airway disease (17). In the present study, the failure of the airways to constrict after smoked placebo might have been due to a balancing out of the constrictor effect of inhaled irritants either by unidentified bronchodilator compounds in marijuana that are not alcohol-extractable, or by a nonspecific placebo bronchodilator response to the expectation of a pleasant experience. In a prior study, it was shown that the airways of normal subjects also did not constrict after the smoking of the placebo preparation but did constrict after cigarette smoking (3). The fact that pulse rate decreased after placebo, in contrast to the significant and expected increase (18) after 2 per cent marijuana (figure 3), suggests a placebo phenomenon rather than a pharmacologic response to a bronchodilator substance in the THC-extracted marijuana preparation. Although the maximal mean change in SGaw after smoking of 2 per cent marijuana (48 per cent) was less than that after inhalation of 1,250 mcg of isoproterenol HCL (69 per cent), the bronchodilator effect of marijuana was more sustained than that of isoproterenol, consistent with the metabolism of delta-9-THC to physiologically active compounds (19), in contrast to the rapid conversion of isoproterenol to inactive metabolites (20). The pharmacologic bronchodilator principal in marijuana might have been expected to produce a fractionally greater bronchodilator effect in subjects with bronchospastic disease compared with healthy subjects by analogy with the greater bronchodilator response to inhaled isoproterenol in asthmatic compared with normal subjects. Our observation that marijuana smoking resulted in a similar, rather than greater, magnitude of bronchdilatation in asthmatic subjects compared with that previously noted in normal persons (3) might possibly have been due to the following reasons. Although an attempt was made to standardize the technique of marijuana smoking, it is possible that the asthmatic subjects delivered less THC to their airways because of relative inexperience with the smoking technique compared with healthy chronic smokers; the bronchial irritant effect of marijuana smoke might have tended to produce more bronchoconstriction in subjects with hyper-reactive airways compared with normal persons, thereby offsetting a potentially greater fractional bronchodilator response to the pharmacologic agent (THC) in marijuana smoke in subjects with bronchospastic disease; because repeated exposure to marijuana is believed to lead to induction of enzymes needed to convert delta-9-THC to the active 11-hydroxy metabolite (19), less extensive metabolism of delta-9-THC to the active form in our asthmatic subjects with relatively little previous marijuana experience might have accounted for a lesser magnitude of physiologic effect than would have resulted had they been chronic users. The maximal average per cent increase in heart rate after marijuana smoking in the present study was only 22 per cent as opposed to the 55 per cent increase previously reported in healthy, experienced subjects smoking the same quantity of THC (3). Possible explanations for this discrepancy in the magnitude of marijuana-induced tachycardia in asthmatic subjects compared with normal subjects include the following reasons: (1) the fact that our asthmatic subjects were relatively inexperienced marijuana smokers might have resulted in reduced delivery of marijuana smoke to the airways and, consequently, reduced systemic absorption of THC; (2) more uneven distribution of marijuana smoke and increased mucus and inflammatory changes in the tracheobronchial tree of asthmatic patients might have resulted in decreased or delayed absorption of THC from the airways; (3) there might have been less conversion of delta-9-THC to the active 11-hydroxy metabolite in our relatively naive asthmatic smokers; (4) there might be basic differences in myocardial tissue responsiveness to THC in asthmatic subjects compared with healthy persons. The small but significant increases in SGaw and decreases in Raw after oral delta-9-THC indicated that this component of natural marijuana has a systemically active bronchodilator effect in asthmatic patients beginning 1 hour and lasting as long as 4 hours after ingestion of the drug; however, this bronchodilator effect was fractionally smaller in magnitude than that previously noted in normal subjects after the same dose of THC (3). Moreover, heart rate did not increase significantly (maximal mean increase, 9 + 5 per cent) after oral administration of 15 mg of delta-9-THC in our asthmatic subjects in contrast with the significant increases (19 + 7 per cent) previously noted in normal subjects (3). These discrepancies in the responses to oral THC of normal experienced Cannabis users and relatively inexperienced asthmatic persons might have been due to differences in absorption of the drug from the gastrointestinal tract, metabolism of THC to the active agent, or tissue responsiveness. With regard to the first 2 possibilities, comparison of plasma concentrations of delta-9-THC and its metabolites after oral administration of the drug in both experienced and naive persons with and without asthma would be of interest. We can conclude that in clinically stable asthmatic subjects with minimal to moderate bronchospasm, both smoked marijuana and oral delta-9-THC resulted in bronchodilatation lasting as long as 2 hours and 4 hours, respectively. Further studies to evaluate the effects of smoked marijuana and oral delta-9-THC on bronchomotor tone during spontaneous or experimentally induced asthmatic attacks would be of interest. Because only the acute effects of marijuana smoking on airway dynamics in subjects with bronchospastic disease were studied, the results did not preclude the possibility of an aggravation of existing bronchial pathology secondary to chronic marijuana smoking in these same persons. Furthermore, the profound psychotropic effect of marijuana and delta-9-THC, in addition to such side effects as tachycardia and the atropine-like drying effect, might severely limit any clinical therapeutic usefulness. Acknowledgment The writers are indebted to Dr. Stephen Szara, National Institutes of Mental Health, for advice in the experimental design of the study; to Dr. Daniel H. Simmons, for help in review of the manuscript; to Mr. Richard N. Bleich, Senior Pharmacist, for assistance in the double-blind aspects of the study, and to Mr. Enoch Lee and Mr. Charles Harper, for their invaluable technical assistance. References 1. Grinspoon, L: Marijuana, Sci. Amer., 1969, 221, 17. 2. Vachon, L., Fitzgerald, M.X., Solliday, N.H., Gould, I.A., and Gaensler, E.A.: Single-dose effect of marijuana smoke. Bronchial dynamics and respiratory-center sensitivity in normal subjects, New Eng. J. Med., 1973, 288, 985. 3. Tashkin, D.P., Shapiro, B.J., and Frank, I.M.: Acute pulmonary physiological effects of smoked marijuana and oral delta-9-tetrahydrocannabinol in healthy young men, New Eng. J. Med., 1973, 289, 336. 4. Waldman, M.M.: Marijuana bronchitis, J.A.M.A., 1970, 211, 501. 5. Chopra, I.C., and Chopra, R.N.: The use of the Cannabis drugs in India, Bull. Narcotics, 1957, 9, 4. 6. American Thoracic Society: Chronic bronchitis, asthma and pulmonary emphysema, A statement on Diagnostic Standards of Nontuberculous Respiratory Diseases, Amer. Rev. Resp. Dis., 1962, 85,762. 7. Ogilvie, C.M., Forster, R.E., Blakemore, W.S., and Morton, J.W.: A standardized breath holding technique for the clinical measurement of the diffusing capacity of the lung for carbon monoxide, J. Clin. Invest., 1957, 36,1. 8. Dubois, A.B., Botelho, S.Y., and Comroe, J.H., Jr.: A new method for measuring airway resistance in many using a body plethysmograph: Values in normal subjects and patients with respiratory disease, J. Clin. Invest., 1956, 35, 327. 9. Dubois, A.B., Botelho, S.Y., Bedell, G.N., Marshall, R., and Comroe, J.H., Jr.: A rapid plethysmographic method for measuring thoracic gas volume, J. Clin. Invest., 1956, 35, 322. 10. Briscoe, W.A., and Dubois, A.B.: Relation between airway resistance, airway conductance and lung volume in subjects of different age and body size, J. Clin. Invest, 1958, 37, 1279. 11. Kory, R.C., Callahan, R., Boren, H.G., and Syner, J.C.: The Veterans Administration-Army cooperative study of pulmonary function. I. Clinical spirometry in normal men, Amer. J. Med., 1961, 30, 243. 12. Cotes, J.E.: Lung Function, F.A. Davis Company, Philadelphia, 1965. 13. Luparello, T., Lyons, H.A., Bleecker, E.R., and McFadden, E.R., Jr.: Influences of suggestionon airway reactivity in asthmatic subjects, Psychosom. Med., 1968, 30, 819. 14. Moore, N.: Behavior therapy in bronchial asthma; a controlled study, J. Psychosom. Res., 1965, 9, 257. 15. Shapiro, B.J., Tashkin, D.p., and Frank, I: Mechanism of increased specific airway conductance with marijuana smoking in healthy young men, Ann. Intern. Med., 1973, 78, 832. 16. Nadel, J.A., Comroe, J.H., Jr.: Acute effects of inhalation of cigarette smoke on airway conductance, J. Appl. Physiol., 1961, 16, 16 713. 17. Devries, K., Booij-Noord, H., Goei, J.T., and orie, N.G.M.: Hyperreactivity of the bronchial tree to drugs, chemical and physical agents, in Bronchitis, N.G.M. Orie and H.G. Sluiter, ed., Royal VanGorcum, Assen, Netherlands, 1964, p. 167. 18. Galanter, M., Wyatt, R.J., Lemberger, L., Weingartner, H., Vaughan, T.B., and Roth, W.T.: Effects on humans of delta-9-tetrahydrocannabinol administered by smoking, Science, 1972, 176, 934. 19. Lemberger, L., Axelrod, J., and Kopin, I.J.: Metabolism and dispostition of delta-9-tetrahydrocannabinol in man, Pharmacol. Rev., 1971, 23, 371. 20. Lyons, H.A., Ayres, S.M., Dworetzky, M., Falliers, C.J., Harris, M.C., Dollery, C.T., and Gandevia, B.: Symposium on isoproterenol therapy in asthma, Ann. Allerg., 1973, 311, 1 source: http://www.ukcia.org...InAsthmatic.php
  2. EDDIEKIRK

    Diabetes

    Diabetes Diabetes is a condition wherein the body either produces inadequate amounts of insulin or fails to utilize available insulin properly. An estimated 1 million Americans suffer from Type 1 diabetes, which develops in childhood. Another 15 million suffer from Type 2 diabetes, also known as adult onset diabetes, which develops later in life. Symptoms generally include an imbalance of blood sugar levels and a high level of sugar excreted through the urine. Initial studies showed that cannabis has no effect on blood sugar levels. A recent test-tube study showed that very high doses of synthetic THC might aggravate diabetes, but that same research also indicates that continued use of cannabis creates a tolerance to the potential aggravation. [ii] No human studies have found that cannabis or synthetic cannabinoids contribute to symptoms of diabetes. At the same time, no human studies have been undertaken to prove or disprove the reports of long-term diabetics who claim that cannabis use causes an immediate lowering of abnormally high blood sugar levels. [iii] Some diabetics also claim that cannabis helps stabilize blood sugar levels and maintain mental stability, or correct mood swings caused by fluctuating blood sugar levels. [iv] Separating the apparent blood sugar response from the anti-anorexic properties of cannabis is currently a matter for further investigation. Diabetics are frequently instructed to refrain from alcohol use because of its high caloric content. Cannabis may provide a psychologically valuable alternative to alcohol in stress reduction, a major factor in managing the potentially life threatening symptoms of diabetes. Hence, cannabis may function in several ways to reduce and stabilize blood sugar levels for patients suffering from diabetes. However, regardless of mounting anecdotal evidence in medical practice, including medical testimony before a district court in California, [v] no scientific papers have been published on the effectiveness of cannabis in treating diabetes. While cannabis has been used as a replacement for insulin, diabetics are strongly advised to continue their physician’s prescribed treatment plan. Maugh, “Inhaled formed of insulin passes first test.” Los Angeles Times/Seattle Times, June 17, 1998 [ii] Hollister, “Health aspects of marijuana.” Pharmacological Review, Vol. 38, No. 1, 1986 [iii] Grinspoon, “Anecdotal surveys on diabetes.” The Forbidden Medicine Website, http://www.rxmarijuana.com [iv] Diabetic reports from Seattle and from the Sonoma Alliance for Medical Marijuana, 1998 [v] “Pot garden’s size brought case to court.” Sonoma Union Democrat (California), March 19, 1998 Drinking Chamomile Tea May Help Fight Complications Of Diabetes ScienceDaily (Sep. 16, 2008) — Drinking chamomile tea daily with meals may help prevent the complications of diabetes, which include loss of vision, nerve damage, and kidney damage, researchers in Japan and the United Kingdom are reporting. -------------------------------------------------------------------------------- The findings could lead to the development of a new chamomile-based drug for type 2 diabetes, which is at epidemic levels in this country and spreading worldwide, they note. Their study appears in the Sept. 10 issue of the ACS' Journal of Agricultural and Food Chemistry, a bi-weekly publication. In the new study, Atsushi Kato and colleagues point out that chamomile, also known as manzanilla, has been used for years as a medicinal cure-all to treat a variety of medical problems including stress, colds, and menstrual cramps. Scientists recently proposed that the herbal tea might also be beneficial for fighting diabetes, but the theory hasn't been scientifically tested until now. To find out, the researchers fed chamomile extract to a group of diabetic rats for 21 days and compared the results to a group of control animals on a normal diet. The chamomile-supplemented animals showed a significant decrease in blood glucose levels compared with the controls, they say. The extract also showed significant inhibition of both ALR2 enzymes and sorbitol, whose elevated levels are associated with increased diabetic complications, the scientists say. source: http://www.sciencedaily.com/releases/2008/...80915164519.htm Non-Psychoactive Cannabinoid Reduces Incidence Of Diabetes, Study Says Non-Psychoactive Cannabinoid Reduces Incidence Of Diabetes, Study Says - NORML Marijuana Compound May Help Stop Diabetic Retinopathy Marijuana Compound May Help Stop Diabetic Retinopathy Anticoagulant Effects of a Cannabis Extract in an Obese Rat Model Anticoagulant effects of a Cannabis extract in an obese rat model. Neuroprotective and Blood-Retinal Barrier-Preserving Effects of Cannabidiol Neuroprotective and Blood-Retinal Barrier-Preserving Effects of Cannabidiol in Experimental Diabetes -- El-Remessy et al. 168 (1): 235 -- American Journal of Pathology The Cannabinergic System as a Target for Anti-inflammatory Therapies http://www.ingentaconnect.com/conten...00013/art00008 Effect of tetrahydrocurcumin on blood glucose, plasma insulin and hepatic key enzymes Unbound MEDLINE | Effect of tetrahydrocurcumin on blood glucose, plasma insulin and hepatic key enzymes in streptozotocin induced diabetic rats. Journal article Cannabidiol reduces the development of diabetes in an animal study IACM-Bulletin Getting Eye On Cannabinoids Getting Eye On Cannabinoids: The Hempire - [cannabis, britain] Marijuana compound could prevent eye damage in diabetics Marijuana compound could prevent eye damage in diabetics: The Hempire - [cannabis, hemp] The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice Diabetes | Evolutionism | Dr. Bob Melamede Cannabidiol arrests onset of autoimmune diabetes in NOD mice CSA: Cannabis Research - Diabetes Cannabidiol attenuates high glucose-induced endothelial cell inflammatory response and barrier disruption Cannabidiol attenuates high glucose-induced endothelial cell inflammatory response and barrier disruption Biological effects of THC and a lipophilic cannabis extract on normal and insulin resistant 3T3-L1 adipocytes Unbound MEDLINE | Biological effects of THC and a lipophilic cannabis extract on normal and insulin resistant 3T3-L1 adipocytes. Journal article Beneficial effects of a Cannabis sativa extract on diabetes induced neuropathy and oxidative stress. Unbound MEDLINE | Beneficial effects of a Cannabis sativa extract treatment on diabetes-induced neuropathy and oxidative stress. Journal article Beneficial effects of a Cannabis sativa extract treatment on diabetes-induced neuropathy and oxidative stress. Unbound MEDLINE | Beneficial effects of a Cannabis sativa extract treatment on diabetes-induced neuropathy and oxidative stress. Journal article Happy reading!
  3. Hey there, Friends! Thought I might start trying to compile a more current list of high CBD strains for patents who are looking to grow or want to know what to look for before they go strain shopping. Cannatonic and Harlequin are fairly well-known, but I am certain there must be others. The lists I have found on the Net are fairly old. The CBD.org site is the best I've fond, but it's a bit clunky and doesn't seem to be updated regularly. I imagine that some of you are tied into what's going on in the world of MMJ breeding and could provide better and/or more up to date info. The more details you can provide about a strain, the better the list will be. Thanks so much for sharing your knowledge.
  4. From the album: EDDIEKIRK

    Potential Therapeutic Uses of medical Cannabis

    © Eddie Kirk

  5. THIS IS THE HIDDEN PICTURE OF THE ZIPPO LIGHTER BRING US THIS LINK AND YOU WIN THE LIGHTER SHOWN AS WELL AS FREE SHIPPING/ (must be a private member to claim prize) Contest won 2-2-2014 by soulreaper Why you should injest cannabis if you have MS, arthritis, epilepsy,spinal cord injury, stroke etc. A doctor told me that those who have immune system disorders (ie. lupus, rheumatoid arthritis) or any disease that affects the brain (neurons) like ALS, alzheimers, parkinsons, epilepsy, etc. should be injesting cannabis...either with tincture, capsules, medibles, edibles etc. Cannabis works over 4 times stronger when injested. You can just juice mature leaves, or cook the leaf/bud mix in with alcohol or fat because it's alcohol/fat soluable. I can't stand the taste, so I prefer capsules! Having said you need to be injesting.....you have to be VERY careful not to overdose. It is not an experience you ever want to repeat. If you are new to injesting, ask those who have had experience with it. Injest only with experienced friends. Some panic and go to the er where they can't do anything for you an experienced person could do. Which is to lie down, try to drink and eat or go to sleep(if you're lucky)!! So what I've learned is to take a drop (if it's tinc you prefer) before bedtime and see how it hits you. If you don't notice it, do 2 drops the next night. Ditto until you find the dose for you. I've had patients that could only take a drop for the first week. Now they are up to a teaspoon 4 times a day! Another thing I learned from the medical marijuana conference is that if you take hemp milk or hemp protein powder or hemp nuts...anything hemp along with your cannabis, they help boost the effects of cannabis. Never seen the stuff you ask!! I've seen it at Fred Meyers, new seasons & whole foods (aka whole paycheck)! Sorry if this is redundant! Happy, safe, effective medicating!
  6. Cannabinoids for Fibromyalgia Syndrome FibroAction has got an article discussing a recent journal article from Fibromyalgia Syndrome (Fibro) expert, Dr Roland Staud MD, and EB Koo, an undergraduate student at the University of Florida, discussing whether cannabinoids are a new treatment option for Fibromyalgia Syndrome. This is in light of the study by Skrabek et al, who carried out what was apparently the first randomized, controlled trial to assess the benefit of nabilone, a synthetic cannabinoid, on pain reduction and quality of life improvement in patients with Fibro. FibroAction is a new organisation, basd in the UK, which aims to make accurate, up-to-date information about Fibromyalgia Syndrome (Fibro) readily available, as well as raise awareness of the condition. My link Cannabinoids for Fibromyalgia Syndrome An article has been e-published ahead of print in the journal Nature Clinical Practice. Rheumatology by Fibromyalgia Syndrome expert, Dr Roland Staud MD, and EB Koo, an undergraduate student at the University of Florida, discussing whether cannabinoids are a new treatment option for Fibromyalgia Syndrome. [1] Dr Staud, author of 'Fibromyalgia for Dummies', is Professor of Medicine at the College of Medicine and Director of the Center for Musculoskeletal Pain Research at the University of Florida. The article discusses cannabinoids as a treatment option for Fibromyalgia Syndrome in light of the study by Skrabek et al, discussed in an article in the February issue of the Journal of Pain. [2] Skrabek et al carried out what was apparently the first randomized, controlled trial to assess the benefit of nabilone, a synthetic cannabinoid, on pain reduction and quality of life improvement in patients with Fibromyalgia Syndrome. [2] The randomized, double-blind, placebo-controlled trial was carried out on 40 patients with Fibromyalgia Syndrome. The primary outcome measure, visual analog scale (VAS) for pain, and the secondary outcome measures, number of tender points, the average tender point pain threshold, and the Fibromyalgia Impact Questionnaire (FIQ), were evaluated at 2 and 4 weeks into the trial and then again after a 4-week washout period. [2] Skrabek et al's trial found that there were significant decreases in the VAS (-2.04, P < .02), FIQ (-12.07, P < .02), and anxiety (-1.67, P < .02) in the nabilone treated group at 4 weeks, and that after the 4-week wash-out period, all benefits were lost, with the nabilone treated group returning to their baseline levels of pain and quality of life. There were no significant improvements in the placebo group. The treatment group experienced more side effects per person at 2 and 4 weeks (1.58, P < .02 and 1.54, P < .05), respectively, and although nabilone was not associated with serious adverse effects, some patients did experience drowsiness, dry mouth, vertigo and ataxia. [2] Skrabek et al said that: "Nabilone appears to be a beneficial, well-tolerated treatment option for fibromyalgia patients, with significant benefits in pain relief and functional improvement. ... As nabilone improved symptoms and was well-tolerated, it may be a useful adjunct for pain management in fibromyalgia." Nabilone, a synthetic cannabinoid, is used to treat chemotherapy-induced nausea and vomiting in patients who do not respond well to other anti-emetics. However, it has also been studied for use in treating cancer pain and neuropathic pain. Cannabinoids are chemicals that are structurally similar to cannabis or THC (the main psychoactive substance found in cannabis), or that bind to cannabinoid receptors. References: Staud R, Koo EB. Are cannabinoids a new treatment option for pain in patients with fibromyalgia? Nat Clin Pract Rheumatol. 2008 Jun 3. [Epub ahead of print]. Skrabek RQ, Galimova L, Ethans K, Perry D. Nabilone for the treatment of pain in fibromyalgia. J Pain. 2008 Feb;9(2):164-73. Epub 2007 Nov 5. Fibromyalgia and Alternative Treatments From acupuncture to chiropractic, from massage to meditation, alternative treatments are in great demand. That's especially true for people with pain-related illnesses such as fibromyalgia. Alternative medicine, including herbal therapy and homeopathy, is a form of "drug-free" doctoring that views the mind and body as a fully integrated system. For people with fibromyalgia, some alternative treatments work well. That's because holistic therapies influence your total being. In that way, they may allow you to reduce your medications and increase your normal activities. Study findings show that standard acupuncture may be effective in treating some people with fibromyalgia. Both biofeedback and electroacupuncture have also been used for relief of fibromyalgia symptoms. However, before you try alternative treatments, talk with your doctor. Check to see what limitations might apply to you. Working with your doctor, you can find an acceptable way to blend conventional medicine with alternative treatments or natural remedies. When you do, you may be able to increase restful sleep and reduce your fibromyalgia pain. Can acupuncture treat fibromyalgia? With acupuncture, a practitioner inserts one or more dry needles into the skin and underlying tissues at specific points. Gently twisting or otherwise manipulating the needles causes a measurable release of endorphins into the bloodstream. Endorphins are the body's natural opioids. In addition, according to acupuncture practitioners, energy blocks are removed. Removing them is said to restore the flow of energy along the meridians, which are specific energy channels. Studies show that acupuncture may alter brain chemistry. It appears to do this by changing the release of neurotransmitters. These neurotransmitters stimulate or inhibit nerve impulses in the brain that relay information about external stimuli and sensations such as pain. In this way, the patient's pain tolerance is increased. One acupuncture treatment in some patients may last weeks to help alleviate chronic pain. What is electroacupuncture? Electroacupuncture is another way of stimulating the acupuncture points. It uses a needle hooked up to small wires connected to very slight electrical currents. Heat - moxibustion -- and massage - acupressure -- can also be used during this electroacupuncture process. Laser acupuncture is yet another offshoot of this alternative therapy. It may occasionally be effective for the treatment of carpal tunnel syndrome. While it uses the same points, there are no needles involved. There are precautions to take if you want to try acupuncture. First, make sure you find a licensed acupuncturist who has a lot of experience. Also, make sure the acupuncturist uses only disposable needles. There are multiple styles of acupuncture. The style used depends on where the practitioner studied. For instance, Chinese acupuncture depends on larger bore needles and the practitioner may be more aggressive with moving them. Japanese acupuncture uses thinner bore needles with a relatively gentle approach. You'll need to find the style that suits your fibromyalgia needs. My link Marijuana Ingredient May Cut Fibromyalgia Pain Preliminary Study Shows Less Pain, Better Quality of Life in Fibromyalgia Patients Taking Nabilone By Miranda Hitti WebMD Health NewsReviewed by Brunilda Nazario, MDFeb. 19, 2008 -- Nabilone, a pain drug based on marijuana's active ingredient, may ease fibromyalgia pain. So say Canadian researchers, based on a preliminary, short-term study. The study included 40 fibromyalgia patients. First, they did three things: Rate the intensity of their fibromyalgia pain. The rating scale ranged from 0 (no pain) to 10 (the worst pain imaginable). Their average rating was about 6. Rate their quality of life. The rating scale ranged from 0 to 100, with higher scores indicating worse quality of life. Their average rating was 66. Get a check of their tender points -- parts of the body that are often sensitive in fibromyalgia patients. The researchers then split the patients into two groups. For a month, one group of patients took nabilone daily. The other group took a placebo pill. The patients didn't know which pill they were taking. After a month of nabilone treatment, fibromyalgia pain was less intense and quality of life had improved. No such changes were seen with the placebo. Nabilone treatment didn't affect the patients' number of tender points. And it didn't cure fibromyalgia pain -- when patients stopped taking nabilone, their fibromyalgia pain returned to its former intensity. Nabilone was well tolerated, but side effects were more commonly reported in the nabilone group. Those side effects -- which included drowsiness, dry mouth, vertigo, and movement problems -- were "generally mild," write the researchers. Longer studies are needed to track the long-term effects, note the University of Manitoba's Ryan Quinlan Skrabek, MD, and colleagues. Their study appears in the February edition of The Journal of Pain. source: http://www.webmd.com/fibromyalgia/news/200...?src=RSS_PUBLIC Pot Drug May Cut Fibromyalgia Pain Preliminary Study Shows Less Pain, Better Quality of Life in Fibromyalgia Patients Taking Nabilone By Miranda Hitti WebMD Health News Reviewed By Brunilda Nazario, MD Feb. 19, 2008 -- Nabilone, a pain drug based on marijuana's active ingredient, may ease fibromyalgia pain. So say Canadian researchers, based on a preliminary, short-term study. The study included 40 fibromyalgia patients. First, they did three things: Rate the intensity of their fibromyalgia pain. The rating scale ranged from 0 (no pain) to 10 (the worst pain imaginable). Their average rating was about 6. Rate their quality of life. The rating scale ranged from 0 to 100, with higher scores indicating worse quality of life. Their average rating was 66. Get a check of their tender points -- parts of the body that are often sensitive in fibromyalgia patients. The researchers then split the patients into two groups. For a month, one group of patients took nabilone daily. The other group took a placebo pill. The patients didn't know which pill they were taking. After a month of nabilone treatment, fibromyalgia pain was less intense and quality of life had improved. No such changes were seen with the placebo. Nabilone treatment didn't affect the patients' number of tender points. And it didn't cure fibromyalgia pain -- when patients stopped taking nabilone, their fibromyalgia pain returned to its former intensity. Nabilone was well tolerated, but side effects were more commonly reported in the nabilone group. Those side effects -- which included drowsiness, dry mouth, vertigo, and movement problems -- were "generally mild," write the researchers. Longer studies are needed to track the long-term effects, note the University of Manitoba's Ryan Quinlan Skrabek, MD, and colleagues. Their study appears in the February edition of The Journal of Pain. SOURCES: Skrabek, R. The Journal of Pain, February 2008; vol 9: pp 164-173. © 2008 WebMD Inc. All rights reserved. source: http://www.rxlist.co...rticlekey=87306 Clinical endocannabinoid deficiency (CECD): can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? Russo EB. Source GW Pharmaceuticals, 2235 Wylie Avenue, Missoula, MT 59802, USA. erusso@montanadsl.net Abstract OBJECTIVES: This study examines the concept of clinical endocannabinoid deficiency (CECD), and the prospect that it could underlie the pathophysiology of migraine, fibromyalgia, irritable bowel syndrome, and other functional conditions alleviated by clinical cannabis. METHODS: Available literature was reviewed, and literature searches pursued via the National Library of Medicine database and other resources. RESULTS: Migraine has numerous relationships to endocannabinoid function. Anandamide (AEA) potentiates 5-HT1A and inhibits 5-HT2A receptors supporting therapeutic efficacy in acute and preventive migraine treatment. Cannabinoids also demonstrate dopamine-blocking and anti-inflammatory effects. AEA is tonically active in the periaqueductal gray matter, a migraine generator. THC modulates glutamatergic neurotransmission via NMDA receptors. Fibromyalgia is now conceived as a central sensitization state with secondary hyperalgesia. Cannabinoids have similarly demonstrated the ability to block spinal, peripheral and gastrointestinal mechanisms that promote pain in headache, fibromyalgia, IBS and related disorders. The past and potential clinical utility of cannabis-based medicines in their treatment is discussed, as are further suggestions for experimental investigation of CECD via CSF examination and neuro-imaging. CONCLUSION: Migraine, fibromyalgia, IBS and related conditions display common clinical, biochemical and pathophysiological patterns that suggest an underlying clinical endocannabinoid deficiency that may be suitably treated with cannabinoid medicines. Republished from Neuro Endocrinol Lett. 2004 Feb-Apr;25(1-2):31-9. Fibromyalgia (FM) is a chronic pain syndrome of unknown etiology. The disease is characterized by widespread musculoskeletal pain, fatigue and multiple tender points in the neck, spine, shoulders and hips. An estimated 3 to 6 million Americans are afflicted by fibromyalgia, which is often poorly controlled by standard pain medications. Fibromyalgia patients frequently self-report using cannabis therapeutically to treat symptoms of the disease,[1-2] and physicians – in instances where it is legal for them do so – often recommend the use of cannabis to treat musculoskeletal disorders.[3-4] To date however, there are few clinical trials assessing the use of cannabinoids to treat the disease. Previous clinical and preclinical trials have shown that both naturally occurring and endogenous cannabinoids hold analgesic qualities,[9-12] particularly in the treatment of pain resistant to conventional pain therapies. (Please see the 'Chronic Pain' section of this book for further details.) As a result, some experts have suggested that cannabinoids are potentially applicable for the treatment of chronic pain conditions such as fibromyalgia,[13] and have theorized that the disease may be associated with an underlying clinical deficiency of the endocannabinoid system.[14] REFERENCES [1] Swift et al. 2005. Survey of Australians using cannabis for medical purposes. Harm Reduction Journal 4: 2-18. [2] Ware et al. 2005. The medicinal use of cannabis in the UK: results of a nationwide survey. International Journal of Clinical Practice 59: 291-295. [3] Dale Gieringer. 2001. Medical use of cannabis: experience in California. In: Grotenhermen and Russo (Eds). Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. New York: Haworth Press: 153-170. [4] Gorter et al. 2005. Medical use of cannabis in the Netherlands. Neurology 64: 917-919. [5] Schley et al. 2006. Delta-9-THC based monotherapy in fibromyalgia patients on experimentally induced pain, axon reflex flare, and pain relief. Current Medical Research and Opinion 22: 1269-1276. [6] Skrabek et al. 2008. Nabilone for the treatment of pain in fibromyalgia. The Journal of Pain 9: 164-173. <a href="http://norml.org/library/item/fibromyalgia#b7">[7] Ware et al. 2010. The effects of nabilone on sleep in fibromyalgia: results of a randomized controlled trial. Anesthesia and Analgesia 110: 604-610. [8] Fiz et al. 2011. Cannabis use in patients with fibromyalgia: Effect on symptoms relief and health-related quality of life. PLoS One 6. [9] Burns and Ineck. 2006. Cannabinoid analgesia as a potential new therapeutic option in the treatment of chronic pain. The Annals of Pharmacotherapy 40: 251-260. [10] David Secko. 2005. Analgesia through endogenous cannabinoids. CMAJ 173. [11] Wallace et al. 2007. Dose-dependent effects of smoked cannabis on capsaicin-induced pain and hyperalgesia in healthy volunteers. Anesthesiology 107:785-96. [12] Cox et al. 2007. Synergy between delta9-tetrahydrocannabinol and morphine in the arthritic rat. European Journal of Pharmacology 567: 125-130. [13] Lynch and Campbell. 2011. op. cit. [14] Ethan Russo. 2004. Clinical endocannabinoid deficiency (CECD): Can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? Neuroendocrinology Letters 25: 31-39. My link
  7. A preliminary controlled study to determine whether whole plant cannabis extracts can improve ... Investigating abnormal protein is already promi- nent in neuroscientific research for neurodegenerative conditions (eg CJD, and Huntington's disease) PDF download Nabilone Could Treat Chorea and Irritability in Huntington’s Disease Adrienne Curtis, B.A., B.Sc. and Hugh Rickards, M.D., M.R.C.Psych., Department of Psychiatry, University of Birmingham, Birmingham, United Kingdom SIR: Huntington’s disease causes chorea and psychiatric abnormalities. Psychiatric symptoms were found in one study in 51 out of 52 patients.1 Dysphoria, agitation, irritability, apathy, and anxiety were found in above 50% of the patients sampled. Many sources postulate that cannabinoids could have a beneficial effect on the symptoms of Huntington’s disease, especially on choreatic movements.2–4 As well as providing possible symptomatic relief in Huntington’s disease, there is also some evidence5 that cannabinoids might have a neuroprotective effect which could delay the onset of symptoms by delaying or preventing the death of striatal neurons. This neuroprotective effect has also been postulated by other sources.6–8 To date there are only two reports on the use of cannabinoids in Huntington’s disease in the literature. Cannabidiol, a nonpsychotropic cannabinoid, had no effect on chorea severity in 15 patients.9 In one single patient, single dose, uncontrolled open clinical trial using nabilone, 1.5mg, the chorea increased significantly.10 We present a case of a female patient with irritability, which improved after the introduction of cannabis. This improvement was maintained by treatment with nabilone. Case Report The patient was a 43-year-old female who died in December 2003. She developed symptoms of Huntington’s disease at the age of 24 and her husband gave up paid employment to care for her in 1990 when she was 30 years old. In 1995, he reported difficulties in caring for his wife. These difficulties were related to personality changes due to her illness. She increasingly resisted help from professionals, especially care assistants, and refused any suggestion of short-term respite care. She became disinhibited and frequently undressed herself and walked around naked inside and occasionally outside the house. She exhibited a number of dangerous behaviors, such as leaving taps running and fires burning, and leaving burning cigarettes around. Her husband became concerned about the effect that the care for his chronically ill wife was having on his son, who was born in 1984. The patient went into residential care in 1996. The patient’s husband visited two or three times every week and he always took his wife out for a trip. These trips were difficult because of the patient’s refusal to be strapped into the car or her wheelchair, which sometimes resulted in falls caused by violent choreic movements when he was unable to physically hold her in the chair because he was using his hands for some other purpose. In 2001, he began to give his wife cannabis to smoke when he took her out on these regular trips. When he returned his wife to the nursing home after these visits the staff were aware of a significant difference in the patient. The cannabis appeared to improve her mood and she was calmer and more relaxed. Prior to the introduction of cannabis she was extremely impatient and would get angry if required to wait even a few minutes for a cigarette. After taking cannabis, she was able to wait a while without screaming and throwing things. The patient also willingly accepted the use of a car seat belt and wheelchair harness. In December 2001, the local general practitioner prescribed a regimen of nabilone, a synthetic 9-keto cannabinoid, which the patient began taking, 1mg each day. The husband and the nursing home staff both reported improvements in behavior and reduction of chorea coinciding with the introduction of cannabis and maintained by daily taking nabilone. Comment This report has many limitations. It is a single case report and no measurements were taken at the time of the introduction of cannabis and nabilone. The information was obtained by interviewing the husband and staff from the care home in 2005. The symptoms of Huntington’s disease do change over time and the movements are different in the later stages of the disease. However both the husband and the staff are sure that the introduction of cannabis was beneficial and greatly improved the patient’s quality of life in her last years. There is need for further trials to establish the therapeutic use of cannabinoids in the symptomatic treatment of Huntington’s disease. ACKNOWLEDGMENTS The first author receives an unrestricted educational grant from Cambridge Laboratories, which holds the European marketing rights for nabilone. REFERENCES 1. Paulsen JS, Ready RE, Hamilton JM, et al: Neuropsychiatric aspects of Huntington’s disease. J Neurol Neurosurg Psychiatry 2001; 71:310–314[Abstract/Free Full Text] 2. Consroe P: Brain cannabinoid systems as targets for the therapy of neurological disorders. Neurobiol Dis 1998; 5:534–551[CrossRef][Medline] 3. Craufurd D, Thompson JC, Snowden JS: Behavioral changes in Huntington disease. Neuropsychiatry Neuropsychol Behav Neurol 2001; 14:219–226[Medline] 4. Goutopoulos A, Makriyannis A: From cannabis to cannabinergics: new therapeutic opportunities. Pharmacol Therapeutics 2002; 95:103–117[CrossRef][Medline] 5. Aiken CT, Tobin AJ, Schweitzer ES: A cell-based screen for drugs to treat Huntington’s disease. Neurobiol Dis 2004; 16:546–555[CrossRef][Medline] 6. Baker D, Pryce G: The therapeutic potential of cannabis in multiple sclerosis. Expert Opin Investig Drugs 2003; 12:561–567[CrossRef][Medline] 7. Croxford JL, Miller SD: Towards cannabis and cannabinoid treatment of multiple sclerosis. Drugs Today 2004; 40:663–676[CrossRef][Medline] 8. Russo E: Future of cannabis and cannabinoids in therapeutics. J Cannabis Therapeutics 2003; 3:163–174 9. Consroe P, Laguna J, Allender J, et al: Controlled clinical trial of cannabidiol in Huntington’s disease. Pharmacol Biochem Behav 1991; 40:701–708[CrossRef][Medline] 10. Muller-Vahl KR, Schneider U, Emrich HMl: Nabilone increases choreatic movements in Huntington’s disease. Mov Disord 1999; 14:1038–1040[CrossRef][Medline] My link Longitudinal Evaluation of Neuropsychiatric Symptoms in Huntington's Disease Jennifer C. Thompson, Ph.D., Jenny Harris, B.Sc., Andrea C. Sollom, M.A., Cheryl L. Stopford, Ph.D., Elizabeth Howard, MBChB, Julie S. Snowden, Ph.D., David Craufurd, M.Sc. The Journal of Neuropsychiatry and Clinical Neurosciences, Jan 2012; 24 (1); 53-60. doi: 10.1176/appi.neuropsych.11030057 /Images/icons/at05_pdf.png PDF EFFECTS OF CANNABIDIOL IN HUNTINGTON'S DISEASE Neurology 36 (Suppl 1) April 1986 p. 342 Reuven Sandyk, Paul Consroe, Lawrence Z. Stern, and Stuart R. Snider, Tucson, AZ Cannabidiol (CBD) is a major nonpsychoactive cannabinoid of marijuana. Based on reports indicating possible efficacy of CBD in dystonic movements (Neurology 1984; 34 [suppl 1]: 147 and 1985; 35 [suppl 1]: 201), we tried CBD in three patients with Huntington's disease (HD). The patients;, aged 30 to 56, had HD of 7 to 12 years' duration. Their condition has been slowly progressive and unresponsive to prior therapy with neuroleptics. Orally administered CBD was initiated at 300 mg/d and increased 1 week later to 600 mg/d for the next 3 weeks. Mild improvement ( 5 to 15%) in the choreic movements was documented using the tongueprotrusion test (Neurology [Minneap} 1972; 22: 929-33) and a chorea severity evaluation scale (Br J Clin Pharmacol 1981; 11: 129-51) after the first week. Further improvement (20 to 40%) was noticed after the second week of CBD, and this remained stable for the following 2 weeks. Except for transient, mild hypotension, no side effects were recorded, and laboratory tests were normal. Withdrawal of CBD after 48 hours resulted in return of choreic movements to the pre-CBD state. (Supported in part by NINCDS grant #NS15441) source: http://www.druglibrary.org/ Huntington’s disease (HD) is a neurodegenerative autosomal dominant disorder that usually presents in the midlife and is ultimately fatal. The genetic defect affects the IT15 gene located in the short arm of chromosome 4 and that encodes a protein called huntingtin (The Huntington’s Disease Collaborative Group, 1993). The mutation consists of an enlarged repeat of CAG triplets in the 5' coding region, that result in an abnormal polyglutamine tract in the amino-terminal portion of this protein (reviewed by Cattaneo et al., 2005). Normal gene contains between 6 and 35 repeats. Incomplete penetrance was seen for repeats between 36 and 39, whereas the pathology develops with a number of repeats higher than 40 (Landes and Bates, 2004). Mutated huntingtin becomes toxic preferentially for striatal medium-spiny neurons that project to the globus pallidus and the substantia nigra. This produces a progressive degeneration of the striatum that results in a biphasic pattern of motor abnormalities that evolves from an early hyperkinetic phase (choreic movements) to a late akinetic and more disabling phase (reviewed by Walker, 2007). The disease also presents cortical degeneration which originates cognitive dysfuntion and psychiatric symptoms, which are more evident at advanced phases. Despite the fact that the mutated gene responsible for HD has been already identified, the precise molecular and cellular mechanisms underlying striatal degeneration are still unknown and, consequently, the therapeutic outcome for HD patients is still too poor. Several types of compounds are presently under clinical evaluation, including minocycline, coenzyme Q10, unsaturated fatty acids and inhibitors of histone deacetylases (reviewed by Stack and Ferrante, 2007), and a great promise has been concentrated with the case of cannabinoid-based compounds, which have been reported to alleviate motor abnormalities and/or to serve as potential neuroprotective molecules (reviewed by Sagredo et al., 2007). Cannabinoid-based compounds are a large series of compounds able to target different elements of the so-called cannabinoid system, an intercellular signaling system active in the brain and also in the periphery (reviewed by Mackie and Stella, 2006). This includes selective agonists or antagonists for the CB1 or CB2 receptors, and also for other related receptor types (e.g. TRPV1 receptors), non-selective agonists, and inhibitors of the endocannabinoid generation or inactivation (reviewed by Fowler, 2007). Some of these compounds have been recently examined in animal or cellular models of HD and, although the matter is still far to be completely elucidated, some results have provided promising expectatives for a clinical evaluation in patients (reviewed by Sagredo et al., 2007). Thus, several studies have demonstrated that the loss of CB1 receptor-mediated signaling observed in the basal ganglia of HD patients and animal models (Maccarrone et al., 2007) is a very early event that takes place before the appearance of major neuropathological signs and functional abnormalities, and that it is susceptible of pharmacological correction (Sagredo et al., 2007). In parallel to this progressive decrease experienced by CB1 receptors during the course of this disease, CB2 receptors, whose presence in the healthy striatum is relatively modest, are, however, markedly up-regulated in reactive microglial cells in response to the striatal damage, thus representing a novel target to reduce the toxic influence of these cells on neuronal homeostasis (Fernández-Ruiz et al., 2007). These two observations have served as a basis to explore, at the preclinical level, the potential of both cannabinoid receptor types, and also of other elements of this signaling system in HD. For example, CB1 receptor agonists and inhibitors of the endocannabinoid inactivation have been examined for their possible antihyperkinetic effect, presumably exerted through acutely recovering the neurochemical deficits typical of first grades of this disorder (reviewed by Lastres-Becker et al., 2003). This potential, however, seems to be restricted to certain cannabinoids that combine the capability to enhance the cannabinoid signaling and also to activate TRPV1 receptors (reviewed by Fernández-Ruiz and González, 2005). In addition, cannabinoid agonists can also serve as neuroprotective agents in HD being capable to delay the progression of the striatal degeneration in different experimental models of this disease (reviewed by Sagredo et al., 2007). The neuroprotective effect of cannabinoids would be exerted through three key mechanisms: (i) their capability to normalize glutamate homeostasis, an effect mediated by CB1 receptors, that would allow to reduce excitotoxic events that occur in this pathology (reviewed by Sagredo et al., 2007); (ii) the antioxidant potential of certain cannabinoids, that would be exerted through cannabinoid receptor-independent mechanisms and that would allow to reduce the oxidative injury that also takes place in HD (reviewed by Sagredo et al., 2007); and (iii) their activity at the CB2 receptors to control the microglial influence on neuronal survival, thus reducing the local inflammatory events that are associated with the striatal degeneration (reviewed by Fernández-Ruiz et al., 2007). My link What is Huntington's Disease? http://www.youtube.com/watch?v=4HgFUvVyHYQ Huntington's disease could be helped through new developments in Scotland involving the medicinal properties of cannabis. The team of experts at the University of Aberdeen discovered that a naturally-occurring molecule in marijuana - cannabidiol - does not provide the high associated with tetrahydrocannabinol (THC) and as such could be used as an "acceptable drug treatment". It is believed that many strains of production cannabis are aimed at ramping up the THC content at the expense of cannabidiol, meaning that smoking marijuana could, if anything, exacerbate the problems associated with Huntington's disease and multiple sclerosis. Dr Bettina Platt, commenting on the findings, said: "We are hoping that our findings can instruct the development of cannabidiol-based treatments for disorders related to mitochondrial dysfunction such as Parkinson's disease or Huntington's disease." Earlier this month, the NHS reported findings from research in the US published in journal Cancer which linked testicular cancer to the use of cannabis by young males. My link Chemical in Cannabis Helps Cells Grow Last Updated (Friday, 01 May 2009 14:56) Written by InfoWeb The fact that cannabis is forbidden in most countries is only a recent event. In the past, starting centuries ago, people always smoked pot for various reasons, including leisure, resting purposes, going into trance, or for medicinal use. In Western societies, it has been mostly forbidden, even though not all of its effects have been fully understood up to this point. This is evidenced by the fact that only recently have researchers managed to identify a substance in cannabis that actually promotes cell growth and helps our bodies function properly. Out of the 60+ active substances that can be found in the average cannabis or marijuana strain, science has only been able to analyze and assess the threat levels of just a few until now. Yet, there are strict laws in place in every country that forbid the use of the plant, even though you can, for instance, buy flamethrowers in the US, as they pose no danger to anyone. A team of researchers from the University of Aberdeen describes the roles and functions of cannabidiol, a molecule that is naturally synthesized in the cannabis plant, publishing its finds in the Journal of Neuroscience. It appears that this substance, also known as CBD, has great potential to relieve pain, even though it's not the substance that gives pot its “high” label. Even though physicians have known for quite a long time that the compound can make pains felt by multiple sclerosis patients more bearable, they have never focused on harnessing this power to do good. Now, UA School of Medical Sciences researcher Dr Bettina Platt, has found out that CBD doesn't actually act on the peripheral nervous system, like other drugs do, but on the brain cells, or neurons themselves, influencing the activity of mitochondria, which are a sort of mini power plants for the cells. Understandably, influencing such an important cellular component into producing more energy is not a bad thing, yet the plant remains illegal because some believe that the other components may indeed be dangerous. However, no one takes the time to actually check them one by one. “We are hoping that our findings can instruct the development of cannabidiol based treatments for disorders related to mitochondrial dysfunction such as Parkinson's disease or Huntington's disease. There are different strains of cannabis out there and many no longer contain cannabidiol. In fact, these have been deliberately bred out to enhance the THC content,” Platt says, while drawing attention to the fact that smoking cannabis will not necessarily cure these conditions. In turn, she advocates the extraction of CBD from plants for scientific reasons. It could then be used to synthesize various drugs, which, with some luck, could offer much-needed pain relief for people suffering from some of the worse medical conditions known to man. source: GOOGLE WIKIPEDIA
  8. Study: Cannabinoid Reduces Breast Cancer Cell Aggression Saturday, November 24 2007 @ 12:31 AM EST Edited by: Michael Hess Cannabidiol may be helpful in reducing the aggressiveness of breast cancer cells BBSNews 2007-11-24 -- (IACM) In a mouse model of metastatic breast cancer the natural non- psychotropic cannabinoid cannabidiol (CBD) reduced the aggressiveness of breast cancer cells. CBD inhibited a protein called Id-1. Id proteins play an important role in tumour cell biology. The researchers of the California Pacific Medical Center Research Institute concluded that "CBD represents the first nontoxic exogenous agent that can significantly decrease Id- 1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness." The authors stressed that they were not suggesting patients smoke cannabis. They added that it would be highly unlikely that effective concentrations of CBD could be reached by smoking cannabis. Lead researcher Dr. Sean McAllister said: "Right now we have a limited range of options in treating aggressive forms of cancer. Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients. This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects." (Sources: BBC News of 19 November 2007; McAllister SD, Christian RT, Horowitz MP, Garcia A, Desprez PY. Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells. Mol Cancer Ther 2007;6(11):2921-7.) source: http://bbsnews.net/a...071124003153693 The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation Luciano De Petrocellis*,†, Dominique Melck*,‡, Antonella Palmisano§, Tiziana Bisogno‡, Chiara Laezza¶, Maurizio Bifulco¶, and Vincenzo Di Marzo‡,‖ +Author Affiliations †Istituto di Cibernetica and ‡Istituto per la Chimica di Molecole di Interesse Biologico (affiliated with the National Institute for the Chemistry of Biological Systems, Consiglio Nazionale delle Ricerche), Consiglio Nazionale delle Ricerche, Via Toiano 6, 80072 Arco Felice, Naples, Italy; § Istituto di Ricerche sull’Adattamento dei Bovini e dei Bufali all’Ambiente del Mezzogiorno, Consiglio Nazionale delle Ricerche, Ponticelli, 80147 Naples, Italy; and ¶Centro di Studio der l’Endocrinologia e l’Oncologia Sperimentale, Consiglio Nazionale Delle Richerche and Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli ‘Federico II,’ 80131 Naples, Italy Communicated by Rita Levi-Montalcini, Institute of Neurobiology, Consiglio Nazionale delle Ricerche, Rome, Italy (received for review March 6, 1998) Abstract Anandamide was the first brain metabolite shown to act as a ligand of “central” CB1 cannabinoid receptors. Here we report that the endogenous cannabinoid potently and selectively inhibits the proliferation of human breast cancer cells in vitro. Anandamide dose-dependently inhibited the proliferation of MCF-7 and EFM-19 cells with IC50 values between 0.5 and 1.5 μM and 83–92% maximal inhibition at 5–10 μM. The proliferation of several other nonmammary tumoral cell lines was not affected by 10 μM anandamide. The anti-proliferative effect of anandamide was not due to toxicity or to apoptosis of cells but was accompanied by a reduction of cells in the S phase of the cell cycle. A stable analogue of anandamide ®-methanandamide, another endogenous cannabinoid, 2-arachidonoylglycerol, and the synthetic cannabinoid HU-210 also inhibited EFM-19 cell proliferation, whereas arachidonic acid was much less effective. These cannabimimetic substances displaced the binding of the selective cannabinoid agonist [3H]CP 55,940 to EFM-19 membranes with an order of potency identical to that observed for the inhibition of EFM-19 cell proliferation. Moreover, anandamide cytostatic effect was inhibited by the selective CB1 receptor antagonist SR 141716A. Cell proliferation was arrested by a prolactin mAb and enhanced by exogenous human prolactin, whose mitogenic action was reverted by very low (0.1–0.5 μM) doses of anandamide. Anandamide suppressed the levels of the long form of the prolactin receptor in both EFM-19 and MCF-7 cells, as well as a typical prolactin-induced response, i.e., the expression of the breast cancer cell susceptibility gene brca1. These data suggest that anandamide blocks human breast cancer cell proliferation through CB1-like receptor-mediated inhibition of endogenous prolactin action at the level of prolactin receptor. source: http://www.pnas.org/...4/8375.abstract Suppression of Nerve Growth Factor Trk Receptors and Prolactin Receptors by Endocannabinoids Leads to Inhibition of Human Breast and Prostate Cancer Cell Proliferation1 Dominique Melck, Luciano De Petrocellis, Pierangelo Orlando, Tiziana Bisogno, Chiara Laezza, Maurizio Bifulco and Vincenzo Di Marzo Istituto per la Chimica di Molecole di Interesse Biologico (D.M., T.B., V.D.M.), Istituto di Cibernetica (L.D.P.), and Istituto di Biochimica delle Proteine ed Enzimologia (P.O.), Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA); and Centro di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, and Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli Federico II (C.L., M.B.), 80131 Naples, Italy Address all correspondence and requests for reprints to: Dr. Vincenzo Di Marzo, Istituto per la Chimica di Molecole di Interesse Biologico, Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA), Italy. E-mail: vdm@trinc.icmib.na.cnr.it. Anandamide and 2-arachidonoylglycerol (2-AG), two endogenous ligands of the CB1 and CB2 cannabinoid receptor subtypes, inhibit the proliferation of PRL-responsive human breast cancer cells (HBCCs) through down-regulation of the long form of the PRL receptor (PRLr). Here we report that 1) anandamide and 2-AG inhibit the nerve growth factor (NGF)-induced proliferation of HBCCs through suppression of the levels of NGF Trk receptors; 2) inhibition of PRLr levels results in inhibition of the proliferation of other PRL-responsive cells, the prostate cancer DU-145 cell line; and 3) CB1-like cannabinoid receptors are expressed in HBCCs and DU-145 cells and mediate the inhibition of cell proliferation and Trk/PRLr expression. ß-NGF-induced HBCC proliferation was potently inhibited (IC50 = 50–600 nM) by the synthetic cannabinoid HU-210, 2-AG, anandamide, and its metabolically stable analogs, but not by the anandamide congener, palmitoylethanolamide, or the selective agonist of CB2 cannabinoid receptors, BML-190. The effect of anandamide was blocked by the CB1 receptor antagonist, SR141716A, but not by the CB2 receptor antagonist, SR144528. Anandamide and HU-210 exerted a strong inhibition of the levels of NGF Trk receptors as detected by Western immunoblotting; this effect was reversed by SR141716A. When induced by exogenous PRL, the proliferation of prostate DU-145 cells was potently inhibited (IC50 = 100–300 nM) by anandamide, 2-AG, and HU-210. Anandamide also down-regulated the levels of PRLr in DU-145 cells. SR141716A attenuated these two effects of anandamide. HBCCs and DU-145 cells were shown to contain 1) transcripts for CB1 and, to a lesser extent, CB2 cannabinoid receptors, 2) specific binding sites for [3H]SR141716A that could be displaced by anandamide, and 3) a CB1 receptor-immunoreactive protein. These findings suggest that endogenous cannabinoids and CB1 receptor agonists are potential negative effectors of PRL- and NGF-induced biological responses, at least in some cancer cells. source: http://endo.endojour...tract/141/1/118 CHEMOTHERAPY, ANTIBIOTICS, AND GENE THERAPY Antitumor Activity of Plant Cannabinoids with Emphasis on the Effect of Cannabidiol on Human Breast Carcinoma Alessia Ligresti, Aniello Schiano Moriello, Katarzyna Starowicz, Isabel Matias, Simona Pisanti, Luciano De Petrocellis, Chiara Laezza, Giuseppe Portella, Maurizio Bifulco, and Vincenzo Di Marzo Endocannabinoid Research Group, Istituto di Chimica Biomolecolare (A.L., A.S.M., K.S., I.M., V.D.M.), and Istituto di Cibernetica (A.S.M., L.D.P.), Consiglio Nazionale delle Ricerche Pozzuoli, Italy; Dipartimento di Biologia e Patologia Cellulare e Molecolare "L. Califano", Università di Napoli "Federico II", Napoli, Italy (S.P., C.L., G.P., M.B.); and Dipartimento di Scienze Farmaceutiche, Università degli Studi di Salerno, Fisciano, Italy (S.P., M.B.) 9-Tetrahydrocannabinol (THC) exhibits antitumor effects on various cancer cell types, but its use in chemotherapy is limited by its psychotropic activity. We investigated the antitumor activities of other plant cannabinoids, i.e., cannabidiol, cannabigerol, cannabichromene, cannabidiol acid and THC acid, and assessed whether there is any advantage in using Cannabis extracts (enriched in either cannabidiol or THC) over pure cannabinoids. Results obtained in a panel of tumor cell lines clearly indicate that, of the five natural compounds tested, cannabidiol is the most potent inhibitor of cancer cell growth (IC50 between 6.0 and 10.6 µM), with significantly lower potency in noncancer cells. The cannabidiol-rich extract was equipotent to cannabidiol, whereas cannabigerol and cannabichromene followed in the rank of potency. Both cannabidiol and the cannabidiol-rich extract inhibited the growth of xenograft tumors obtained by s.c. injection into athymic mice of human MDA-MB-231 breast carcinoma or rat v-K-ras-transformed thyroid epithelial cells and reduced lung metastases deriving from intrapaw injection of MDA-MB-231 cells. Judging from several experiments on its possible cellular and molecular mechanisms of action, we propose that cannabidiol lacks a unique mode of action in the cell lines investigated. At least for MDA-MB-231 cells, however, our experiments indicate that cannabidiol effect is due to its capability of inducing apoptosis via: direct or indirect activation of cannabinoid CB2 and vanilloid transient receptor potential vanilloid type-1 receptors and cannabinoid/vanilloid receptor-independent elevation of intracellular Ca2+ and reactive oxygen species. Our data support the further testing of cannabidiol and cannabidiol-rich extracts for the potential treatment of cancer source: http://jpet.aspetjou...ract/318/3/1375 9-Tetrahydrocannabinol Inhibits Cell Cycle Progression in Human Breast Cancer Cells through Cdc2 Regulation María M. Caffarel1, David Sarrió2, José Palacios2, Manuel Guzmán1 and Cristina Sánchez1 1 Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University and 2 Breast and Gynecological Cancer Group, Molecular Pathology Programme, Centro Nacional de Investigaciones Oncológicas, Madrid, Spain Requests for reprints: Cristina Sánchez, Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain. Phone: 34-913944668; Fax: 34-913944672; E-mail: csg@bbm1.ucm.es. It has been proposed that cannabinoids are involved in the control of cell fate. Thus, these compounds can modulate proliferation, differentiation, and survival in different manners depending on the cell type and its physiopathologic context. However, little is known about the effect of cannabinoids on the cell cycle, the main process controlling cell fate. Here, we show that 9-tetrahydrocannabinol (THC), through activation of CB2 cannabinoid receptors, reduces human breast cancer cell proliferation by blocking the progression of the cell cycle and by inducing apoptosis. In particular, THC arrests cells in G2-M via down-regulation of Cdc2, as suggested by the decreased sensitivity to THC acquired by Cdc2-overexpressing cells. Of interest, the proliferation pattern of normal human mammary epithelial cells was much less affected by THC. We also analyzed by real-time quantitative PCR the expression of CB1 and CB2 cannabinoid receptors in a series of human breast tumor and nontumor samples. We found a correlation between CB2 expression and histologic grade of the tumors. There was also an association between CB2 expression and other markers of prognostic and predictive value, such as estrogen receptor, progesterone receptor, and ERBB2/HER-2 oncogene. Importantly, no significant CB2 expression was detected in nontumor breast tissue. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.(Cancer Res 2006; 66(13): 6615-21) source: http://cancerres.aac...ract/66/13/6615 Science: A combination of THC and prochlorperazine effective in reducing nausea and vomiting in women following breast surgery Researchers of the University of Arkansas and the Central Arkansas Veterans Hospital System investigated the effects of 5 mg oral THC and 25 mg rectal prochlorperazine on the rate of nausea and vomiting in women following breast surgery under general anaesthesia. The rate of nausea decreased from 59 per cent to 15 per cent and the rate of vomiting from 29 per cent to 3 per cent compared to non-treated patients. A retrospective review of 242 eligible patients, who underwent surgery between July 2001 and March 2003 was performed. 127 patients received surgery before September 2002 and did not receive a prophylaxis. 115 patients received surgery after September 2002 and were treated before surgery with oral THC (dronabinol) and rectal prochlorperazine. Data were collected from hospital records. Researchers concluded that post-operative nausea and vomiting (PONV) is a "significant problem in breast surgical patients. Preoperative treatment with dronabinol and prochlorperazine significantly reduced the number and severity of episodes of PONV." source: http://www.cannabis-...el.php?id=219#1 Science: Cannabidiol inhibits tumour growth in leukaemia and breast cancer in animal studies Italian researchers investigated the anti-tumour effects of five natural cannabinoids of the cannabis plant (cannabidiol, cannabigerol, cannabichromene, cannabidiol-acid and THC-acid) in breast cancer. Cannabidiol (CBD) was the most potent cannabinoid in inhibiting the growth of human breast cancer cells that had been injected under the skin of mice. CBD also reduced lung metastases deriving from human breast cancer cells that had been injected into the paws of the animals. Researchers found that the anti-tumour effects of CBD were caused by induction of apoptosis (programmed cell death). They concluded that their data "support the further testing of cannabidiol and cannabidiol-rich extracts for the potential treatment of cancer." These observations are supported by investigations of US scientists who found out that exposure of leukaemia cells to CBD led to a reduction in cell viability and induction of apoptosis. In living animals CBD caused a reduction in number of leukaemia cells. The scientists noted that CBD "may be a novel and highly selective treatment for leukemia." source: http://www.cannabis-...el.php?id=220#2 Science: A combination of THC and prochlorperazine effective in reducing nausea and vomiting in women following breast surgery Researchers of the University of Arkansas and the Central Arkansas Veterans Hospital System investigated the effects of 5 mg oral THC and 25 mg rectal prochlorperazine on the rate of nausea and vomiting in women following breast surgery under general anaesthesia. The rate of nausea decreased from 59 per cent to 15 per cent and the rate of vomiting from 29 per cent to 3 per cent compared to non-treated patients. A retrospective review of 242 eligible patients, who underwent surgery between July 2001 and March 2003 was performed. 127 patients received surgery before September 2002 and did not receive a prophylaxis. 115 patients received surgery after September 2002 and were treated before surgery with oral THC (dronabinol) and rectal prochlorperazine. Data were collected from hospital records. Researchers concluded that post-operative nausea and vomiting (PONV) is a "significant problem in breast surgical patients. Preoperative treatment with dronabinol and prochlorperazine significantly reduced the number and severity of episodes of PONV." source: http://www.cannabis-...el.php?id=219#1 “Medical Marijuana” Takes On New Meaning for Metastatic Breast Cancer If you have breast cancer, you may have considered the use of “medical marijuana” at some point during your chemo treatment. Smoking marijuana has provided some women with relief from the nausea and vomiting that can accompany chemo, relief that the range of normal side effect drugs weren’t able to give. Some states permit the legal use of medical marijuana; most don’t. Nevertheless, most women who want to try marijuana seem to be able to get it. Personally, I didn’t experience any severe problems with nausea. But I was astounded at the number of people who, prior to treatment, offered to get me a supply if I thought I needed it! Now, doctors at the California Pacific Medical Center Research Institute in San Francisco have released a study, in the current issue of Molecular Cancer Therapeutics, that may in the future open the door to a much more critical use of marijuana: stopping the spread of metastatic breast cancer. It seems that a compound found in cannabis (the scientific name for marijuana), CBD, has been shown (in the lab) to stop the human gene Id-1 from directing cancer cells to multiply and spread. California Pacific Senior researcher Pierre-Yves Desprez, in an interview with HealthDay News, noted that the Id-1 genes “are very bad. They push the cells to behave like embryonic cells and grow. They go crazy, they proliferate, they migrate. We need to be able to turn them off." Desprez and fellow researcher Sean D. McAllister joined forces just two years ago. Desprez had been studying the Id-1 gene for 12 years; McAllister was a cannabis expert, but not involved in cancer research. Together they found that Id-1 is the “orchestra conductor” that directs breast cancer cells to grow and spread. And that CBD inhibits Id-1; it turns it off, puts it to sleep, pick your metaphor. Bottom line, it neutralizes it. And the cancer stops spreading. Both researchers pointed out that CBD is non-toxic and non-psychoactive. In other words, patients wouldn’t get high taking it. And its non-toxicity is an important attribute; Desprez and McAllister predict that, to be effective, patients might have to take CBD for several years. They also cautioned that smoking marijuana isn’t going to cure metastatic breast cancer; the level of CBD necessary to inhibit Id-1 simply can’t be obtained that way. While studies are still very much in the preliminary stages, it’s interesting to think that a plant that has been used medicinally for nearly 5,000 years may in the future be a key element in controlling cancer. As recently as 1937 (when it was outlawed in the U.S.), marijuana (“cannabis sativa”) was being touted as an analgesic, anti-emetic, narcotic, and sedative. Parke-Davis, once America’s oldest and largest drug manufacturer (and now a division of drug giant Pfizer), offered “Fluid Extract Cannabis” via catalogs. Until the invention of aspirin in the mid-1800s, cannabis was the civilized world’s main pain reliever. Now it’s illegal. Here’s hoping that someday soon cannabis returns, this time as a successful treatment for metastatic breast cancer. source: http://www.healthcen...6/takes-cancer/ Marijuana Compound May Stop Breast Cancer From Spreading, Study Says A compound found in cannabis may stop breast cancer from spreading throughout the body, according to a new study by scientists at California Pacific Medical Center Research Institute. The researchers are hopeful that the compound called CBD, which is found in cannabis sativa, could be a non-toxic alternative to chemotherapy. "Right now we have a limited range of options in treating aggressive forms of cancer," said lead researcher Dr. Sean D. McAllister, a cancer researcher at CPMCRI, in a news release. "Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients. This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects." The researchers tested CBD to inhibit the activity of a gene called Id-1, which is believed to be responsible for the aggressive spread of cancer cells throughout the body, away from the original tumor site. "We know that Id-1 is a key regulator of the spread of breast cancer," said Dr. Pierre-Yves Desprez, a cancer researcher at CPMCRI and the senior author of the study, in a news release. "We also know that Id-1 has also been found at higher levels in other forms of cancer. So what is exciting about this study is that if CBD can inhibit Id-1 in breast cancer cells, then it may also prove effective at stopping the spread of cancer cells in other forms of the disease, such as colon and brain or prostate cancer." Comparing it with another ingredient isolated from marijuana called THC, which is used in some medical treatments, the researchers said CBD does not have any psychoactive properties, so using it would not violate any state or federal laws. However, the researchers stressed that they are not suggesting that breast cancer patients smoke marijuana. They say it is highly unlikely that effective concentrations of CBD could be reached by smoking pot. The study is published in the latest issue of the journal Molecular Cancer Therapeutics. source: http://www.foxnews.c...,312132,00.html Sean D. McAllister, PhD Introduction Our research team is studying the potential of the endocannabinoid system to control cell fate with the goal of developing therapeutic interventions for aggressive cancers. This newly discovered biological system can be regulated by many different classes of cannabinoid compounds that work through specific cellular receptors. The cloned cannabinoid receptors have been termed cannabinoid 1 (CB1) and (CB2). ∆9-tetrahydrocannabinol (THC), a mixed CB1 and CB2 receptor agonist, is the primary active constituent of Cannabis sativa and is currently being used in a clinical trial for the treatment of aggressive recurrent glioblastoma multiforme (GBM). Cannabinoids are also being used in clinical trials for purposes unrelated to their direct anticancer activity. The compounds have been reported to be well tolerated during chronic oral and systemic administration. In addition to Δ9-THC, cannabidiol (CBD), cannabinol (CBN) and cannabigerol (CBG) are also present in reasonable quantities in Cannabis. CBN has low affinity for CB1 and CB2 receptors, whereas the non-psychotropic cannabinoids, CBD and CBG, have negligible affinity for the cloned receptors. We have determined that these additional cannabinoids are also effective and inhibiting aggressive cancers. Importantly, we have discovered in vitro that a synergistic increase in the antiproliferative and apoptotic activity of cannabinoids can be produced by combining specific ratios of CB1 and CB2 receptors agonists with non-psychotropic cannabinoids. We are currently determining the molecular mechanism that may explain the synergistic increase in anticancer activity that is observed with the combination treatments. We are also studying whether this combination strategy will lead to greater antitumor activity in vivo. In addition to the combination therapy project, we are working in collaboration with Dr. Pierre Desprez to develop novel inhibitors of Id-1 using cannabinoid compounds. Id-1 is a helix-loop-helix protein that acts as an inhibitor of basic helix-loop-helix transcription factors that control cell differentiation, development and carcinogenesis. Past research of Id-1 expression in normal and cancerous breast cells, as well as in mouse mammary glands and in human breast cancer biopsies, demonstrated that increased Id-1 expression was associated with a proliferative and invasive phenotype. Specifically, it was found that Id-1 was constitutively expressed at a high level in aggressive breast cancer cells and human biopsies, and that aggressiveness was reverted in vitro and in vivo when Id-1 expression was targeted using antisense technology. Importantly, we have recently discovered that CBD, a nontoxic cannabinoid that lacks psychoactivity, can inhibit Id-1 gene expression in metastatic breast cancer cells and consequently their aggressive phenotype. The down-regulation of expression was the result of the inhibition of the endogenous Id-1 promoter and corresponding mRNA and protein levels. CBD and compounds based off of its structure can therefore potentially be used as therapeutic agents. CBD also inhibits breast cancer metastasis in vivo. Based off of our recent findings, we are currently involved in 1) developing novel CBD analogs for the treat of aggressive breast cancers 2) discovering the detailed mechanisms through which cannabinoid compounds regulate Id-1 expression. source: http://www.cpmc.org/...ience/sean.html McAllister SD, Christian RT, Horowitz MP, Garcia A, Desprez PY. California Pacific Medical Center, Research Institute, 475 Brannan Street, San Francisco, CA 94107, USA. mcallis@cpmcri.org Invasion and metastasis of aggressive breast cancer cells is the final and fatal step during cancer progression, and is the least understood genetically. Clinically, there are still limited therapeutic interventions for aggressive and metastatic breast cancers available. Clearly, effective and nontoxic therapies are urgently required. Id-1, an inhibitor of basic helix-loop-helix transcription factors, has recently been shown to be a key regulator of the metastatic potential of breast and additional cancers. Using a mouse model, we previously determined that metastatic breast cancer cells became significantly less invasive in vitro and less metastatic in vivo when Id-1 was down-regulated by stable transduction with antisense Id-1. It is not possible at this point, however, to use antisense technology to reduce Id-1 expression in patients with metastatic breast cancer. Here, we report that cannabidiol (CBD), a cannabinoid with a low-toxicity profile, could down-regulate Id-1 expression in aggressive human breast cancer cells. The CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. CBD was able to inhibit Id-1 expression at the mRNA and protein level in a concentration-dependent fashion. These effects seemed to occur as the result of an inhibition of the Id-1 gene at the promoter level. Importantly, CBD did not inhibit invasiveness in cells that ectopically expressed Id-1. In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness. source: http://www.ncbi.nlm....Pubmed_RVDocSum N. California Researchers Testing Whether Marijuana Chemical Can Slow Cancer Growth, With Funding by Susan G. Komen for the Cure® Largest Breast Cancer Organization Investing $60 Million to Research Despite Down Economy SAN FRANCISCO, April 9 /PRNewswire-USNewswire/ -- Testing whether a powerful ingredient in marijuana can help slow the growth of aggressive breast cancer cells is just one of six Bay Area breast cancer studies being funded this year by Susan G. Komen for the Cure®, the global leader in the breast cancer movement announced today. The projects are part of a $60 million portfolio of 2009 research grants that Komen for the Cure is investing with scientists worldwide to find the cures for breast cancer. "Breast cancer doesn't care about the economy, and with more than 1.3 million new cases of breast cancer expected this year, the need for new research is more urgent than ever," said Hala Moddelmog, Komen's CEO and president. In the Bay Area this year, Komen's $1.8 million in grants will go to the University of California at San Francisco, Stanford University School of Medicine and California Pacific Medical Center. The UCSF study will try to improve bilingual communication and education between Latinas and their health care providers. One Stanford grant, if successful, could reverse some of the debilitating neurological and cognitive side effects of brain metastases, halt the progression of disease and possibly reduce mortality. And CPMC researchers will test whether cannabidiol - an ingredient in marijuana - can inhibit the aggressive growth of some breast cancers. "Komen's infusion of millions of dollars into research projects means that promising research that is designed to treat and ultimately eradicate breast cancer will continue," said Eric Winer, M.D., Komen's chief scientific advisor. During the past 27 years, Komen has invested $400 million to fund research globally, starting with Komen's first grant in 1982 for $28,000. A decade later, the annual total had grown to 21 grants worth $590,000 and 10 years after that, Komen distributed $21 million in research funds. This year, Komen is providing researchers worldwide with $60 million. In the last three years alone, Komen has invested nearly $237 million for breast cancer research. In 2008, Komen created Promise Grants - a new category of multi-year, multi-million dollar grants designed to discover and deliver cures for breast cancer more quickly. Here is a list of local institutions, the researchers and the projects Komen is funding this year, pending agreements: University of California at San Francisco *Celia Kaplan, $450,185, Breast Cancer Risk Reduction in Primary Care Clinics: A Bilingual Intervention for Women and Physicians Stanford University School of Medicine *Irene Wapnir, $600,000, From Bench to Bedside: Treatment of Breast Cancer Brain Metastasis with 131I and Radiosensitizers *Roeland Nusse, $180,000, 'Wnt signaling in human breast cancer stem cells. *Michael Clarke, $180,000, Functions of microRNAs in metastatic tumor initiating cells of human breast cancer *Howard Chang, $180,000, Noncoding RNA, Polycomb and Breast Cancer Progression California Pacific Medical Center *Sean McAlister, $593,713, Inhibition of Breast Cancer Cell Aggressiveness by Cannabidiol About Susan G. Komen for the Cure® Nancy G. Brinker promised her dying sister, Susan G. Komen, she would do everything in her power to end breast cancer forever. In 1982, that promise became Susan G. Komen for the Cure and launched the global breast cancer movement. Today, Komen for the Cure is the world's largest grassroots network of breast cancer survivors and activists fighting to save lives, empower people, ensure quality care for all and energize science to find the cures. Thanks to events like the Komen Race for the Cure®, we have invested more than $1.3 billion to fulfill our promise, becoming the largest source of nonprofit funds dedicated to the fight against breast cancer in the world. For more information about Susan G. Komen for the Cure, breast health or breast cancer, visit www.komen.org or call 1-877 GO KOMEN. SOURCE Susan G. Komen for the Cure source: http://news.prnewswi...C...3872&EDATE= Cannabis compound 'halts cancer' The CBD compound found in cannabis is non-toxicA compound found in cannabis may stop breast cancer spreading throughout the body, US scientists believe.The California Pacific Medical Center Research Institute team are hopeful that cannabidiol or CBD could be a non-toxic alternative to chemotherapy. Unlike cannabis, CBD does not have any psychoactive properties so its use would not violate laws, Molecular Cancer Therapeutics reports. The authors stressed that they were not suggesting patients smoke marijuana. They added that it would be highly unlikely that effective concentrations of CBD could be reached by smoking cannabis. This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects <br clear="all"> Lead researcher Dr Sean McAllister CBD works by blocking the activity of a gene called Id-1 which is believed to be responsible for the aggressive spread of cancer cells away from the original tumour site - a process called metastasis. Past work has shown CBD can block aggressive human brain cancers. The latest work found CBD appeared to have a similar effect on breast cancer cells in the lab. Future hope Lead researcher Dr Sean McAllister said: "Right now we have a limited range of options in treating aggressive forms of cancer. "Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients. "This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects." Dr Joanna Owens of Cancer Research UK said: "This research is at a very early stage. "The findings will need to be followed up with clinical trials in humans to see if the CBD is safe, and whether the beneficial effects can be replicated. "Several cancer drugs based on plant chemicals are already used widely, such as vincristine - which is derived from a type of flower called Madagascar Periwinkle and is used to treat breast and lung cancer. It will be interesting to see whether CBD will join them." Maria Leadbeater of Breast Cancer Care said: "Many people experience side-effects while having chemotherapy, such as nausea and an increased risk of infection, which can take both a physical and emotional toll. "Any drug that has fewer side-effects will, of course, be of great interest." But she added: "It is clear that much more research needs to be carried out." Caution content may be shocking! WHAT IS BREAST CANCER? Breast cancer itself is a malignant tumor than can form in one or both breasts, and usually develops in the milk-producing ducts of the breast, known as the the lobules. According to the website www.Cancer.org: Breast cancer is the most common cancer among women in the United States, other than skin cancer. It is the second leading cause of cancer death in women, after lung cancer. The chance of a woman having invasive breast cancer some time during her life is a little less 1 in 8. The chance of dying from breast cancer is about 1 in 35. Now Breast Cancer isn't only found in women, it can also occur in men, although not as common, but just as deadly. The most recent statistics for 2011 from the American Cancer Society estimate as follows: About 230,480 new cases of invasive breast cancer in women About 57,650 new cases of carcinoma in situ (CIS) will be found (CIS is non-invasive and is the earliest form of breast cancer). About 39,520 deaths from breast cancer (women) HOW CAN YOU PREVENT IT? THE GENETIC FACTORSBecause there is a higher chance of cancer in women with a family history, women should consult a medical professional who is specifically trained in risk assessment in order to help you decide the best methods for early detection. In Western countries, up to 10% of breast cancer is attributed to genetic predisposition. It can be transmitted through either the mother or father, with the possibility of either parent transmitting the abnormality without ever developing it -- as in, they're simply carriers. However, an excess of ovarian, colon, prostatic, and other cancers are inherited in the same abnormal mutation as breast cancer, so if any of these are present in family members, it is recommended that you take precautions. Most breast cancers are due to genetic mutations, with women who get the disease at an early age predisposed to the development of breast cancer. Mentioned on www.MindFully.org: WHERE IN THE WORLD IS CANCER?
  9. CANCER- PANCREATIC/ and use of Cannabis Molecule That Facilitates Cancer Spread In Both Cells And Their Surroundings Found ScienceDaily (Jan. 21, 2008) — The discovery that a molecule drives local tumor growth, as well as its ability to flourish and spread, opens a new window for understanding and treating cancer by taking aim at both cancer cells and their surrounding environment. A Dartmouth Medical School team led by Dr. Murray Korc found that a member of a common molecular family plays a role in the progress of a particularly resilient and aggressive pancreatic cancer, and that its influence is not restricted to that cancer. The work builds on studies by Korc, professor and chair of medicine at DMS, and colleagues at University of California, Irvine on glypican molecules, which interact with many growth factors implicated in cancer. A receptor called glypican-1 (GPC1) is abnormally abundant in pancreatic ductal adenocarcinoma, the most common and deadliest form of pancreatic cancer, often diagnosed after it has spread or metastasized. Human pancreatic cells deprived of their own GPC1 had reduced growth in culture, as well as when they were transplanted into immunocompromised mice (known as athymic for the lack of a thymus gland) that don't reject human cancer cells, the researchers demonstrated. "Tumors grow more slowly and are smaller. Interestingly, they also have less angiogenesis (blood vessel growth) and less metastasis," said Korc, also a professor pharmacology and toxicology and member of the Norris Cotton Cancer Center. Since GPC1 is common in many tissues, the researchers wanted to determine its role in the host environment, or how it functions in a patient. Knocking out the gene for GPC1 in mice, they created an athymic mouse population that lacked GPC1; then they introduced cancer cells. Host mice devoid of GPC1 had smaller pancreatic tumors that were less angiogenic and less metastatic when exposed to tumor cell lines with normal levels of GPC1. The metastatic potential of mouse melanoma (skin cancer) cells injected into mice with no GPC1 was also greatly decreased, the researchers found. "We've shown that GPC1 in the cancer cells and in the host—that is, the patient—is important not only for tumor growth, but for tumor angiogenesis and metastasis, Korc said. "This raises the possibility for therapeutic manipulations that will target GPC1 in both cancer cells and in patients to slow tumor growth and to prevent metastasis." Zeroing in on mechanisms that allow metastasis to occur more efficiently -namely, presence of GPC1—in either the cancer cells or the host, offers new options against cancer. The approach seems promising because, added Korc, "Host-cancer interactions are becoming significant as clinicians and cancer researchers realize that the environment around cancer cells is just as important as the cancer cells themselves." This research was reported in the January Journal of Clinical Investigation. Co-authors on the research are Takuma Aikawa, Chery A. Whipple, Jason Gunn, Alison Young, of DMS, and Martha E. Lopez and Arthur D. Lander of UC Irvine. Adapted from materials provided by Dartmouth Medical School. source: http://www.scienceda...80117180113.htm Pancreatic cancer has one of the highest morbidity rates due mainly to the fact that early detection is rare. The symptom profile of most patients is not very distinct. I would encourage folks who have ANY issues with digestion or elimination to get it thoroughly checked A.S.A.P. This is one you don't want to mess with. Regardless of the type of treatment, early detection is the key to survival. Experimental Therapeutics, Molecular Targets, and Chemical Biology Cannabinoids Induce Apoptosis of Pancreatic Tumor Cells via Endoplasmic Reticulum Stress–Related Genes Arkaitz Carracedo1, Meritxell Gironella2, Mar Lorente1, Stephane Garcia2, Manuel Guzmán1, Guillermo Velasco1 and Juan L. Iovanna2 1 Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid, Spain and 2 U624 Institut National de la Sante et de la Recherche Medicale, Marseille, France Requests for reprints: Guillermo Velasco, Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, c/ José Antonio Novais s/n, 28040 Madrid, Spain. Phone: 34-91-394-4668; Fax: 34-91-394-4672; E-mail: gvd@bbm1.ucm.es. Pancreatic adenocarcinomas are among the most malignant forms of cancer and, therefore, it is of especial interest to set new strategies aimed at improving the prognostic of this deadly disease. The present study was undertaken to investigate the action of cannabinoids, a new family of potential antitumoral agents, in pancreatic cancer. We show that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumor biopsies at much higher levels than in normal pancreatic tissue. Studies conducted with MiaPaCa2 and Panc1 cell lines showed that cannabinoid administration (a) induced apoptosis, ( increased ceramide levels, and © up-regulated mRNA levels of the stress protein p8. These effects were prevented by blockade of the CB2 cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo. Knockdown experiments using selective small interfering RNAs showed the involvement of p8 via its downstream endoplasmic reticulum stress–related targets activating transcription factor 4 (ATF-4) and TRB3 in 9-tetrahydrocannabinol–induced apoptosis. Cannabinoids also reduced the growth of tumor cells in two animal models of pancreatic cancer. In addition, cannabinoid treatment inhibited the spreading of pancreatic tumor cells. Moreover, cannabinoid administration selectively increased apoptosis and TRB3 expression in pancreatic tumor cells but not in normal tissue. In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB2 receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress–related genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer. (Cancer Res 2006; 66(13): 6748-55) Source: http://cancerres.aac...ract/66/13/6748 Cannabinoids Halt Pancreatic Cancer, Breast Cancer Growth, Studies Say by Paul Armentano, NORML, Cancer Research July 1st, 2006 Madrid, Spain: Compounds in cannabis inhibit cancer cell growth in human breast cancer cell lines and in pancreatic tumor cell lines, according to a pair of preclinical trials published in the July issue of the journal of the American Association for Cancer Research. In one trial, investigators at Complutense University in Spain and the Institut National de la Sante et de la Recherche Medicale (INSERM) in France assessed the anti-cancer activity of cannabinoids in pancreatic cancer cell lines and in animals. Cannabinoid administration selectively increased apoptosis (programmed cell death) in pancreatic tumor cells while ignoring healthy cells, researchers found. In addition, "cannabinoid treatment inhibited the spreading of pancreatic tumor cells ... and reduced the growth of tumor cells" in animals. "These findings may contribute to ... a new therapeutic approach for the treatment of pancreatic cancer," authors concluded. In the second trial, investigators at Spain's Complutense University reported that THC administration "reduces human breast cancer cell proliferation [in vitro] by blocking the progression of the cell cycle and by inducing apoptosis." Authors concluded that their findings "may set the bases for a cannabinoid therapy for the management of breast cancer." Previous preclinical data published in May in the Journal of Pharmacological and Experimental Therapeutics reported that non-psychoactive cannabinoids, particularly cannabidiol (CBD), dramatically halt the spread of breast cancer cells and recommended their use in cancer therapy. Separate trials have also shown cannabinoids to reduce the size and halt the spread of glioma (brain tumor) cells in animals and humans in a dose dependent manner. Additional preclinical studies have demonstrated cannabinoids to inhibit cancer cell growth and selectively trigger malignant cell death in skin cancer cells, leukemic cells, lung cancer cells, and prostate carcinoma cells, among other cancerous cell lines. source: http://safeaccessnow...cle.php?id=3563 Molecule That Facilitates Cancer Spread In Both Cells And Their Surroundings Found ScienceDaily (Jan. 21, 2008) — The discovery that a molecule drives local tumor growth, as well as its ability to flourish and spread, opens a new window for understanding and treating cancer by taking aim at both cancer cells and their surrounding environment. A Dartmouth Medical School team led by Dr. Murray Korc found that a member of a common molecular family plays a role in the progress of a particularly resilient and aggressive pancreatic cancer, and that its influence is not restricted to that cancer. The work builds on studies by Korc, professor and chair of medicine at DMS, and colleagues at University of California, Irvine on glypican molecules, which interact with many growth factors implicated in cancer. A receptor called glypican-1 (GPC1) is abnormally abundant in pancreatic ductal adenocarcinoma, the most common and deadliest form of pancreatic cancer, often diagnosed after it has spread or metastasized. Human pancreatic cells deprived of their own GPC1 had reduced growth in culture, as well as when they were transplanted into immunocompromised mice (known as athymic for the lack of a thymus gland) that don't reject human cancer cells, the researchers demonstrated. "Tumors grow more slowly and are smaller. Interestingly, they also have less angiogenesis (blood vessel growth) and less metastasis," said Korc, also a professor pharmacology and toxicology and member of the Norris Cotton Cancer Center. Since GPC1 is common in many tissues, the researchers wanted to determine its role in the host environment, or how it functions in a patient. Knocking out the gene for GPC1 in mice, they created an athymic mouse population that lacked GPC1; then they introduced cancer cells. Host mice devoid of GPC1 had smaller pancreatic tumors that were less angiogenic and less metastatic when exposed to tumor cell lines with normal levels of GPC1. The metastatic potential of mouse melanoma (skin cancer) cells injected into mice with no GPC1 was also greatly decreased, the researchers found. "We've shown that GPC1 in the cancer cells and in the host—that is, the patient—is important not only for tumor growth, but for tumor angiogenesis and metastasis, Korc said. "This raises the possibility for therapeutic manipulations that will target GPC1 in both cancer cells and in patients to slow tumor growth and to prevent metastasis." Zeroing in on mechanisms that allow metastasis to occur more efficiently -namely, presence of GPC1—in either the cancer cells or the host, offers new options against cancer. The approach seems promising because, added Korc, "Host-cancer interactions are becoming significant as clinicians and cancer researchers realize that the environment around cancer cells is just as important as the cancer cells themselves." This research was reported in the January Journal of Clinical Investigation. Co-authors on the research are Takuma Aikawa, Chery A. Whipple, Jason Gunn, Alison Young, of DMS, and Martha E. Lopez and Arthur D. Lander of UC Irvine. Adapted from materials provided by Dartmouth Medical School. source: http://www.scienceda...80117180113.htm Q. I would like you to know about medical marijuana for cancer. In her late 30s, my wife was diagnosed with pancreatic cancer, stage 4a. It was a 6 cm tumor that had grown around the hepatic artery and portal vein. At first I thought marijuana was just for nausea caused by her chemo, but then I found a study in the journal Cancer Research (July 1, 2006). It showed that cannabinoids specifically fight pancreatic tumor cells. I changed her diet and started her on a regimen and she is now cancer free. The regimen is being studied at the University of Wisconsin. I hope others can benefit from medical marijuana. A. For years, marijuana research was suspected of being a way to rationalize people getting high. But as a recent article in Science News points out, scientists are now starting to take it seriously (June 19, 2010). The article you cite demonstrates that compounds from marijuana make pancreatic tumor cells commit suicide. Other cancer researchers have followed up with studies on its effectiveness against a range of tumors in test tubes, including breast, colon, glioblastoma brain tumors and lymphoma, a blood cancer. None are yet in clinical trials, but this will be an interesting field to watch. We are delighted your wife got such a good response for such a difficult-to-treat cancer.
  10. OBESITY - Cannabis Obesity to be cured by Marijuana? A British pharmaceuticals company is planning to start trials on humans for a treatment for [tag-tec]obesity[/tag-tec] using [tag-tec]marijuana[/tag-tec]. They hasten to add that at this stage it is purely experimental. Of course marijuana has long been known to be a stimulus for hunger but GW pharma plc claim that they have derived a treatment from marijuana itself that could help suppress hunger. They go on to explain that the [tag-tec]marijuana plant[/tag-tec] has 70 different [tag-tec]cannabinoids[/tag-tec] in it and that each of these has an entirely different effect on the human body. Some stimulate your hunger whilst others suppress your hunger. GW say that they will begin trials later in 2007. All drugs have to pass a rigorous three stages of tests before it can be assessed by regulators and only then can a new drug be released. They added that this could take several years. I will keep my ear to the ground and let you know of any developments, as and when they happen. source: http://www.dreambody...d-by-marijuana/ How marijuana could help cure obesity-related diseases A British company says that two compounds found in marijuana leaves could treat patients whose weight puts them at high risk for heart disease and stroke According to a new British study, marijuana leaves (not the buds that Willie Nelson loves so dearly) contain two compounds that boost the metabolism of mice, leading to lower levels of fat and cholesterol in the body — the latest addition to a growing body of evidence that marijuana may be useful in countering ailments related to obesity. One study in March found that a brain chemical similar in structure to an active compound in cannibis could help people shed weight, while another study last September concluded that pot smokers were less likely to be obese than non-potheads, though for reasons that remain unclear. The researchers at Britain's GW Pharmaceuticals who are responsible for the latest weed development are already testing the two compounds on humans. Here, a guide to their findings: So the company is allowed to grow and dispense marijuana? Yes. Although marijuana is illegal in England, says Doug Barry at Jezebel, GW Pharmaceuticals, an "enormous multinational drug corporation equipped with all the magic passwords for dodging government regulations," was granted a license to grow the plant in specially constructed greenhouses at a secret location in the south of England. SEE MORE: Invented: Marijuana that doesn't get you high http://www.youtube.com/watch?v=u8WCdANlf_I London -- Human trials of an experimental treatment for obesity derived from cannabis, which is commonly associated with stimulating hunger, are scheduled to begin in the second half of this year, Britain's GW Pharmaceuticals Plc announced Tuesday. Several other companies, such as Sanofi-Aventis, which is investigating Acomplia, are working on new drugs that will switch off the brain circuits that make people hungry when they smoke cannabis. GW Pharma, however, says it has derived a treatment from cannabis that could help suppress hunger. "The cannabis plant has 70 different cannabinoids in it and each has a different affect on the body," GW Managing Director Justin Gover told Reuters in a telephone interview. "Some can stimulate your appetite, and some in the same plant can suppress your appetite. It is amazing both scientifically and commercially," he said. Drugs have to pass three stages of tests in humans before being eligible for approval by regulators in a process that takes many years. Sanofi-Aventis' Acomplia, which it believes can achieve $3 billion in annual sales, is already on sale in Europe and it is waiting for a U.S. regulatory decision in April. Several other big drug companies also already have similar products to Acomplia in clinical trials. GW is best known for developing Sativex, a treatment derived from cannabis that fights spasticity in multiple sclerosis patients. Sativex, an under-the-tongue spray, has been approved in Canada, but has hit delays with regulators in Britain. GW submitted Sativex for assessment by several European regulators in September, and hopes to secure approval for the UK, Denmark, Spain and the Netherlands in the second half of this year at the earliest, the company said on Tuesday. GW's marijuana plants are grown indoors in a secret location in Southern England. ScienceDaily (May 8, 2008) — Anti-obesity drugs that work by blocking brain molecules similar to those in marijuana could also interfere with neural development in young children, according to a new study from MIT's Picower Institute for Learning and Memory. Marijuana is known to be an appetite stimulant, and a new class of anti-obesity drugs--such as rimonabant (trade name Acomplia) developed by Sanofi-Aventis and awaiting approval for use in the United States--work by blocking brain receptors that bind to marijuana and other cannabinoids. Marijuana, derived from the plant Cannabis sativa, contains special active compounds that are referred to collectively as cannabinoids. But other cannabinoids (endocannabinoids) are generated naturally inside the body. The MIT study, which was done in mice, found that blocking cannabinoid receptors could also suppress the adaptive rewiring of the brain necessary for neural development in children. The work is reported in the May 8 issue of Neuron. "Our finding of a profound disruption of cortical plasticity in juvenile mice suggests caution is advised in the use of such compounds in children," wrote lead author Mark F. Bear, director of the Picower Institute and Picower Professor of Neuroscience. The researchers investigated plasticity--the brain's ability to change in response to experience--by temporarily depriving newborn mice of vision in one eye soon after birth. This well-known experiment induces a long-lasting loss of synapses that causes blindness in the covered eye, while synapses shift to the uncovered eye. How and where this synaptic shift occurs in the primary visual cortex has remained controversial. Understanding the mechanism behind this phenomenon is key because the same brain mechanisms are used for normal development and may go awry in conditions that cause developmental delays in humans, and may reappear in old age and contribute to synaptic loss during Alzheimer's disease, Bear said. In mice, the MIT researchers found, even one day of deprivation from one eye starts the shift to dominance of the uncovered eye. But injecting the mice with a cannabinoid receptor blocker halted the shift in certain brain regions, indicating that cannabinoids play a key role in early synaptic development. Blocking cannabinoids receptors could thwart this developmental process, the researchers said. This work is supported by the National Eye Institute and the National Institute of Mental Health. source: http://www.scienceda...80507133326.htm
  11. Multiple Sclerosis / Muscle Spasms A.D.A.M. Medical Encyclopedia. Multiple sclerosis MS; Demyelinating diseaseLast reviewed: September 26, 2011. Multiple sclerosis is an autoimmune disease that affects the brain and spinal cord (central nervous system). Causes, incidence, and risk factors Multiple sclerosis (MS) affects women more than men. The disorder is most commonly diagnosed between ages 20 and 40, but can be seen at any age. MS is caused by damage to the myelin sheath, the protective covering that surrounds nerve cells. When this nerve covering is damaged, nerve signals slow down or stop. The nerve damage is caused by inflammation. Inflammation occurs when the body's own immune cells attack the nervous system. This can occur along any area of the brain, optic nerve, and spinal cord. It is unknown what exactly causes this to happen. The most common thought is that a virus or gene defect, or both, are to blame. Environmental factors may play a role. You are slightly more likely to get this condition if you have a family history of MS or live in an part of the world where MS is more common. Symptoms Symptoms vary, because the location and severity of each attack can be different. Episodes can last for days, weeks, or months. These episodes alternate with periods of reduced or no symptoms (remissions). Fever, hot baths, sun exposure, and stress can trigger or worsen attacks. It is common for the disease to return (relapse). However, the disease may continue to get worse without periods of remission. Because nerves in any part of the brain or spinal cord may be damaged, patients with multiple sclerosis can have symptoms in many parts of the body. Muscle symptoms: Loss of balance Muscle spasms Numbness or abnormal sensation in any area Problems moving arms or legs Problems walking Problems with coordination and making small movements Tremor in one or more arms or legs Weakness in one or more arms or legs Bowel and bladder symptoms: Constipation and stool leakage Difficulty beginning to urinate Frequent need to urinate Strong urge to urinate Urine leakage (incontinence) Eye symptoms: Double vision Eye discomfort Uncontrollable rapid eye movements Vision loss (usually affects one eye at a time) Numbness, tingling, or pain Facial pain Painful muscle spasms Tingling, crawling, or burning feeling in the arms and legs Other brain and nerve symptoms: Decreased attention span, poor judgment, and memory loss Difficulty reasoning and solving problems Depression or feelings of sadness Dizziness and balance problems Hearing loss Sexual symptoms: Problems with erections Problems with vaginal lubrication Speech and swallowing symptoms: Slurred or difficult-to-understand speech Trouble chewing and swallowing Fatigue is a common and bothersome symptoms as MS progresses. It is often worse in the late afternoon. Signs and tests Symptoms of MS may mimic those of many other nervous system disorders. The disease is diagnosed by ruling out other conditions. People who have a form of MS called relapsing-remitting may have a history of at least two attacks, separated by a period of reduced or no symptoms. The health care provider may suspect MS if there are decreases in the function of two different parts of the central nervous system (such as abnormal reflexes) at two different times. A neurological exam may show reduced nerve function in one area of the body, or spread over many parts of the body. This may include: Abnormal nerve reflexes Decreased ability to move a part of the body Decreased or abnormal sensation Other loss of nervous system functions An eye examination may show: Abnormal pupil responses Changes in the visual fields or eye movements Decreased visual acuity Problems with the inside parts of the eye Rapid eye movements triggered when the eye moves Tests to diagnose multiple sclerosis include: Lumbar puncture (spinal tap) for cerebrospinal fluid tests, including CSF oligoclonal banding MRI scan of the brain and MRI scan of the spine are important to help diagnose and follow MS Nerve function study (evoked potential test) Is marijuana an effective treatment for spasticity disorders such as multiple sclerosis? Movement Disorders stated in a Sep. 2004 article titled "Survey on Cannabis Use in Parkinson's Disease" by researchers from the Movement Disorders Centreat the Department of Neurology at Charles University, Prague, Czech Republic: "An anonymous questionnaire sent to all patients attending the Prague Movement Disorder Centre revealed that 25% of 339 respondents had taken cannabis and 45.9% of these described some form of benefit.... The late onset of cannabis action is noteworthy. Because most patients reported that improvement occurred approximately two months after the first use of cannabis, it is very unlikely that it could be attributed to a placebo reaction." More Pro's and Cons People with multiple sclerosis and other diseases that cause severe muscle spasms, spasticity and tremors have used cannabis for a very long time, and have consistently reported that it relieves their symptoms. In what is perhaps the earliest medical report on the use of cannabis to treat muscle spasms, Dr. William O’Shaughnessy, a British physician working in India, reported in 1842 that cannabis extracts effectively controlled the spasticity he observed in cases of tetanus, and in 1890 More Cannabis has also been shown to be effective in relieving muscle spasms and spasticity associated with a number of other illnesses such as irritable bowel syndrome, premenstrual dysphoric disorder (PMDD) and PMS, cerebral palsy, Parkinson’s Disease, amyotrophic lateral sclerosis (Lou Gehrig’s disease), spinal cord injury and other nerve injuries, and may also relieve the bronchial spasms that cause asthma, though little formal research has been done on cannabis in any of these conditions. Alan Shackelford, M.D., graduated from the University of Heidelberg School of Medicine and trained at major teaching hospitals of Harvard Medical School in internal medicine, nutritional medicine and hyperalimentation and behavioral medicine. He is principle physician for Intermedical Consulting, LLC and Amarimed of Colorado, LLC and can be contacted at Amarimed.com. Article from Culture Magazine and republished with special permission The question of whether marijuana (Cannabis sativa) should be used for symptom management in MS is a complex one. It is generally agreed that better therapies are needed for distressing symptoms — including pain, tremor, and spasticity — that may not be sufficiently relieved by available treatments. Yet there are serious uncertainties about the benefits of marijuana relative to its side effects. The fact that marijuana is an illegal drug in many states and by federal statute (see in the News) further complicates the issue. Some people with MS report that smoking marijuana relieves several of their MS symptoms. However, for any therapy to be recognized as an effective treatment, this kind of subjective, anecdotal reporting needs to be supported by carefully gathered objective evidence of safety and benefit. Unfortunately, it has proven difficult to do carefully controlled clinical trials of marijuana. One reason for this is that marijuana is psychoactive and makes people feel "high." This means that people taking the active drug during a clinical trial usually become aware of it — thus "unblinding" the study and possibly biasing results. Studies completed thus far have not provided convincing evidence that marijuana or its derivatives provide substantiated benefits for symptoms of MS. Conflicting results of previous research, coupled with the need for additional therapies to treat symptoms of MS, make it important that more research be done on the potential of marijuana and its derivatives. The National MS Society is funding a well controlled study on the effectiveness of different forms of marijuana to treat spasticity in MS, and established a task force to examine the use of Cannabis in MS to review what is currently known about its potential. This task force had made specific recommendations on the research that still needs to be done to answer pressing questions about the potential effectiveness and safety of marijuana and its derivatives in treating MS. Download Recommendations Regarding the Use of Cannabis in Multiple Sclerosis (.pdf) Early Studies Showed Mixed Results and Some Side Effects Well known for its mind-altering properties, marijuana is produced from the flowering top of the hemp plant, Cannabis sativa. Early studies explored the role of THC (tetrahydrocannabinol — an active ingredient in marijuana) or smoked marijuana in treating spasticity, tremor, and balance control in small numbers of people with MS. Most of these studies were done with THC. Because THC can be given by mouth, it is easier to control the dose. The results of these studies were mixed, and participants reported a variety of uncomfortable side effects. In addition, smoked marijuana poses health risks that are at least as significant as those associated with tobacco. For spasticity (unusual muscle tension or stiffness) Studies of THC for spasticity have had mixed results. While some people reported feeling "looseness" and less spasticity, this could not always be confirmed by objective testing done by physicians. Even at its best, effects lasted less than three hours. Side effects, especially at higher doses, included weakness, dry mouth, dizziness, mental clouding, short-term memory impairment, space-time distortions and lack of coordination. For tremor (uncontrolled movements) In a small study of THC involving eight seriously disabled individuals with significant tremor and ataxia (lack of muscle coordination), two people reported improvement in tremor that could be confirmed by an examination by a physician and another three reported improvement in tremor that could not be confirmed. All eight patients taking THC experienced a "high," and two reported feelings of discomfort and unease. For balance Smoked marijuana was shown to worsen control of posture and balance in 10 people with MS and 10 who did not have MS. All 20 study participants reported feeling "high." National Academy of Sciences/ Institute of Medicine Report A 1999 report by the National Academy of Sciences/Institute of Medicine on the medical uses of marijuana raised additional questions. While the report concluded that smoked marijuana does not have a role in the treatment of MS, there remained the possibility that specific compounds derived from marijuana might reduce some MS symptoms, particularly MS-related spasticity. Well designed and controlled studies of the therapeutic potential of marijuana compounds (called cannabinoids) were indicated, in conjunction with the development of safe, reliable drug delivery technology. Study on Marijuana Derivatives in Mice Investigators in the United Kingdom and United States tested the ability of two marijuana derivatives and three synthetic cannabinoids to control spasticity and tremor, symptoms of the MS-like disease, EAE, in mice. The results, published in the March 2, 2000 issue of Nature, suggested that four different cannabinoids could temporarily relieve spasticity and/or tremor. While the study suggested that similar derivatives of marijuana might be developed for human use, it was clear that the psychoactive effects of these cannabinoids would need to be reduced sufficiently to make them a safe and comfortable treatment for people with MS. Received 18 August 1999;accepted 20 January 2000 References 1. Baker, D. et al. Induction of chronic relapsing experimental allergic encephalomyelitis in Biozzi mice. J. Neuroimmunol. 28, 261-270 (1990). 2. Consroe, P., Musty, R., Rein, J., Tillery, W. & Pertwee, R. The perceived effects of smoked cannabis on patients with multiple sclerosis. Eur. Neurol. 38, 44-48 (1997). 3. Consroe, P. Cannabinoid systems as targets for the therapy of neurological disorders. Neurobiol. Dis. 5, 534-551 (1998). Links 4. Petro, D. J. & Ellenberger, C. Treatment of human spasticity with 9- tetrahydrocannabinol. J. Clin. Pharmacol. 21 (suppl.), 413-416 (1981). 5. Clifford, D. B. Tetrahydrocannabinol for tremor in multiple sclerosis. Ann. Neurol. 13, 669-671 (1983). Links 6. Ungerleider, J. T., Andyrsiak, T., Fairbanks, L., Ellison, G. W. & Myers, L. W. 9-THC in the treatment of spasticity associated with multiple sclerosis. Adv. Alcohol Substance Abuse 7, 39-50 (1987). 7. Martyn, C. N., Illis, L. S. & Thom, J. Nabilone in the treatment of multiple sclerosis. Lancet 345, 579 (1995). Links 8. Pertwee, R. G. Pharmacology of cannabinoid receptor ligands. Curr. Med. Chem. 6, 635-664 (1999). Links 9. Lyman, W. D., Sonett, J. R., Brosnan, C. F., Elkin, R. & Bornstein, M. B. 9-tetrahydrocannabinol: a novel treatment for experimental autoimmune encephalomyelitis. J. Neuroimmunol. 23, 73-81 (1989). Links 10. Wirguin, I. et al. Suppression of experimental autoimmune encephalomyelitis by cannabinoids. Immunopharmacology 28, 209-214 (1994). Links 11. Heller, A. H. & Hallet, M. Electrophysiological studies with the spastic mutant mouse. Brain Res. 234, 299-308 (1982). Links 12. Chai, C. K. Hereditary spasticity in mice. J. Heredity 52, 241-243 (1961). 13. Pertwee, R. G. Pharmacology of cannabinoid CB1 and CB2 receptors. Pharmacol. Therapeut. 74, 129-180 (1997). 14.Breivogel, C. S. & Childers, S. R. The functional neuroanatomy of brain cannabinoid receptors. Neurobiol. Dis. 5, 417-431 (1998). Links 15. Landsman, R. S., Burkey, T. H., Consroe, P., Roeske, W. R. & Yamamura, H. I. SR141716A is an inverse agonist at the human cannabinoid CB1 receptor. Eur. J. Pharmacol. 334, R1-R2 (1997). Links 16. Portier, M. et al. SR144528, an antagonist for the peripheral cannabinoid receptor that behaves as an inverse agonist. J. Pharmacol Exp. Ther. 288, 582-589 (1999). Links 17. Calignano, A., La Rana, G., Giuffrida, A. & Piomelli, D. Control of pain initiation by endogenous cannabinoids. Nature 394, 277-281 (1998). Links 18. Giuffrida, A. et al. Dopamine activation of endogenous cannabinoid signalling in dorsal striatum. Nature Neurosci. 2, 358-363 (1999). Links 19. Huffman, J. W. et al. 3-(1,1-Dimethylbutyl)-1-deoxy-9-THC and related compounds: synthesis of selective ligands for the CB2 receptor. Bioorg. Med. Chem. 7, 2905-2914 (1999). Links 20. Noth, J. Trends in the pathophysiology and pharmacotherapy of spasticity. J. Neurol. 238, 131-139 (1991). Links Acknowledgements. The authors would like to thank the Multiple Sclerosis Society of Great Britain and Northern Ireland, the Medical Research Council, the National Institute on Drug Abuse and the Wellcome Trust for their financial support. Nature © Macmillan Publishers Ltd 2000 Registered No. 785998 England. Smoked Cannabis Reduces Some Symptoms of Multiple Sclerosis Controlled trial shows improved spasticity, reduced pain after smoking medical marijuana A clinical study of 30 adult patients with multiple sclerosis (MS) at the University of California, San Diego School of Medicine has shown that smoked cannabis may be an effective treatment for spasticity – a common and disabling symptom of this neurological disease. The placebo-controlled trial also resulted in reduced perception of pain, although participants also reported short-term, adverse cognitive effects and increased fatigue. The study will be published in the Canadian Medical Association Journal on May 14. Principal investigator Jody Corey-Bloom, MD, PhD, professor of neurosciences and director of the Multiple Sclerosis Center at UC San Diego, and colleagues randomly assigned participants to either the intervention group (which smoked cannabis once daily for three days) or the control group (which smoked identical placebo cigarettes, also once a day for three days). After an 11-day interval, the participants crossed over to the other group. “We found that smoked cannabis was superior to placebo in reducing symptoms and pain in patients with treatment-resistant spasticity, or excessive muscle contractions,” said Corey-Bloom. Earlier reports suggested that the active compounds of medical marijuana were potentially effective in treating neurologic conditions, but most studies focused on orally administered cannabinoids. There were also anecdotal reports of MS patients that endorsed smoking marijuana to relieve symptoms of spasticity. However, this trial used a more objective measurement, a modified Ashworth scale which graded the intensity of muscle tone by measuring such things as resistance in range of motion and rigidity. The secondary outcome, pain, was measured using a visual analogue scale. The researchers also looked at physical performance (using a timed walk) and cognitive function and – at the end of each visit – asked patients to assess their feeling of “highness.” Although generally well tolerated, smoking cannabis did have mild effects on attention and concentration. The researchers noted that larger, long-terms studies are needed to confirm their findings and determine whether lower doses can result in beneficial effects with less cognitive impact. The current study is the fifth clinical test of the possible efficacy of cannabis for clinical use reported by the University of California Center for Medicinal Cannabis Research (CMCR). Four other human studies on control of neuropathic pain also reported positive results. “The study by Corey Bloom and her colleagues adds to a growing body of evidence that cannabis has therapeutic value for selected indications, and may be an adjunct or alternative for patients whose spasticity or pain is not optimally managed,” said Igor Grant, MD, director of the CMCR, which provided funding for the study. Additional contributors include Tanya Wolfson, Anthony Gamst, PhD, Shelia Jin, MD, MPH, Thomas D. Marcotte, PhD, Heather Bentley and Ben Gouaux, all from UC San Diego School of Medicine. Press Release From University Of California, San Diego
  12. PAU D'ARCO TEA - HEALTH BENEFITS The following is a summary of some of the effects of pau d'arco / lapacho and/or any of its constituents that have been validated by modern research: 1. PAU D'ARCO TEA - Laxative effect. Regular use of lapacho will maintain regularity of bowel movements. This property is undoubtedly due to the presence of the napthaquinones and anthraquinones. Users of lapacho universally report a pleasant and moderate loosening of the bowels that leads to greater regularity without any unpleasant side-effects such as diarrhea. 2. PAU D'ARCO TEA - Anti-cancer effect. The greater part of the basic research on lapacho, both in the United States and in other countries has dealt directly with the cancer question. Obviously, this issue is of great importance. The absence of side effects makes lapacho a treatment of choice even in conjunction with standard forms of therapy. The user has nothing to lose and much to gain from the judicious use of Pau d'arco. "I had a large tumor in my brain. Traditional treatment produced only minor success. Then I began to use lapacho tea. After several weeks a CAT scan showed that the tumor was totally gone. The doctors couldn't believe it because they had classified my case as basically untreatable." 3. PAU D'ARCO TEA - Anti-oxidant effect. In vitro trials show definite inhibition of free radicals and inflammatory leukotrienes by lapacho constituents. This property might underlie the effectiveness of lapacho against skin cancer, and definitely helps to explain observed anti-aging effects. Modern science has recently uncovered the importance of free radicals in the generation of many debilitating diseases, from cancer to arthritis. Among the antioxidants few have greater potency than lapacho and other constituents of lapacho. 4. PAU D'ARCO TEA - Analgesic effect. The administration of lapacho is consistently credited in reports issuing from South American clinics as a primary modality for lessening the pain associated with several kinds of cancer, especially cancer of the prostate, liver or breast. Arthritic pain has also been relieved with lapacho ingestion. 5. PAU D'ARCO TEA - Antimicrobial/anti-parisiticidal effects. includes inhibition and destruction of gram positive and acid-fast bacteria (B. subtilis, M. pyogenes aureus, etc.), yeasts, fungi, viruses and several kinds of parasites. Two troublesome families of viruses inhibited by lapachol are noteworthy: Herpes viruses and HIV's. Together, these viruses account for much of the misery of mankind. The anti malarial activity of lapacho spawned a great deal of research interest in the early decades of this century. A 1948 article reviewed the progress and indicated that the N-factors, especially lapachol, were among the most promising anti malarial substances known at that time. Lapacho's immunostimulating action is due in part to its rather potent antimicrobial effects. "I began using pau d'arco tea about 3 mos. ago. I immediately experienced a surge of energy within half-an-hour I was up dancing which is pretty amazing considering I've got MS and spent most of the Spring in a wheelchair. Within 2 days I noticed a lessening of pain and muscle spasms which was fantastic . . . my urinary, bowel and digestive functions have vastly improved . . . There is no doubt that the MS has greatly improved with the herbs as I quit using them for a week and all the old symptoms return. I start the tea again and they subside., I've repeated this scenario three times." 6. PAU D'ARCO TEA - Anti-fungal effect. Lapacho is often singled out as the premier treatment for Candida or yeast infections. Lapachol, N-factors and xyloidone appear to be the primary active principles.9/10 By the mid 70's the list of N-factors that inhibited Candida albicans and other fungi had grown to several dozen. It would be misleading to categorically state that the N-factors in lapacho have proven antimicrobial and anti fungal activity in and of themselves. Studies have shown that the manner in which they occur in the plant must be taken into consideration. We know, for example, that anti fungal activitys lost when the N-factors are tightly bound to highly water-soluble or highly fat-soluble groups. It has not been clearly determined how the N-factors occur in lapacho. N-factors, obtainable from various chemical supply companies, have become favorite testing agents in government/university labs due to the rise in yeast infections resulting from increased use of cytotoxic drugs, corticosteroids, antibiotics and immunosuppressants. An interesting application has been reported in which toe and fingernail fungi infections are relieved by soaking these appendages in lapacho tea off and on for a couple of weeks. 7. PAU D'ARCO TEA - Anti-inflammatory. The anti-inflammatory and healing action of lapacho extracts was demonstrated in a study in which purple lapacho extract was administered to patients with cervicitis and cervico-vaginitis, conditions resulting variously from infections (candida albicans, trichomonas vaginalis), chemical irritations and mechanical irritation. The lapacho extract was applied intra-vaginally via gauze tampons soaked in the extract, and renewed every 24 hours. The treatment proved to be highly effective. One wonders what might happen were the tampon method combined with the ingestion of strong teas. The anti-inflammatory action of lapacho might also account for its observed tendency to reduce the pain, inflammation and other symptoms of arthritis. Anecdotal accounts of complete recovery are even available. As yet virtually untested in research settings, the purported ability of this plant to reduce symptoms of joint disease may be ultimately validated and added to the growing list of benefits to be enjoyed by the daily ingestion of lapacho tea. "I recently had a violent M.S. attack. I lost my balance, lost vision in my left eye and had excruciating pain in my left leg. I went to bed, took the anti-siezure medication and an analgesic. I drank about 1-1/2 quarts of lapacho. Within 6 hours I was up stuffing turkey. Usually these episodes lay me up for weeks. I am convinced the lapacho and mate made the difference." 8. PAU D'ARCO TEA - Other beneficial effects. Routine screenings have revealed several minor properties of lapacho that might occur if needed in certain individuals: diuretic, sedative, decongestant, and hypotensive, to name a few. "I started drinking the red lapacho because I had read a testimonial letter that indicated that its daily use had been effective against the pain of arthritis. I was skeptical to say the least. Prior to drinking the tea I could not stand on a hard surface for more than 5 minutes because the pain was excruciating in my hip . . . Since drinking the red lapacho regularly I have been on my feet for two or three hours without pain. Now the doctor tells me the tissues in my hip are regenerating!" "During exploratory surgery it was noted that I had ovarian, stomach, intestine & liver cancer. I was told I had approximately 4 to 6 months to live. I made up my mind to fight. I went for chemotherapy, drank a quart of red lapacho tea, an ounce of aloe vera juice and took various vitamins daily. After 11 mos. the physicians could not believe what they found (no cancer). I continue to have regular check-ups and have proved to be a 'miracle case'." A Note on Nausea: In the human study reported above, some patients dropped out of the experiment due to nausea. This is a common observation in some, but certainly not all, people who begin to experience the cleansing action of lapacho (and other healthful herbs). As toxins (and toxic medicines) and wastes are drawn out of the cells, or flushed out, or physiologically expelled from the cells, through the action of the herb, they tend at times to accumulate in the blood, lymph, lymph nodes, skin, liver and kidneys awaiting the opportunity to be expelled from the body. Backing up, they can, on occasion produce sensations such as nausea; the body may even try to rid itself of some toxic substances by vomiting. Not to worry. These transient signs dissipate once the toxins are moving freely from the body. They are a positive sign that the herb is working. Remember the body only has three basic processes for getting rid of wastes: lower bowel movement, sweating, urinating. The use of lapacho can so overload these processes in the early stages that discomfort may be produced. "My wife was dying of cancer. She has a malignant tumor on her temple. The pain was so intense the doctors wanted to keep her sedated in the hospital until she died. We decided not to give up. For three weeks now she has been drinking purple lapacho tea. The tumor looks much better; it began draining and no longer looks so 'angry.' The pain is much less, and she can get up and move around the house. Our M.D. is impressed! . . . Now we have hope!" TOXICITY While there can be no doubt that lapacho is very toxic to many kinds of cancer cells, viruses, bacteria, fungi, parasites and other kinds of microorganisms, the substance appears to be without any kind of significant toxicity to healthy human cells. The side-effects mainly encountered, and usually with isolated lapacho constituents, are limited to nausea and anticoagulant effects in very high doses, a tendency to loosen the bowels, and diarrhea in very high doses. As indicated earlier, some nausea should be expected as a natural consequence of the detoxification process. The FDA gave lapacho a clean bill of health in 1981. Some trials have indicated that lapachol has anti-vitamin K action. Other constituents have a pro-vitamain K action; it is likely, therefore, that the two actions cancel each other out (except possibly when one or the other is necessary--as one would expect from an herbal tonic). Perhaps the most significant study on toxicity was published in 1970 by researchers from the Chase Pfizer & Co., Inc. Looking specifically at lapachol, these investigators found that all signs of lapachol toxicity in animals were completely reversible and even self limiting, i.e., over time the signs of toxicity decreased and even disappeared within the time constraints of the study. The most severe kinds of self-limiting side-effects they observed were an anti-vitamin K effect, anemia, and significant rises of metabolic and protein toxins in the blood stream. The diminution of these signs indicates that lapacho initiates an immediate "alterative" or "detoxification" effect on the body's cells. Once the cells are "cleaned up," the signs of toxicity disappear. This effect is quite common among herbal tonics. Clinical studies showed that Pau D'Arco has no contraindications, no incompatabilities, and has been proven to be non-toxic. However, the most innocuous of agents, even oxygen, could finally become toxic if taken in too large enough amounts. A little common sense goes a long way!
  13. AMYOTROPHIC LATERAL SCLEROSIS Edit by Author, 1/15/2013 Some of the source links below are now dead. I was only allowed to take one third of the original content. And leave links. I give you permission to use one third also. Or search out the videos first and and take them from there. http://www.youtube.com/watch?v=Dp4q8YNF9o4 What Types of Nerves Make Your Body Work Properly? (from Living with ALS, Manual 1: What's It All About?) The body has many kinds of nerves. There are those involved in the process of thinking, memory, and of detecting sensations (such as hot/cold, sharp/dull), and others for vision, hearing, and other bodily functions. The nerves that are affected when you have ALS are the motor neurons that provide voluntary movements and muscle power. Examples of voluntary movements are your making the effort to reach for the phone or step off a curb; these actions are controlled by the muscles in the arms and legs. The heart and the digestive system are also made of muscle but a different kind, and their movements are not under voluntary control. When your heart beats or a meal is digested, it all happens automatically. Therefore, the heart and digestive system are not involved in ALS. Breathing also may seem to be involuntary. Remember, though, while you cannot stop your heart, you can hold your breath - so be aware that ALS may eventually have an impact on breathing. Although the cause of ALS is not completely understood, the recent years have brought a wealth of new scientific understanding regarding the physiology of this disease. Source Marijuana's Potential Exciting Researchers in Treatment of ALS, Parkinson's Disease A Legal Mood Lifter: Researchers are investigating a new antidepressant and pain reliever that works like cannabis (marijuana), without the illegal side effects. A decade ago, when Daniele Piomelli went to scientific conferences, he was often the only researcher studying cannabinoids, the class of chemicals that give marijuana users a high. His work often drew snickers and jokes, but no more. At the annual Society for Neuroscience conference recently, scientists here delivered almost 200 papers on the subject. Why the attention? Many scientists believe cannabis-like drugs might be able to treat a wide range of diseases, far beyond the nausea and chronic pain typically treated with medical cannabis. Researchers here presented tantalizing evidence that cannabinoid drugs can help treat amyotrophic lateral sclerosis, known as ALS or Lou Gehrig's disease, Parkinson's disease and obesity. Other researchers are studying whether the compounds can help victims of stroke and multiple sclerosis. Although the chemicals work on the same area of the nervous system, the new drugs are much more refined and targeted than cannabis, with few of its side effects. "Cannabinoids have a lot of pharmaceutical potential," said Piomelli, a neuroscientist at the University of California at Irvine. "A lot of people are very excited" Although the federal government opposes the use of medical marijuana, it generally doesn't restrict cannabinoid research, most of which doesn't involve the cannabis plant itself. Scientists who use Marinol, a legal but tightly regulated marijuana-like drug, do need government permission. Because the cannabinoid system wasn't discovered until the late 1980s, decades after serotonin, dopamine and other neurotransmitters, researchers still know relatively little about how it works. Like all neurotransmitter networks, the cannabinoid system consists of a series of chemical pathways through the brain and nervous system. Cannabis produces its effects by activating this pathway, primarily through the effects of tetrahydrocannabinol, or THC, the drug's main active ingredient. Over the past decade, researchers have been following these abundant trails to determine their real purpose. "You don't have them there to get stoned. So, there must be internal reasons," said Andrea Giuffrida, a neuroscientist at the University of Texas Health Sciences Center in San Antonio. Researchers have learned that endogenous cannabinoids, internal brain chemicals that activate the system, play a role in tissue protection, immunity and inflammation, among other functions. The cannabinoid system also appears to exert wide influence, modulating the release of dopamine, serotonin and other neurotransmitters. Giuffrida and others believe cannabinoids can treat degenerative disorders such as Parkinson's disease and ALS. At the conference, Giuffrida announced that a cannabinoid drug wards off Parkinson's-like effects in mice. The disorder, which afflicts more than 1 million Americans, destroys neurons in a key part of the brain, causing patients to lose control over movement. Giuffrida, with colleagues David Price and James Roberts, injected mice with a chemical called MPTP, which mimics Parkinson's damage. When some of the animals subsequently received a drug that blocks cannabinoid receptors, their nerve cells suffered far less damage than did the cells of the other mice. This was the first demonstration that a cannabinoid drug can have this effect. Although he is not sure how the anti-cannabinoid compound works, Giuffrida suspects it protects neurons by reducing inflammation, a key component in Parkinson's. Cannabinoids might also slow down ALS, which destroys neurons that control muscles until victims become paralyzed, unable to breathe on their own. Neuroscientist Mary Abood first became interested in cannabinoids after hearing about ALS patients who got some relief from smoking cannabis. So she began animal experiments at the California Pacific Medical Center in San Francisco. In her study, mice with a variant of ALS were given a combination of THC and cannabidiol, another compound found in cannabis. Both substances are cannabinoid agonists, chemicals that activate the cannabinoid system. Abood measured the course of the ailment by testing how long the mice could stand on a rod that was slowly rotating. The treatment delayed disease progression by more than seven days and extended survival by six days. In human terms, this would amount to about three years. That's a significant improvement over the only existing ALS drug, riluzole, which extends life by two months. "I was very excited when I got my initial results," Abood said. Also at the conference, researchers at the Institute of Neurology in London announced results that corroborated her findings. Cannabinoids have also helped some human ALS patients in one small trial, and Abood is trying to get funding for a larger one. If cannabinoids can shield human neurons from harm, researchers say, they might prove useful against other neurological diseases, including mental illness. Scientists are looking at whether cannabinoids can treat multiple sclerosis, epilepsy and Huntington's disease, while Giuffrida is beginning a study of their effect on schizophrenia. Advocates of medical cannabis have long argued that the drug can be useful for treating many conditions, particularly chronic pain, nausea and glaucoma (in the latter, cannabis works by temporarily decreasing pressure around the eye). Although they don't dispute this view, most researchers believe there are better, more precise ways to stimulate the cannabinoid system. They believe cannabis has too many negatives to be a truly effective drug, with side effects that include memory problems, decreased immunity and possibly addiction. (Some researchers dispute this "addictive" claim.) Cannabis has another drawback. From a scientific standpoint, Giuffrida says, it's "a very dirty drug." It contains more than 300 compounds, 60 of which affect the cannabinoid system. Scientists don't understand what most of these substances do or how they work together. This complexity makes it hard for researchers to pinpoint cannabis' effects. One cannabinoid, Marinol, is available legally. The compound, which contains THC in a pill form, is usually prescribed for nausea and for appetite loss among AIDS patients. But Marinol has the same psychoactive effects as cannabis. "So the key", Piomelli says, "is getting the effects without the side effects." To that end, Piomelli has developed a compound called URB597, which doesn't flood the body with cannabinoids, as Marinol and cannabis do. Instead, it slows the breakdown of the cannabinoids in the system. He thinks the drug may help treat pain, anxiety and even depression without making patients stoned and forgetful. He and others are testing it on animals. SOURCE http://www.illinoisn...ent/view/600/1/ http://www.youtube.com/watch?v=-qFSMXEYC3c Survey of Cannabis Use in Patients with Amyotrophic Lateral Sclerosis Dagmar Amtmann, PhD Patrick Weydt, Md Kurt L. Johnson, PhD Mark P. Jensen, PhD Gregory T. Carter, M.D. Abstract Cannabis (marijuana) has been proposed as treatment for a widening spectrum of medical condtions and has many properties that may be applicable to the management of amyotrophic lateral sclerosis (ALS). This study is the first, anonymous survey of persons with ALS regarding the use of cannabis. There were 131 respondents, 13 of whom reported using cannabis in the last 12 months. Although the small number of people with ALS that reported using cannabis limits the interpretation of the survey findings, the results indicate that cannabis may be moderately effective at reducing symptoms of appetite loss, depression, pain, spasticity, and drooling. Cannabis was reported ineffective in reducing difficulties with speech and swallowing, and sexual dysfuction. The longest relief was reported for depression (approximately two to three hours). Key words: pain, palliative care, cannabis, medicinal marijuana, amyotrophic lateral sclerosis. Introduction Amyotrophic lateral sclerosis (ALS), with an incident rate of five to seven per 100,000 population, is the most common form of adult motor neuron disease.1-3 ALS is a rapidly progerssive neuromuscular disease that destroys both upper and lower motor neurons, ultimately causing death, typically from respiratory failure. The vast majority of ALS is acquired and occurs sporadically. There is not yet a known cure for ALS. 4-6 ALS patients may present with any number of clinical symptoms, including weakness, spasticity, cachexia, dysarthria and drooling, and pain secondary to immobility, among others.7-8 Previous studies have reported both direct and theoretical applications for using cannabis to manage some of these ALS symptoms.9-11 Cannabis has easily observable clinical effects with rapid onset (e.g., analgesia, muscle relaxation, dry mouth). Moreover, some components of marijuana (not inhaled smoke) have been shown in laboratory studiues to have neuroprotective properties that may help prolong neuronal cell survival over extended time.12-16 Marijuana is a complex plant, containing over 400 chemicals.17 Approximately 60 are cannabinoids, chemically classified as 21 carbon terpenes.17,18 Among the most psychoactive of these is delta-9-tetrahydrocannabinol (THC).17,18 Because of this biochemical complexity, characterizing the clinical pharmacology of marijuana is difficult. The clinical pharmacology of marijuana containing high concentrations of THC may well differ from plant material containing small amounts of THC and higher amounts of the other cannabinoids. The bioavailability and pharmacokinetics of inhaled marijuana are also substantially different from those taken by ingestion. The cannabinoids are all lipid soluble compounds and are not soluble in water.19 Besides THC, which is the active ingredient in dronabinol, varying proportions of other cannabinoids, mainly cannabidiol (CBD) and cannabinol (CBN), are also present in marijuana and may modify the pharmacology of the THC as well as have distinct effects of their own. CBD is not psychoactive but has significant anticonvulsant and sedative pharmacologic properties and may interact with THC.20-21 The concentration of THC and other cannabinoids in marijuana varies greatly depending on growing conditions, plant genetics, and processing after harvest.21 In the usual mixture of leaves and stems distributed as marijuana, concentration of THC ranges from 0.3 percent to 4 percent by weight.21,22 However, specially grown and selected marijuana can contain 15 percent or more THC. Thus, one gram of marijuana might contain as little as three milligrams of THC or more than 150 mg.21 THC is a potent psychoactive drug, and large doses may produce mental and perceptual effects similar to hallucinogenic drugs.23,24 Despite this, THC and other cannabinoids have low toxicity, and lethal doses in humans have not been described.25,26 Despite risk for bronchitis, the main advantage of smoking is rapid onset of effect and easy dose titration. When marijuana is smoked, cannabinoids in the form of an aerosol in the inhaled smoke are rapidly absorbed and delivered to the brain, as would be expected of a highly lipid-soluble drug.27,28 However, smoking anything, including marijuana, carries health risks for the lungs and airway system. A healthier option is vaporization. Because the cannabinoids are volatile, they will vaproize at a temperature much lower than actual combustion.24 Heated air can be drawn through marijuana and the active compounds will vaporize, which can then be inhaled. This delivers the substance in a rapid manner that can be easily titrated to desired effect.29 Vaporization therefore removes most of the health hazards of smoking.27 The medicinal use of cannabis is better documented in multiple sclerosis (MS) than in other clinical conditions, although evidence tends to be anecdotal, and no controlled clinical trials of medicinal marujuana use in MS have been published.30-39 With respect to pain, the concominant use of cannabis with narcotics may be beneficial, because the cannabinoid receptor system appears to be discrete from that of opioids.40-45 In that regard, the antiemetic effect of cannabis may also help with the nausea sometimes associated with narcotic medications. Untoward effects of cannabis include potentially significant psychoactive properties, which may produce a sense of well-being or euphoria but can also induce anxiety, confusion, paranoia, and lethargy.46 To date there have not yet been any empirical studies to investigate the use of cannabis for medicinal purposes in ALS. The purpose of this survey was to gather preliminary data on the extent of use of cannabis among persons with ALS (PALS) and to learn which of the symptoms experienced by PALS are reported to be alleviated by the use of cannabis. Metohdology Participants in this survey were recruited from the ALS Digest (the Digest), an electronic discussion list published weekly to serve the worldwide ALS community, including patients, families, caregivers, and providers. The Digest serves as a forum for discussion of issues related to ALS and is not intended to provide medical advice on individual health matters. The Digest can be viewed at www.alslinks.com. Currently there are over 5,600 subscribers in 80 countries worldwide. However, the number of subscribers with ALS is not known. The editor is not a physician and the Digest is not peer reviewed. An e-mail invitation to participate was posted to the Digest four times over two months. The survey was available online from January 6 through March 2, 2003, approximately eight consecutive weeks. Any subscriber with ALS was invited to participate on a voluntary and anonymous basis. The sponsoring institution human subjects review board approved the study protocol. A Web-based survey tool developed by the University of Washignton was used to collect responses. The tool uses SSL encryption for transferred data, and all identifying information was stored in a code translation table separate from the actual data to protect the privacy of respondents. The University of Washington human subjects review board has approved this tool for research purposes. PALS who wanted to participate were given a Web site address that introduced the survey and provided a link to the survey site. The invitation to participate did not mention cannabis or marijuana, in order to discourage participation by individuals who do not have ALS but might otherwise be interested in promoting legalization of marijuana. The sruvey was titled "A survey of ALS Patients Who Use Alternative Therapies to Treat Symptoms." It was presumed by the investigatiors that the diagnostic information provided by the survey participants was accurate (i.e., no medical records were reviewed to confirm their diagnosis). In addition to a series of questions related to the ALS symptoms, the use of cannabis, and its effectiveness in alleviating the symptoms of ALS, participants were also asked to provide demographic and diagnostic information. The survey was anonymous and it is therefore impossible to conclusively determine whether all respondents were individuals with ALS. However, the first six questions of the survey asked about how and when the respondent was diagnosed with ALS and specifically asked those who were not diagnosed with ALS by a physician to not fill out the survey. The authors carefully studied the demographic and diagnostic information provided by each respondent for completeness, consistency, and plausiblity. Records with the diagnostic information missing were excluded from the analysis. Many participants offered extensive information about other alternative therapies they use, and the general comments appeared to reflect experiences of individuals living with ALS. Results A total of 137 responses were received. Four responses were excluded because of duplicate submission (i.e. the same person inadvertently submitting more than one survey by hitting the submit key more than once) and two because of failure to complete most of the questions of the survey. Eletronic logs of all submissions were inspected for repeated entries from the same Internet protocol (IP) address. None were found. A total of 131 responses were retained for analysis. The demographics of the sample are shown in Table 1. Seventy-five percent of the respondents were male and 90 percent were caucasian. The average age of participants was 54 years [standard deviation(sd)=11], with no significant difference between the genders [Mean(M) mean(m)=54 for=for males,=males, sd=12.5 m=53 females,=females,]. Eighty-four percent of the respondents were married or living with a significant other, 17 percent were employed (full time or part-time), 64 percent were unemployed or retired due to disability, and 18 percent were retired due to age. Respondents reported high levels of education, with only 13 percent with high school education or less and 62 percent with college education or higher. The time since ALS diagnosis ranged from one month to 24 years. The median time since diagnosis (i.e., duration) was three years, the mean duration was approximately four years (M=4.4, SD=4.0). About a half of the sample reported they used a wheelchair usually or always, and about 20 percent reported no restrictions in mobility. Eighty-one percent of the respondents filled out the survey independently while 19 percent reported that they required assistance from others. One-half of the participants were taking Riluzole. The majority of participants (69 percent) reported that they live in the Unted States, 8 percent in Canada, and 5 percent in Australia. Six percent of the participants live in Europe, while the rest (12 percent) of the respondents reported that they were from Africa, India, Israel, Brazil, Ecuador, Guatemala, or Argentina. Fifty-three participants (41 percent) reported drinking alcohol, 14 (11 percent) reported that they use tobacco, and four (3 percent) reported consuming both alcohol and tobacco. Use of cannabis Seventy-seven respondents (60 percent) reported that they never used cannabis, and 41 (31 percent) used cannabis in teenage or college years only. Thirteen respondents (10 percent) reported using cannabis in the last 12 months, and their demographics are outlined in Table 2. Those who reported using cannabis in the last 12 months were all male and all lived in the US. Ten of those who reported using cannabis in the last 12 months also responded affirmatively to the question that asked about the use of cannabis during the teenage, college, and adult years. All of those who reported using cannabis in the last 12 months also reported that they used cannabis at some point in their lives before they were diagnosed with ALS. Six of the cannabis users reported that they lived in a state where medical cannabis is legal, and four lived in a state where medical cannabis is illegal. The remaining three respondents were not sure whteher medical cannabis was legal in their state. There were no statistcally significant differences between the cannabis users and non-users (see Table 2) on any demographic variable (age, marital status, employment status, education level, time since diagnosis, mobility status). None of those who reported using cannabis in the past 12 months reported tobacco use, but all reported drinking alcohol. Eight cannabis users reported smoking cannabis in the last three months. Two respondents reported smoking cannabis infrequently (less often than once a month), one reported smoking one to two times a week, and three reported daily use. No respondents reported only breathing vaporized cannabis, although one participant reported using vaporized cannabis in addition to smoking and using medicinal cannabis. Two participants reported eating cannabis, one in addition to smoking it. Three respondents used medicinal cannabinoids (i.e., Dronabinol). Of the three respondents who used medicinal cannabinoids, one reported using only medicinal cannabinoids, one also smoked cannabis, and one both smoked as well as breathed vaporized cannabis. Symptoms The intensity of ALS-related symptoms was quantified by asking respondents to rate how much they experience each of the symptoms on a five-point scale ranging from "not at all" (0) to "very much" (4). The most frequent sympotm was weakness, followed by speech difficulties, drooling and swalowing difficulties. The intnesity of symptoms reported by respondents who did not use cannabis was not statistically significantly idfferent from the symptom intensity reported by the cannabis users [F(10, 120)=120) 1.07,=1.07, p=.39]. A summary of symptoms and their intensity is listed in Table 3. The ammount of relief attributed to cannabis use was assessed by asking the respondents to rate the degree to which cannabis alleviates each symptom on a five-point scale ranging from "not at all" (0) to "completely relieves the symptom" (4). Respondents reported that the use of cannabis helped moderately for depression, appetite loss, spasticity, drooling, and pain. All cannabis users who reported symptoms of appetite loss and depression also reported that cannabis reduced these symptoms. None of the cannabis users reported any reduction in difficulties with swallowing and speech or sexual dysfunction. The duration of symptom relief was measured on a scale from 0 (no relief) to 6 (more than nine hours). Respondents reported the most lasting relief (on average two to three hours) for depression. The loss of appetite, drooling, shortness of breath, spasticity, and pain were reported to be relieved on average for approximately one hour or less. Table 4 provides a summary of symptoms reported by the cannabis users. Level of relief was reported on a five-point scale ranging from "not at all" (0) to "completely relieves the symptom" (4). The duration of sumptom relief was measured on a scale from "no relief" (0), "less than one hour" (1), "two to three hours" (2), "four to five hours" (3), "six to seven hours" (4), "eight to nine hours" (5), "more than nine hours" (6). Discussion There is an increasing amount of research concerning the medicinal effects of cannabinoids. For example, cannabinoids have been reported to reduce chemotherapy-induced nausea and vomiting, lower intraocular pressure in patients with glaucoma, reduce anorexia in patients with cancer and AIDS-associated weight loss, and reduce pain and spasticity in MS.30-39 Cannabinoids, the active ingredients in marijuana, may also have properties that may be applicable to the management of ALS.9,10 However, to date no empirical studies of use and effectiveness of cannabis for symptom management by PALS have been published. Approximately 10 percent of the survey respondents reported using cannabis. This is a lower rate than the frequency of use reported by other patient populations, including MS, AIDS, and cancer patients.10,30,31 However, the pattern of symptom relief reported by the small number of PALS who reported using cannabis for symptom management by people with other conditions, including MS.30,35,36 Cannabis users reported that cannabis smoking was most effective at reducing depression, appetite loss, pain, spasticity, drooling, and weakness. The factor that most predicted current use of cannabis by PALS was reported previous use (presumably recreational). The survey had a number of limitations. First, the survey results reported here are based on a relatively small number of respondents (131) and on reports of 13 cannabis users, and may not be representative of the patterns of cannabis use in the ALS population by people with ALS in general. Second, 75 percent of the respondents were male, 25 percent were female. Men appear to be about 1.5 times more likely to be affected with ALS than women,7,8 so the percentage of female participants is slightly lower than expected in the general ALS population (about 33 percent). Published studies of Internet use consistently report that females are less likely to use the Internet for reasons that may be independent of income and estimate that only about one-third of Internet users are women.47,48 This may account for the lower than expected participation by women with ALS. A third limitation of the study is that a disproportionate number of the survey respondents were white (90 percent) and all cannabis users were white. There is some evidence that whites may be at higher risk for ALS though most researchers agree that ALS equally affects people of all races.49,50 Racial discrepancies in rates of ALS may be due to poorer access to healthcare for minority populations in the US, particularly access to tertiary referral centers, where the ALS diagnosis is often made. Published studies report that over 80 percent of Internet users are white;48 this is the most likely explanation for the disproportionate perticipation by Caucasians in this survey. Fourth, Internet users tend to be highly educated. Almost 60 percent repoert having at least one degree.48 Those with higher education are more likely to own computer equipment and to use it to connect to the Internet.51 The results of the survey we report here provide further evidence for this trend, with only 13 respondents (10 percent) reported having high school education or less. Finally, none of the participants from the countries where cannabis use is prevalent (India) or legal for medical uses (Australia, Canada) reported using cannabis. The most likely explanation for this finding is the small number of perticipants from these countries; only one respondent was from India, six from Australia, and eleven from Canada. In general, professionals with university degrees living in households with disposable incomes sufficient to purchase technology tools are likely to be over-represented in Internet surveys. Women, minorities, the elderly, those who liveon social assistance disability payments, or who earn minimum wages, are much less likely to participate.48,51 Privacy is a major issue associated with Web-based methodology. When the Internet is used for research, especially for research on sensitive issues (such as using substances that are illegal under federal law and most state laws), protecting the privacy of the participants is paramount. By making the survey anonymous, the authors protected the privacy of the respondents but gave up the ability to verify respondent' diagnoses or prevent repeated or malicious submittals. Although the records showed that no two responses were submitted from the same IP address, the IP address identifies the computer, not the user. Therefore, it cannot be conclusively determined that one respondent did not submit more than one response using different computers. The low response rate might be explained by many factors. First, we do not know how many participants in the electronic discussion list that was used to recruit participants have ALS. It is possible, even likely, that a large majority of the participants are family members, service providers, and advocates. Second, the respondents who do not use alternative therapies may have been less likely to respond. It is unclear what percentage of people with ALS use alternative therapies. A recent survey from Germany suggests that about half of the ALS patients there use complementary and alternative medicine.52 Some respondents who do not use alternative therapies such as vitamins and supplements, but do use cannabis to manage their symptoms may not have considered cannabis to be an "alternative therapy" and decided not to participate. Many respondents provided information on vitamins, supplements, and other alternative therapies in the write-in spaces of the survey even though they were nto asked about these therapies directly, probably because the respondents had anticipated the survey would gather informationon those topics. Third, even though the invitation as well as the introduction to the survey clearly stated that the survey was anonymous and there was no way for the researchers to associate a specific response with a specific respondent, many may have been individuals who are generally suspicious of providing information via the Internet and may have decided not to participate for this reason. Despite the limitations of this study noted above, these preliminary findings support the need for further research into the potential benefits of cannabis use for the clinical management of some ALS symptoms. These include pain, which was one of the symptoms identified in a recent study as not being sufficiently addressed in ALS.53 Further research is needed to see if the current findings can be confirmed using non-Internet-based survey methodology with a defined sample. It would also be informative to inquire about cannabis use within the context of subject beliefs about the efficacy of various alternative and complimentary approaches and their engagement and satisfaction with those approaches. Acknowledgements Funding for this research was provided by grants from the National Institute on Disability and Rehabilitation Research, Washington, DC and from the National Institutes of Health References 1. Norris F, Sheperd R, Denys E, Et al.: Onset, natural history and outcome in idiopathic adult motor neuron disease. J Neurol Sci. 1993; 118(1); 48-55. 2. Ringel SP, Murphy JR, Alderson MK, et al.: The natural history of amyotrophic lateral sclerosis. Neurology. 1993; 43(7): 1316-1322. 3. Neilson S, Tobinson I, Nymoen EH: Longitudinal analysis of amyotrophic lateral sclerosis mortality in Norway, 1966-1989: Evidence for a susceptible subpopulation. J Neurol Sci. 1994; 122(2): 148-154. 5. Eisen A: Amyotropic lateral sclerosis is a multifactorial disease. Muscle Nerve. 1995; 18(7): 741-752. 6. Eisen A, Schulzer M, MacNeil M, et al.: Duration of amyotrophic lateral sclerosis is age dependent. Muscle Nerve. 1993; 16: 27-32. 7. Carter GT, Miller RG: Comprehensive management of amyotrophic lateral sclerosis. Phys Med Rehabil Clin N Am. 1998; 9(1): 271-284. 8. Carter GT, Krivickas LS: Adult motor neuron disease. In Kirshblum S, Campagnolo DL, DeLisa JA, (eds.): Spinal Cord Injury Medicine. Philadelphia: Lippincott, Williams, and Wilkins, 2002. 9. Carter GT, Rosen BS: Marijuana in the management of amyotrophic lateral sclerosis. Am J Hosp Palliat Care. 2001; 18(4): 264-270. 10. Carter GT, Weydt P. Cannabis: Old medicine with new promise for neurological disorders. Curr Opin Investig Drugs. 2002; 3(3): 437-440. 11. Weydt P, Weiss MD, Moller T, et al.: Neuroinflammation as a therapeutic target in amyotrophic lateral sclerosis. Curr Opin Investig Drugs. 2002; 3(12): 1720-1724. 12. Hampson AJ, Grimaldi M, Axelrod J, et al.: Cannabidiol and (-)Delta9-tetrahydrocannabinol are neuroprotective antioxidants. Proc Natl Acad Sci USA 1998; 95(14): 8268-8273. 13. Hampson AH, Grimaldi M, Lolic M, et al.: Neuroprotective antioxidants from marijuana. Ann NY Acad Sci. 2000; 899: 274-282. 14. Nagayama T, Sinor AD, Simon RP, et al.: Cannabinoids and neuroprotection in global and focal cerebral ischemia and in neuronal cultures. J Neurosci. 1999; 19(8): 2987-2995. 15. Chen Y, Buck J: Cannabinoids protect cells from oxidative cell death: A receptor-independent mechanism. J Pharmacol Exp Ther. 2000; 293(3): 807-812. 16. Eshhar N, Striem S, Biegon A: HU-211, a non-psychotropic cannabinoid, rescues cortical neurones from excitatory amino acid toxicity in culture. Neuroreport. 1993; 5(3): 237-240. 17. Adams IB, Martin BR: Cannabid: Pharmacology and toxicoloty in animals and humans. Addiction. 1996; 91(11): 1585-1614. 18. Agurell S, Halldin M, Lindgren Je, et al.: Pharmacokinetics and metabolism of delta 1-tetrahydrocannabinol and other cannabinoids with emphasis on man. Pharmacol Rev. 1986; 38(1): 21-43. 19. Johansson E, Halldin MM, Agurell S, et al.: Terminal elimination plasma half-life of delta 1-tetrahydrocannabinol (delta 1-THC) in heavy users of Marijuana. Eur J Clin Pharmacol. 1989; 37(3): 273-277. 20. Thomas BF, Adams IB, Mascarella SW, et al.: Structure-activity analysis of anandamide analogs: Relationship to a cannabinoid pharmacophore. J Med Chem. 1996, 39(2): 471-497. 21. Mechoulam R, Davane WA, Breuer A, et al.: A random walk whrough a cannabis field. Special Issue: Pharmacological, chemical, biochemical and behavioral research on cannabis and the cannabinoids. Pharmacol Biochem Behav. 1991; 40(3): 461-464. 22. Conrad C: Hemp for Health: The Medicinal and Nutritional Uses of Cannabis Sativa. Rochester, Vermont: Healing Arts Press, 1997. 23. Jones RT: Drug of abuse profile: Cannabis. Clin Chem. 1987; 33(11 Suppl): 72B-81B. 24. Jones RT, Beonwitz NL, Herning RI: Clinical relevance of cannabis tolerance and dependence. J Clin Pharmacol.. 1981; 21: 143S-152S. 25. Polen MR, Sidney S, Tekawa IS, et al.: Health care use by frequent marijuana smokers who do not smoke tobacco. West J Med. 1993; 158(6): 596-601. 26. Pope HG, Yurgelun-Todd D: The residual cognitive effects of heavy marijuana use in college students. JAMA 1996; 275(7): 521-527. 27. Renn E, Mandel S, Mandel E: The medicinal uses of marijuana. Pharm Ther. 2000; 25(10: 536-524. 28. Gurley RJ, Aranow R, Katz M: Medicinal marijuana: A comprehensive review. J Psycho-active Drugs. 1998; 30(2): 137-147. 29. Voth EA, Schwartz RH: Medicinal applications of delta-9-tetrahydrocannabinol and marijuana. Ann Intern Med. 1997; 126(10): 791-798. 30. Cosroe P, Musty R, Rein J, et al.: The perceived effects of smoked cannabis on patients with multiple sclerosis. Eur Neurol. 1997; 38: 44-48 31. Beal JE, Olson DO, Laubenstein L, et al.: Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS. J Pain Symptom Manage. 1995; 10: 89-97. 32. Foltin RW, Fischman MW, Byrne MF: Effects of smoked marijuana on food intake and body weight of humans living in a residential laboratory. Appetite. 1988; 11: 1-14. 33. Greenberg I, Kuehnle J, Mendelson JH: Effects of marijuana use on body weight and caloric intake in humans. Psychopharmacology (Berl). 1976; 49: 79-84. 34. Nelson K, Walsh D, Deeter P, et al.: A phase II study of delta-9-tetrahydrocannabinol for appetite stimulation in cancer-associated anorexia. J Palliat Care. 1994; 10(1): 14-18. 35. Meinck HM, Schonle PW, Conrad B: Effects of cannabinoids on spasticity and ataxia in multiple sclerosis. J Neurol. 1989; 263(2): 120-122. 36. Greenberg HS, Weiness AS, Pugh JE: Short term effects of smoking marijuana on balance in patients with multiple sclerosis and normal volunteers. Clin Pharmacol Ther. 1994; 55: 324-328. 37. Renn E, Mandel S, Mandel E: The medicinal uses of marijuana. Pharm Ther. 2000; 25(10): 536-524. 38. Gurley RJ, Aranow R, Katz M: Medicinal marijuana: A comprehensive review. J Psychoactive Drugs. 1998; 30(2): 137-147. 39 Voth EA, Schwartz RH: Medicinal applications of delta-9-tetrahydrocannabinol and marijuana. Ann Intern Med. 1997; 126(10): 791-798. 40. Meng Id, Manning BH, Martin WJ, et al.: An analgesia circuit activated by cannabinoids. Nature. 1998; 395(6700): 381-383. 41. Noyes R, Brunk SF, Baram DA, et al.: Analgesic effect of delta-9-tetrahydrocannabinol. J Clin Pharmacol. 1975a; 15(2-3): 139-143. 42. Zeltser R, Seltzer Z, Eisen A, et al.: Suppression of neuropathic pain behavior in rats by a non-psychotropic synthetic cannabinoid with NMDA receptor-blocking properties. Pain. 1991; 47(1): 95-103. 43. Noyes R, Brunk SF, Avery DAH, et al.: The analgesic properties of delta-9-tetrahydracannabinol. Clin Pharmacol Ther. 1975b; 18(1):84-89. 44. Richardson JD. Cannabinoids modulate pain by multiple mechanisms of action. J Pain. 2000; 1(1): 1-20. 45. Carter GT, Butler LM, Abresch RT, et al.: Expanding the role of hospice in the care of amyotrophic lateral sclerosis. Am J Hosp Palliat Care. 1999; 16(6): 707-710. 46. National Institute on Drug Abuse. Reserach Report Series: Marijuana Abuse. Bethesda, MD: National Institutes on Health, 2003. 47. Edsworth SM: World Wide Web: Opportunities, challenges, and threats. Lupus. 1999; 8: 596-605. 48. Kehoe C, Pitkow J, Sutton K, et al.: Results of GVU's Tenth World Wide Web User Survey. Georgia Institute of Technology, Graphics Visualization and Usability Center, College of Computing, Atlanta, Georgia. Available at WWW.gvu.gatech.edu/user_surveys/survey-1998-10/tenthreport.html. Accessed May 14, 1999. 49. Leone M, Chandra V, Schoenberg BS: Motor neuron disease in the United States, 1971 and 1973-1978: Patterns of mortality and associated conditions at the time of death. Neurology. 1987; 37(8): 1339-1343. 50. Lilenfeld DE, Chan E, Ehland J, et al.: Rising mortality from motoneuron disease in the USA, 1962-84. Lancet. 1989; 1(8640): 710-713. 51. Kaye S: Computer and Internet Use Among People with Disabilities. Washington, DC: NIDRR, US Dept. of Education, 2000. 52. Wasner M, Klier H, Borasio GD: The use of alternative medicine by patients with amyotrophic lateral sclerosis. J Neurol Sci. 2001; 191(1-2): 151-154. 53. Mandler RN, Anderson FA, Miller RG, et al.: ALS C.A.R.E. Study Group. The ALS patient care database: insights in to end-of-life care in ALS. Amyotroph Lateral Scler Other Motor Neruon Disord. 2001; 2(4): 203-208 source: http://www.cannabism...rts/carter4.php Amyotrophic lateral sclerosis: delayed disease progression in mice by treatment with a cannabinoid. Raman C, McAllister SD, Rizvi G, Patel SG, Moore DH, Abood ME. Forbes Norris MDA/ALS Research Center, 2351 Clay Street, Suite 416, California Pacific Medical Center, San Francisco, CA 94115, USA. Effective treatment for amyotrophic lateral sclerosis (ALS) remains elusive. Two of the primary hypotheses underlying motor neuron vulnerability are susceptibility to excitotoxicity and oxidative damage. There is rapidly emerging evidence that the cannabinoid receptor system has the potential to reduce both excitotoxic and oxidative cell damage. Here we report that treatment with Delta(9)-tetrahydrocannabinol (Delta(9)-THC) was effective if administered either before or after onset of signs in the ALS mouse model (hSOD(G93A) transgenic mice). Administration at the onset of tremors delayed motor impairment and prolonged survival in Delta(9)-THC treated mice when compared to vehicle controls. In addition, we present an improved method for the analysis of disease progression in the ALS mouse model. This logistic model provides an estimate of the age at which muscle endurance has declined by 50% with much greater accuracy than could be attained for any other measure of decline. In vitro, Delta(9)-THC was extremely effective at reducing oxidative damage in spinal cord cultures. Additionally, Delta(9)-THC is anti-excitotoxic in vitro. These cellular mechanisms may underlie the presumed neuroprotective effect in ALS. As Delta(9)-THC is well tolerated, it and other cannabinoids may prove to be novel therapeutic targets for the treatment of ALS. source: http://www.ncbi.nlm....Pubmed_RVDocSum
  14. Cannabis cured my Cancer Causes, incidence, and risk factors Prostate cancer is the most common cause of death from cancer in men over age 75. Prostate cancer is rarely found in men younger than 40. People who are at higher risk include: African-American men, who are also likely to develop cancer at every age Men who are older than 60 Men who have a father or brother with prostate cancer Other people at risk include: Men who have been around agent orange Men who use too much alcohol Farmers Men who eat a diet high in fat, especially animal fat Tire plant workers Painters Men who have been around cadmium Prostate cancer is less common in people who do not eat meat (vegetarians). A common problem in almost all men as they grow older is an enlarged prostate. This is called benign prostatic hyperplasia, or BPH. It does not raise your risk of prostate cancer. However, it can increase your PSA blood test results. Symptoms The PSA blood test is often done to screen men for prostate cancer. Because of PSA testing, most prostate cancers are now found before they cause any symptoms. The symptoms listed below can occur with prostate cancer, usually at a late stage. These symptoms can also be caused by other prostate problems: Delayed or slowed start of urinary stream Dribbling or leakage of urine, most often after urinating Slow urinary stream Straining when urinating, or not being able to empty out all of the urine Blood in the urine or semen Bone pain or tenderness, most often in the lower back and pelvic bones (only when the cancer has spread) Signs and tests A biopsy is needed to tell if you have prostate cancer. A sample of tissue is removed from the prostate and sent to a lab. Your doctor may recommend a prostate biopsy if: You have high PSA level A rectal exam shows a large prostate or a hard, uneven surface The results are reported using what is called a Gleason grade and a Gleason score. The Gleason grade tells you how fast the cancer might spread. It grades tumors on a scale of 1 - 5. You may have different grades of cancer in one biopsy sample. The two main grades are added together. This gives you the Gleason score. The higher your Gleason score, the more likely the cancer is to have spread past the prostate: Scores 2 - 5: Low-grade prostate cancer Scores 6 - 7: Intermediate- (or in the middle-) grade cancer. Most prostate cancers fall into this group. Scores 8 - 10: High-grade cancer The following tests may be done to determine whether the cancer has spread: CT scan Bone scan The PSA blood test will also be used to monitor your cancer after treatment. Often, PSA levels will begin to rise before there are any symptoms. An abnormal digital rectal exam may be the only sign of prostate cancer (even if the PSA is normal). Treatment Treatment depends on many things, including your Gleason score and your overall health. Your doctor will discuss your treatment options. For early-stage prostate cancer, this may include: Surgery (radical prostatectomy) Radiation therapy, including brachytherapy and proton therapy If you are older, your doctor may recommend simply monitoring the cancer with PSA tests and biopsies. If the prostate cancer has spread, treatment may include: Hormone therapy (medicines to reduce testosterone levels) Surgery Chemotherapy Surgery, radiation therapy, and hormone therapy can affect your sexual desire or performance. Problems with urine control are common after surgery and radiation therapy. Discuss your concerns with your health care provider. After treatment for prostate cancer, you will be closely watched to make sure the cancer does not spread. This involves routine doctor check-ups, including PSA blood tests (usually every 3 months to 1 year). See also: Prostate cancer - stages Prostate radiation - discharge Support Groups You can ease the stress of illness by joining a support group whose members share common experiences and problems. See: Support group - prostate cancer Expectations (prognosis) How well you do depends on whether the cancer has spread outside the prostate gland and how abnormal the cancer cells are (the Gleason score) when you are diagnosed. Many patients can be cured if their prostate cancer has not spread. Some patients whose cancer has not spread very much outside the prostate gland can also be cured. Hormone treatment can improve survival, even in patients who cannot be cured. Complications The complications of prostate cancer are mostly due to different treatments. Calling your health care provider Discuss the advantages and disadvantages to PSA screening with your health care provider. Prevention You may lower your risk of prostate cancer by eating a diet that is: High in omega-3 fatty acids Low-fat Similar to the traditional Japanese diet Vegetarian Finasteride (Proscar, generic) and dutasteride (Avodart) are drugs used to treat prostate enlargement (benign prostatic hyperplasia, or BPH). If you do not have prostate cancer and your PSA score is 3.0 or lower, ask your health care provider about the pros and cons of taking these drugs to prevent prostate cancer. References Theoret MR, Ning YM, Zhang JJ, et al. The risks and benefits of 5a-reductase inhibitors for prostate-cancer prevention. N Engl J Med. 2011 Jun 15. Antonarakis ES, Eisenberger MA. Expanding treatment options for metastatic prostate cancer. N Engl J Med. 2011 May 26;364:2055-2058. Andriole GL, Crawford ED, Grubb RI 3rd, Buys SS, Chia D, Church TR, et al. Mortality results from a randomized prostate-cancer screening trial. N Engl J Med. 2009;360:1310-1319. Babaian RJ, Donnelly B, Bahn D, Baust JG, Dineen M, Ellis D, et al. Best practice statement on cryosurgery for the treatment of localized prostate cancer. J Urol. 2008;180:1993-2004. Schrader FH, Hugosson J, Roobol MJ, Tammela TL, Ciatto S, Nelen V, et al. Screening and prostate-cancer mortality in a randomized European study. N Engl J Med. 2009;360:1320-1328. Walsh PC. Chemoprevention of prostate cancer. N Engl J Med. 2010 Apr 1;362(13):1237-8. Wilt TJ, MacDonald R, et al. Systematic review: comparative effectiveness and harms of treatments for clinically localized prostate cancer. Ann Intern Med. 2008;148(6):435-448. Review Date: 9/19/2011. Reviewed by: Louis S. Liou, MD, PhD, Chief of Urology, Cambridge Health Alliance, Visiting Assistant Professor of Surgery, Harvard Medical School. Also reviewed by David Zieve, MD, MHA, Arachidonoylglycerol A Novel Inhibitor of Androgen-Independent Prostate Cancer Cell Invasion Kasem Nithipatikom1, Michael P. Endsley1, Marilyn A. Isbell1, John R. Falck3, Yoshiki Iwamoto2, Cecilia J. Hillard1 and William B. Campbell1 Departments of 1 Pharmacology and Toxicology and 2 Urology, Medical College of Wisconsin, Milwaukee, Wisconsin; and 3 Departments of Biochemistry and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas Endocannabinoids have been implicated in cancer. Increasing endogenous 2-arachidonoylglycerol (2-AG) by blocking its metabolism inhibits invasion of androgen-independent prostate cancer (PC-3 and DU-145) cells. Noladin ether (a stable 2-AG analog) and exogenous CB1 receptor agonists possess similar effects. Conversely, reducing endogenous 2-AG by inhibiting its synthesis or blocking its binding to CB1 receptors with antagonists increases the cell invasion. 2-AG and noladin ether decrease protein kinase A activity in these cells, indicating coupling of the CB1 receptor to downstream effectors. The results suggest that cellular 2-AG, acting through the CB1 receptor, is an endogenous inhibitor of invasive prostate cancer cells. source: http://cancerres.aac...ract/64/24/8826 Activation of Signal Transducer and Activator of Transcription 5 in Human Prostate Cancer Is Associated with High Histological Grade Hongzhen Li1, Tommi J. Ahonen4, Kalle Alanen5, Jianwu Xie1, Matthew J. LeBaron1, Thomas G. Pretlow7, Erica L. Ealley1, Ying Zhang2, Martti Nurmi6, Baljit Singh3,1, Paula M. Martikainen8 and Marja T. Nevalainen1 Departments of 1 Oncology, 2 Biostatistics Unit, and 3 Pathology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington DC; Departments of 4 Anatomy and Cell Biology and 5 Pathology, Institute of Biomedicine, University of Turku, Turku, Finland; 6 Department of Surgery, University Hospital of Turku, Turku, Finland; 7 Department of Pathology, Case Western Reserve Medical Center, Cleveland, Ohio; and 8 Deptartment of Pathology, Tampere University Hospital, Tampere, Finland We have recently identified signal transducer and activator of transcription 5 (Stat5) as a critical survival factor for prostate cancer cells. We now report that activation of Stat5 is associated with high histological grade of human prostate cancer. Specifically, immunohistochemical analysis demonstrated a strong positive correlation with activation of Stat5 and high Gleason score in 114 human prostate cancers. To investigate the mechanisms underlying constitutive activation of Stat5 in prostate cancer, a dominant-negative mutant of Janus kinase 2 (Jak2) was delivered by adenovirus to CWR22Rv cells. Dominant-negative-Jak2 effectively blocked the activation of Stat5 whereas wild-type Jak2 enhanced activation, indicating that Jak2 is the main kinase that phosphorylates Stat5 in human prostate cancer cells. A ligand-induced mechanism for activation of Stat5 in prostate cancer was suggested by the ability of prolactin (Prl) to stimulate activation of both Jak2 and Stat5 in CWR22Rv human prostate cancer cells and in CWR22Rv xenograft tumors. In addition, Prl restored constitutive activation of Stat5 in five of six human prostate cancer specimens in ex vivo long-term organ cultures. Finally, Prl protein was locally expressed in the epithelium of 54% of 80 human prostate cancer specimens with positive correlation with high Gleason scores and activation of Stat5. In conclusion, our data indicate that increased activation of Stat5 was associated with more biologically aggressive behavior of prostate cancer. The results further suggest that Jak2 is the principal Stat5 tyrosine kinase in human prostate cancer, possibly activated by autocrine/paracrine Prl. source: http://cancerres.aac...ract/64/14/4774 Suppression of Nerve Growth Factor Trk Receptors and Prolactin Receptors by Endocannabinoids Leads to Inhibition of Human Breast and Prostate Cancer Cell Proliferation1 Dominique Melck, Luciano De Petrocellis, Pierangelo Orlando, Tiziana Bisogno, Chiara Laezza, Maurizio Bifulco and Vincenzo Di Marzo Istituto per la Chimica di Molecole di Interesse Biologico (D.M., T.B., V.D.M.), Istituto di Cibernetica (L.D.P.), and Istituto di Biochimica delle Proteine ed Enzimologia (P.O.), Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA); and Centro di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, and Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli Federico II (C.L., M.B.), 80131 Naples, Italy Address all correspondence and requests for reprints to: Dr. Vincenzo Di Marzo, Istituto per la Chimica di Molecole di Interesse Biologico, Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA), Italy. E-mail: vdm@trinc.icmib.na.cnr.it. Anandamide and 2-arachidonoylglycerol (2-AG), two endogenous ligands of the CB1 and CB2 cannabinoid receptor subtypes, inhibit the proliferation of PRL-responsive human breast cancer cells (HBCCs) through down-regulation of the long form of the PRL receptor (PRLr). Here we report that 1) anandamide and 2-AG inhibit the nerve growth factor (NGF)-induced proliferation of HBCCs through suppression of the levels of NGF Trk receptors; 2) inhibition of PRLr levels results in inhibition of the proliferation of other PRL-responsive cells, the prostate cancer DU-145 cell line; and 3) CB1-like cannabinoid receptors are expressed in HBCCs and DU-145 cells and mediate the inhibition of cell proliferation and Trk/PRLr expression. ß-NGF-induced HBCC proliferation was potently inhibited (IC50 = 50–600 nM) by the synthetic cannabinoid HU-210, 2-AG, anandamide, and its metabolically stable analogs, but not by the anandamide congener, palmitoylethanolamide, or the selective agonist of CB2 cannabinoid receptors, BML-190. The effect of anandamide was blocked by the CB1 receptor antagonist, SR141716A, but not by the CB2 receptor antagonist, SR144528. Anandamide and HU-210 exerted a strong inhibition of the levels of NGF Trk receptors as detected by Western immunoblotting; this effect was reversed by SR141716A. When induced by exogenous PRL, the proliferation of prostate DU-145 cells was potently inhibited (IC50 = 100–300 nM) by anandamide, 2-AG, and HU-210. Anandamide also down-regulated the levels of PRLr in DU-145 cells. SR141716A attenuated these two effects of anandamide. HBCCs and DU-145 cells were shown to contain 1) transcripts for CB1 and, to a lesser extent, CB2 cannabinoid receptors, 2) specific binding sites for [3H]SR141716A that could be displaced by anandamide, and 3) a CB1 receptor-immunoreactive protein. These findings suggest that endogenous cannabinoids and CB1 receptor agonists are potential negative effectors of PRL- and NGF-induced biological responses, at least in some cancer cells. source: http://endo.endojour...tract/141/1/118 Cannabinoids Induce Apoptosis of Pancreatic Tumor Cells via Endoplasmic Reticulum Stress–Related Genes Arkaitz Carracedo1, Meritxell Gironella2, Mar Lorente1, Stephane Garcia2, Manuel Guzmán1, Guillermo Velasco1 and Juan L. Iovanna2 1 Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid, Spain and 2 U624 Institut National de la Sante et de la Recherche Medicale, Marseille, France Requests for reprints: Guillermo Velasco, Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, c/ José Antonio Novais s/n, 28040 Madrid, Spain. Phone: 34-91-394-4668; Fax: 34-91-394-4672; E-mail: gvd@bbm1.ucm.es. Pancreatic adenocarcinomas are among the most malignant forms of cancer and, therefore, it is of especial interest to set new strategies aimed at improving the prognostic of this deadly disease. The present study was undertaken to investigate the action of cannabinoids, a new family of potential antitumoral agents, in pancreatic cancer. We show that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumor biopsies at much higher levels than in normal pancreatic tissue. Studies conducted with MiaPaCa2 and Panc1 cell lines showed that cannabinoid administration (a) induced apoptosis, ( increased ceramide levels, and © up-regulated mRNA levels of the stress protein p8. These effects were prevented by blockade of the CB2 cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo. Knockdown experiments using selective small interfering RNAs showed the involvement of p8 via its downstream endoplasmic reticulum stress–related targets activating transcription factor 4 (ATF-4) and TRB3 in 9-tetrahydrocannabinol–induced apoptosis. Cannabinoids also reduced the growth of tumor cells in two animal models of pancreatic cancer. In addition, cannabinoid treatment inhibited the spreading of pancreatic tumor cells. Moreover, cannabinoid administration selectively increased apoptosis and TRB3 expression in pancreatic tumor cells but not in normal tissue. In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB2 receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress–related genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer. (Cancer Res 2006; 66(13): 6748-55) source: http://cancerres.aacrjournals.org/cgi/cont...ract/66/13/6748
  15. Int J Oncol. 2012 May 14. doi: 10.3892/ijo.2012.1476. [Epub ahead of print] Cannabinoid-associated cell death mechanisms in tumor models (Review). Calvaruso G, Pellerito O, Notaro A, Giuliano M. Source Department of Experimental Biomedicine and Clinical Neuroscience, Section of Biochemical Sciences, University of Palermo, 90129 Palermo, Italy. Abstract In recent years, cannabinoids (the active components of Cannabis sativa) and their derivatives have received considerable interest due to findings that they can affect the viability and invasiveness of a variety of different cancer cells. Moreover, in addition to their inhibitory effects on tumor growth and migration, angiogenesis and metastasis, the ability of these compounds to induce different pathways of cell death has been highlighted. Here, we review the most recent results generating interest in the field of death mechanisms induced by cannabinoids in cancer cells. In particular, we analyze the pathways triggered by cannabinoids to induce apoptosis or autophagy and investigate the interplay between the two processes. Overall, the results reported here suggest that the exploration of molecular mechanisms induced by cannabinoids in cancer cells can contribute to the development of safe and effective treatments in cancer therapy. PMID:22614735 [PubMed - as supplied by publisher] My link Anti-tumoral action of cannabinoids: Involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation Δ9-Tetrahydrocannabinol, the main active component of marijuana, induces apoptosis of transformed neural cells in culture. Here, we show that intratumoral administration of Δ9-tetrahydrocannabinol and the synthetic cannabinoid agonist WIN-55,212-2 induced a considerable regression of malignant gliomas in Wistar rats and in mice deficient in recombination activating gene 2. Cannabinoid treatment did not produce any substantial neurotoxic effect in the conditions used. Experiments with two subclones of C6 glioma cells in culture showed that cannabinoids signal apoptosis by a pathway involving cannabinoid receptors, sustained ceramide accumulation and Raf1/extracellular signal-regulated kinase activation. These results may provide the basis for a new therapeutic approach for the treatment of malignant gliomas. My link 15 Rats with "incurable" brain tumors treated with THC infusions:3 die, 9 live up to twice as long as untreated Rats, 3 had tumors completely eliminated.Effective treatment: 60% Complete cure: 20% Cancer Killed by Cannabis - Weed - Pot - Marijuana finds UCLA research and others Full-length Doc Marijuana cures cancer - US government has known since 1974
  16. Marijuana Chemical May Fight Brain Cancer Active Component In Marijuana Targets Aggressive Brain Cancer Cells, Study Says By Kelli Miller Stacy WebMD Health News Reviewed by Louise Chang, MD The active chemical in marijuana promotes the death of brain cancer cells by essentially helping them feed upon themselves, researchers in Spain report. Guillermo Velasco and colleagues at Complutense University in Spain have found that the active ingredient in marijuana, THC, causes brain cancer cells to undergo a process called autophagy. Autophagy is the breakdown of a cell that occurs when the cell essentially self-digests. The team discovered that cannabinoids such as THC had anticancer effects in mice with human brain cancer cells and people with brain tumors. When mice with the human brain cancer cells received the THC, the tumor growth shrank. Two patients enrolled in a clinical trial received THC directly to the brain as an experimental treatment for recurrent glioblastoma multiforme, a highly aggressive brain tumor. Biopsies taken before and after treatment helped track their progress. After receiving the THC, there was evidence of increased autophagy activity. The findings appear in the April 1 issue of the Journal of Clinical Investigation. The patients did not have any toxic effects from the treatment. Previous studies of THC for the treatment of cancer have also found the therapy to be well tolerated, according to background information in journal article. Study authors say their findings could lead to new strategies for preventing tumor growth. source : http://www.webmd.com...ht-brain-cancer Marijuana May Stall Brain Tumor Growth Active Ingredient in Marijuana Inhibits Cancer Growth in Early Study By Jennifer Warner WebMD Health News Reviewed by Michael W. Smith, MD Aug. 15, 2004 -- The active ingredient in marijuana may help fight brain tumors, a new study suggests. Researchers say the cannabinoids found in marijuana may aid in brain tumor treatment by targeting the genes needed for the tumors to sprout blood vessels and grow. Their study showed that cannabinoids inhibited genes needed for the production of vascular growth factor (VEGF) in laboratory mice with glioma brain tumors and two patients with late-stage glioblastoma multiforme, a form of brain cancer. VEGF is a protein that stimulates blood vessels to grow. Tumors need an abundant blood supply because they generally grow rapidly. So when VEGF is blocked, tumors starve from lack of blood supply and nutrients. Blocking of VEGF constitutes one of the most promising tumor-fighting approaches currently available, says researcher Manuel Guzman, professor of biochemistry and molecular biology, at the Complutense University in Madrid, Spain, in a news release. Guzman says the findings suggest VEGF may be a new target for cannabinoid-based treatments. Previous studies have shown that cannabinoids could inhibit the growth of tumor-associated blood vessels in mice, but until now little was known about how they worked. The results of the study appear in the Aug. 15 issue of the journal Cancer Research. Cannabinoids May Help Starve Tumors In the study, researchers looked at the effects of cannabinoid treatment on gliobastoma multiforme, a form of brain cancer that affects about 7,000 Americans each year. It's considered one of the deadliest forms of cancer and usually results in death within one to two years after diagnosis. Treatment typically involves surgery, followed by radiation and/or chemotherapy. But despite these efforts to destroy the tumor, this type of brain tumor often survives and starts growing again, which is why researchers are looking for novel ways to attack it. In order to grow, all tumors require a network of blood vessels to feed them, and they create this network through a process known as angiogenesis. VEGF is critical to this process. In the first part of the study, researchers induced brain cancer in mice and then treated them with cannabinoids. They then analyzed the genes associated with the growth of blood vessels in the tumor and found that cannabinoids inhibited several of the genes related to VEGF. In the second part of the study, researchers injected cannabinoids into tumor samples taken from two human glioblastoma patients. "In both patients, VEGF levels in tumor extracts were lower after cannabinoid inoculation," says Guzman. Researchers say more study is needed but the results suggest that cannabinoid-based therapies may offer a new alternative for treatment of these otherwise untreatable brain tumors. source: http://www.webmd.com...in-tumor-growth http://www.youtube.com/watch?v=HVGlfcP3ATI Human Brains Make Their Own 'Marijuana' ScienceDaily (Apr. 20, 2009) — U.S. and Brazilian scientists have discovered that the brain manufactures proteins that act like marijuana at specific receptors in the brain itself. This discovery may lead to new marijuana-like drugs for managing pain, stimulating appetite, and preventing marijuana abuse. "Ideally, this development will lead to drugs that bind to and activate the THC receptor, but are devoid of the side effects that limit the usefulness of marijuana," said Lakshmi A. Devi of the Department of Pharmacology and Systems Therapeutics at Mount Sinai School of Medicine in New York and one of the senior researchers involved in the study. "It would be helpful to have a drug that activated or blocked the THC receptor, and our findings raise the possibility that this will lead to effective drugs with fewer side effects." Scientists made their discovery by first extracting several small proteins, called peptides, from the brains of mice and determining their amino acid sequence. The extracted proteins were then compared with another peptide previously known to bind to, but not activate, the receptor (THC) affected by marijuana. Out of the extracted proteins, several not only bound to the brain's THC receptors, but activated them as well. "The War on Drugs has hit very close to home," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Last year, scientists found that our skin makes its own marijuana-like substance. Now, we see that our brain has been making proteins that act directly on the marijuana receptors in our head. The next step is for scientists to come up with new medicines that eliminate the nasty side of pot—a better joint, so to speak." source: http://www.scienceda...90420151240.htm Active Ingredient in Marijuana Kills Brain Cancer Cells Experts say finding worth further study, but patients shouldn't light up just yet Posted April 1, 2009 By Alan Mozes HealthDay Reporter WEDNESDAY, April 1 (HealthDay News) -- New research out of Spain suggests that THC -- the active ingredient in marijuana -- appears to prompt the death of brain cancer cells. The finding is based on work with mice designed to carry human cancer tumors, as well as from an analysis of THC's impact on tumor cells extracted from two patients coping with a highly aggressive form of brain cancer. Explaining that the introduction of THC into the brain triggers a cellular self-digestion process known as "autophagy," study co-author Guillermo Velasco said his team has isolated the specific pathway by which this process unfolds, and noted that it appears "to kill cancer cells, while it does not affect normal cells." Velasco is with the department of biochemistry and molecular biology in the School of Biology at Complutense University in Madrid. The findings were published in the April issue of The Journal of Clinical Investigation. The Spanish researchers focused on two patients suffering from "recurrent glioblastoma multiforme," a fast-moving form of brain cancer. Both patients had been enrolled in a clinical trial designed to test THC's potential as a cancer therapy. Using electron microscopes to analyze brain tissue taken both before and after a 26- to 30-day THC treatment regimen, the researchers found that THC eliminated cancer cells while it left healthy cells intact. The team also was able, in what it described as a "novel" discovery, to track the signaling route by which this process was activated. These findings were replicated in work with mice, which had been "engineered" to carry three different types of human cancer tumor grafts. "These results may help to design new cancer therapies based on the use of medicines containing the active principle of marijuana and/or in the activation of autophagy," Velasco said. Outside experts suggested that more research is needed before advocating marijuana as a medicinal intervention for brain cancer. Dr. John S. Yu, co-director of the Comprehensive Brain Tumor Program in the Maxine Dunitz Neurosurgical Institute at Cedars-Sinai Medical Center in Los Angeles, said the findings were "not surprising." "There have been previous reports to this effect as well," he said. "So this is yet another indication that THC has an anti-cancer effect, which means it's certainly worth further study. But it does not suggest that one should jump at marijuana for a potential cure for cancer, and one should not urge anyone to start smoking pot right away as a means of curing their own cancer." But that's exactly what many brain cancer patients have been doing, said Dr. Paul Graham Fisher, the Beirne Family director of Neuro-Oncology at Stanford University. "In fact, 40 percent of brain tumor patients in the U.S. are already using alternative treatments, ranging from herbals to vitamins to marijuana," he said. "But that actually points out a cautionary tale here, which is that many brain cancer patients are already rolling a joint to treat themselves, but we're not really seeing brain tumors suddenly going away as a result, which we clearly would've noticed if it had that effect. So we need to be open-minded. But this suggests that the promise of THC might be a little over-hoped, and certainly requires further investigation before telling people to go out and roll a joint." source: http://health.usnews...ain-cancer.html Ted Kennedy's Brain Cancer Can Be Fought The senator, like the author, was struck by a sudden seizure. She has outlasted a grim prognosis By Bernadine Healy, M.D. Posted May 20, 2008 I have been praying for Sen. Ted Kennedy since Saturday, when he was rushed to the hospital because of an out-of-the-blue seizure. I knew all too well that the most likely diagnosis, considering his presentation and age, was a brain tumor. Today we hear it's a malignant glioma in the left parietal lobe of his brain, a dominant area that controls, among other functions, the ability to comprehend and express words. As he and his family are trying hard, no doubt, to digest this shocking news, they must also face the dark stories that are being blasted all over the airways about his illness—almost as if he were no longer with us. It brings chills to me, not just as a doctor who has cared for many with serious illness but also as a patient who, like the senator, once had a sudden seizure that led to the detection of a malignant glioma. Mine, too, was in the left parietal lobe. As I commented in my book Living Time and in an excerpt in U.S.News last year about my own battle with brain cancer, gliomas are rare and often forgotten tumors that strike fear into anyone's heart—in part because we have known so little about them. Though the senator's doctors have not yet shared details of his exact tumor type, those particulars will be crucial, because all malignant gliomas are not created equal. In the coming days we will learn more about his outlook. But it is worth remembering that prognoses are estimates—and can be misleading. When I was diagnosed, it looked like I would not see my 12-year-old daughter complete middle school. This past weekend, she graduated from college. To a large degree, the prognosis in brain cancer depends on a given tumor's characteristics—how it looks under the microscope, its genetic profile (which increasingly guides newer and better therapies), and, importantly, how it responds to treatment. In other words, Senator Kennedy's outlook depends on the traits of his particular tumor—as well as the patient himself. And if there is one thing we know about this patient, it's that he's a determined fighter. http://health.usnews...lated-links:TOP Can Cannabis Cure Brain Cancer? Apr 3, 2009 In another boost for the cred of marijuana as a potential valuable medicine, researchers in Spain have found that cannabis could be a treatment and perhaps a future cure for brain cancer - in a study done on both rats and humans: Hope Ted Kennedy gets the word. WASHINGTON (AFP) — The main chemical in marijuana appears to aid in the destruction of brain cancer cells, offering hope for future anti-cancer therapies, researchers in Spain wrote in a study released Thursday. The authors from the Complutense University in Madrid, working with scientists from other universities, found that the active component of marijuana, tetrahydrocannabinol (THC), causes cancer cells to undergo a process called autophagy -- the breakdown that occurs when the cell essentially self-digests. The research, which appears in the April edition of US-published Journal of Clinical Investigation, demonstrates that THC and related "cannabinoids" appear to be "a new family of potential antitumoral agent." The authors wrote that the chemical may prove useful in the development of future "antitumoral agents." source: http://www.fodors.co...rain-cancer.cfm The active chemical in marijuana promotes the death of brain cancer cells by essentially helping them feed upon themselves, researchers in Spain report. Guillermo Velasco and colleagues at Complutense University in Spain have found that the active ingredient in marijuana, THC, causes brain cancer cells to undergo a process called autophagy. Autophagy is the breakdown of a cell that occurs when the cell essentially self-digests. The team discovered that cannabinoids such as THC had anticancer effects in mice with human brain cancer cells and people with brain tumors. When mice with the human brain cancer cells received the THC, the tumor growth shrank. Two patients enrolled in a clinical trial received THC directly to the brain as an experimental treatment for recurrent glioblastoma multiforme, a highly aggressive brain tumor. Biopsies taken before and after treatment helped track their progress. After receiving the THC, there was evidence of increased autophagy activity. The findings appear in the April 1 issue of the Journal of Clinical Investigation. The patients did not have any toxic effects from the treatment. Previous studies of THC for the treatment of cancer have also found the therapy to be well tolerated, according to background information in journal article. Study authors say their findings could lead to new strategies for preventing tumor growth. Ref: http://www.webmd.com...ht-brain-cancer How Medical Marijuana Works The Therapeutic Uses of Cannabis and Cannabinoids There are over 400 natural compounds in medical marijuana and, of these, eighty are only found in cannabis plants. These eighty special compounds are known as cannabinoids. Cannabinoids relieve symptoms of illness by attaching to receptors in the brain that look for similar compounds that occur in the human body, such as dopamine. There are five major cannabinoids in medical marijuana that are particularly effective for relieving symptoms of illness, and each one produces different physical and psychological effects. This is why certain strains of medical marijuana are bred to have different amounts of each cannabinoid and are recommended for different conditions. Major Cannabinoids in Medical Marijuana What THC Is and Its Effects THC stands for delta-9-tetrahydrocannibinol. It is probably the best known cannabinoid present in medical marijuana. Physically it acts as a muscle relaxant and anti-inflammatory and psychologically it acts as a stimulant. This makes medical marijuana strains high in THC a good choice for patients who need relief while also to remain alert and active. THC in medical marijuana acts in the following ways: anti-epileptic anti-inflammatory anti-depressant stimulates appetite lowers blood pressure What CBD Is and Its Effects CBD stands for cannabidiol. Cannabidiol actually reduces the psychological effects of medical marijuana. For most patients, a strain that has high THC and high cannabidiol will have fewer “mental” effects and more physical ones. High cannabidiol medical marijuana strains, like Blueberry and Harlequin, are especially effective for illnesses with strong physical symptoms. Cannabidiol’s effects include: reduced pain reduced anxiety reduced nausea sedative effects anti-convulsive anti-schizophrenic What CBN Is and Its Effects CBN is cannabinol, not to be confused with Cannabidiol. Cannabinol is very similar to THC, but has less psychological effects. It is produced as THC breaks down within the medical marijuana plant. High THC will make cannabinol’s effects stronger, and very high cannabinol concentrations can produce undesirably strong head highs. Cannabinol levels tend to be high in medical marijuana strains like Strawberry Haze and Blue Rhino, which can be particularly helpful for: lowering pressure in the eye (such as with glaucoma) analgesic anti-seizure What CBC Is and Its Effects CBC stands for cannabichromene. Cannabichromene’s main action is to enhance the effects of THC. High cannabichromene levels will make a high-THC medical marijuana strain much more potent. Cannabichromene working together with THC is known to be a: sedative analgesic anti-inflammatory What CBG Is and Its Effects CBG is an abbreviation for cannabigerol. Cannabigerol has no psychological effects on its own, and is not usually found in high amounts in most medical marijuana. Scientists believe that cannabigerol is actually one of the oldest forms of cannabinoids, meaning it is essentially a “parent” to the other cannabinoids found in medical marijuana. It also has anti-microbial properties. Cannabigerol has physical effects such as: lowering pressure in the eye anti-inflammatory sedative sleep assistance Combining Strains Alone, none of the five major cannabinoids are as effective as when they work together. These five cannabinoids also work with the minor compounds in marijuana, and this is probably one reason that medical marijuana replacements like Marinol do not work very well. Professional medical marijuana growers can analyze their medical marijuana strains to breed and grow medication for patients with the desired range of levels of each major cannabinoid. Using this knowledge of what each compound does helps medical marijuana pharmacists, or budtenders, find the right combination for patients to treat specific conditions and find maximum relief.
  17. http://www.youtube.com/watch?v=yj72e5q61Fs Marijuana and ADD By: Kort E Patterson Year Written: 2000 Therapeutic uses of Medical Marijuana in the treatment of Attention Deficit Disorder --------------------------------- Note: The following research was part of a petition filed in 1999 to add Attention Deficit Disorder to the Oregon Medical Marijuana Act. The Oregon Health Division continues to refuse to add mental conditions such as ADD to the list of OMMA "covered conditions". The Health Division claims that medical marjuana isn't effective for mental conditions even though the primary justification for marijuana prohibition is its alleged psycho-active effectiveness. --------------------------------- At first glance it might seem counter-intuitive to use a medication that has a public perception of decreasing attention to treat a condition whose primary symptom is a deficit of attention. But just as taking stimulants often calms those with hyperactivity, medical marijuana improves the ability to concentrate in some types of ADD. Categorizing The Condition Attention Deficit Disorder (ADD) is a very broad category of conditions that share some symptoms but appear to result from different underlying causes. Most seem to involve, at least in part, imbalances in neural transmitter levels and functions. Some experts in the field expect that the broad category of ADD will be refined in the future, with many conditions that are now diagnosed as ADD being recognized as separate disorders. The particular type of ADD under consideration for treatment with medical marijuana might better be termed "Racing Brain Syndrome" (RBS). A useful analogy for this mental condition is that of a centrifugal pump that is being over-driven. As the pump speed increases, cavitation sets in and the pump's output decreases. The faster the pump is driven the greater the cavitation until a point is reached where large amounts of energy are being input but nothing is being output. Without medication there is a sensation that thoughts flash through the brain too fast to "think" them. Medical marijuana slows the brain down sufficiently to achieve impressive improvements in functionality. This syndrome probably only afflicts a small minority of all those diagnosed with ADD. The condition doesn't respond to the standard ADD medications, indicating that it results from different underlying processes than other forms of ADD. Individuals with types of ADD that do respond to the standard ADD medications also tend to have a far different reaction to medical marijuana than those with RBS. At this point in our limited understanding of the condition, it appears that RBS would make a good candidate to be redefined as a separate condition outside of the general diagnosis of ADD. Treating ADD/RBS With Medical Marijuana There is some evidence available that medical marijuana has been found to be an effective medication for some types of ADD by other researchers in the field.(1) Unfortunately, ADD encompasses such a variety of conditions that the limited amount of research in the field leaves many of the effective therapeutic mechanisms under-investigated. Considering the regulatory difficulties in researching the effects of medical marijuana, it isn't surprising that the information regarding medical marijuana and ADD is largely anecdotal(2). Individuals with RBS tend to have a very low tolerance for most stimulants, and report even caffeine aggravates their disorder. The one exception appears to be low doses of Dextrostat. While Dextrostat does have a calming effect, it fails to address the higher level mental functions needed for complex intellectual demands. Larger doses of Dextrostat tend to produce undesirable mental and physical stimulation, greatly limiting the level of medication that can be tolerated. Medical marijuana remains the only single medication that provides an adequate solution for RBS, and remains a necessary component in a multi-drug approach. Dextrostat does appear to reduce the amount of medical marijuana needed by individuals with RBS to achieve a functional mental state. This reduction probably justifies continuing with Dextrostat as a means of reducing the quantity of medical marijuana that must consumed, as well as allow those with RBS to gain the maximum benefit possible within the quantity limitations of the OMMA. The green leaves of certain strains of medical marijuana appear to provide the best therapeutic effects for RBS. Experiments with Marinol seem to indicate that THC is involved, but is not the primary therapeutic agent. The therapeutic agent(s) most useful in treating RBS appear to be present in relatively low concentrations in medical marijuana. As such those with this condition must consume a larger quantity of medical marijuana in order to ingest a sufficient dosage of the target agent(s). This would explain why dried low-THC green leaves appear to be the most effective treatment. The patient can consume enough of this low-THC marijuana to acquire the levels of the needed active agent(s) necessary to treat the condition without in the process consuming sufficient THC to become intoxicated. Underlying Cause of RBS It has long been suspected that RBS involved a deficit of one or more neural transmitters. It was observed as long ago as the 1970's that high levels of adrenaline had a residual therapeutic effect in those with RBS. The effect was first noted in those engaged in such activities as skydiving. Individuals with RBS reported that their mental functions were improved in the days following skydiving. It was first assumed that adrenaline stimulated the production of all neural transmitters - including those that were in deficit. It's now thought that while adrenaline initially acts as a stimulant of neural transmitter production, it has a secondary effect of depleting neural transmitters. The limited effectiveness of Dextrostat, as well as additional information about the secondary effects of adrenaline, suggests the possibility that at least part of the underlying cause of RBS may also be a surplus of one or more neural transmitters. The partial solution offered by Dextrostat also suggests that at least some part of the condition results from those neural transmitters and/or hormones that are influenced by both Dextrostat and medical marijuana. The failure of Dextrostat to provide a complete solution suggests two possible alternatives: (1) that the effects of Dextrostat and medical marijuana are additive - with both influencing the same neural transmitters and/or hormones, and together delivering the required level of therapeutic effect; or (2) that the condition is the result of multiple imbalances, some of which are unaffected by Dextrostat, but all of which appear to be affected by medical marijuana. Potential Beneficial Therapeutic Effects The research that has been done on the therapeutic effects of medical marijuana on other conditions provides a number of potential mechanisms that may be involved in RBS. The following are documented effects of medical marijuana that appear to have some potential for involvement. Perhaps the most obvious possibility is suggested by the fact that both Dextrostat and medical marijuana influence the release and/or functions of serotonin(3)(4). Since both Dextrostat and medical marijuana appear to decrease the apparent availability and effectiveness of serotonin, it would appear possible that a surplus of serotonin is involved in some way. There are over 60 cannabinoids and cannabidiols present in medical marijuana. The effect of most of these substances is at present largely unknown.(5) The discovery of a previously unknown system of cannabinoid neural transmitters is profound.(6) The different cannabinoid receptor types found in the body appear to play different roles in normal human physiology.(5) An endogenous cannabinoid, arachidonylethanolamide, named anandamide, has been found in the human brain. This ligand inhibits cyclic AMP in its target cells, which are widespread throughout the brain, but demonstrate a predilection for areas involved with nociception. The exact physiological role of anandamide is unclear, but preliminary tests of its behavioral effects reveal actions similar to those of THC.(7) Cannabinoid receptors appear to be very dense in the globus pallidus, substantia nigra pars reticulata (SNr), the molecular layers of the cerebellum and hippocampal dentate gyrus, the cerebral cortex, other parts of the hippocampal formation, and striatum - with the highest density being in the SNr. The Neocortex has moderate receptor density, with peaks in superficial and deep layers. Very low and homogeneous density was found in the thalamus and most of the brainstem, including all of the monoamine containing cell groups, reticular formation, primary sensory, visceromotor and cranial motor nuclei, and the area postrema. The hypothalamus, basal amygdala, central gray, nucleus of the solitary tract, and laminae I-III and X of the spinal cord showed slightly higher but still sparse receptor density.(5) While there are cannabinoid receptors in the ventromedial striatum and basal ganglia, which are areas associated with dopamine production, no cannabinoid receptors have been found in dopamine-producing neurons. According to the congressional Office of Technology Assessment, research over the last 10 years has proved that marijuana has no effect on dopamine-related brain systems.(6) However, cannabidiol has been shown to exert anticonvulsant and antianxiety properties, and is suspected by some to exert antidyskinetic effects through modulation of striatal dopaminergic activity.(3) It's been suggested that the cannabinoid receptors in the human brain play a role in the limbic system, which in turn plays a central role in the mechanisms which govern behavior and emotions. The limbic system coordinates activities between the visceral base-brain and the rest of the nervous system. Cannabis acts on memory by way of the receptors in the limbic system's hippocampus, which "gates" information during memory consolidation.(6) In addition, some effects of cannabinoids appear to be independent of cannabinoid receptors. The variety of mechanisms through which cannabinoids can influence human physiology underlies the variety of potential therapeutic uses for medical marijuana.(8) When the effects of cannabis on a "normal" brain are tracked on an electroencephalogram (EEG), there is an initial speeding up of brain wave activity and a reactive slowing as the drug effects wear off. The higher the dosage, the more intense the effects and longer the experience. There is an increase in mean-square alpha energy levels and a slight slowing of alpha frequency.(5) There is also an increase of beta waves reflecting increased cognitive activity. The distortion of time resulting from the "speeding up of thoughts" causes a subjective perception that there is a slowing of time.(9) As the cannabis effects wear off, stimulation gives way to sedation. The cognitive activity of the beta state gives way to alpha and theta frequencies. Theta waves are commonly associated with visual imagery. These images interact with thinking and disrupt the train of thought. Thinking can be distracted by these intrusions, with thought contents being modified to some extent depending on dose, expectations, setting, and personality.(9) Cannabis decreases emotional reactivity and intensity of affect while increasing introspection as evidenced by the slowing of the EEG after initial stimulation. Obsessive and pressured thinking is replaced by introspective free associations. Emotional reactivity is moderated and worries become less pressing.(10) Cannabis causes a general increase in cerebral blood flow (CBF). This increase in blood circulation is due to decreased peripheral resistance, which is in turn due to the dilation of the capillaries in the cerebral cortex. Changes in CBF affect the mental processes of the brain, with increases stimulating cognition, while decreases accompany sedation.(9) Relative Safety of Medical Marijuana "Marijuana is the safest therapeutically active substance known to man... safer than many foods we commonly consume." DEA Judge Francis L. Young, Sept. 6, 1988 "After carefully monitoring the literature for more than two decades, we have concluded that the only well-confirmed deleterious physical effect of marihuana is harm to the pulmonary system." Grinspoon M.D., James B. Bakalar, Medical Marijuana has been in use for thousands of years, and in spite of substantial efforts to find adverse effects, it remains the safest medication available for RBS. There has never been a single known case of lethal overdose. The ratio of lethal to effective dose for medical marijuana is estimated to be as 40,000 to 1. By comparison, the ratio is 3-50 to 1 for secobarbital and 4-10 to 1 for alcohol.(11) During the 1890s the Indian Hemp Drugs Commission interviewed some eight hundred people and produced a report of more than 3000 pages. The report concluded that "there was no evidence that moderate use of cannabis drugs produced any disease or mental or moral damage, or that it tended to lead to excess any more than the moderate use of whiskey."(12) The Mayor's Committee on Marihuana examined chronic users in New York City who had averaged seven marihuana cigarettes a day for eight years and "showed no mental or physical decline."(13) Several later controlled studies of chronic heavy use failed to establish any pharmacologically induced harm.(14) A subsequent government sponsored review of cannabis conducted by the Institute of Medicine, a branch of the National Academy of Sciences, also found little evidence of its alleged harmfulness.(15) Several studies in the United States found that fairly heavy marihuana use had no effects on learning, perception, or motivation over periods as long as a year.(16) Studies of very heavy smokers in Jamaica, Costa Rica, and Greece "found no evidence of intellectual or neurological damage, no changes in personality, and no loss of the will to work or participate in society."(17) The Costa Rican study showed no difference between heavy users (seven or more marihuana cigarettes a day) and lighter users (six or fewer cigarettes a day).(18) In addition, none of the studies involving prolonged and heavy use of medical marijuana have shown any effects on mental abilities suggestive of impairment of brain or cerebral function and cognition.(2) The inhalation of the combustion products of burning plant material is the cause of the only well-confirmed deleterious physical effects of medical marijuana. These adverse effects can be eliminated by using one of the non-combustion means of ingesting the mediation. Marijuana can be eaten in foods or inhaled using a vaporizer. The therapeutic agents in medical marijuana vaporize at around 190 degrees centigrade, while it takes the heat of combustion of around 560 degrees centigrade to generate the harmful components of marijuana smoke. A vaporizer heats the medical marijuana to the point where the therapeutic agents are released and can be inhaled, without getting the plant material hot enough to burn.(19) Cannabis And Blood Pressure Research Proposal 1. Possible Therapeutic Cannabis Applications for Psychiatric Disorders, Tod H. Mikuriya, M.D. 2. Marihuana, The Forbidden Medicine, Lester Grinspoon M.D., James B. Bakalar, Yale University Press, 1997 3. MARIJUANA AND TOURETTE'S SYNDROME, Journal of Clinical Psychopharmacology, Vol. 8/No. 6, Dec 1988 4. CANNABINOIDS BLOCK RELEASE OF SEROTONIN FROM PLATELETS INDUCED BY PLASMA FROM MIGRAINE PATIENTS, Int J Clin Pharm. Res V (4) 243-246 (1985), Volfe Z., Dvilansky A., Nathan I. Blood Research, Faculty of Health Sciences, Soroka Medical Center, Ben-Gurion University of the Negev, P.O. Box 151, Beer-Sheva 84101, Israel. 5. Nelson, P. L. (1993). A critical review of the research literature concerning some biological and psychological effects of cannabis. In Advisory Committee on Illicit Drugs (Eds.), Cannabis and the law in Queensland: A discussion paper (pp. 113-152). Brisbane: Criminal Justice Commission of Queensland. 6. Marijuana And the Brain, by John Gettman, High Times, March, 1995 7. Cannabis for Migraine Treatment: The Once and Future Prescription?: An Historical and Scientific Review; Ethan B. Russo, M.D. 8. Marijuana and Medicine, Assessing the Science Base, Janet E. Joy, Stanley J. Watson, Jr., and John A. Benson, Jr., Editors Division of Neuroscience and Behavioral Health, INSTITUTE OF MEDICINE 9. Marijuana Medical Handbook, by Tod Mikuriya, M.D. 10. Medicinal Uses of Cannabis, Tod H. Mikuriya, M.D. ©1998 11. Marihuana as Medicine: A Plea for Reconsideration; Lester Grinspoon M.D., James B. Bakalar; Journal of the American Medical Association (JAMA); June 1995 12. Report of the Indian Hemp Drugs Commission, 1893-1894, 7 vols. (Simla: Government Central Printing Office, 1894); D. Solomon, ed., The Marihuana Papers (Indianapolis: Bobbs-Merrill, 1966). 13. Mayor's Committee on Marihuana, The Marihuana Problem in the City of New York (Lancaster, Pa.: Jacques Cattell, 1944). 14. M. H. Beaubrun and F Knight, "Psychiatric Assessment of Thirty Chronic Users of Cannabis and Thirty Matched Controls," American journal of Psychiatry 130 (1973): 309; M. C. Braude and S. Szara, eds., The Pharmacology of Marihuana, 2 vols. (New York: Raven, 1976); R. L. Dombush, A. M. Freedman, and M. Fink, eds., "Chronic Cannabis Use," Annals of New Yorh Academy of Sciences 282 (1976); J. S. Hochman and N. Q. Brill, "Chronic Marijuana Use and Psychosocial Adaptation," American journal of Psychiatry 130 (1973):132; Rubin and Comitas, Ganja in Jamaica. 15. Institute of Medicine, Marijuana and Health (Washington, D.C.: National Academy of Sciences, 1982). 16. C. M. Culver and F W King, "Neurophysiological Assessment of Undergraduate Marihuana and LSD Users," Archives of General Psychiatry 31 (1974): 707-711; P.J. Lessin and S. Thomas, "Assessment of the Chronic Effects of Marijuana on Motivation and Achievement: A Preliminary Report," in Pharmacology of Marihuana, ed. Braude and Szara, 2:681-684. 17. Cognition and Long-Term Use of Ganja (Cannabis), Reprint Series, 24 July 1981, Volume 213, pp. 465-466 SCIENCE, Jeffrey Schaeffer, Therese Andrysiak, and J. Thomas Ungerleider Copyright 1981 by the American Association for the Advancement of Science 18. Rubin and Comitas, Ganja in Jamaica; W E. Carter, ed., Cannabis in Costa Rica: A Study of Chronic Marihuana Use (Philadelphia: Institute for the Study of Human Issues, 1980); C. Stefariis, J. Boulougouris, and A. I-iakos, "Clinical and Psychophysiological Effects of Cannabis in Long-term Users," in Pharmacology of Marihuana, ed. Braude and Szara, 2:659-666; P Satz, J. M. Fletcher, and L. S. Sutker, "Neurophysiologic, Intellectual, and Personality Correlates of Chronic Marihuana Use in Native Costa Ricans," Annals of the New York Academy of Sciences 282 (1976): 266-306. 19. Is Marijuana The Right Medicine For You?; Bill Zimmerman Ph.D., Rick Bayer M.D., and Nancy Crumpacker M.D.; (1998): pp. 125; Keats Publishing Inc. source: http://www.kortexplores.com/node/133 © International Association for Cannabis as Medicine1Case report Cannabis improves symptoms of ADHD http://66.218.69.11/...&...=1&.intl=us Cannabis as a medical treatment for attention deficit disorder "Why would anyone want to give their child an expensive pill... with unacceptable side effects, when he or she could just go into the backyard, pick a few leaves off a plant and make tea for him or her instead? Cannabinoids are a very viable alternative to treating adolescents with ADD and ADHD" WASHINGTON - As a California pediatrician and 49-year-old mother of two teenage daughters, Claudia Jensen says pot might prove to be the preferred medical treatment for attention deficit disorder - even in adolescents. While some wonder whether Jensen was smoking some wacky weed herself, the clinician for low-income patients and professor to first-year medical students at the University of Southern California said her beliefs are very grounded: The drug helps ease the symptomatic mood swings, lack of focus, anxiety and irritability in people suffering from neuropsychiatric disorders like ADD and attention deficit/hyperactivity disorder. "Cannabinoids are a very viable alternative to treating adolescents with ADD and ADHD.I have a lot of adult patients who swear by it." Under California state law, physicians are allowed to recommend to patients the use of cannabis to treat illnesses, although the federal government has maintained that any use of marijuana - medicinal or otherwise - is illegal. The federal courts have ruled that physicians like Jensen cannot be prosecuted for making such recommendations. Jensen said she regularly writes prescriptions recommending the use of cannabis for patients -particularly those suffering pain and nausea from chronic illnesses, such as AIDS, cancer, glaucoma and arthritis. She has also worked with one family of a 15-year-old - whose family had tried every drug available to help their son, who by age 13 had become a problem student diagnosed as suffering from ADHD. Under Jensen’s supervision, he began cannabis treatment, settling it on in food and candy form, and he has since found equilibrium and regularly attends school. But not everyone is so high on the idea of pot for students with neurological illnesses. Subcommittee Chairman Mark Souder, R-Ind., who invited Jensen to testify after reading about her ideas in the newspaper, was hardly convinced by her testimony. "I do believe that Dr. Jensen really wants to help her patients, but I think she is deeply misguided when she recommends cannabis to teenagers with attention deficit disorder or hyperactivity," he told Foxnews.com. "There is no serious scientific basis for using marijuana to treat those conditions, and Dr. Jensen didn’t even try to present one." Dr. Tom O’Connell, a retired chest surgeon who now works with patients at a Bay Area clinic for patients seeking medical marijuana recommendations, is working on it. He said cannabis not only helps pain, but also can treat psychological disorders. He is currently conducting a study of hundreds of his patients, whom he said he believes have been self-medicating with pot and other drugs for years, and he hopes to publish a paper on the subject soon. "My work with cannabis patients is certainly not definitive at this point, but it strongly suggests that the precepts upon which cannabis prohibition have been based are completely spurious," O’Connell said. Worse yet, he added, the prohibition has successfully kept certain adolescents away from pot who now turn to tobacco and alcohol instead. Jensen, who said she believes Souder invited her to testify to "humiliate me and incriminate me in some way," suggested that a growing body of evidence is being developed to back medical cannabis chiefly for chronic pain and nausea. She said it is difficult, however, for advocates like herself to get the funding and permission to conduct government-recognized tests on ADD/ADHD patients. "Unfortunately, no pharmaceutical companies are motivated to spend the money on research, and the United States government has a monopoly on the available cannabis and research permits," she told Congress. Studies done on behalf of the government, including the 1999 Institute of Medicine’s "Marijuana and Medicine: Assessing the Science Base," found that cannabis delivers effective THC and other cannabinoids that serve as pain relief and nausea-control agents. But these same studies warn against the dangers of smoking cannabis and suggest other FDA-approved drugs are preferable. "We know all too well the dangerous health risks that accompany (smoking)," said Rep. Elijah Cummings, D-Md., ranking member on the subcommittee, who like Souder, was not impressed by Jensen’s arguments. "It flies in the face of responsible medicine to advocate a drug that had been known to have over 300 carcinogens and has proven to be as damaging to the lungs as cigarette smoking," added Jennifer Devallance, spokeswoman for the White House Office of Drug Control Policy. The government points to Food and Drug Administration-approved Marinol, a THC-derived pill that acts as a stand-in for marijuana. But many critics say there are nasty side effects, and it’s too expensive for the average patient. On the other hand, Jensen and others say cannabinoids can be made into candy form, baked into food or boiled into tea. They say that despite the FDA blessing, giving kids amphetamines like Ritalin for ADD and other behavioral disorders might be more dangerous. "Ritalin is an amphetamine - we have all of these youngsters running around on speed," said Keith Stroup, spokesman for the National Organization for the Reform of Marijuana Laws. "Although it flies in the face of conventional wisdom, it’s nevertheless true that cannabis is far safer and more effective than the prescription agents currently advocated for treatment of ADD-ADHD," O’Connell said. Stroup said if Souder’s intention was to harangue Jensen, he was unsuccessful in the face of her solid and articulate testimony on April 1."It was a good day for her, and a good day for medical marijuana in Congress," he said. Nick Coleman, a subcommittee spokesman, said Souder doesn’t "try to humiliate people. "But to promote medical cannabis for teenagers with ADD... he does not feel that is a sound and scientific medical practice," Coleman said. While the issue of treating adolescents with medical marijuana is fairly new, the idea of using pot to treat chronically and terminally ill patients is not. Nine states currently have laws allowing such practices. A number of lawmakers on both sides of the aisle have added that they want the states to decide for themselves whether to pursue medical marijuana laws. Among those lawmakers are Reps. Ron Paul, R-Texas, a physician; Dana Rohrabacher, R-Calif.; and Barney Frank, D-Mass. "(Rep. Paul) believes there are some legitimate applications," like for pain and nausea, said spokesman Jeff Deist. "But the real issue is that states should decide for themselves." source: http://www.chanvre-i...-treatment.html Marijuana and ADD Therapeutic uses of Medical Marijuana in the treatment of Marijuana and ADD By Kort E Patterson Sam’s Story; Autism & Medical Marijuana Sam’s Story, Using Medical Cannabis to Treat Autism Spectrum Disorder ADD, ADHD & Medical Marijuana It was mentioned in the Portland newspaper that the Oregon Health Division is considering allowing medical marijuana to be used to treat Attention Deficit Disorder (ADD) under the Oregon Medical Marijuana Act. At first glance it might seem counter-intuitive to use a medication that has a public perception of decreasing attention to treat a condition whose primary symptom is a deficit of attention. But just as taking stimulants often calms those with hyperactivity, medical marijuana improves the ability to concentrate in some types of ADD. Categorizing The Condition Attention Deficit Disorder (ADD) is a very broad category of conditions that share some symptoms but appear to result from different underlying causes. Most seem to involve, at least in part, imbalances in neural transmitter levels and functions. Some experts in the field expect that the broad category of ADD will be refined in the future, with many conditions that are now diagnosed as ADD being recognized as separate disorders. The particular type of ADD under consideration for treatment with medical marijuana might better be termed "Racing Brain Syndrome" (RBS). A useful analogy for this mental condition is that of a centrifugal pump that is being over-driven. As the pump speed increases, cavitation sets in and the pump's output decreases. The faster the pump is driven the greater the cavitation until a point is reached where large amounts of energy are being input but nothing is being output. Without medication there is a sensation that thoughts flash through the brain too fast to "think" them. Medical marijuana slows the brain down sufficiently to achieve impressive improvements in functionality. This syndrome probably only afflicts a small minority of all those diagnosed with ADD. The condition doesn't respond to the standard ADD medications, indicating that it results from different underlying processes than other forms of ADD. Individuals with types of ADD that do respond to the standard ADD medications also tend to have a far different reaction to medical marijuana than those with RBS. At this point in our limited understanding of the condition, it appears that RBS would make a good candidate to be redefined as a separate condition outside of the general diagnosis of ADD. Treating ADD/RBS With Medical Marijuana There is some evidence available that medical marijuana has been found to be an effective medication for some types of ADD by other researchers in the field.(1) Unfortunately, ADD encompasses such a variety of conditions that the limited amount of research in the field leaves many of the effective therapeutic mechanisms under-investigated. Considering the regulatory difficulties in researching the effects of medical marijuana, it isn't surprising that the information regarding medical marijuana and ADD is largely anecdotal(2). Individuals with RBS tend to have a very low tolerance for most stimulants, and report even caffeine aggravates their disorder. The one exception appears to be low doses of Dextrostat. While Dextrostat does have a calming effect, it fails to address the higher level mental functions needed for complex intellectual demands. Larger doses of Dextrostat tend to produce undesirable mental and physical stimulation, greatly limiting the level of medication that can be tolerated. Medical marijuana remains the only single medication that provides an adequate solution for RBS, and remains a necessary component in a multi-drug approach. Dextrostat does appear to reduce the amount of medical marijuana needed by individuals with RBS to achieve a functional mental state. This reduction probably justifies continuing with Dextrostat as a means of reducing the quantity of medical marijuana that must consumed, as well as allow those with RBS to gain the maximum benefit possible within the quantity limitations of the OMMA. The green leaves of certain strains of medical marijuana appear to provide the best therapeutic effects for RBS. Experiments with Marinol seem to indicate that THC is involved, but is not the primary therapeutic agent. The therapeutic agent(s) most useful in treating RBS appear to be present in relatively low concentrations in medical marijuana. As such those with this condition must consume a larger quantity of medical marijuana in order to ingest a sufficient dosage of the target agent(s). This would explain why dried low-THC green leaves appear to be the most effective treatment. The patient can consume enough of this low-THC marijuana to acquire the levels of the needed active agent(s) necessary to treat the condition without in the process consuming sufficient THC to become intoxicated. Underlying Cause of RBS It has long been suspected that RBS involved a deficit of one or more neural transmitters. It was observed as long ago as the 1970's that high levels of adrenaline had a residual therapeutic effect in those with RBS. The effect was first noted in those engaged in such activities as skydiving. Individuals with RBS reported that their mental functions were improved in the days following skydiving. It was first assumed that adrenaline stimulated the production of all neural transmitters - including those that were in deficit. It's now thought that while adrenaline initially acts as a stimulant of neural transmitter production, it has a secondary effect of depleting neural transmitters. The limited effectiveness of Dextrostat, as well as additional information about the secondary effects of adrenaline, suggests the possibility that at least part of the underlying cause of RBS may also be a surplus of one or more neural transmitters. The partial solution offered by Dextrostat also suggests that at least some part of the condition results from those neural transmitters and/or hormones that are influenced by both Dextrostat and medical marijuana. The failure of Dextrostat to provide a complete solution suggests two possible alternatives: (1) that the effects of Dextrostat and medical marijuana are additive - with both influencing the same neural transmitters and/or hormones, and together delivering the required level of therapeutic effect; or (2) that the condition is the result of multiple imbalances, some of which are unaffected by Dextrostat, but all of which appear to be affected by medical marijuana. Potential Beneficial Therapeutic Effects The research that has been done on the therapeutic effects of medical marijuana on other conditions provides a number of potential mechanisms that may be involved in RBS. The following are documented effects of medical marijuana that appear to have some potential for involvement. Perhaps the most obvious possibility is suggested by the fact that both Dextrostat and medical marijuana influence the release and/or functions of serotonin(3)(4). Since both Dextrostat and medical marijuana appear to increase the apparent availability and effectiveness of serotonin, it would appear possible that a deficit of serotonin is involved in some way. There are over 60 cannabinoids and cannabidiols present in medical marijuana. The effect of most of these substances is at present largely unknown.(5) The discovery of a previously unknown system of cannabinoid neural transmitters is profound.(6) The different cannabinoid receptor types found in the body appear to play different roles in normal human physiology.(5) An endogenous cannabinoid, arachidonylethanolamide, named anandamide, has been found in the human brain. This ligand inhibits cyclic AMP in its target cells, which are widespread throughout the brain, but demonstrate a predilection for areas involved with nociception. The exact physiological role of anandamide is unclear, but preliminary tests of its behavioral effects reveal actions similar to those of THC.(7) Cannabinoid receptors appear to be very dense in the globus pallidus, substantia nigra pars reticulata (SNr), the molecular layers of the cerebellum and hippocampal dentate gyrus, the cerebral cortex, other parts of the hippocampal formation, and striatum - with the highest density being in the SNr. The Neocortex has moderate receptor density, with peaks in superficial and deep layers. Very low and homogeneous density was found in the thalamus and most of the brainstem, including all of the monoamine containing cell groups, reticular formation, primary sensory, visceromotor and cranial motor nuclei, and the area postrema. The hypothalamus, basal amygdala, central gray, nucleus of the solitary tract, and laminae I-III and X of the spinal cord showed slightly higher but still sparse receptor density.(5) While there are cannabinoid receptors in the ventromedial striatum and basal ganglia, which are areas associated with dopamine production, no cannabinoid receptors have been found in dopamine-producing neurons. According to the congressional Office of Technology Assessment, research over the last 10 years has proved that marijuana has no effect on dopamine-related brain systems.(6) However, cannabidiol has been shown to exert anticonvulsant and antianxiety properties, and is suspected by some to exert antidyskinetic effects through modulation of striatal dopaminergic activity.(3) It's been suggested that the cannabinoid receptors in the human brain play a role in the limbic system, which in turn plays a central role in the mechanisms which govern behavior and emotions. The limbic system coordinates activities between the visceral base-brain and the rest of the nervous system. Cannabis acts on memory by way of the receptors in the limbic system's hippocampus, which "gates" information during memory consolidation.(6) In addition, some effects of cannabinoids appear to be independent of cannabinoid receptors. The variety of mechanisms through which cannabinoids can influence human physiology underlies the variety of potential therapeutic uses for medical marijuana.(8) When the effects of cannabis on a "normal" brain are tracked on an electroencephalogram (EEG), there is an initial speeding up of brain wave activity and a reactive slowing as the drug effects wear off. The higher the dosage, the more intense the effects and longer the experience. There is an increase in mean-square alpha energy levels and a slight slowing of alpha frequency.(5) There is also an increase of beta waves reflecting increased cognitive activity. The distortion of time resulting from the "speeding up of thoughts" causes a subjective perception that there is a slowing of time.(9) As the cannabis effects wear off, stimulation gives way to sedation. The cognitive activity of the beta state gives way to alpha and theta frequencies. Theta waves are commonly associated with visual imagery. These images interact with thinking and disrupt the train of thought. Thinking can be distracted by these intrusions, with thought contents being modified to some extent depending on dose, expectations, setting, and personality.(9) Cannabis decreases emotional reactivity and intensity of affect while increasing introspection as evidenced by the slowing of the EEG after initial stimulation. Obsessive and pressured thinking is replaced by introspective free associations. Emotional reactivity is moderated and worries become less pressing.(10) Cannabis causes a general increase in cerebral blood flow (CBF). This increase in blood circulation is due to decreased peripheral resistance, which is in turn due to the dilation of the capillaries in the cerebral cortex. Changes in CBF affect the mental processes of the brain, with increases stimulating cognition, while decreases accompany sedation.(9) Relative Safety of Medical Marijuana "Marijuana is the safest therapeutically active substance known to man... safer than many foods we commonly consume." DEA Judge Francis L. Young, Sept. 6, 1988 "After carefully monitoring the literature for more than two decades, we have concluded that the only well-confirmed deleterious physical effect of marihuana is harm to the pulmonary system." Grinspoon M.D., James B. Bakalar, Medical Marijuana has been in use for thousands of years, and in spite of substantial efforts to find adverse effects, it remains the safest medication available for RBS. There has never been a single known case of lethal overdose. The ratio of lethal to effective dose for medical marijuana is estimated to be as 40,000 to 1. By comparison, the ratio is 3-50 to 1 for secobarbital and 4-10 to 1 for alcohol.(11) During the 1890s the Indian Hemp Drugs Commission interviewed some eight hundred people and produced a report of more than 3000 pages. The report concluded that "there was no evidence that moderate use of cannabis drugs produced any disease or mental or moral damage, or that it tended to lead to excess any more than the moderate use of whiskey."(12) The Mayor's Committee on Marihuana examined chronic users in New York City who had averaged seven marihuana cigarettes a day for eight years and "showed no mental or physical decline."(13) Several later controlled studies of chronic heavy use failed to establish any pharmacologically induced harm.(14) A subsequent government sponsored review of cannabis conducted by the Institute of Medicine, a branch of the National Academy of Sciences, also found little evidence of its alleged harmfulness.(15) Several studies in the United States found that fairly heavy marihuana use had no effects on learning, perception, or motivation over periods as long as a year.(16) Studies of very heavy smokers in Jamaica, Costa Rica, and Greece "found no evidence of intellectual or neurological damage, no changes in personality, and no loss of the will to work or participate in society."(17) The Costa Rican study showed no difference between heavy users (seven or more marihuana cigarettes a day) and lighter users (six or fewer cigarettes a day).(18) In addition, none of the studies involving prolonged and heavy use of medical marijuana have shown any effects on mental abilities suggestive of impairment of brain or cerebral function and cognition.(2) The inhalation of the combustion products of burning plant material is the cause of the only well-confirmed deleterious physical effects of medical marijuana. These adverse effects can be eliminated by using one of the non-combustion means of ingesting the mediation. Marijuana can be eaten in foods or inhaled using a vaporizer. The therapeutic agents in medical marijuana vaporize at around 190 degrees centigrade, while it takes the heat of combustion of around 560 degrees centigrade to generate the harmful components of marijuana smoke. A vaporizer heats the medical marijuana to the point where the therapeutic agents are released and can be inhaled, without getting the plant material hot enough to burn.(19) References: 1. Possible Therapeutic Cannabis Applications for Psychiatric Disorders, Tod H. Mikuriya, M.D. 2. Marihuana, The Forbidden Medicine, Lester Grinspoon M.D., James B. Bakalar, Yale University Press, 1997 3. MARIJUANA AND TOURETTE'S SYNDROME, Journal of Clinical Psychopharmacology, Vol. 8/No. 6, Dec 1988 4. CANNABINOIDS BLOCK RELEASE OF SEROTONIN FROM PLATELETS INDUCED BY PLASMA FROM MIGRAINE PATIENTS, Int J Clin Pharm. Res V (4) 243-246 (1985), Volfe Z., Dvilansky A., Nathan I. Blood Research, Faculty of Health Sciences, Soroka Medical Center, Ben-Gurion University of the Negev, P.O. Box 151, Beer-Sheva 84101, Israel. 5. Nelson, P. L. (1993). A critical review of the research literature concerning some biological and psychological effects of cannabis. In Advisory Committee on Illicit Drugs (Eds.), Cannabis and the law in Queensland: A discussion paper (pp. 113-152). Brisbane: Criminal Justice Commission of Queensland. 6. Marijuana And the Brain, by John Gettman, High Times, March, 1995 7. Cannabis for Migraine Treatment: The Once and Future Prescription?: An Historical and Scientific Review; Ethan B. Russo, M.D. 8. Marijuana and Medicine, Assessing the Science Base, Janet E. Joy, Stanley J. Watson, Jr., and John A. Benson, Jr., Editors Division of Neuroscience and Behavioral Health, INSTITUTE OF MEDICINE 9. Marijuana Medical Handbook, by Tod Mikuriya, M.D. 10. Medicinal Uses of Cannabis, Tod H. Mikuriya, M.D. ©1998 11. Marihuana as Medicine: A Plea for Reconsideration; Lester Grinspoon M.D., James B. Bakalar; Journal of the American Medical Association (JAMA); June 1995 12. Report of the Indian Hemp Drugs Commission, 1893-1894, 7 vols. (Simla: Government Central Printing Office, 1894); D. Solomon, ed., The Marihuana Papers (Indianapolis: Bobbs-Merrill, 1966). 13. Mayor's Committee on Marihuana, The Marihuana Problem in the City of New York (Lancaster, Pa.: Jacques Cattell, 1944). 14. M. H. Beaubrun and F Knight, "Psychiatric Assessment of Thirty Chronic Users of Cannabis and Thirty Matched Controls," American journal of Psychiatry 130 (1973): 309; M. C. Braude and S. Szara, eds., The Pharmacology of Marihuana, 2 vols. (New York: Raven, 1976); R. L. Dombush, A. M. Freedman, and M. Fink, eds., "Chronic Cannabis Use," Annals of New Yorh Academy of Sciences 282 (1976); J. S. Hochman and N. Q. Brill, "Chronic Marijuana Use and Psychosocial Adaptation," American journal of Psychiatry 130 (1973):132; Rubin and Comitas, Ganja in Jamaica. 15. Institute of Medicine, Marijuana and Health (Washington, D.C.: National Academy of Sciences, 1982). 16. C. M. Culver and F W King, "Neurophysiological Assessment of Undergraduate Marihuana and LSD Users," Archives of General Psychiatry 31 (1974): 707-711; P.J. Lessin and S. Thomas, "Assessment of the Chronic Effects of Marijuana on Motivation and Achievement: A Preliminary Report," in Pharmacology of Marihuana, ed. Braude and Szara, 2:681-684. 17. Cognition and Long-Term Use of Ganja (Cannabis), Reprint Series, 24 July 1981, Volume 213, pp. 465-466 SCIENCE, Jeffrey Schaeffer, Therese Andrysiak, and J. Thomas Ungerleider Copyright 1981 by the American Association for the Advancement of Science 18. Rubin and Comitas, Ganja in Jamaica; W E. Carter, ed., Cannabis in Costa Rica: A Study of Chronic Marihuana Use (Philadelphia: Institute for the Study of Human Issues, 1980); C. Stefariis, J. Boulougouris, and A. I-iakos, "Clinical and Psychophysiological Effects of Cannabis in Long-term Users," in Pharmacology of Marihuana, ed. Braude and Szara, 2:659-666; P Satz, J. M. Fletcher, and L. S. Sutker, "Neurophysiologic, Intellectual, and Personality Correlates of Chronic Marihuana Use in Native Costa Ricans," Annals of the New York Academy of Sciences 282 (1976): 266-306. 19. Is Marijuana The Right Medicine For You?; Bill Zimmerman Ph.D., Rick Bayer M.D., and Nancy Crumpacker M.D.; (1998): pp. 125; Keats Publishing Inc. source: http://www.onlinepot...cal/add&mmj.htm
  18. WWII Chemical Exposure Spurs Obesity, Autism, Researcher Says May 21 (Bloomberg) -- The World War II generation may have passed down to their grandchildren the effects of chemical exposure in the 1940s, possibly explaining current rates of obesity, autism and mental illness, according to one researcher. David Crews, professor of psychology and zoology at the University of Texas at Austin, theorized that the rise in these diseases may be linked to environmental effects passed on through generations. His research showed that descendants of rats exposed to a crop fungicide were less sociable, more obese and more anxious than offspring of the unexposed. The results, published today in the Proceedings of the National Academy of Sciences, are part of a growing field of study that suggests environmental damage to cells can cause inherited changes and susceptibility to disease. Crews said his findings are applicable to humans. "We should be very careful about overstating what looks like basic science with public health implications," Feinberg said in an interview. "Currently we don't have enough evidence showing that these fungicides are causing common human disease through an epigenetic mechanism. It's research that's well worth doing, but it's clear that that hasn't been shown." Read more: http://www.sfgate.co...L#ixzz1vYC5xs9j KTLA 5 news Los Angeles has reported on a family in southern California who, after a series of worsening autism symptoms exhibited by their son, resorted to medical marijuana. The results have been wonderful, according to the boy's parents. Ten-year -old Sam's father told reporter Cher Calvin that his son had been hurting other children at school, pulling the television down, destroying furniture, etc .He would have to put the boy in a hold for an hour, while he had spasms, until he eventually calmed down. The parents had consulted the conventional 'experts'; doctors who put Sam on prescription drugs, which resulted in the boy gaining twenty pounds. "He was getting more dangerous, bigger, stronger", recalled Sam's mom. Within 20 minutes effects were clear, recalls the reporter who spent some time with the family. He was "calm, relaxed and social" after taking his "spec of hash" in front of the news crew. "The more I tell people the more comfortable I am", says the mother when asked how she explains this treatment to others. A Dr. Tolcher, consulted by KTLA, says this is intriguing, but needs more research. Read the full article here... Sam’s Story: Using Medical Cannabis to Treat Autism Spectrum Disorder Background on Sam Sam is an eight-year-old male. He was diagnosed with Pervasive Developmental Delay- Not Otherwise Specified (PDD-NOS) when he was two and one-half years old by a pediatric psychiatrist at the M.I.N.D. Institute, UC Davis Medical Center. He was re-diagnosed at the M.I.N.D. Institute in October of 2007 with Autism Spectrum Disorder (ASD). As the psychiatrist told Sam’s mom and I, “Sam is a poster child for ASD”. Sam has lowered cognitive abilities and lowered verbal skills. Sam lives with his mom, dad and his younger sister who is six years of age. She is a typical child with no physical or mental health issues. Sam was adopted at birth. He had no prenatal issues and was a healthy infant. At around 18 months of age he began exhibiting ASD like behaviors and after six months of reassurances by his primary doctors that he was fine Sam was diagnosed with ASD. Since his diagnoses he has received special education services, speech therapy, occupational therapy, and behavioral therapy. He had been on the Gluten-Casein Free Diet (GCFD). He has been treated by a doctor (supposedly one of the best in the country) who treats ASD patients following the Defeat Autism Now (DAN) protocol which emphasizes a “BioMedical” approach established by Dr. Rimland the founder of Autism Society of America and the Autism Research Institute in San Diego, CA. As a family we have spent tens of thousands of dollars trying to help Sam. Even though as a teacher I have full coverage insurance, many of the services and doctors Sam has seen are not covered under my plan. Blue Cross of California still categorizes ASD as a “mental illness” instead of an “organic disorder” which precludes it from receiving the coverage a typical physical illness would be granted. I only mention this because since Sam was diagnosed with ASD we have devoted ourselves to helping him. This devotion has been in the forms of time, effort, education, therapy cost, medical costs, conferences, parent support groups, and most importantly love. Sam’s Strengths Sam loves people and he loves to “be on the go”. He has been to Disneyland four times, been camping many times, and has been to San Diego to visit the zoo, Wild Animal Park and Sea World. Sam loves to go to San Francisco Giant and Sacramento Kings games and loves to travel to San Francisco. Sam is our gift from God and we love him just as he is. Many tears have been shed from worry and from the joy of watching Sam achieve things parents of typical children take for granted. There have many moments of laughter and warmth given to us by our quirky, sweet, lovable, little boy. Purpose of this Journal I write this journal for Sam and other children like him. We almost lost our little boy to ASD and pharmaceuticals. By the grace of God and the help of a little Medical Cannabis (MC) we have him back. Maybe this journal can give other parents hope when all else seems dark and hopeless. Maybe this journal can prompt others to tell their stories if they have treated their ASD child with Medical Cannabis (MC). Even more important would be some legitimate scientific studies conducted to determine the effectiveness of MC to treat symptoms of Autism. I never wanted to be an advocate for Medical Cannabis (MC). I do not drink alcohol, take marijuana, or any other psychoactive drug. However, this experience has been so profound and dramatic that I feel no choice but to speak out on the issue. I understand the political and legal sensitivity of giving an eight-year-old child medical cannabis but if one child and family can be helped from my disclosure any risk to myself is acceptable. As a parent, I only want to help my son. No one ever questioned our decision to give our son the potpourri of pharmaceuticals prescribed by his doctors that, in my opinion, almost destroyed him. My wife and I both have very conservative parents and families who are very much opposed to any type of “illegal” drug use. We have their complete support. They witnessed Sam’s deterioration over the last year and they saw his almost miraculous turn around once we started using the MC. We have only disclosed treating Sam with MC to our closest family. We have shared the information with Sam’s primary pediatrician on the recommendation of Sam’s MC Doctor. The pediatrician has been supportive in an “off the record” manner. He has been Sam’s pediatrician since birth and he knows that we are responsible parents. Sam’s Educational Background Sam has had significant difficulty in school. He did well in preschool but began having constant problems once he entered Kindergarten. After a few months in a Kindergarten Special Day Class (SDC) Sam was removed from his neighborhood school and placed in a more specialized program for children with ASD. In 1st grade he was removed from that program and placed in a very restrictive setting that deals only with ASD kids (also public school). The population of that program was much lower than Sam, i.e., he was the only verbal child out of 12. Throughout this time Sam continued to have severe behavioral problems. To begin the 2007-08 school year he was placed back at his home school. His negative acting out became so intense and frequent that he was only able to attend school for 3 hours each day and was getting sent home at least 2 days each week. He was extremely unhappy at school and this unhappiness seemed to compound the increasing difficulty he was having at home. In December of 2007 Sam was placed in a Non Public School setting due to his aggressive, destructive, unsafe and antisocial behaviors. Data from a Functional Analysis Assessment done over a month period of time by a Behavioral Intervention Specialists (BIP) showed that Sam was having anywhere from 10-20 hitting, pushing, knocking things over, running off incidents per each 3 hour day. In summary, school was a disaster. Sam wasn’t learning anything and the teacher and his one-on-one aide were just trying to prevent him from hurting himself, them, or other children. Medical Intervention with Pharmaceuticals Throughout this time we were encouraged by school personnel and his doctors to keep trying different medications until we found one that would help him. We were told that this could be a long process because kids with ASD were extremely sensitive to medications in general and that there was no one drug that worked for every kid. We were constantly reminded of the success stories of other children. Unfortunately, taking any of the medications prescribed by his doctors never helped Sam. On the contrary, Sam’s mom and I were seeing a dramatic escalation of his anti social behaviors at school and at home. We had never had such intense problems at home. Sam’s condition imminently threatened the safety of our six-year-old daughter whom he began hitting on a regular basis. There were times when I would have to physically restrain Sam because he was in such a rage. He would go around the house yelling and knocking things over as if he were going crazy. He would try to run out of the house at 10 PM in the rain with no shoes on. Our home became a lock down facility. We were all miserable and Sam just kept getting worse. The future looked bleak. All this time we were going through a litany of medications to "help" him. Over a two-year period we did trials with Respirdol and Abilify (atypical antipsychotics), Ritalin and Adderall (amphetamines), Prosac, Paxil and Celexa (serotonin reuptake meds), and Tenex (Guanfacine), which is a blood pressure medication. We have a cupboard full of prescriptions for Sam. We tried different versions of the same type medications. We were encouraged to keep trying a medication until we knew for sure it worked or didn't work. The problem was he was having significant negative reactions to each medication he would try. He gained 10 pounds in 6 weeks on the Respirdol. Some of the meds, like the amphetamines, were obviously ineffective but others like the Abilify, Resperdal, and Paxil took time to develop negative side effects. The last medicine we tried was the Celexa. He was on it for 2 days in December and had a severe negative reaction. To put it bluntly, he "flipped out" on the medication. We stopped giving it to him immediately but the negative effects lingered with Sam for weeks. At that point we took Sam off all medication. His doctors recommended we try Depakote next. At this point, we were fearful that we would be able to manage him at home either with or without medication. Decision to Use Medical Cannabis At this point it was clear that the medications being prescribed by his doctors were not only failing to help Sam but they were harming him. He had gained significant weight, had an increase of aggressive and unpredictable behaviors and, most alarmingly to us, became very distant to those he had always loved so much. He began hitting his grandmothers and sister, and did not engage with his parents as he once did. He even became distant to me, his dad, the one person whom he had always had the most attachment. It was heartbreaking to watch him slip away. It was like the Sammy we had known was disappearing and we feared that he would steadily slip into greater isolation. There were several episodes that were so bad that we considered taking him to the hospital. My wife came to me with the suggestion that we consider treating Sam with Medical Cannabis. She had found information on the Internet that documented another parent’s success in treating her son who had similar characteristics to Sam with Medical Cannabis. I researched the subject myself and found an article written by Dr. Bernard Rimland from the Autism Research Institute that authenticated the parent’s story and stated the he would be more in favor of trying MC before he would more “toxic” pharmaceuticals. The article can be found at the following address (http://www.autism.org/marijuana.html). After discussing it with my wife and Sam’s grandparents, we decided to pursue it further. I knew very little about getting a recommendation from a doctor but was able to contact a doctor in my local area who recommends MC to patients. We had no idea how to obtain marijuana and we didn’t want to do anything illegal. We made an appointment with the MC doctor and gathered up all Sam’s medical and school records The doctor reviewed the case, examined Sam, and educated us on Medical Cannabis. He also made it clear that we would need to share information with Sam’s primary pediatrician. Additionally, we discussed the sensitivity of the issue and the risk that we were taking. As a team, we decided to maintain a “need to know policy” regarding Sam’s new medication. It was decided that school personnel did not need to know. Sam’s mom and I learned that in California a physician can “recommend” MC. It is not called a prescription but a recommendation. We also discovered that we would be able to obtain the MC locally through a Cooperative. Using Medical Cannabis to Treat Sam I have been keeping a journal since the trial began. The entries were daily to begin. After the first three weeks I reported every three to four days. I am not including every journal entry in this paper because it would be too long. January 8th, 2008 Today was the first day we gave Sam MC. We obtained the medicine around 3:00 PM. Because Sam is such a finicky eater we were very concerned about putting the medicine in baked goods. We wanted to give him the same amount of medicine at the same times each day and we knew that the baked goods could be problematic. Sam doesn’t like to eat breakfast before school and has an almost uncanny ability to detect anything that we place in his food. Often, he smells food before eating. Due to these considerations, we decided to give him the MC orally, in the form of Hashish. At 4:00 PM we administered his first dose. We gave him an amount that was about the size of a BB. We rolled the dose into a tight ball and buried it in a spoonful of yogurt. We told him he was taking a new medicine. He chewed the MC when he discovered it in the yogurt. He complained of the taste. We wanted to start out with a very small dose. Sam had been having another horrible day before the dose. After 30 minutes we could see the MC was beginning to have an effect. Sam’s eyes got a little red and got a bit droopy. His behavior became relaxed and far less anxious than he had been at the time we gave him the MC. He started laughing for the first time in weeks. My wife and I were astonished with the effect. It was as if all the anxiety, rage and hostility that had been haunting him melted away. That afternoon and evening his behavior was steady and calm. He started talking to us and interacting with us again. Sam’s was physically more relaxed and began initiating physical contact with the motivation being affection instead of aggression. It was amazing! He went to sleep that night with no problem and slept through the night. January 9th, 2008 Gave Sam about ½ dose (1/2 BB) of MC at 7:00 AM. He was not attending his new school yet so spent the day with Grandparent while we were at work. He had rough morning. Hitting, yelling, non-compliance, trying to jump in their freezing cold pool, and running out the front door. Re-dosed Sam at 3:30 PM when I got home from work. I gave him a BB sized dose, as I had the previous day. I feared that our experience was an anomaly and that, like all the other meds, it was just false hope. After 30 minute of giving Sam the dose his behavior deescalated to the levels it was the previous night. He was calm, happy, affectionate, more verbal, more compliant, and much more predictable. I noticed that he was open to conversation and even receptive to some short reading instruction. His reduced anxiety level made his behavior manageable and even agreeable. He was perseverating about certain things far less and we were able to redirect him far more quickly and effectively when he did get upset or need correction. January 10th, 2008 Gave him BB sized dose at 7:00 AM. He was staying with his Grandparents again for the day because he was not in school and we had to work. Before 8:00 AM he had a few episodes of acting out. He was becoming agitating and anxious and then around 8:20 my mom noticed that the MC was beginning to take effect. She described it to me as follows. “It was like a wave of calmness just swept over him and he changed from being a monster into a loveable, little boy”. When I got home from work he was still doing great. I didn’t give him an afternoon dose and he was fine for the rest of the day. Slept fine that night. January 11th, 2008 BB sized dose at 7:00 AM. Spent day with his mom. Had one blow out on walk when he wanted to jump in a small creek. No PM dose was necessary. Improved cooperative play with his sister. His sister came to me in disbelief when Sam was playing with her. She said’ “Sam is acting like a regular brother today”. When she told me that I just cried because here was this little girl who had lived in such fear, for so long, finally getting a brother she could love. Sam laughed and played. Again, the results we were getting far exceeded anything we could have imagined. January 12th, 2008 ¾ BB sized dose at 8:00 AM. It is a Saturday. Did Ok up to 2:00 PM and started to get agitated and anxious for an hour or so. Re-dosed him at 3:00 PM with ¾ size BB and within 1 hour he has calm again. That afternoon around 4:00 PM he lay down on our bed and took a nap. He rarely naps but fell asleep for an hour. Woke up happy and had a good evening. January 13th, 2008 8:00 AM dose; 1 BB size; Sunday; plans to go to Boat and RV show. Sam did great at the boat show. No running off, easily redirected, no yelling, and happy. It’s like he is a bit elevated and tipsy. He does look a bit “high” to us but it would never be noticeable to anyone else. His speech is clear (no slurring) and his gross or fine motor coordination are normal. In fact, his speech is moderately improved on the medication (both expressively and receptively). His anxiety level is greatly reduced and it just seems that he can concentrate better for longer stretches of time. This may contribute to the improved language skills we are noticing. If I scaled his anxiety from 1-10, (10 being extreme anxiety and 1 being no anxiety at all) I would place him at a 3 for today. Prior to the MC trial that began Jan. 8th, I would have placed him at a 10. No aggressive behaviors. No hitting, kicking, or threatening to do so. Sam is displaying much greater affection and is more compliant and social. He still has deficits in these social areas but far less pronounced than before the MC trial. January 18th, 2008 The following dosage is what we give Sam. The form of MC is hashish. ¾ BB size dose of MC at 7:00 AM ¾ BB size dose of MC at 3:00-4:00 PM (if necessary) The MC continues to be a very effective medication. Sam aggression has decrease dramatically. Prior to the medication trial, Sam was averaging 4-5 major outbursts per hour at home and an even greater frequency at school (see Functional Analysis Data Summary). An outburst could last minutes or hours. The behaviors included hitting, threatening to hit, kicking, throwing things, knocking things over, destroying property, yelling, crying, running off, and doing other unsafe acts like climbing over fences and leaving the house without supervision at night. Once Sam got into an agitated state it was extremely difficult to redirect him or get him to “move on” to something more positive. I really like the flexibility we have with the MC. There have been afternoons where a dose hasn’t been necessary. We don’t want to give him any medication unless we see symptoms that justify it. The AM dose is consistent because he is going to school but the PM dose can be eliminated. We have been giving him the PM dose 4 out of 5 days on average. Another convenience of the MC is that we can adjust his dose slightly depending on certain variables. If we something special planned, we can adjust the dose. For example, last night our daughter was given a Student of the Month award. There was a ceremony at the school board meeting that lasted 45 minutes or so. Sam was able attend and sit throughout the ceremony without incident. He was able to enjoy it and obviously, for us as parents, it was great that we were both able to be there for our daughter. This is in complete contrast to what usually happened to us when we had to take Sam somewhere like this. Before Christmas and prior to him being on MC, our daughter performed in a school musical. Within 10 minutes, I had to leave with Sam because he would not sit down and he began yelling when we tried to get him to stay and watch. This incident pretty much illustrates what life was like for us before this medication. I am not saying that this wouldn’t happen again but now we feel we have a chance for Sam to be successful in situations where we had little hope before. January 20th, 2008 Since the MC trial began, Sam has not had one act of hitting, kicking or threatening to hit. This includes school and home. SAM HASN’T GONE THIS LONG WITHOUT AGGRESSIVE BEHAVIORS IN YEARS. Additionally, the following improvements have occurred. I have classified these behavioral improvements into the three categories; Reduced Behaviors, Significant Improvements, and Mild Improvements. Reduced Behaviors Reduced aggression Reduced anxiety Reduced mood swings Reduced crying for no reason Reduced negative self talk Reduced obsessive/compulsive behavior Reduced non compliance Reduced running off and escape behaviors Significant Improvements Improved attitude and happier. Shares happiness with others appropriately. (Before the MC trial, the only time Sam laughed was when others were angry, crying or hurt) Increased flexibility to changes in routine or plans Quicker transition from being upset to being OK Improved affection to others Improved concentration and on task behavior at school Improved physical well-being. Far less complaining of stomachaches (probably because of being off other prescriptions) and more typical diet (the pharmaceuticals either made him habitually starving (Respirdol and Abilify) not hungry at all (Adderall, Ritalin) or caused him to have stomach irritation (Paxil, and Celexa). As I’ve stated, we feel much better about giving Sam MC that we did giving him the pharmaceuticals. Mild Improvements Improved language (receptive and expressive) Reduced self stimulation with finger play and fingers to mouth Reduced hyperactivity Increased ability to learn new information Improved sociability with peers February 21st, 2008 Sam continues to do great! He is getting great reports from school. His teachers write daily in a school journal. There has not been one negative entry and they are considering placing him in a more typical setting. Here are a few entries. 2-7-08 “Sam had another great day. He is such a joy to be around. His all day smiles and giggles are contagious.” 2-8-08 “John and I are so proud of Sam. He had a great day! He earned a trip to the barn this afternoon.” 2-20-08 “Sam did great! Today was the “Safety Fair”. Sam was awesome. He participated at each booth.” 2-21-08 “Another great day. We are currently working with Judith to develop a reading program that meets his needs. He always seems so excited to do his work and does great transitioning”. 2-27-08 Sam did great today! He was so awesome at the talent show. We won 3rd place!” Removing the Medical Cannabis After discussing the matter with Sam’s MC doctor, we decided to not give Sam any Medical Cannabis before school for a week or so to see if some of the negative behaviors returned. I concluded there were three main variables that could have accounted for Sam’s major improvement. One was the medical cannabis, two was his new school, and three was that he was no longer on any kind of prescription pharmaceuticals. On February 28th and February 29th (Thursday and Friday) Sam went to his new school for the first time without MC. On both days Sam had acting out behavior that his teachers had not previously seen. He didn’t hit but he did knock things over in his classroom and did a lot of negative self-talk. The staff was able to get him turned around pretty quickly but they were concerned that he was acting out at all. They had not seen any of this behavior since he started there. Conclusions
  19. Curing Addiction With Cannabis Medicines? Addiction is a real target — researchers like Professor Kendall believe the endocannabinoids could be a crucial link to addictive behaviour: “We know that the endocannabinoid system is intimately involved in reward pathways and drug seeking behaviour. So this tends to indicate that that if the link involving endocannabinoids and the reward pathway, using inhibitors, can be interrupted, it could turn down the drive to seek addictive agents like nicotine.” Because cannabinoids have also been shown to bring down blood pressure, it is hoped that related compounds can be used in patients with conditions like hypertension. Dr Michael Randall, a cardiovascular pharmacologist at the University has looked at how endocannabinoids cause blood vessels to relax. “This could have many implications,” Dr Randall said. “The endocannabinoids appear to lower blood pressure under certain conditions; states of shock for example. If the endocannabinoids are of physiological importance, this could have real therapeutic possibilities.” “In terms of getting better medicines the endocannabinoid system has a lot to offer,” said Dr Alexander. “The range of cannabis-related medicines is currently limited, but by increasing our knowledge in this area we can increase our stock.” Short break.. watch this Addiction is generally defined as a physical or psychological dependence on a substance, especially alcohol or other dugs, with use of increasing amounts.[1] For the sake of clarification, physical addiction is covered separately from psychological dependence on this website. (See also the section titled Dependence.) Scientific research on cannabinoid compounds has not demonstrated a strong association with biochemical addiction. In their exhaustive quest for evidence of addiction, federally funded researchers have resorted to relying on questionable data, such as the withdrawal symptoms reported by children who were referred to social service and criminal justice agencies. These researchers may argue that the court-ordered testimony of troubled youths “proves” that marijuana is addictive;[2] however, such questionable data is not scientific evidence of chemical addiction. In another case, an addictions researcher reported on his experiment in which rats displayed withdrawal symptoms upon a sudden discontinuation of THC. Critics point out that the reported withdrawal effects were created with very high doses of THC, and by the introduction of a second drug, a THC-blocking agent used to trigger the withdrawal symptoms. Withdrawal symptoms are not found in rats without using a THC-blocking agent,[3] and even among troubled youths, withdrawal symptoms are relatively mild and of short duration. [4], [5] Dopamine, a neurochemical produced in the central cortex of the brain, is thought to provide the brain’s “reward system.” Interference with dopamine production is considered a major symptom of biochemical addiction. While two studies alleged a minor link between THC and dopamine production in the brains of rats,[6] these were refuted by several subsequent studies showing that cannabis does not radically affect dopamine levels.[7], [8], [9] In assessing the importance of a possible link between cannabis use and dopamine levels, it should be noted that dopamine activity has also been detected in the brains of video game players who were paid money every time they reached a new level of the game.[10] Clearly, minor evidence of dopamine activity is not the sloe indicator of addiction. If it were, than all pleasurable activities would be defined as addictive. Moreover, the scientific evidence that cannabis use produces any amount of increased dopamine activity remains entirely inconclusive. Assessing the scientific literature on marijuana’s addictive potential for the Criminal Justice Commission of Australia, Peter Nelson reported, “… involvement with the ventromedial striatum suggests connections to dopamine circuits. However, the expected reinforcing properties usually associated with these dopamine pathways are difficult to demonstrate in the case of THC.”[11] Cannabinoids bond to anandamide nerve receptors that are primarily concentrated in the frontal lobes of the brain,[12], [13] rather than in the central cortex where dopamine is produced. THC is mild, with effects resembling those of caffeine or chocolate rather than classic addictive drugs such as alcohol, amphetamines, cocaine, opiates, and nicotine. In fact, a 1996 report from Daniele Piomelli of the Neurosciences Institute in San Diego indicated that chocolate contains three compounds that are chemically similar to cannabinoids. Studies involving rats showed that cannabinoid chemicals found in chocolate amplify the effect of natural cannabinoids found in the brain. The article published in Nature concluded that these compounds may, “participate in the subjective feelings of eating chocolate.”[14] In the April 1999 issue of Nature Neuroscience, Piomelli and colleagues at the University of California, Irvine reported that anandamide acts as an inhibitor of dopamine neurons.[15] Far from triggering chemical addiction in the brain, THC, the natural anandamide analogue, may actually help to balance erratic dopamine levels. The common scientific criteria for determining the addictive quality of a drug are examples of animal studies in which subjects self-administer an addictive substance. When given the choice between food and narcotics, for example, animals commonly self-administer the drug to the exclusion of all other activity, often starving themselves to death. Unlike heroin, cocaine, and other substances of abuse, there are no clinical studies showing animals self-administering cannabinoid compounds. In 1993, the Congressional Office of Technology Assessment reached this conclusion: While marijuana produces a feeling of euphoria in humans, in general, animals will not self-administer THC in controlled studies. Also, canabinoids generally do not lower the threshold needed to get animals to self-stimulate the brain reward system as do other drugs of abuse.[16] Clinical studies indicate a very low potential for addiction to cannabinoid drugs. In addition, there is no real-world evidence suggesting that THC is chemically addictive.[17] Epidemiological studies show that the large majority of people who try marijuana do not continue to use it on a regular basis. Moreover, the majority of people who ever use cannabis stop using it entirely before the age of thirty. Of an estimated 65 million “experimenters,”[18] only about 0.8% of Americans use cannabis on a daily basis.[19] The fact that millions of Americans have stopped using marijuana voluntarily and without difficulty is strong epidemiological evidence that cannabis is not chemically addictive. Despite federally funded sociological and scientific findings that marijuana produces only mild dependence in some heavy users,[20], [21] the federal government has officially classified cannabis as a Schedule I substance that has “a high potential for abuse.” Recent research determining that cannabinoids are not chemically addictive and do not have a high potential for abuse forms the basis of a petition filed with the Drug Enforcement Administration. That petition prompted the federal drug agency to enter into a legally binding review of the existing evidence by the US Department of Health and Human Services in 1997.[22] Two years later, investigative authors of the 1999 Institute of Medicine report determined that, “… marijuana was not particularly addictive.”[23] Yet cannabis is still classified as having, “no medical value and a high potential for abuse.” In 1999, Dr. Podrebarac wrote to the White House Office of National Drug Control Policy: “The recently released Institute of Medicine (IOM) study on the medical use of marijuana clearly supports rescheduling it for medical use.” The US Drug Czar’s office refused to comment on the rescheduling issue. Cannabis authority Tod Mikuria wrote extensively on the value of cannabis in treating addiction. Consider the following excerpt: “In 1839, William B. O’Shaughnessy visited cannabis buyers’ centers in India and mingled with the “dissolute and depraved” to learn about the preparations of this social drug for clinical medical trials and found it to be useful in the treatment of tetanus and seizures. In 1843, Clendinning utilized cannabis substitution for the treatment of alcoholism and opium addiction. Potter recommended full-dose Squibb cannabis extract for withdrawal from opium addiction. In 1894, the Indian Hemp Drugs Commission Report recognized the comparative safety of cannabis in its unsurpassed ethnographic studies within different cultures with a concern that if prohibited it would cause the use of more dangerous drugs. McMeens, citing Fronmueller in 1860, found that the use of cannabis in place of, or combined with, opiates reduced harm from increased dose, tolerance, dependance, and side effects of opiates. In 1897, cannabis was confirmed as useful in the treatment of delirium tremens and as an alternative to opium for analgesia. Dutt independently described the comparative safety of cannabis in Materia medica of the Hindus. Yeo and calleagues warned about addiction to morphine in the treatment of neuralgia and suggested cannabis as an alternative.” The connection between dependency on drugs and mood disorders may be caused by unsuccessful attempts to self-medicate uncomfortable feelings with the “cure,” causing more harm and aggravation of the underlying condition. Moreau described cannabis as being useful in the treatment of depression in 1845. Throughout the late nineteenth and early twentieth centuries, the drug was listed in medical texts and pharmaceutical catalogues for treatment f melancholia or mania. Notwithstanding some polysubstance abusers who maladaptively combine cannabis with other psychoactives, there appears to be a significant number of persons who have learned that cannabis can totally substitute for other psychoactive drugs. Following the therapeutic paths of Clendinning, throughout the nineteenth and twentieth century, cannabis was found useful in the treatement of opiate and sedative abuse. Brunton described the use of cannabis for the treatment of opiate dependence or as a substitute when opiates were not tolerated. Shoemaker found cannabis to be used for the cure of opium or chloral habits. Birch advocated for the use of Indian hemp in the treatment of chronic chloral and opium poisoning. Mattison, an early addcition specialist, recommended cannabis as a substitute for morphine and cautioned his fellow physicians about hypodermic use of the opiate. Alcohol abuse, stimulant, sedative, and opioid abuse and dependence are conditions potentially treatable with cannabis substitution. All of these conditions involve management of mood and emotional reactivity. Although there have been numerous synthetic homologues developed, short-acting psychotropic drugs continue to have high potential for dependency and abuse. The quality of immediacy for mood management would appear to be inseparable from abuse potential but cannabis appears to be the exception because of lesser or milder withdrawal symptoms. California cannabis center members and patients in my private practice independently rediscovered and confirmed that cannabis is a safer substitute for many prescribed and most nonmedical psychoactive drugs in the control of depression, anger, and anxiety. Cannabis substitution may be a gateway drug back to sobriety and dealing with the underlying psychopathalogic etiologies.[24] -------------------------------------------------------------------------------- [1] Taber’s Cyclopedic Medical Dictionary. Philedelphia: F.A. Davis Company, 1987 [2] “US Study: Marijuana is addictive.” Reuters, March 31, 1998 [3] “New Scientist special report on marijuana.” New Scientist, February 21, 1998 [4] “US Study: Marijuana is addictive.” op. cit. [5] Institute of Medicine, Marijuana and Medicine: Assessing the Science Base. Washington, DC: National Academy Press, 1999 [6] “Similar effects found in pot, harder drugs.” Maugh, Los Angeles Times, June 27, 1997 [7] Castaneda, et al., “THC does not affect striatal dopamine release: microdialysis in freely moving rats.” 1991 [8] Gifford, Gardner, and Ashby, “The effects of intravenous administration of delta-9-tetrahydrocannabinol on the activity of the A 10 dopamine neurons recorded in vivo in anesthetized rats.” Neuropsychopharmacology Vol. 36, No. 2, pp. 96-99, 1997 [9] “The July 1995 Gettman/High Times petition to repeal marijuana prohibition: An extensive review of relevant legal and scientific findings.” Source: www.hightimes.com/ht/new/petition/jgpetition/index.html [10] "Researchers watch dopamine changes in brain of video game players.” Associated Press, May 21, 1998 [11] Nelson, “A Critical Review of the Research Literature Concerning Some Biological and Psychological Effects of Cannabis.” Advisory Committee on Illicit Drugs, Cannabis and the Law in Queensland, pp. 113-152, Source: Schaffer Library of Drug Policy, www.druglibrary.org [12] Piomelli, “Functional role of high-affinity anamdamide transport, as revealed by selective inhibition.” Science, Vol. 277, No. 5329, p. 1094(4), August 22, 1997 [13] Gettman, op. cit. See also: Gettman, “Marijuana and the human brain.” High Times, March 1995 [14] “Chocolate and Cannabinol.” The Washington Post, August 26, 1996 [15] Stein, “Bits and Pieces.” Geriatric Psychiatry News, Issue 3, No. 7, June/July 1999 [16] U.S. Congress OTA, 1993 [17] Grinspoon, Bakalar, Zimmer, and Morgan, “Marijuana Addiction.” Science, Vol. 277, p. 749, August 8, 1997 [18] Annas, “Reefer Madness—The federal response to California’s medical-marijuana law.” The New England Journal of Medicine, Vol. 337, No. 6, August 7, 1997 [19] Zimmer and Morgan, Marijuana Myths: Marijuana Facts. New York: The Lindesmith Center, 1997 [20] U.S. Code Congressional and Administrative News, 1970 [21] Institute of Medicine, Marijuana and Medicine: Assessing the Science Base. Washington, DC: National Academy Press, 1999 [22] “DEA refers marijuana rescheduling petition to HHS.” The Law Offices of Michael Kennedy, NY, 1998 [23] “Official report backs medical use of marijuana.” Reuters, March 17, 1999 [24] Mikuriya, “Dependency and Cannabis.” Chapter 20, p. 225-227 source: http://www.cannabismd.net/addiction/ Run From The Cure The Rick Simpson Story (Full Version) http://www.youtube.com/watch?v=dvosdIXyjWM Following the therapeutic paths of Clendinning, throughout the nineteenth and twentieth century, cannabis was found useful in the treatment of opiate and sedative abuse. Brunton described the use of cannabis for the treatment of opiate dependence or as a substitute when opiates were not tolerated. Shoemaker found cannabis to be used for the cure of opium or chloral habits. Birch advocated for the use of Indian hemp in the treatment of chronic chloral and opium poisoning. Mattison, an early addcition specialist, recommended cannabis as a substitute for morphine and cautioned his fellow physicians about hypodermic use of the opiate. Alcohol abuse, stimulant, sedative, and opioid abuse and dependence are conditions potentially treatable with cannabis substitution. All of these conditions involve management of mood and emotional reactivity. Although there have been numerous synthetic homologues developed, short-acting psychotropic drugs continue to have high potential for dependency and abuse. The quality of immediacy for mood management would appear to be inseparable from abuse potential but cannabis appears to be the exception because of lesser or milder withdrawal symptoms. Cannabis, also known as marijuana[1] (from the Mexican Spanish marihuana) and by other names,a[›] is a preparation of the Cannabis plant intended for use as a psychoactive drug and as medicine.[2][3][4] Chemically, the major psychoactive compound in cannabis is delta-9-tetrahydrocannabinol (Δ9-THC); it is one of 400 compounds in the plant, including other cannabinoids, such as cannabidiol (CBD), cannabinol (CBN), and tetrahydrocannabivarin (THCV), which can produce sensory effects unlike the psychoactive effects of THC.[5] Contemporary uses of cannabis are as a recreational drug, as religious or spiritual rites, or as medicine; the earliest recorded uses date from the 3rd millennium BC.[6] In 2004, the United Nations estimated that global consumption of cannabis indicated that approximately 4.0 percent of the adult world population (162 million people) used cannabis annually, and that approximately 0.6 percent (22.5 million) of people used cannabis daily.[7] Since the early 20th century cannabis has been subject to legal restrictions with the possession, use, and sale of cannabis preparations containing psychoactive cannabinoids currently illegal in most countries of the world; the United Nations has said that cannabis is the most used illicit drug in the world.[8][9] wekipeda Sources: Journal reference: Br J Pharmacol 153 Theme Issue: http://www.nature.co...3/n2/index.html @ommpeddie EddieKirks Blog
  20. 5 Marijuana Compounds That Could Help Combat Cancer, Alzheimers, Parkinsons (If Only They Were Legal) September 14, 2012 | Imagine there existed a natural, non-toxic substance that halted diabetes, fought cancer, and reduced psychotic tendencies in patients with schizophrenia and other psychiatric disorders. You don’t have to imagine; such a substance is already here. It’s called cannabidiol (CBD). The only problem with it is that it’s illegal. Cannabidiol After THC, CBD is by far the most studied plant cannabinoid. First identified in 1940 (though its specific chemical structure was not identified until 1963), many researchers now describe CBD as quite possibly the most single important cannabinoid in the marijuana plant. That is because CBD is the cannabinoid that arguably possesses the greatest therapeutic potential. Cannabinol Cannabinol (CBN) is largely a product of THC degradation. It is typically available in cannabis in minute quantities and it binds relatively weakly with the body’s endogenous cannabinoid receptors. Scientists have an exceptionally long history with CBN, having first isolated the compound in 1896. Yet, a keyword search on PubMed reveals fewer than 500 published papers in the scientific literature specific to cannabinol. Of these, several document the compound’s therapeutic potential – including its ability to induce sleep, ease pain and spasticity, delay ALS (Lou Gehrig’s Disease) symptoms, increase appetite, and halt the spread of certain drug resistant pathogens, like MRSA (aka ‘the Superbug’). In a 2008 study, CBN was one of a handful of cannabinoids found to be “ exceptional” in its ability to reduce the spread MRSA, a skin bacteria that is resistant to standard antibiotic treatment and is responsible for nearly 20,000 hospital-stay related deaths annually in the United States. Cannabichromene Cannabichromene (CBC) was first discovered in 1966. It is typically found in significant quantities in freshly harvested, dry cannabis. To date, the compound has not been subject to rigorous study; fewer than 75 published papers available on PubMed make specific reference to CBC. According to a 2009 review of cannabichromine and other non-psychotropic cannabinoids, “CBC exerts anti-inflammatory, antimicrobial, and modest analgesic activity.” CBC has also been shown to promote anti-cancer activity in malignant cell lines and to possess bone-stimulating properties. More recently, a 2011 preclinical trial reported that CBC influences nerve endings above the spine to modify sensations of pain. “[This] compound might represent [a] useful therapeutic agent with multiple mechanisms of action,” the study concluded. Cannabigerol Similar to CBC, cannabigerol (CBG) also has been subject to relatively few scientific trials since its discovery in 1964. To date, there exist only limited number of papers available referencing the substance – a keyword search on PubMed yields fewer than 55 citations – which has been documented to possess anti-cancer, anti-inflammatory, analgesic, and anti-bacterial properties. Tetrahydrocannabivarin Discovered in 1970, tetrahydrocannabivarin (THCV) is most typically identified in Pakistani hashish and cannabis strains of southern African origin. Depending on the dose, THCV may either antagonize some of the therapeutic effects of THC (e.g., at low doses THCV may repress appetite) or promote them. (Higher doses of THCV exerting beneficial effects on bone formation and fracture healing in preclinical models, for example.) Unlike, CBD, CBN, CBC, CBG, high doses of THCV may also be mildly psychoactive (but far less so than THC). http://www.alternet.org/drugs/5-marijuana-compounds-could-help-combat-cancer-alzheimers-parkinsons-if-only-they-were-legal?page=0%2C0
  21. Nausea / Chemotherapy Is marijuana an effective treatment for reducing nausea and vomiting from chemotherapy? Cancer Monthly, a cancer treatment website, stated in its May 2006 e-newsletter article "Medical Marijuana - The FDA Loses More Credibility": "There are literally hundreds of articles that appear in the peer reviewed medical and scientific literature that discuss marijuana's effects in pain relief, control of nausea and vomiting, and appetite stimulation... Obviously smoking marijuana is not risk-free especially to respiratory organs and tissue. However, compared to the risks of a typical chemotherapy agent such as cytoxan which includes: urinary bladder, myeloproliferative, or lymphoproliferative malignancies, potential sterility, urinary system hemorrhagic cystitis, hematuria, cardiac toxicity, anaphylactic reactions, significant suppression of immune responses, and sometimes fatal, infections; the risks of marijuana pale in comparison. And for cancer patients with advanced cancers who want to improve the quality of their life, a risk versus benefit analysis weighs heavily on the benefit side. More Pro's and Con's How does marijuana help a cancer patient undergoing chemotherapy? Chemotherapy comes with some pretty common, and unpleasant, side effects. Many patients lose their desire to eat and experience nausea and vomiting. Still others develop a condition called cachexia, in which they lose a significant portion of their body weight, both fat and muscle. This condition, especially when combined with the loss of appetite and nausea, can cause those being treated for cancer to feel physically weak and emotionally drained. The National Cancer Institute (NCI) explains that maintaining an adequate weight and absorbing sufficient nutrients can help patients feel, look, and function better, and may even help their bodies tolerate cancer therapy. Traditionally, patients are given drugs called antiemetics in tandem with their chemotherapy in order to reduce nausea and increase appetite. But not all people respond adequately to these medications. That's where marijuana comes in. It has been know for years that THC (delta-9-tetrahydrocannabinol), the main chemical component of marijuana, tends to stimulate one's appetite. In fact, THC has been available since the mid-1980s for cancer patients in a synthetically engineered capsule form. This medication, known as dronabinol in the medical world, has been shown to reduce nausea, increase appetite, and help patients gain weight. Right now there is a study under way, supported by the NCI, which is designed to measure the impact THC therapy, as dronabinol, has on the management of these symptoms in cancer patients. Click here to get more information about this study. There is also research being done on the medical use of THC by people with AIDS and those with glaucoma. More I have a friend who will be going through chemotherapy and radiation. What can she do to build herself up to keep her body in the best condition possible? Chemotherapy and radiation — using drugs and radiation to kill cancer cells — can be tough on both the body and the mind. As you suggest, advance preparation can make the process easier. While it is unclear how much time your friend has before she begins her treatment, the following suggestions may offer some sense of direction in preparing for therapy. Eat right. In order to keep the body working at its best to prepare for treatment, nutrition is important. Typically, a healthy eating plan includes lots of whole grains, fresh fruits and vegetables, and moderate amounts of low-fat meats and dairy products. The nutritional needs of people with cancer, including those who are preparing for chemotherapy or radiation, however, may require high-calorie, high-protein foods, such as milk, cream, cheese, and cooked eggs. Other recommendations may include cooking with more sauces, gravies, butter, margarine, or oil. While the emotional stress of cancer and beginning treatment can affect appetite, these extra nutrients may help to ensure that people with cancer will be able to commence treatment with the energy reserves needed. Your friend needs to consult with her cancer treatment team, which may include a nutritionist, before her sessions begin for specific recommendations tailored to her cancer and the chemotherapy and radiation treatments she will be given. (During treatment, these calorie- and protein-rich food recommendations may change.) More f your friend is having trouble sleeping or relieving stress, or just wants someone to talk with about her treatment, an appointment with a counselor might be helpful. If she's a student at Columbia, she can look at the Counseling and Psychological Services (CPS) web page for info on setting up an appointment, or call x4-2878. To find out more about preparing for cancer treatment, you and your friend can visit the American Cancer Society's site on What to Do Before Treatment Begins. Also, consider a visit to the American Academy of Family Physicians' Cancer: Preparing for Treatment webpage for more ways to make the time and experience during treatment easier. If you or your friend prefers books, pick up The Chemotherapy and Radiation Therapy Survival Guide by Judith McKay and Nancee Hirano. It's great that you're being so supportive before your friend's treatment — she's lucky to have a friend like you! Safety of cannabis Various strains of medical marijuana in front of a vaporizer According to an approved statement from the US Department of Justice in 1988, "Nearly all medicines have toxic, potentially lethal effects. But cannabis is not such a substance. There is no record in the extensive medical literature describing a proven, documented cannabis-induced fatality. In practical terms, cannabis cannot induce a lethal response as a result of drug-related toxicity."[53] From January 1997 to June 2005, the U.S. Food and Drug Administration (FDA) reported zero deaths caused by the primary use of cannabis. In contrast, common FDA-approved drugs which are often prescribed in lieu of cannabis (such as anti-emetics and anti-psychotics), were the primary cause of 10,008 deaths.[54] wiki Cannabidiol Main article: Cannabidiol Cannabidiol has been shown to relieve convulsions, inflammation, anxiety, cough, congestion and nausea, and it inhibits cancer cell growth.[80] Cannabidiol (CBD) is a major constituent of medical cannabis. CBD represents up to 40% of extracts of medical cannabis.[81] Cannabidiol has been shown to relieve convulsion, inflammation, anxiety, cough, congestion and nausea, and it inhibits cancer cell growth.[80] Recent studies have shown cannabidiol to be as effective as atypical antipsychotics in treating schizophrenia.[82] Because cannabidiol relieves the aforementioned symptoms, cannabis strains with a high amount of CBD may benefit people with multiple sclerosis, frequent anxiety attacks and Tourette syndrome.[57][80][83]Source Difference between Cannabis indica and Cannabis sativa Cannabis sativa, Cannabis indica, and Cannabis ruderalis A Cannabis indica plant may have a CBD/THC ratio 4-5 times that of Cannabis sativa. Cannabis with relatively high ratios of CBD:THC is less likely to induce anxiety than vice versa. Indica has more cannabidiol and sativa has more THC.[105] This might partially be due to CBD's antagonist effects at the cannabinoid receptor, compared to THC's partial agonist effect.[106] The relatively large amount of CBD contained in Cannabis indica, means, compared to an Cannabis sativa, the effects are modulated significantly. The effects of sativa are well known for its cerebral high, hence used daytime as medical cannabis, while indica is well known for its sedative effects and preferred night time as medical cannabis. Indica plants are normally shorter and stockier plants than sativas. They have wide, deeply serrated leaves and a compact and dense flower cluster. The effects of indicas are predominantly physical and sedative. Due to the relaxing nature of indicas, they are best used for non-active times of the day, and before bed. Indica strains generally have higher levels of C.B.D and C.B.N and lower levels of T.H.C.[107] Harm reduction Aspergillus fumigatus The harm caused by smoking can be minimized or eliminated by the use of a vaporizer[127] or ingesting the drug in an edible form. Vaporizers are devices that heat the active constituents to a temperature below the ignition point of the cannabis, so that their vapors can be inhaled. Combustion of plant material is avoided, thus preventing the formation of carcinogens such as polyaromatic hydrocarbons, benzene and carbon monoxide. A pilot study led by Donald Abrams of UC San Francisco showed that vaporizers eliminate the release of irritants and toxic compounds, while delivering equivalent amounts of THC into the bloodstream.[128] According to Matthew Seamon and his co-authors “Vaporizers are the optimal route of administration because they allow for rapid and complete absorption with minimal combustible byproducts, often considered the major health risk associated with smoking tobacco.”[129] In order to kill microorganisms, especially the molds A. fumigatus, A. flavus and A. niger, Levitz and Diamond suggested baking marijuana at 150 °C (302 °F) for five minutes. They also found that tetrahydrocannabinol (THC) was not degraded by this process.[130] Marijuana Component Could Ease Pain from Chemotherapy Drugs, Study Suggests ScienceDaily (Oct. 6, 2011) — A chemical component of the marijuana plant could prevent the onset of pain associated with drugs used in chemo therapy, particularly in breast cancer patients, according to researchers at Temple University's School of Pharmacy. The researchers published their findings in the journal Anesthesia and Analgesia. The researchers developed animal models and tested the ability of the compound cannabidiol, which is the second most abundant chemical found in the marijuana plant, to relieve chemo-induced neuropathic pain, said Sara Jane Ward, research assistant professor of pharmaceutical sciences in Temple's School of Pharmacy and the study's lead author. "We found that cannabidiol completely prevented the onset of the neuropathic, or nerve pain caused by the chemo drug Paclitaxel, which is used to treat breast cancer," said Ward, who is also a research associate professor in Temple's Center for Substance Abuse Research More n addition to Ward, Temple researchers involved in the study included Michael David Ramirez, Harshini Neelakantan and Ellen Ann Walker. The study was supported by grants from the National Institutes of Health and the Peter F. McManus Charitable Trust.
  22. Pain / Analgesia Is medical marijuana an effective treatment for patients suffering from severe / chronic pain? The National Institutes of Health (NIH) stated the following in a report to the NIH Director titled "Workshop on the Medical Utility of Marijuana," that was compiled by the self-titled Ad Hoc Group of Experts during a two day meeting held Feb. 19-20, 1997: "A number of studies have been conducted on the antinociceptive [increased pain tolerance] or analgesic [pain reducing] effect of tetrahydrocannabinol (THC) or marijuana in both animals and human subjects; the results have been conflicting...Cannabinoids have been shown to be possibly analgesic in animal models of neuropathic pain... Since oral Delta-9-THC has some analgesic activity, it is highly likely that smoked marijuana has some analgesic activity in some kinds of clinical pain...If marijuana is to be a useful analgesic, healthcare providers need to know how it compares in efficacy and safety to at least a few of the standard analgesics that would be used in managing a particular kind of pain...There appear to be no controlled analgesic studies of smoked marijuana in patients with naturally occurring pain." More on Pro's and Con's Tetrahydrocannabinol (THC) and some other cannabinoids, either from the Cannabis sativa plant or synthetic, have analgesic properties, although the use of cannabis derivatives is currently illegal in many countries. A recent study finds that inhaled cannabis is effective in alleviating neuropathy and pain resulting from e.g. spinal injury and multiple sclerosis.[13] Other psychotropic analgesic agents include ketamine (an NMDA receptor antagonist), clonidine and other a2-adrenoreceptor agonists, and mexiletine and other local anaesthetic analogues. wikipedia "Cananbinoid-induced analgesia appears linked to the same system by which opioids [synthetic narcotics] produce pain relief. But different from opioids, cannabinoids are also effective in a rat model of neuropathic pain, which means pain cased by nerves. For those of us that care for people with HIV—we know about the painful, peripheral neuropathy they get—very painful numb tingling feet. We often start these patients on a trial of drugs that lead ultimately to morphine, because there isn’t anything effective." [26] Dr. Abrams conducted a valuable human study of 50 HIV patients who used smoked marijuana cigarettes three times per day. Subjects showed positive results in daily pain, hyperalgesia, and a 30% reduction in pain. [27] My link A research paper fone at Hammersmith Hospital in London confirmed cannabis’ analgesic effects in the first UK clinical trial. The paper’s abstract began, “Cannabinoids have analgesic and, possibly, anti-inflammatory properties but their clinical use has been restricted by legislation.” That same abstract calling for further studies concluded, “Cannabis naïve patients would tolerate investigations but may generate medicolegal problems.” [28] The use of cannabis for pain relief was widespread in the membership of legitimate medical marijuana groups under attack by the US government. [29] In 1998, federal law enforcers closed San Francisco Bay Area Cannabis Clubs, forcing over 10,000 seriously ill patients to support nefarious “street” sources and pay outrageous black market prices for non-medical grade marijuana. In the following year, the government sponsored Institute of Medicine report elevated pain relief to the top of the list of marijuana’s medical benefits. [30] Due to cannabis prohibition and the bias of research regulation by the National Institutes on Drug Abuse, human studies of the pain relieving qualities of cannabis are limited. Grotenherman writes: " Few clinical studies of cannabinoids in painful conditions exist. In two trials, oral THC proved to be effective against cancer pain in doses of 15 and 20 mg, respectively. However, some patients experienced intolerable side effects. In a single case double-blind study a patient with familial Mediterranean fever clearly reduced his need for opiates while receiving THC (50 mg per day divided in five doses) in comparison to placebo."[31] However, the fascinating new view of the body's endocannabinoid systems provide ample scientific evidence to justify the widespread popularity of cannabis as an analgesic, partivcularly in cases of nerve or neurological pain. Consider the following excerpts from a recent paper titled “Mechanisms of Cannabinoid Analgesia”: “Within the central nervous system, cannabinoids, like opioids, act at both spine (intrathecal) and supraspinal (intracerebroventricular) levels to produce analgesia. Cannabinoid-induced analgesia is not mediated by opioid receptors because it is unaffected by opioid antagonists. However, cannabinoid and opioid agonists have synergistic analgesic affects.” “In vivo electrophysiological studies indicate that, like opioids, cannabinoids suppress the activity of neurons involved in the ascending transmission of nociceptive information. Systemic administration of cannabinoid agonists inhibits noxious stimulus-evoked firing in neurons of the spinal cord dorsal horn and thalamus. Cannabinoids also inhibit windup (a neuronal correlate of hyperalgesia), which is the augmentation of the response of spinal neurons to repetitive noxious electrical stimuli.” “It is now becoming apparent that, like opioids, cannabinoids act via specific receptors within pain pathways to produce analgesia. The distinct anatomical receptors within pain pathways suggests that they may be useful for management of different pain sites. The distinction between cannabinoids and opioids is emphasized by more recent electrophysiological studies and provides a cellular basis for their synergistic analgesic actions. These findings suggest that cannabinoids warrant urgent study as therapeutic agents, particularly with the emergence of novel cannabinoid drugs.”[32] IN 2008, i nvestigators at the University of California at Davis, in conjunction with the University of California Center for Medical Cannabis Research (CMCR), assessed the efficacy of inhaled cannabis on pain intensity among 38 patients with central and/or peripheral neuropathic pain in a randomized, placebo-controlled, crossover trial. Researchers reported that smoking low-grade (3.5 percent THC) and mid-grade (7 percent THC) cannabis equally reduced patients’ perception of spontaneous pain. They concluded: "In the present experiment, cannabis reduced pain intensity and unpleasantness equally. Thus, as with opioids, cannabis does not rely on a relaxing or tranquilizing effect, but rather reduces both the core component of nociception (nerve pain) and the emotional aspect of the pain experience to an equal degree." The study is the second clinical trial conducted by CMCR investigators to conclude that inhaled cannabis significantly reduces chronic neuropathy, a condition that is typically unresponsive to both opioids and non-steroidal anti-inflammatory drugs such as ibuprofen.[33] GW Pharmeceuticals is a company that has isolated canabinoid compounds in arosol sprays for medical use. Another recent study shows that GW's product, Sativex, sowed remarkable value in trating neuropathic pain. Forty-one patients with multiple sclerosis and central neuropathic pain completed the double blind, placebo-controlled "randomized withdrawal" study. Volunteers in the study were administered either Sativex or a placebo daily for four weeks following their long-term use of the cannabis spray. Previous trials of Sativex have reported that patients required fewer daily doses of the drug and reported lower median pain scores the longer they took it.[34] Recent studies have located and determined exact mechanisms of cannabis analgesia through the body's endocannabinoid receptors. The following is an excert from "Endocannabinoids and pain: spinal and peripheral analgesia in inflammation and neuropathy" from theInperial College of Science in London: "Local administration, peptide release and electrophysiological studies support the concept of spinally mediated endocannabinoid-induced analgesia. Whilst a proportion of the peripheral analgesic effect of endocannabinoids can be attributed to a neuronal mechanism acting through CB(1) receptors expressed by primary afferent neurones, the antiinflammatory actions of endocannabinoids, mediated through CB(2) receptors, also appears to contribute to local analgesic effects." [35] Related sections: Addiction, Arthritis, Neuralgia, Psychoactivity, Replacement of Medications [1] “Doctor urges war on pain, more use of opium-based drugs.” Miami Hearald, January 29, 1998 [2] Stolberg, “Study Finds Elderly Receive Little Pain Treatment in Nursing Homes.” June 17, 1998 [3] “Doctor urges war on pain, more use of opium-based drugs.” Miami Hearald, January 29, 1998 [4] “Researchers say many cancer patients suffer needless pain.” Associated Press, June 17, 1998 [5] Drug Enforcement Administration, “Statement of policy for the use and handling of controlled substances in the treatment of pain.” 1998 [6] Kassirer, “Federal foolishness and marijuana.” Editorial, The New England Journal of Medicine, January 30, 1997 [7] Russo "Cannabinoids in the management of difficult to treat pain" Therapeutics and Clinical Risk Management" 2008-4(1) 245-259 [8] Mikuriya, Marijuana Medical Papers: 1839-1972. Oakland: Medi-comp Press, 1973 [9] Grinspoon, Marijuana Reconsidered. 3rd ed. San Francisco: Quick American Archives, 1971 [10] Russo, "The Role of Cannabis and Cannabinoids in Pain Management" Weiner's Pain Mnagement Guide, 7th ed. American Academy of Pain Management 2006 [11] Noyes and Baram, “Cannabis analgesia.” Comprehensive Psychiatry. Vol. 15, No. 6, 1974 [12] Beltramo and Piomelli, “Functional role of high-affinity anandamide transport, as revealed by selective inhibition.” Science, Vol. 277, No. 5329, p1094(4), 1997 [13] Russo, "The Role of Cannabis and Cannabinoids in Pain Management" Weiner's Pain Mnagement Guide, 7th ed. American Academy of Pain Management 2006 [14] Formukong, Evans, and Evans, “Analgesic and anti-inflammatory activity of constituents of cannabis sativa L.” Inflammation, Vol. 12, No. 4, pp.361-371, 1988 [15] Maurer, Henn, Dittrich, and Hoffman, “Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double blind trial.” European Archive of Psychiatry and Neurological Science. Vol. 240, No. 1, pp. 1-4, 1990 [16] “Cannabidiol, Wonder drug of the 21st century?” Source: Schaffer Library of Drug Policy, www.druglibrary.org [17] “Pre-clinical studies show CT-3 reduces chronic and acute inflammation and reduces destruction of joints.” BW HealthWire, January 1998 [18] "Curative Leaf - Compound in marijuana reduces inflammation without the psychological effects", Amy Maxmen, Science News, June 23rd, 2008, www.sciencenews.com [19] “Medical marijuana: Doing the science.” Synapse, 1998, www.itsa.ucsf.edu/synapse/ [20] Symposium Syllabus, Functional Role of Cannabinoid Receptors. Press Conference, August 26, 1998, Source: Medical Marijuana Magazine, www.marijuanamagazine.com [21] “Study reveals pot chemicals can relieve serious pain.” Los Angeles Times, October 27, 1998 [22] Ibid. [23] Morin, “Research into cannabinoids provides evidence that the use of marijuana to treat pain and nausea should not e so easily dismissed.” May 1998, Source: Morin@Brown.edu [24] Cowen, “Science journal reports that cannabinoid receptors located outside the brain and spine are affected when the skin or flesh is cut or hurt.” July 16, 1998, www.marijuananews.com [25] Widener, “Study: Marijuana, morphine work on same area of brain.” The Seattle Times, September 25, 1998 [26] “Diagnosis: Smoke Pot to Relieve Pain.” The University of Washington Daily, May 1997 [27] Abrams, Lindesmith Center Lecture, San Francisco, May 17, 1999 [28] Holdcroft et al., “Pain relief with oral cannabinoids in familial Mediterranean fever.” Anesthesia, Vol. 52, No. 5, pp. 483-486, May 1997 [29] San Francisco Chronicle, San Francisco Examiner, Associated Press, May 1998 [30] Institute of Medicine: Marijuana and Medicine: Assessing the Science Base. Washington DC: National Academy Press [31] Grotenhermen, “Review of Therapeutic Effects.” Chapter 11, p. 126-128 (see Absracts and Studies section of this website) [32] Vaughn and Christie, “Mechanisms of Cannabinoid Analgesia.” Chapter 8, p. 90-95 [33] Inhaled Cannabis Reduces Central And Peripheral Neuropathic Pain, Study Says, NORML News, May 3rd, 2008 See: www.NORML.org [34] Cannabis Spray Demonstrates Long Term Efficacy In Neuropathic Pain, Study Says, NORML News, 9/11/08, See: www.NORML.org [35] “Endocannabinoids and pain: spinal and peripheral analgesia in inflammation and neuropathy”, Rice AS, Farquhar-Smith WP, Nagy I., Department of Anaesthetics, Pain Research Group, Inperial College of Science, Technology and Medicine, Chelsea and Westminster Hospital Campus, 369 Fulham Road, London SW10 9NH, UK. a.rice@ic.ac.uk My link Researchers at University of California Davis examined whether marijuana produces analgesia for patients with neuropathic pain. Thirty-eight patients were examined. They were given either high-dose (7%), low-dose (3.5%) or placebo cannabis. The authors reported that identical levels of analgesia were produced at each cumulative dose level by both concentrations of the agent. As with opioids, cannabis does not rely on a relaxing or tranquilizing effect, but reduces the core component of nociception and the emotional aspect of the pain experience to an equal degree. There were undesirable consequences observed from cannabis smoking, such as feeing high or impaired, but they did not inhibit tolerability or cause anyone to withdraw from the study. In general, side effects and mood changes were inconsequential. It was noted by the authors that since high and low dose cannabis produced equal analgesic efficacy, a case could be made for testing lower concentrations to determine if the analgesic profile can be maintained while reducing potential cognitive decline. In addition, the authors said further research could probe whether adding the lowest effective dose of cannabis to another analgesic drug might lead to more effective neuropathic pain treatment for patients who otherwise are treatment-resistant n a randomized, double-blinded, placebo controlled, crossover trial in fifteen healthy volunteers, we evaluated the effects of low, medium, and high dose smoked cannabis (respectively 2%, 4%, and 8% 9-delta-tetrahydrocannibinol by weight) on pain and cutaneous hyperalgesia induced by intradermal capsaicin. Capsaicin was injected into opposite forearms 5 and 45 minutes after drug exposure and pain, hyperalgesia, tetrahydrocannibinol plasma levels, and side effects were assessed. Five minutes after cannabis exposure, there was no effect on capsaicin-induced pain at any dose. By 45 minutes after cannabis exposure, however, there was a significant decrease in capsaicin-induced pain with the medium dose and a significant increase in capsaicin-induced pain with the high dose. There was no effect seen with the low dose nor was there an effect on the area of hyperalgesia at any dose. Significant negative correlations between pain perception and plasma delta-9-tetrahydrocannibinol levels were found after adjusting for the overall dose effects. There was no significant difference in performance on the neuropsychological tests. This study suggests that there is a window of modest analgesia for smoked cannabis with lower doses decreasing pain and higher doses increasing pain. The full results of this study were published in the journal Anesthesiology. ABSTRACT: By every criteria (deterioration in quality of life; loss of work days, and therapy directed dollars) pain is appreciated to be a major medical problem. Recent findings in the molecular biology and the pharmacology of pain transmission have shed light on mechanisms of nociceptive processing and the activity of a variety of "novel therapeutic" modalities that include the cannabinoids. Although the pre-clinical literature suggests that the cannabinoids produce antinociception and anti-hyperalgesic effects, the efficacy of the cannabinoids in the human pain state is unclear. As an experimental variable, clinical pain is a multidimensional phenomenon with few objective physical correlates. Many other factors such as emotional status and coping skills, make "pain" difficult to study in the clinical setting. An important development has been the implementation of well-controlled experimental pain models to investigate the sensory components of pain processing and to use these models in the assessment of analgesic efficacy in normal volunteers. To the degree that human experimental pain models can predict analgesic efficacy of novel agents, the role of mechanisms defined in preclinical studies can be translated to the human experience under well-controlled conditions. Human experimental pain has been used to test a wide range of currently available analgesics. Knowing the effect of these agents on human experimental pain, I now wish to study the effects of cannabis on human experimental pain and how this compares to commonly used analgesics. PUBLICATIONS: Type: Title: Journal Article Wallace M, Schulteis G, Atkinson JH, Wolfson T, Lazzaretto D, Bentley H, Gouaux B, Abramson I. Dose-dependent Effects of Smoked Cannabis on Capsaicin-induced Pain and Hyperalgesia in Healthy Volunteers. Anesthesiology. 107(5):785-796, November 2007. The most frequent complaint that patients look for medical help with is pain. There are several different types of pain, and unfortunately none of the currently-prescribed pharmacological treatments for pain work completely for certain types. A particular example is that of pain caused by damaged nerves (such as that which causes phantom limb pain), which does not respond well to existing medications. Severe chronic pain is usually treated with opiates, but these are addictive, and tolerance develops so that the dose has to be increased. The risk of severe side effects such as nausea is great, and additionally the user feels drugged, and finds it difficult to function properly. Family life may suffer as patients find it hard to relate to other people, and even reading to children is difficult. Synthetic analgesics are non-addictive but they are not powerful enough. Cannabis has fewer side effects than other analgesics, and users report it "rounds off" the pain quickly after smoking. An Institute of Medicine report contains a minimal list of 5 situations in which cannabis-based medicines are of use in treating pain: There are medical conditions or patients in which they are more effective than any currently available medication. They have a broad clinical spectrum of efficacy and a unique side effect profile that differs from other analgesics. They have synergistic interactions with other analgesics. They exhibit "side effects" which are considered useful in certain clinical situations. Their efficacy is enhanced in patients who have developed tolerance to opioids. Some people have used cannabis to control pain for 20 years or more, and many report that they were able to kick their addiction to opiates with small amounts of cannabis. One strange fact is that more experienced users get a greater pain-relieving effect from cannabis than novices. Experienced users also are able to function normally and ignore the psychoactive effects. Cannabis may be better at controlling the different types of pain. Cannabis has had a long history of use as an analgesic, and was widely used in 19th century Britain, including in the royal household. Dr. J. Russell Reynolds, Fellow of the Royal Society and Physician to Queen Victoria reported in the Lancet in 1890 that he had been prescribing cannabis for 30 years and considered it "one of the most valuable medicines we possess". According to Reynolds indian hemp remained effective as an analgesic for months and even years without an increase in the dose. It seems that cannabis shares some method of action with opioids, but the mechanism with which it accomplishes its analgesic effects differs. This indicates that they may produce an additive effects when used in conjunction with current medicines. In addition they might provide help to patients who do not react satisfactorily to other treatments. Much anecdotal evidence seems to indicate that this is the case. Indeed, the British Medical Association has gone on record as stating that 'the prescription of nabilone, THC and other cannabinoids...should be permitted for patients with intractable pain'. Other official bodies have found similar results. A House of Lords report summed up the situation stating that 'there is scientific evidence that cannabinoids possess painrelieving properties, and some clinical evidence to support their medical use in this indication'. In a press conference on October 26th 1997, the US Society for Neuroscience claimed that 'substances similar to or derived from marijuana...could benefit the more than 97 million Americans who experience some form of pain each year'. Patients' testimonies The medical testimonies database contains 51 testimonies from cannabis users with pain . NameDate Amanda Mon 01 Nov 2010 Annon Mon 01 Nov 2010 Mund Mon 01 Nov 2010 jimmy Mon 01 Nov 2010 Mr Dmoore Mon 02 Nov 2009 Anonymous Mon 02 Nov 2009 Anonymous Sun 06 Dec 2009 Anonymous Wed 02 Dec 2009 Anonymous Wed 02 Dec 2009 Anonymous Sun 02 Nov 2008 Annamarie Grogan Tue 02 Dec 2008 Anonymous Thu 02 Nov 2006 Stephen Livingston Sat 09 Dec 2006 Ian Lunar Module Wed 06 Dec 2006 Anonymous Sat 02 Dec 2006 Roger Pigott Fri 01 Dec 2006 GC Mon 31 Oct 2005 Eleanor Sun 04 Dec 2005 Ronald Roberson Sat 03 Dec 2005 Maggie Froud Fri 02 Dec 2005 Terry Sun 05 Dec 2004 vanessa Fri 03 Dec 2004 gruf Sun 02 Nov 2003 J. Gribbin Sat 01 Nov 2003 Welshstoner Fri 31 Oct 2003 Nicolas Tue 09 Dec 2003 George Lister Sun 07 Dec 2003 Sonia Fri 05 Dec 2003 Bob Mon 01 Dec 2003 John Sat 02 Nov 2002 Anonymous Sat 02 Nov 2002 Winston Matthews Fri 01 Nov 2002 Stacey H Thu 31 Oct 2002 Carl Thu 31 Oct 2002 Steven Mon 09 Dec 2002 Garry Pearson Sat 07 Dec 2002 Missi Fri 06 Dec 2002 Hugh Tue 03 Dec 2002 Russ Points Fri 02 Nov 2001 Puffs Thu 01 Nov 2001 Phil James Thu 01 Nov 2001 Anonymous Sun 09 Dec 2001 Anonymous Mon 03 Dec 2001 Anonymous Sun 02 Dec 2001 Sybil Sun 02 Dec 2001 Anonymous Sun 02 Dec 2001 Anonymous Tue 31 Oct 2000 Anonymous Sat 09 Dec 2000 Nigel Pearson Sat 09 Dec 2000 Anonymous Thu 07 Dec 2000 Anonymous Thu 07 Dec 2000 For the complete collection of testimonies from medical users of cannabis, see our medical testimony database. Do you find that cannabis helps you with this, or any other, medical condition? If so, please tell us about how it benefits you via this form. Anonymous submissions welcome! Scientific evidence Despite the long history of use of cannabis as an analgesic, and the obvious problems with synthetic drugs, the War on Drugs prevented people from reconsidering cannabis until the mid-seventies, when several studies were published. Patients suffering from cancer usually suffer from severe pain. This can be for a number of reasons, such as the invasion of their bones, inflammation or damage caused to nerves. It is a form of pain which is notoriously hard to treat effectively. At the University of Iowa Noyes et al (1975a) gave oral THC or a placebo at random to hospitalised cancer patients who were in severe pain. The THC relieved pain for several hours at very low doses and longer periods at higher doses (15 - 20 mg). It also acted as a sedative at the higher dose. It had fewer physical side effects than other commonly used analgesics. There was no incidence of nausea or vomiting unlike many other analgesics - indeed more than half of the patients had an increased appetite. Then Noyes et al conducted another study (1975b). This time they gave codeine, THC and placebo to 36 patients with advanced cancer. Codeine and cannabis were equally effective, but some patients found the psychoactive effects of THC uncomfortable. However these people did not know they were going to take a psychoactive drug and were obviously frightened. If they had been told beforehand perhaps they would not have been uncomfortable. Many of the patients however felt they generally had a sense of well-being that was absent before. As a result of this experiment, the researchers estimated that 10mg of THC was roughly equivalent to 60mg of codeine. A study revealing potential additive effects of THC on standard medication was done by Holdcroft et al (1997). It centred on a patient who had severe chronic pain of gastrointestinal origin. The patient used morphine as an analgesic.It was found that the patient required a substantially lower amount of morphine when they were treated with oral THC in the form of cannabis oil. The differing mechanism of analgesic action cannabis uses compared to existing (mainly opioid) medications means that not only are additive effects likely, but it could be useful in patients resistant to existing medications, and be useful in treating pain which existing medications fail to deal with adequately. The National Institutes of Health suggested that 'Neuropathic pain represents a treatment problem for which currently available analgesics are, at best, marginally effective. ...THC...may be useful in this inadequately treated type of pain'. The findings of Growing et al (1998) concurred with this conclusion, and suggested that this might be the area of greatest medical potential. Maurer et al (1990) found that a paraplegic patient, who suffered leg pain, gained pain-relief after taking a single dose of THC. Staquet et al (1978) did a trial using a nitrogen analogue of THC. This too showed significant analgesic effects, and was effective as both codeine and secobarbital. A further study using the synthetic THC analogue Levonantradol was done by Jain et al (1981). The trial population was patients who had moderate to severe post-operative pain. They were administered Levonantrodol by injection, and found significant pain relief as a result. In Canada, Milstein et al (1975) studied the analgesic effect of smoked cannabis in normal subjects. Half of them had used cannabis before. The researchers caused pain by pressing onto the subjects thumbnails. The subjects were able to withstand more pressure after they had smoked cannabis. Strangely, the analgesic effect was greater in the experienced users. A article by Noyes and Baram (1974) showed that cannabis relieved the pain of a headache in three patients with an equivalent or better efficacy than aspirin or ergotamine tartrate. Petro (1980) found that two patients suffering pain from a muscle spasticity disorder had a reduction in their discomfort after inhaling cannabis. Recently, it has been found that the body's natural cannabinoid, anandamide is involved in the control of pain. Calignano et al (1998) found that rats release anandamide when cells are damaged. This then causes seemingly pain-relieving effects in the areas of the brain and spinal cord that process pain stimuli. An ACM bulletin in 1998 demonstrated that when anandamide is used with another naturally occuring compound in the body, palmitylethanolamide, pain was reduced by up to 100 times. References Calignano A. et al (1998) Control of pain by endogenous cannabinoids, Nature 394: 277-281. Growing L et al (1998) Therapeutic use of cannabis: clarifying the debate, Drug and Alcohol Review 17: 445-452. Holdcroft A et al (1997) Pain relief with oral cannabinoids in familial Mediterranean fever. Anaesthesia, 52: 483 House of Lords Select Committee on Science and Technology (1998) Science and Technology - Ninth report. Science and Technology Committee Publications, UK. Institute of Medicine (1999) Marijuana and medicine: Assessing the science base. National Academy Press Jain AK, Ryan JR, McMahon FG, Smith G. (1981) Evaluation of intramuscular levonantradol and placebo in acute postoperative pain. Journal of Clinical Pharmacology 21 :320S-326S. Maurer M. et al. (1990) Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double-blind trial. European Archives of Psychiatry and Clinical Neuroscience 240: 1-4. Milstein S.L., MacCannell K., Karr, G. and Clark S. (1975) Marijuana-produced changes in pain tolerance: Experienced and non-experienced subjects. International Pharmacopsychiatry 10: 177-182. National Institutes of Health (1997) Workshop on the Medical Utility of Marijuana: Report to the Director. Washington, D.C. Noyes R., Baram D. (1974) Cannabis analgesia. Compr. Psychiatry 15 : 531. Noyes R., Brunk S.F., Baram D.A. and Canter A. (1975a) Analgesic effect of delta-9-tetrahydrocannabinol. Journal of Clinical Pharmacology 15: 139-143. Noyes R., Brunk S.F., Avery D.H. and Canter A. (1975b) The analgesic properties of delta-9-tetrahydrocannabinol and codeine. Clinical Pharmacology and Therapeutics 18: 84-89. Petro D. (1980) Marihuana as a therapeutic agent for muscle spasm and spasticity. Psychosomatics 21: 81-85. Reynolds J.R. (1890) Therapeutic uses and toxic effects of Cannabis indica. Lancet 1: 637 Science: Cannabinoid/anandamide-receptor systems involved in peripheral control of pain, ACM Bulletin, July 26, 1998. Staquet M, Gantt C, Machin D. (1978) Effect of a nitrogen analog of tetrahydrocannabinol on cancer pain. Clinical Pharmacology and Therapeutics 23:397401. For a large collection of research materials, see our research page. Use of Marijuana in Neurological and Movement Disorders Medical Marijuana Use of Marijuana in Neurological and Movement Disorders 1. What research has been done and what is known about the possible medical uses of marijuana? There have been numerous studies both in animals and in various clinical states on the use of cannabinoids on neurological and various movement disorders. These results range from anecdotal reports to surveys and clinical trials. Marijuana or tetrahydrocannabinol (THC) is reported to have some antispasticity, analgesic, antitremor, and antiataxia actions, as well as some activity in multiple sclerosis (MS) and in spinal cord injury patients. The spasticity and nocturnal spasms produced by MS and partial spinal cord injury have been reported to be relieved by smoked marijuana and to some extent by oral THC in numerous anecdotal reports. The effect seems to appear rapidly with smoked marijuana; patients are able to titrate the dose by the amount they smoke. No large-scale controlled studies or studies to compare either smoked or oral THC with other available therapies have been reported. Several relatively good therapeutic alternatives exist. There is no published evidence that the cannabinoid drugs are superior or even equivalent. Substantial experimental animal literature exists showing that various cannabinoids, given primarily by parenteral routes, have a substantial anticonvulsant effect in the control of various models of epilepsy, especially generalized and partial tonic-clonic seizures. Scant information is available about the human experience with the use of marijuana or cannabinoids for the treatment of epilepsy. This is an area of potential value, especially for cannabis therapies by other than the smoked route. Several single case histories have been reported indicating some benefit of smoked marijuana for dystonic states. It must be remembered that dystonia is a clinical syndrome with numerous potential causes, and the information available now does not differentiate which causes are most likely to be improved. Smoked marijuana and oral THC have been tested in the treatment of Parkinson's disease and Huntington's chorea without success. The cannabinoids also have been used as experimental immunologic modifiers to treat such conditions as the animal models of experimental allergic encephalomyelitis (EAE) and neuritis. Parenteral cannabinoids have been successful in modifying EAE in animals, suggesting that cannabinoids may be of value in a more fundamental way by altering the root cause of a disease such as MS rather than simply treating its symptoms. Smoked marijuana would not be acceptable for such a role because of the variability of dose with the smoked route. 2. What are the major unanswered scientific questions? The discovery of dedicated systems of central nervous system (CNS) neurons approximately 8 years ago, which express receptors specific for the cannabinoids, is of major scientific interest and importance. The distribution of these cannabinoid receptor-bearing neurons corresponds well with the clinical effects of smoked marijuana; for instance, their presence in the forebrain may relate to adverse changes in short-term memory, but perhaps positively in the control of epilepsy. Cannabinoid receptors in the brainstem and cerebellum may relate to the recognized incoordination that accompanies smoked marijuana use. The discovery of intrinsic ligands for these receptors in the mammalian brain is also of great importance. This system of cannabinoid receptors and ligands may be analogous to the discovery of opiate receptors and endorphins, which linked various opium derivatives (heroin and morphine) to an intrinsic system of neurons in the CNS. That discovery was of major importance for pain research. The major unanswered scientific questions are: * How useful is smoked marijuana of known specific potency in controlling various neurologic conditions? * In comparative studies, how useful is smoked marijuana in altering objective abnormalities such as spasticity versus current standard therapies that have already been approved for human use? * Can alternative delivery systems (other than the oral route) be developed to provide rapidity of action with more safety than smoked marijuana? * Can available or newly developed synthetic cannabinoids be used more effectively to stimulate or block receptor activity in the cannabinoid system of the CNS? * What are the immune-modulating characteristics of the cannabinoids and can they be used for therapeutic human benefit? * Can the long-term risks of daily smoked marijuana be quantified so that useful risk versus benefit ratios can be determined, especially when considering treatment of long-term conditions such as spasticity or epilepsy? 3. What are the diseases or conditions for which marijuana might have potential as a treatment and which merit further study? Marijuana or the use of other cannabinoids as human therapies might be considered for treating spasticity and nocturnal spasms complicating MS and spinal cord injury, for various active epilepsy states, for some forms of dystonia, and perhaps most interestingly, for treating neuropathic pain (Zeltser et al. 1991). (Also see the chapter titled Analgesia.) Neuropathic pain complicates many CNS diseases. Few available therapies provide even partial relief. Reference Zeltser, R.; Seltzer, Z.; Eisen, A.; Feigenbaum, J.J.; and Mechoulam, R. Suppression of neuropathic pain behavior in rats by a non-psychotropic synthetic cannabinoid with NMDA receptor-blocking properties. Pain 47(1):95-103, October 1991. source: http://www.onlinepot...l/article44.htm
  23. Endocannabinoids potently protect the newborn brain against AMPA-kainate receptor-mediated excitotoxic damage. Abstract Brain lesions induced in newborn mice or rats by the glutamatergic agonists ibotenate (acting on NMDA and metabotropic receptors) or S-bromowillardiine (acting on AMPA-kainate receptors) mimic some aspects of white matter cysts and transcortical necrosis observed in human perinatal brain damage associated with cerebral palsy. Exogenous and endogenous cannabinoids have received increasing attention as potential neuroprotective agents in a number of neurodegenerative disorders of the adult. One recent study showed neuroprotection by the cannabinoid agonist WIN-55212 in a newborn rat model of acute severe asphyxia. The present study was designed to assess the neuroprotective effects of the endogenous cannabinoid anandamide using a well-defined rodent model of neonatal excitotoxic brain lesions. In this model, anandamide provided dose-dependent and long-lasting protection of developing white matter and cortical plate reducing the size of lesions induced by S-bromowillardiine. Anandamide had only marginal neuroprotective effect against ibotenate-induced cortical grey matter lesions. Anandamide-induced neuroprotection against AMPA-kainate receptor-mediated brain lesions were blocked by a CB1 antagonist but not by a CB2 antagonist. Furthermore, anandamide effects were mimicked by a CB1 agonist but not by a CB2 agonist. Real-time PCR confirmed the expression of CB1 receptors, but not CB2 receptors, in the untreated newborn neocortex. Finally, neuroprotective effects of anandamide in white matter involved increased survival of preoligodendrocytes and better preservation of myelination. The present study provides experimental support for the role of endocannabinoids as a candidate therapy for excitotoxic perinatal brain lesions. http://www.youtube.com/watch?v=Jd5aoqtNo8Y CEREBRAL PALSY / CANNABIS Statement Before City Council Re: Medical Marijuana Morgan, MD, John P. "Statement Before City Council Re: Medical Marijuana." Feb. 23, 2004. A comparison of cannabis sativa to papaver somniferum, the opium poppy, is apt. Humans found products of both plants useful and pleasurable under certain circumstances, and began to cultivate them. Products of both were used to relieve symptoms (and for other effects), although the use of both also produced fear and attempts to control their production and use. Thirty to forty years ago the appeal of the poppy to humans was elucidated elegantly. The principal constituent of opium, morphine, was found to produce its effects in animals by interacting with a pre-existing structural and functional component of the brain. Morphine binds to a receptor tissue and that binding, changes the function of cells. Further, the receptors were not waiting for morphine, but were ordinarily activated by compounds produced by the brain which provoked effects which we must assume were useful and part of normal brain function. Understanding of this system has lead to pharmacological exploitation of it. We now produce many versions of morphine which bind to the receptor, may be given by various routes and produce variations in effect. We even produce drugs which block the receptor and are useful under certain circumstances. The “marijuana” (perhaps cannabis is a better term) story is similar and in many ways identical. The effects of cannabis are largely due to the presence of a chemical (delta-9-tetrahydrocannabinol, THC) which binds to pre-existing receptors in human calls and that binding alters cellular function. The receptors are part of a structural and functional system. We produce chemicals which bind to the cannabinoid receptors and it is clear that the system is useful and part of normal brain function. There is now active research producing compounds related to THC and products to deliver THC in various ways. There are even cannabinoid receptor blockers which are chiefly used in research to promote understanding of this built-in cannabinoid system in our brains. Activation of the cannabinoid system by delivering THC to receptor sites provokes a variety of effects. Many of those effects, not all, reduce cellular response to stimuli. There is adequate evidence that THC is therapeutic in diminishing pain perception, diminishing nausea and vomiting in response to many stimuli, and reducing muscle tone and spasm secondary to multiple sclerosis, cerebral palsy and spinal cord injury. Interestingly, THC is one of the very few compounds that humans consistently respond to with increased appetite. The development of fuller understanding and exploitation of the effects of cannabis has been delayed by societal and legislative reactions to the widespread use of cannabis by young people in the Western democracies, beginning in the 1960's, for the purpose of having fun. This negative reaction and aversion to cannabis is also fueled by the fact that it is commonly ingested by smoking it using cigarettes and pipes. Many who wish to use cannabis for apparent medical reasons wish to smoke it, and that act remains usually illegal in the United States. In truth, the current federal administration remains committed to continuing and expanding that criminalization of all cannabis use in the USA at incredible costs to taxpayers, patients and truth. Cannabis smoking is always compared to tobacco smoking in terms of health consequences, and some who might support medical cannabis fear tobacco-like consequences. The current federal administration through its ministry of propaganda (The Office of Drug Control Policy), is actively directing a campaign to frighten Americans into believing that smoking of cannabis might even be worse for human health than the smoking of tobacco. This is not even close to true. Despite dire predictions there is no evidence that the smoking of cannabis alone causes lung cancer. It is with real concern that I tell you that the bronchial cells of cannabis smokers show pre-cancerous changes. This has been known for 20 years. Yet there are no reported cases of cancer in marijuana-only smokers. Further, strong evidence indicates that marijuana smoking even in unusually large doses does not produce the most crippling lung disorder, emphysema. The absence of these toxicities reflects the much lower dose of smoke and its irritants inhaled by users of cannabis. Not only do they smoke fewer cigarettes, but they rarely continue their smoking careers for years in the fixed pattern of tobacco use. I agree with those who think the future of cannabinoid medication may not involve smoking; even though There is meaningful and positive research in using vaporizing devices to reduce the irritant load in cannabis smoke. However currently, there are really no alternatives to smoking cigarette and pipe-delivered plant material, for patients who find benefit in cannabis. I believe strongly that the harm in permitting this kind of use approaches zero. Sincerely, John P. Morgan, M.D. source: http://www.lindesmit...yc_comments.cfm Jaqueline Patterson, Cerebal Palsay video included Cerebral palsy is a group of disorders that affect a person's ability to move and to maintain balance and posture. The disorders appear in the first few years of life. Usually they do not get worse over time. People with cerebral palsy may have difficulty walking. They may also have trouble with tasks such as writing or using scissors. Some have other medical conditions, including seizure disorders or mental impairment. Cerebral palsy happens when the areas of the brain that control movement and posture do not develop correctly or get damaged.There is no cure for cerebral palsy, but treatment can improve the lives of those who have it. Treatment includes medicines, braces, and physical, occupational and speech therapy. - National Institute of Neurological Disorders and Stroke source: http://www.medicalca...documentary.htm Treatment of human spasticity with delta 9-tetrahydrocannabinol. Abstract Spasticity is a common neurologic condition in patients with multiple sclerosis, stroke, cerebral palsy or an injured spinal cord. Animal studies suggest that THC has an inhibitory effect on polysynaptic reflexes. Some spastic patients claim improvement after inhaling cannabis. We tested muscle tone, reflexes, strength and performed EMGs before and after double-blinded oral administration of either 10 or 5 mg THC or placebo. The blinded examiner correctly identified the trials in which the patients received THC in seven of nine cases. For the group, 10 mg THC significantly reduced spasticity by clinical measurement (P less than 0.01). Quadriceps EMG interference pattern was reduced in those four patients with primarily extensor spasticity. THC was administered to eight other patients with spasticity and other CNS lesions. Responses varied, but benefit was seen in three of three patients with "tonic spasms." No benefit was noted in patients with cerebellar disease. Blind Cerebral Palsy Victim Sues City Over Medical Marijuana
  24. Causes, incidence, and risk factors Worldwide, cervical cancer is the third most common type of cancer in women. It is much less common in the United States because of the routine use of Pap smears. Cervical cancers start in the cells on the surface of the cervix. There are two types of cells on the cervix's surface: squamous and columnar. Most cervical cancers are from squamous cells. Cervical cancer usually develops very slowly. It starts as a precancerous condition called dysplasia. This precancerous condition can be detected by a Pap smear and is 100% treatable. It can take years for precancerous changes to turn into cervical cancer. Most women who are diagnosed with cervical cancer today have not had regular Pap smears or they have not followed up on abnormal Pap smear results. Almost all cervical cancers are caused by HPV (human papilloma virus). HPV is a common virus that is spread through sexual intercourse. There are many different types of HPV. Some strains lead to cervical cancer. (Other strains may cause genital warts, while others do not cause any problems at all.) A woman's sexual habits and patterns can increase her risk for cervical cancer. Risky sexual practices include having sex at an early age, having multiple sexual partners, and having multiple partners or partners who participate in high-risk sexual activities. Risk factors for cervical cancer include: Not getting the HPV vaccine Poor economic status Women whose mothers took the drug DES (diethylstilbestrol) during pregnancy in the early 1960s to prevent miscarriage Weakened immune system Symptoms Most of the time, early cervical cancer has no symptoms. Symptoms that may occur can include: Abnormal vaginal bleeding between periods, after intercourse, or after menopause Continuous vaginal discharge, which may be pale, watery, pink, brown, bloody, or foul-smelling Periods become heavier and last longer than usual Cervical cancer may spread to the bladder, intestines, lungs, and liver. Patients with cervical cancer do not usually have problems until the cancer is advanced and has spread. Symptoms of advanced cervical cancer may include: Back pain Bone pain or fractures Fatigue Leaking of urine or feces from the vagina Leg pain Loss of appetite Pelvic pain Single swollen leg Weight loss Signs and tests Precancerous changes of the cervix and cervical cancer cannot be seen with the naked eye. Special tests and tools are needed to spot such conditions. Pap smears screen for precancers and cancer, but do not make a final diagnosis. If abnormal changes are found, the cervix is usually examined under magnification. This is called colposcopy. Pieces of tissue are surgically removed (biopsied) during this procedure and sent to a laboratory for examination. Cone biopsy may also be done. If the woman is diagnosed with cervical cancer, the health care provider will order more tests to determine how far the cancer has spread. This is called staging. Tests may include: Chest x-ray CT scan of the pelvis Cystoscopy Intravenous pyelogram (IVP) MRI of the pelvis Treatment Treatment of cervical cancer depends on: The stage of the cancer The size and shape of the tumor The woman's age and general health Her desire to have children in the future Early cervical cancer can be cured by removing or destroying the precancerous or cancerous tissue. There are various surgical ways to do this without removing the uterus or damaging the cervix, so that a woman can still have children in the future. Types of surgery for early cervical cancer include: Loop electrosurgical excision procedure (LEEP) -- uses electricity to remove abnormal tissue Cryotherapy -- freezes abnormal cells Laser therapy -- uses light to burn abnormal tissue A hysterectomy (removal of the uterus but not the ovaries) is not often performed for cervical cancer that has not spread. It may be done in women who have repeated LEEP procedures. Treatment for more advanced cervical cancer may include: Radical hysterectomy, which removes the uterus and much of the surrounding tissues, including lymph nodes and the upper part of the vagina. Pelvic exenteration, an extreme type of surgery in which all of the organs of the pelvis, including the bladder and rectum, are removed. Radiation may be used to treat cancer that has spread beyond the pelvis, or cancer that has returned. Radiation therapy is either external or internal. Internal radiation therapy uses a device filled with radioactive material, which is placed inside the woman's vagina next to the cervical cancer. The device is removed when she goes home. External radiation therapy beams radiation from a large machine onto the body where the cancer is located. It is similar to an x-ray. Chemotherapy uses drugs to kill cancer. Some of the drugs used for cervical cancer chemotherapy include 5-FU, cisplatin, carboplatin, ifosfamide, paclitaxel, and cyclophosphamide. Sometimes radiation and chemotherapy are used before or after surgery. Support Groups National Cervical Cancer Coalition - http://www.nccc-online.org/ Expectations (prognosis) How well the patient does depends on many things, including: The type of cancer The stage of the disease The woman's age and general physical condition If the cancer comes back after treatment Pre-cancerous conditions are completely curable when followed up and treated properly. The chance of being alive in 5 years (5-year survival rate) for cancer that has spread to the inside of the cervix walls but not outside the cervix area is 92%. The 5-year survival rate falls steadily as the cancer spreads into other areas. Complications Some types of cervical cancer do not respond well to treatment. The cancer may come back (recur) after treatment. Women who have treatment to save the uterus have a high risk of the cancer coming back (recurrence). Surgery and radiation can cause problems with sexual, bowel, and bladder function. Calling your health care provider Call your health care provider if you: Have not had regular Pap smears Have abnormal vaginal bleeding or discharge Prevention A vaccine to prevent cervical cancer is now available. In June 2006, the U.S. Food and Drug Administration approved the vaccine called Gardasil, which prevents infection against the two types of HPV responsible for most cervical cancer cases. Studies have shown that the vaccine appears to prevent early-stage cervical cancer and precancerous lesions. Gardasil is the first approved vaccine targeted specifically to prevent any type of cancer. Practicing safe sex (using condoms) also reduces your risk of HPV and other sexually transmitted diseases. HPV infection causes genital warts. These may be barely visible or several inches wide. If a woman sees warts on her partner's genitals, she should avoid intercourse with that person. To further reduce the risk of cervical cancer, women should limit their number of sexual partners and avoid partners who participate in high-risk sexual activities. Getting regular Pap smears can help detect precancerous changes, which can be treated before they turn into cervical cancer. Pap smears effectively spot such changes, but they must be done regularly. Annual pelvic examinations, including a pap smear, should start when a woman becomes sexually active, or by the age of 20 in a nonsexually active woman. See also: Physical exam frequency If you smoke, quit. Cigarette smoking is associated with an increased risk of cervical cancer. References Noller KL. Intraepithelial neoplasia of the lower genital tract (cervix, vulva): Etiology, screening, diagnostic techniques, management. In: Katz VL, Lentz GM, Lobo RA, Gershenson DM, eds. Comprehensive Gynecology. 5th ed. Philadelphia, Pa: Mosby Elsevier; 2007:chap 28. National Comprehensive Cancer Network. NCCN Practice Guidelines in Oncology: Cervical Cancer Screening. v.1.2011. Smith RA, Cokkinides V, Brooks D, Saslow D, Brawley OW. Cancer screening in the United States, 2010: a review of current American Cancer Society guidelines and issues in cancer screening. CA Cancer J Clin. 2010;60:99-119. Review Date: 12/15/2011. Reviewed by: Yi-Bin Chen, MD, Leukemia/Bone Marrow Transplant Program, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc. Cannabis Slows cervical Cancer in Test Tube Marijuana Ingredients Slow Invasion by Cervical and Lung Cancer Cells By Daniel J. DeNoon WebMD Health NewsReviewed by Louise Chang, MDDec. 26, 2007 -- THC and another marijuana-derived compound slow the spread of cervical and lung cancers, test-tube studies suggest. The new findings add to the fast-growing number of animal and cell-culture studies showing different anticancer effects for cannabinoids, chemical compounds derived from marijuana. Cannabinoids, and sometimes marijuana itself, are currently used to lessen the nausea and pain experienced by many cancer patients. The new findings -- yet to be proven in human studies -- suggest that cannabinoids may have a direct anticancer effect. "Cannabinoids' ... potential therapeutic benefit in the treatment of highly invasive cancers should be addressed in clinical trials," conclude Robert Ramer, PhD, and Burkhard Hinz, PhD, of the University of Rostock, Germany. Might cannabinoids keep dangerous tumors from spreading throughout the body? Ramer and Hinz set up an experiment in which invasive cervical and lung cancer cells had make their way through a tissue-like gel. Even at very low concentrations, the marijuana compounds THC and methanandamide (MA) significantly slowed the invading cancer cells. Doses of THC that reduce pain in cancer patients yield blood concentrations much higher than the concentrations needed to inhibit cancer invasion. "Thus the effects of THC on cell invasion occurred at therapeutically relevant concentrations," Ramer and Hinz note. The researchers are quick to point out that much more study is needed to find out whether these test-tube results apply to tumor growth in animals and in humans. Ramer and Hinz report the findings in the Jan. 2, 2008 issue of the Journal of the National Cancer Institute. source: http://www.webmd.com...er-in-test-tube Cervical Cancer - Radical Trachelectomy http://www.youtube.com/watch?v=NVsczkyLdOA Medicinal Cannabis Fighting cervical cancer and fibromyalgia, Juliet uses a vaporiser to treat her pain with cannabis. http://natgeotv.com/.../?cmp=user_post Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells via aberrantly expressed vanilloid receptor-1 Emmanuel Contassot a, Mirna Tenan a, Valérie Schnüriger a, Marie-Françoise Pelte b and Pierre-Yves Dietrich a, , a Oncology Division, Laboratory of Tumor Immunology, University Hospital, Geneva, Switzerland b Clinical Pathology Department, University Hospital, Geneva, Switzerland Received 9 September 2003. Available online 8 February 2004. References and further reading may be available for this article. To view references and further reading you must purchase this article. Abstract Objective. Δ9-Tetrahydrocannabinol, the active agent of Cannabis sativa, exhibits well-documented antitumor properties, but little is known about the possible effects mediated by endogenous cannabinoids on human tumors. In the present study, we analyzed the effect of arachidonyl ethanolamide (AEA) on cervical carcinoma (CxCa) cell lines. Methods. To assess the sensitivity of CxCa cells to AEA, we selected three cell lines that were exposed to increasing doses of AEA with or without antagonists to receptors to AEA. DNA fragmentation and caspase-7 activity were used as apoptosis markers. The expression of receptors to AEA were analyzed in CxCa cell lines as well as CxCa biopsies. Results. The major finding was that AEA induced apoptosis of CxCa cell lines via aberrantly expressed vanilloid receptor-1, whereas AEA binding to the classical CB1 and CB2 cannabinoid receptors mediated a protective effect. Furthermore, unexpectedly, a strong expression of the three forms of AEA receptors was observed in ex vivo CxCa biopsies. Conclusion. Overall, these data suggest that the specific targeting of VR1 by endogenous cannabinoids or synthetic molecules offers attractive opportunities for the development of novel potent anticancer drugs. Author Keywords: Author Keywords: Arachidonyl ethanolamide; Cervical cancer; Vanilloid receptor; Apoptosis source: and more info http://www.sciencedi...3a344307d083fe1 Please contact us at info@freemygreenpdx.com to add more to this thread
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