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  1. I suffer migraines severally. I have stopped taking the preventative for the migraines, after so long it was making me worse. Today I take Imitrex nasal spray, pill form and injection form. Today I had a shot for the first time in a bit, I don’t like the shots but sometimes one or the other work . Migraines so bad today that I did do the shot. It makes me off for the entire day. I have been told physical mobility would help I am restricted for that as well. So they say you suffer from migraines you Just suffer from severe ones,’keep doing what I am doing. Hoping I can make some type of difference with food etc, I don’t know. Please I am all open to suggestions. Thank you-~B
  2. 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


    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!
  4. Cannabidiol is a popular natural remedy used for many common ailments. Better known as CBD, it is one of the 104 chemical compounds known as cannabinoids found in the cannabis or marijuana plant, Cannabis sativa (1). Tetrahydrocannabinol (THC) is the main psychoactive cannabinoid found in cannabis, and causes the sensation of getting “high” that’s often associated with marijuana. However, unlike THC, CBD is not psychoactive. This quality makes CBD an appealing option for those who are looking for relief from pain and other symptoms without the mind-altering effects of marijuana or certain pharmaceutical drugs. CBD oil is made by extracting CBD from the cannabis plant, then diluting it with a carrier oil like coconut or hemp seed oil. It’s gaining momentum in the health and wellness world, with some scientific studies confirming it may help treat a variety of ailments like chronic pain and anxiety. This article reviews seven science-based health benefits of CBD oil and also explains the potential risks involved with using it. 1. May Relieve Pain Marijuana has been used to treat pain as far back as 2900 B.C. (2). More recently, scientists have discovered that certain components of marijuana, including CBD, are responsible for its pain-relieving effects. The human body contains a specialized system called the endocannabinoid system (ECS), which is involved in regulating a variety of functions including sleep, appetite, pain and immune system response (3). The body produces endocannabinoids, which are neurotransmitters that bind to cannabinoid receptors in your nervous system. Studies have shown that CBD may help reduce chronic pain by impacting endocannabinoid receptor activity, reducing inflammation and interacting with neurotransmitters (4). For example, one study in rats found that CBD injections reduced pain response to surgical incision, while another rat study found that oral CBD treatment significantly reduced sciatic nerve pain and inflammation (5, 6). Several human studies have found that a combination of CBD and THC is effective in treating pain related to multiple sclerosis and arthritis. An oral spray called Sativex, which is a combination of THC and CBD, is approved in several countries to treat pain related to multiple sclerosis. In a study of 47 people with multiple sclerosis, those treated with Sativex for one month experienced a significant improvement in pain, walking and muscle spasms, compared to the placebo group (7). Another study found that Sativex significantly improved pain during movement, pain at rest and sleep quality in 58 people with rheumatoid arthritis (8). SUMMARYCBD, especially in combination with THC, may be effective in reducing pain associated with diseases like multiple sclerosis and rheumatoid arthritis 2. Could Reduce Anxiety and Depression Anxiety and depression are common mental health disorders that can have devastating impacts on health and well-being. According to the World Health Organization, depression is the single largest contributor to disability worldwide, while anxiety disorders are ranked sixth (9). Anxiety and depression are usually treated with pharmaceutical drugs, which can cause a number of side effects including drowsiness, agitation, insomnia, sexual dysfunction and headache (10). What’s more, medications like benzodiazepines can be addictive and may lead to substance abuse (11). CBD oil has shown promise as a treatment for both depression and anxiety, leading many who live with these disorders to become interested in this natural approach. In one study, 24 people with social anxiety disorder received either 600 mg of CBD or a placebo before a public speaking test. The group that received the CBD had significantly less anxiety, cognitive impairment and discomfort in their speech performance, compared to the placebo group (12). CBD oil has even been used to safely treat insomnia and anxiety in children with post-traumatic stress disorder (13). CBD has also shown antidepressant-like effects in several animal studies (14, 15). These qualities are linked to CBD’s ability to act on the brain’s receptors for serotonin, a neurotransmitter that regulates mood and social behavior. SUMMARYUsing CBD has been shown to reduce anxiety and depression in both human and animal studies. 3. May Alleviate Cancer-Related Symptoms CBD may help reduce symptoms related to cancer and side effects related to cancer treatment, like nausea, vomiting and pain. One study looked at the effects of CBD and THC in 177 people with cancer-related pain who did not experience relief from pain medication. Those treated with an extract containing both compounds experienced a significant reduction in pain compared to those who received only THC extract (16). CBD may also help reduce chemotherapy-induced nausea and vomiting, which are among the most common chemotherapy-related side effects for those with cancer (17). Though there are drugs that help with these distressing symptoms, they are sometimes ineffective, leading some people to seek alternatives. A study of 16 people undergoing chemotherapy found that a one-to-one combination of CBD and THC administered via mouth spray reduced chemotherapy-related nausea and vomiting better than standard treatment alone (18). Some test-tube and animal studies have even shown that CBD may have anticancer properties. For example, one test-tube study found that concentrated CBD induced cell death in human breast cancer cells (19). Another study showed that CBD inhibited the spread of aggressive breast cancer cells in mice (20). However, these are test-tube and animal studies, so they can only suggest what might work in people. More studies in humans are needed before conclusions can be made. SUMMARYThough CBD has been shown to help reduce symptoms related to cancer and cancer treatment, and may even have cancer-fighting properties, more research is needed to assess its efficacy and safety. Originally published at hemp4everyone.org
  5. People globally enjoy partaking in the pungent flowers of the Cannabis plant, seeking the euphoric psycho-activity unique to this plant, whether for pain relief, pleasure or pastime. Many people though are unaware of the amazing benefits of Raw, organic Cannabis Juice. In raw form, Cannabis leaves and the tri-chrome covered flowers are concentrated with non-psychoactive, anti-biotic, anti-fungal, anti-viral, antioxidant, anti-inflammatory, immune-regulating and anti-cancer nutrient compounds including lesser-known Tetrahydrocannabicannabidiol (CBD), and Tetrahydrocannabivarin (THCV) both of which are proving to be therapeutic substances capable of preventing and/or reversing a plethora of chronic and debilitating illnesses. When you begin juicing “raw” cannabis, you will consume cannabinoids in their acid forms. The raw form of CBD is CBDA or cannabidiolic acid. The raw form of THC is THCA or tetrahydrocannabinolic acid. These are the A arrangements of the molecules, the non-psychoactive forms. The acids of this plant are not psychoactive unless they are decarboxylated, or heated. When decarboxylation takes place the acids are converted to Δ9-THC and CBD. Recently CBD is making waves in research, being regarding as a highly medicinal substance with unique immune-regulating capabilities. The human body already contains an endogenous cannabinoid system, complete with different types of cannabinoid receptors, introducing cannabinoids to your systems can help normalize the body's functions, including cellular communication, regeneration and repair, as well as regulating immune function. JUICING WORKS! Because it provides the cannabinoid acids, which are potent anti-inflammatory compounds that help activate and regulate the endocannabinoid system. When you juicing is done properly, you should not have to worry about psycho-activity. Though preparing the juice improperly may lead to heating the solution and causing THC to form, this can be said of pasteurization, even flash pasteurization. I utilize the power of raw Cannabis in juiced form myself. This juice possesses a powerful grassy taste, definitely lacking in the flavor department. It is best mixed into a smoothie for those with sensitive palates, chased with apple juice or lemonade or just straight for veterans and die-hards. No matter the taste, it is worth the power-house of nutrients found within. Canna Juicers will notice a strong increase in energy levels, feeling invigorated almost immediately. I am unsure as to why this amount of energy is produced, I am pretty sure it has something to do with the metabolism of the acid components of the juice, leaving it exceptionally beneficial to those with chronic-fatigue issues. This juice has appetite suppressant qualities, as you do not feel the urge to eat as often, and there are no “munchies” associated with raw Cannabis juice. One downfall is, in its raw form Cannabis Juice does not have a long-shelf life. The neon-green juice begins to turn the mucky-brown of oxidation about as quickly as an apple once bitten into. I would not recommend keeping juice longer than 12 hours as the nutritional value begins to degrade. You are able to store the juice in the freezer for a period of 6-12 months, though fresh is best! My friend and Juicing Guru, Dr. William Courtney, of Mendocino County California recommends that patients juice 15-20 leaves per day. Cannabis leaves have the highest CBD levels, and therefore are the best for juicing. Prime juicing material is found when the plants are between 70-85 days old. He believes that individuals with compromised immune systems from autoimmune disorders, cellular dysfunction, chronic inflammation, cancer and various other illnesses can derive a wide range of health-promoting benefits by consuming organic raw Cannabis Juice. I believe that Cannabis, and the compounds found within are vital nutrients missing from our modern, prohibitionist, western diet. Give raw, organic Cannabis juicing a try, feel the benefits for yourself, and then share the news with your friends and loved ones. Don’t be afraid to cure yourself! Cannadad
  6. Migraines Is marijuana an effective treatment for migraines? MedlinePlus, the National Library of Medicine's online Medical Encyclopedia (accessed June 26, 2006), wrote: "A Migraine is a type of primary headache that some people get repeatedly over time. Migraines are different from other headaches because they occur with symptoms such as nausea, vomiting, or sensitivity to light. In most people, a throbbing pain is felt only on one side of the head." Pro Philip Denney, MD, Co-founder of a medical cannabis evaluation practice, in the June 2, 2005 Whittier Daily News is quoted by Shirley Hsu in the article "Migraine Sufferer Finds Relief from Marijuana": "Cannabis is one of the best medicines for migraines. It's so effective - it works rapidly, and it has limited toxicity, although lung damage from smoking is a concern." Con and more
  7. 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!
  8. 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
  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. Cachexia is often seen in end-stage cancer, and in that context is called "cancer cachexia." In patients with congestive heart failure, there is also a cachectic syndrome. Also, a cachexia co-morbidity is seen in patients that have any of the range of illnesses classified as "COPD" (chronic obstructive pulmonary disease), particularly emphysema. Some severe cases of schizophrenia can present this condition where it is named vesanic cachexia (from vesania, a Latin term for insanity).[citation needed] It also can be observed in such parasitic diseases as african trypanosomiasis (Sleeping sickness).[citation needed] In each of these settings there is full-body wasting, which hits the skeletal muscle especially hard, resulting in muscle atrophy and great muscle loss. However, when presenting comorbidly with malabsorbtion syndrome, (as seen, for example, in Crohn's Disease or Celiac Disease) simply consuming more food is not sufficient to reverse wasting and the malabsorbtion must be treated before the patient will be able to stabilize body mass.[5] Cachexia not only worsens survival for people with cancer, but it interferes with quality of life. People with cachexia are less able to tolerate treatments, such as chemotherapy, and often have more side effects. For those who have surgery, postoperative complications are more common. Cachexia also worsens cancer fatigue, one of the most annoying symptoms of cancer. Mechanism The exact mechanism in which these diseases cause cachexia is poorly understood, but there is probably a role for inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), which is also nicknamed cachexin (also spelled cachectin) for this reason, Interferon gamma (IFNγ), and Interleukin 6 (IL-6), as well as the tumor-secreted proteolysis inducing factor (PIF). Related malnutrition syndromes are kwashiorkor and marasmus, although these do not always have an underlying causative illness; they are most often symptomatic of severe malnutrition. Those suffering from the eating disorder anorexia nervosa appear to have high plasma levels of ghrelin. Ghrelin levels are also high in patients who have cancer-induced cachexia.[6] Treatment Currently, there are no widely accepted drugs to treat cachexia and there are no FDA-approved drugs to treat cancer cachexia. Cachexia may be treated by steroids such as corticosteroids or drugs that mimic progesterone, which increase appetite, may reverse weight loss, but have no evidence of reversing muscle loss.[7] Medical marijuana has been allowed for the treatment of cachexia in some US states such as Nevada, Michigan, Washington, Oregon, California, Colorado, New Mexico, and Arizona.[7][8] Evaluation There are several ways that cachexia can be evaluated. Some of these measures include: Body mass index (BMI) -- Body mass index describes not only relative body weight, but can give more information about a healthy weight. BMI is calculated using a formula of height and weight. Lean muscle mass -- Measuring body composition can help determine the ratio of lean muscle mass to body fat. Tests used to do this may include skin folds and bioimpedance. Food intake diaries -- Keeping a food diary is an important activity when looking to prevent or cope with cachexia. At the same time, it's important to keep in mind that the malnutrition of cachexia can occur even with an adequate intake of calories. Blood tests -- Some lab tests that are useful in evaluating cachexia include white blood cell counts (WBC), serum albumin, transferin levels, uric acid, and inflammatory markers, such as C-reactive protein (CRP). Omega-3 fatty acids A 2007 systematic review of n-3 fatty acids and cachexia found seventeen studies, eight of which were high-quality. It concluded that there was evidence that oral n-3 fatty acid supplements benefit cancer patients, improving appetite, weight and quality of life.[9] A 2009 trial found that a supplement of eicosapentaenoic acid helped cancer patients retain muscle mass.[10] source Medical Marijuana and Cachexia Watch this video http://www.youtube.com/watch?v=har8I0Lqsd4 What Is Cachexia? Cachexia is any general reduction in vitality and strength of body and mind resulting from a debilitating chronic disease. Medical Marijuana and Cachexia Cachexia is a wasting syndrome that causes weakness and a loss of weight, fat, and muscle, which affects patients with advanced cancer, AIDS, and some other major chronic progressive diseases. Cachexia and anorexia, or a lack of appetite, often occur together. Currently, there is no widely accepted drug to treat cachexia. Patients are often treated with steroids and/or nutritional supplements that provide easy-to-absorb nutrients. A 2009 trial found that a supplement of eicosapentaenoic acid helped cancer patients retain muscle mass. Scientists are also studying how human growth hormone treatments can help wasting syndrome patients. However, it is extremely expensive and could cost over $40,000 per year to use. In order to manage cachexia, patients must reduce nausea and vomiting in order to increase food intake. And according to scientific and anecdotal evidence, using medical marijuana is a safe, effective way to do so. The National Cancer Institute is in the process of evaluating the effects of THC for treatment-related and cancer-related anorexia and cachexia. Many marijuana states include cachexia on their list of qualifying conditions. Additionally, marijuana side effects are typically mild and are classified as "low risk," with euphoric mood changes among the most frequent side effects. If you or someone you know is looking to find relief from cachexia, MarijuanaDoctors.com can help. We can connect you with hundreds of quality marijuana doctors across the country in all legal marijuana states. Book an appointment today and let us help improve your quality of life! Source Cannabinoids and Cachexia [Cannabinoids in the treatment of the cachexia-anorexia syndrome in palliative care patients]. Nauck F, Klaschik E. Loss of appetite and cachexia are frequent symptoms in palliative care patients. However, therapeutic regimens often prove ineffective, and the quality of life of many patients is significantly impaired by these symptoms. Causes and pathophysiology of anorexia and cachexia are complex and must be identified and treated. Symptomatic pharmacological therapy aims at metabolic, neuroendocrinological and catabolic changes. Prokinetic drugs, corticosteroids and gestagenes are used for symptomatic therapy. Recently, the use of cannabinoids for treatment of loss of appetite and cachexia has become the focus of interest. In cancer patients, cannabinoids proved more effective than placebo but less than gestagenes. Compared to placebo, higher efficacy of cannabinoids could be demonstrated in patients with AIDS as well as in patients with Morbus Alzheimer. However, side effects, such as dizziness, tiredness and daze led to discontinuation of the cannabinoid therapy in some patients. Cancer cachexia and cannabinoids. Gorter RW. Anorexia and cachexia are diagnosed in more than two-thirds of all cancer patients with advanced disease, and are independent risk factors for morbidity and mortality. Anorexia, nausea and vomiting often are described as more significant inhibiting factors for quality of life of cancer patients than even intense pain. In 1986, delta-9-tetrahydrocannabinol (THC), the main effective constituent of cannabis, was licensed as an anti-emetic drug in cancer patients receiving chemotherapy. In addition, in clinical studies THC has shown significant stimulation of appetite and increase of body weight in HIV-positive and cancer patients. The appetite-stimulating effect of cannabis itself has also been well documented in many anecdotal cases. There are strong indications that cannabis is better tolerated than THC alone, because cannabis contains several additional cannabinoids, like cannabidiol (CBD), which antagonize the psychotropic actions of THC, but do not inhibit the appetite-stimulating effect. Therefore, we intend to compare the therapeutic effects of whole-plant extracts of cannabis to those of THC (dronabinol) alone in controlled studies. Abstract and key points • Cannabinoids are components isolated from Cannabis sativa and Cannabis indica plants (hemp). • The antiemetic efficacy of cannabis in chemotherapy-induced nausea/vomiting has been established in a systematic review. • The use of cannabinoids for anorexia-cachexia-syndrome in advanced cancer is not supported by the evidence from randomised controlled trials. • Several randomised controlled trials indicate a mild analgesic effect of cannabinoids in cancer patients. • Dose-limitating central nervous and cardiovascular adverse effects have frequently been observed in clinical studies. Cannabinoids are components isolated from Cannabis sativa and Cannabis indica plants (hemp). This summary deals with cannabinoid products for medical use. Medical cannabinoids are claimed to alleviate nausea and vomiting in chemo-/radiotherapy and in palliative care. They are also recommended for the treatment of anorexia and cachexia in patients with advanced cancer and for the control of chronic tumor pain. The pharmacokinetics of cannabinoids have been intensively investigated and cannabinoid effects in humans have been linked to their agonist activity at two cannabinoid receptors. The antiemetic efficacy of cannabinoids in chemotherapy-induced nausea/vomiting has been established in a systematic review. If cannabinoids can offer improvements over modern antiemetic medication, especially serotonin antagonists, in preventing acute or delayed chemotherapy induced nausea and vomiting is still unclear. Only anecdotal evidence is available to support the use of medical cannabinoids against radiotherapy-related nausea and nausea in palliative care patients. The use of cannabinoids for anorexia-cachexia-syndrome in advanced cancer is not supported by the evidence from randomised controlled trials. Several randomised controlled trials also indicate a mild analgesic effect of cannabinoids in cancer patients. Insufficient evidence is available to support the introduction of cannabinoids into widespread clinical use as analgesics. The main limitation of cannabinoids is seen in the high frequency of serious adverse effects on the central nervous system and the cardiovascular system. Known absolute and relative contraindications and pharmacological interactions should be carefully considered. Medical cannabinoids are subject to country-specific prohibitory legislation. Considering the availability of well-investigated and established medications for chemotherapy-induced nausea and chronic pain, a first-line use of medical cannabinoids is not recommended. Medical cannabinoids might be beneficial in individual cases as adjuncts to other antiemetic or analgesic medication when standard treatment fails in symptom control. Potential hazards and toxicities should be considered. Case notes "It affected everything I did," says Addario, who is alive and well nine years later in San Carlos, Calif. "I literally could not get up and down the stairs." There is a name for what Addario experienced: cachexia. It is the muscle wasting and weight loss that are so often cancer's sidekick. Doctors and patients have long assumed cachexia is an integral part of cancer, and it's rarely discussed. "Ninety percent of oncologists completely ignore the cachexia because there's no known therapy," says Alfred Goldberg, a professor of cell biology who studies protein and muscle breakdown at Harvard Medical School in Boston. But that could soon change as two potential cachexia treatments are now in Phase 3 clinical trials. If studies continue to go well, the drugs could become available for lung cancer patients within the next two to three years. The main goal of both medications is to give people more muscle strength as they fight cancer. But they may do even more, scientists hope. "It's not clear that if you treat cachexia you will prolong life," says Dr. Egidio Del Fabbro, a palliative care physician at the University of Texas M.D. Anderson Cancer Center in Houston, but "we suspect it will." Del Fabbro is not involved with either of the companies developing the drugs,GTx Inc. of Memphis, Tenn., and Helsinn Therapeutics Inc. of Bridgewater, N.J. Cachexia (pronounced kuh-KEK-see-uh) is commonly defined as the unintentional loss of 5% or more of a person's weight within a six-month period. Crucially, it's muscle that slides off one's frame, often with fat as well. It's associated with advanced cancers as well as HIV, heart failure and kidney disease. In layman's terms, it means "the patient looks awful, they look weak, they've lost much of their body mass," Goldberg says. Cachexia is especially prevalent in pancreatic and lung cancers. People with the condition also tend to lose their appetites, but eating more does not help because the body's metabolism is operating at a higher-than-normal rate, says Vickie Baracos, a metabolism researcher at the University of Alberta in Edmonton. "The controls are not operating properly," she says. "It's sort of like having your thermostat turned up and the window left open at the same time." Given current rates of obesity, muscle wasting is sometimes hidden behind a layer of fat. "You can have somebody who technically looks obese, but they have the muscle mass of a concentration camp victim," says Dr. Mitchell Steiner, a urologic oncologist who co-founded GTx and now serves as the company's chief executive. MORE Introduction Cannabis sativa has been cultivated for more than 5000 y both to obtain fibers for manufacturing of textiles and to provide a variety of extracts for medicinal and recreational use. To the present, marijuana and other psychoactive derivatives of Cannabis sativa represent the most widely illegal drug consumed in the Western world. However, despite the social problems related to the abuse of these substances, scientific and social communities have recently started to be aware of the therapeutic potentials of cannabinoids and of new synthetic compounds interfering with the endogenous cannabinoid system. Since 300 AD, it was observed that Cannabis can stimulate hunger and increase appetite, particularly for sweet and palatable food. However, only a few years ago this phenomenon was seriously taken into consideration in research. After the discovery of cannabinoid receptors and their endogenous ligands (endocannabinoids), the existence of an endogenous cannabinoid system has been proposed, providing a physiological basis for the biological effects induced by marijuana and its derivatives. The importance of this system is also underlined by the finding of a high degree of evolutionary conservation across species, emphasizing the fundamental physiological role played by cannabinoids in brain function. The endogenous cannabinoid system Cannabinoid research was largely neglected at the beginning of the 20th century, partly because of the political antimarijuana attitude, which officially started in the United States with the Harrison Act in 1914, leading to full prohibition 20 years later. During the 1960s, the sudden increase of the recreational use of Cannabis stimulated the public concern about its negative effects on the health of the consumers. On the other hand, this renewed interest initiated a series of scientific investigations into the numerous chemical constituents of Cannabis and their mechanisms of action, finally leading to the identification of the structure of 9-tetrahydrocannabinol ( 9-THC), the main psychoactive ingredient of marijuana. However, the definitive breakthrough concerning the importance of this system was given by the discovery of cannabinoid receptors and their endogenous ligands. Cannabinoid receptors In 1990, the first cannabinoid receptor (CB1) was cloned, followed 3 y later by the characterization of a second cannabinoid receptor (CB2). Cannabinoid receptors belong to the G protein-coupled receptor superfamily and, to the present, include CB1, CB2 and a splice variant of the CB1 (for a review see Howlett et al). There is important pharmacological and physiological evidence suggesting the existence of other cannabinoid receptor subtypes that have not yet been cloned. Typically, the activation of cannabinoid receptors modulates adenylate-cyclase, potassium and calcium channels and signal-regulated kinases. Moreover, cannabinoid receptors are able to crosstalk with other neurotransmitter receptor systems, for example, recruiting by this way other intracellular signal transduction pathways. Given its wide distribution in the central nervous system (CNS) CB1 was considered as the 'brain-type' cannabinoid receptor, whereas CB2, mainly expressed in immune cells, was considered as its 'peripheral' counterpart. However, this classification does not hold true anymore as many studies show expression of CB1 also in peripheral tissues. On the other hand, CB2 was also localized in brain-derived immune cells. In the CNS, CB1 is predominantly expressed presynaptically, modulating the release of neurotransmitters, including -aminobutyric acid (GABA), dopamine, noradrenaline, glutamate and serotonin. 9-THC-mediated behavioral effects include ataxia, analgesia, hypothermia, euphoria, short-term memory deficits and other cognitive impairments. They are mediated by CB1 as suggested by the expression of this receptor in brain areas implicated in these functions and by the lack of these effects in CB1-deficient mice. Endogenous cannabinoids The presence of specific receptors mediating the actions of marijuana and its derivatives strongly stimulated the search for endogenous ligands for cannabinoid receptors. The first endogenous cannabinoid, arachidonoyl ethanolamide, was identified from the porcine brain in 1992 and was named anandamide, from the Sanskrit word 'ananda' that means internal bliss. Anandamide is able to reproduce most of the typical behavioral effects of 9-THC in rodents and shares the same G protein-mediated actions on adenylate cyclase and Ca2+ channels with 9-THC (for a review see Di Marzo et al). This substance binds both to CB1 and CB2, with a higher affinity to CB1 and is present at highest concentration in hippocampus, cortex, thalamus and cerebellum of different species including humans. Since the discovery of this ligand, other polyunsaturated fatty acid derivatives, acting as functional agonists of cannabinoid receptors, have been characterized and collectively termed endocannabinoids. As an example, Noladin ether is the most recent ether-type endocannabinoid identified only 1 y ago. Among these compounds, 2-arachidonoylglycerol (2-AG), identified in canine gut in a search for endogenous ligands selective for CB2, displays a lower affinity for CB1; nevertheless, it represents the most abundant endocannabinoid in the brain. In contrast to classical neurotransmitters, endocannabinoids do not appear to be stored in the interior of synaptic vesicles, because of the high lipophilicity of these ligands. In fact, phospholipid molecules within the cellular membrane were shown to serve as precursors and storage depots for anandamide synthesis. Anandamide is produced from such membrane phospholipids (eg N-arachidonoyl phosphatidyl ethanolamine), after cleavage of the phosphodiester bond by an as-yet-unidentified phospholipase D that is activated by Ca2+ ions. Endocannabinoids, like 'classical' neurotransmitters, are released from neurons following membrane depolarization and Ca2+ influx into the cells, are inactivated by a reuptake mechanism, involving facilitated transport by an as-yet-unisolated anandamide membrane transporter, and hydrolyzed by the enzyme fatty acid amide hydrolase in neurons and astrocytes. Cannabis Treatment: Anorexia and Cachexia An appetite enhancing effect of THC is observed with daily divided doses totalling 5 mg. When required, the daily dose may be increased to 20 mg. In a long-term study of 94 AIDS patients, the appetite-stimulating effect of THC continued for months, confirming the appetite enhancement noted in a shorter 6 week study. THC doubled appetite on a visual analogue scale in comparison to placebo. Patients tended to retain a stable body weight over the course of seven months. A positive influence on body weight was also reported in 15 patients with Alzheimer’s disease who were previously refusing food. source Covers body composition and muscle loss in both normal lifespan progression and disease conditions, offering research results and clinical innovation. The first scientific journal dedicated to research on cachexia and sarcopenia Presents research on both typical ageing progression and disease-related changes Covers both research and clinical topics Changes in body composition, especially in skeletal muscle, are key elements in the ageing process and in the pathophysiology of chronic illness. The Journal of Cachexia, Sarcopenia and Muscle presents research on these debilitating conditions, and on body composition and physiological and pathophysiological changes during the lifespan, and in response to disease. more Coverage includes research on the functional importance of fat tissue and mechanisms leading to lipolysis, and studies on mechanisms of muscle wasting, as well as better screening and evaluation options and enhanced biomarkers through validated complementary investigations. The Journal is a reliable resource on clinical care, including patients suffering from AIDS, cancer, chronic heart failure, chronic lung disease, liver cirrhosis, chronic kidney failure, rheumatoid arthritis and sepsis. The Journal of Cachexia, Sarcopenia and Muscle benefits physicians, biochemists, biologists, dieticians, pharmacologists, and students. Related subjects » Family & Geriatric Medicine - Internal Medicine - Molecular Medicine - Oncology & Hematology - Pharmaceutical Science Understanding Cachexia Symptoms, Signs, Causes, and Treatments By Lynne Eldridge MD, About.com Guide Updated April 03, 2012 About.com Health's Disease and Condition content is reviewed by the Medical Review Board My link Cachexia is a syndrome that is characterized by symptoms of unintentional weight loss, progressive muscle wasting, and a loss of appetite. Present in at least 50% of people with advanced cancer, it's estimated that it contributes directly to 20% of cancer deaths. Even though the symptoms and signs of cachexia are usually noticed late in the course of cancer, we're learning that the process leading to muscle wasting begins very early on after a diagnosis of cancer. In such, cachexia is often present before any weight loss occurs. Cachexia is sometimes referred to as a paraneoplastic syndrome, which simply means symptoms that are caused by substances made by a cancer or by the body's reaction to cancer. It might seem like cachexia should be easily treated at first glance, but effective treatments are lacking. This is because cachexia is more than just a lack of calories in the body. Cancer Cachexia Cachexia is seen frequently with cancer, but is also seen with diseases such as AIDS/HIV, heart failure, emphysema, and kidney failure. With regard to cancer, it is seen most frequently with lung cancer, pancreatic cancer, and stomach cancer. Cachexia not only worsens survival for people with cancer, but it interferes with quality of life. People with cachexia are less able to tolerate treatments, such as chemotherapy, and often have more side effects. For those who have surgery, postoperative complications are more common. Cachexia also worsens cancer fatigue, one of the most annoying symptoms of cancer. read more here Signs and Symptoms The major symptoms of cachexia include: Involuntary (unintentional) weight loss -- Weight loss with cachexia is involuntary, meaning that it occurs without trying. Yet it goes further than unintentional weight loss. Weight loss may occur even though you are getting an adequate amount of calories in your diet, and if calorie intake outweighs output of energy. Skeletal muscle wasting -- Muscle wasting is a hallmark of cachexia and occurs along with loss of fat. It can also be fairly insidious. In people who are overweight at the time of their diagnosis, significant loss of muscle mass can occur without an obvious outward appearance of weight loss. Anorexia/loss of appetite -- Loss of appetite is another symptom of cachexia, and again, this symptom is somewhat different than ordinary "loss of appetite" symptoms. With cachexia, it is not simply a decreased desire for food, but more of a loss of a desire to eat. Lowered quality of life -- Muscle wasting can diminish your ability to walk and participate in activities that would ordinarily be enjoyable. What Causes Cachexia? Cachexia may be caused by "tumor factors" -- substances manufactured and secreted by a tumor, or by the "host response." Host response simply means the body's response to a tumor. The response of the immune system to cancer and other causes of cachexia is being studied to try and understand the underlying factors behind cachexia. Cachexia is dominated by catabolic metabolism. If you think of normal metabolism being the building of tissue and muscle (anabolic metabolism), the opposite is true with cachexia, which is the breakdown of normal bodily processes. Evaluation There are several ways that cachexia can be evaluated. Some of these measures include: Body mass index (BMI) -- Body mass index describes not only relative body weight, but can give more information about a healthy weight. BMI is calculated using a formula of height and weight. Lean muscle mass -- Measuring body composition can help determine the ratio of lean muscle mass to body fat. Tests used to do this may include skin folds and bioimpedance. Food intake diaries -- Keeping a food diary is an important activity when looking to prevent or cope with cachexia. At the same time, it's important to keep in mind that the malnutrition of cachexia can occur even with an adequate intake of calories. Blood tests -- Some lab tests that are useful in evaluating cachexia include white blood cell counts (WBC), serum albumin, transferin levels, uric acid, and inflammatory markers, such as C-reactive protein (CRP). Tackling the Conundrum of Cachexia in Cancer Source http://www.cancer.go...in/110111/page5 By some estimates, nearly one-third of cancer deaths can be attributed to a wasting syndrome called cachexia that can be devastating for patients and their families. Characterized by a dramatic loss of skeletal muscle mass and often accompanied by substantial weight loss, cachexia (pronounced kuh-KEK-see-uh) is a form of metabolic mutiny in which the body overzealously breaks down skeletal muscle and adipose tissue, which stores fat. Patients suffering from cachexia are often so frail and weak that walking can be a Herculean task. Cachexia occurs in many cancers, usually at the advanced stages of disease. It is most commonly seen in a subset of cancers, led by pancreatic and gastric cancer, but also lung, esophageal, colorectal, and head and neck cancer. Despite cachexia's impact on mortality and data strongly suggesting that it hinders treatment responses and patients' ability to tolerate treatment, researchers who study muscle wasting say it has not received the attention it deserves. No effective therapies have been developed to prevent or hamper its progression. Even for patients who are able to eat—appetite suppression or anorexia is a common cachexia symptom—improved nutrition often offers no respite. There really is an enormous therapeutic opportunity here. —Dr. GoldbergAnd yet, over the last few years, researchers have begun to better understand the underlying biology of cancer-related cachexia. Findings from several studies point to potentially powerful therapeutic approaches, and a number of clinical trials of investigational drugs and drugs approved for other uses have been conducted or are under way. "It's exciting to see several avenues of investigation coming to the forefront and trials moving forward," said Dr. Aminah Jatoi, a medical oncologist at the Mayo Clinic Comprehensive Cancer Center. "It's important that oncologists be aware of these trials and offer participation to their patients," said Dr. Jatoi, a member of an international group of clinicians and researchers who earlier this year published a consensus statement to more precisely define cancer-related cachexia. The publication also provided a preliminary classification system for the condition—akin in some respects to the staging system used for tumors. (See the sidebar.) Cachexia isn't limited to cancer. It is commonly seen in people with AIDS and chronic forms of kidney disease and heart failure, among other conditions, as well as in those who have suffered severe trauma and burns, said Dr. Alfred Goldberg of the Harvard University School of Medicine, whose research on muscle wasting and protein degradation eventually led to the development of the cancer drug bortezomib (Velcade). With so many potential clinical applications, Dr. Goldberg said, "There really is an enormous therapeutic opportunity here." Why and How Cachexia Happens The consensus statement is a good beginning, according to another co-author, Dr. Mellar Davis of the Cleveland Clinic Taussig Cancer Center. But researchers still need to dig deeper into how cachexia develops in patients with cancer, Dr. Davis continued, and how its course is influenced by everything from nutrition and physical activity to disease-specific factors, such as reduced testosterone levels caused by cancer therapy or opioids to treat pain. Multiple factors are clearly at play in cachexia development and progression, Dr. Goldberg explained. He believes that at its core cachexia is "more of a host response that's evolved to fight fasting, injury, or disease," he said. During this response, the body is trying to obtain additional energy stores from muscle, in the form of amino acids, to convert into glucose to keep the brain functioning. The problem, he continued, "is that we can't turn off this response to the cancer, even when we can provide the patient with essential nutrients." Many studies suggest that inflammation "is a unifying theme of cachexia across many diseases, including cancer," said Dr. Teresa Zimmers of the Jefferson Kimmel Cancer Center in Philadelphia. The inflammation is caused in part by the body's immune response to the tumor, which results in the production of pro-inflammatory cytokines, explained Dr. Konstantin Salnikow, of NCI's Division of Cancer Biology (DCB). Although these cytokines can help to kill tumor cells, some also appear to tilt the body's metabolism toward catabolism, the breakdown of muscle proteins and fat. Elevated levels of several cytokines in particular have been closely associated with cachexia and mortality in cancer patients. In NCI-supported mouse model studies, for example, Dr. Zimmers has shown that elevated levels of the cytokine IL-6 can induce cachexia. She and others have begun to unravel some of the potential mechanisms by which IL-6 may do this. Goverments Search Despite the incomplete understanding of the underlying biology of cancer-related cachexia, a few potential therapies are moving into early human trials. More than one drug will likely be needed to successfully combat cachexia, particularly if it's at an advanced stage, said Dr. Barbara Spalholz, also of DCB. "We may have to hit different combinations of targets, depending on the type of cancer and other factors," she said. 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  11. 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
  12. Did you know that cilantro (aka. coriander, Coriandrum sativum) has been found by scientific research to eliminate highly toxic mercury from the body? A groundbreaking research project conducted at the Heart Disease Research Foundation, New York, USA in the mid to late 1990s discovered this remarkable effect of cilantro. [1][2] Since then, several fascinating follow-up studies have appeared. A 2001 study found that coriander had a preventative effect on lead poisoning in mice. [3] Here is another study of interest, as a completely different industry corroborates the findings: A study by the Department of Atomic Energy in India found cilantro able to remove mercury ions from aqueous solution “with good efficiency”. [4] Also, more recent studies have found that the detox effect was amplified by the inclusion of chlorella [5] – which, interestingly, has also been found able to bind to cadmium – another toxic metal. [6] There is far too much here to ignore: This subject is worthy of more studies, please! In the recent decades, there has an increasing awareness about the serious negative impacts of heavy metals to human body. Extensive scientific studies have been conducted to determine the extent of these damages and how to minimize their undesirable and damaging effects. These heavy / toxic metals include arsenic, beryllium, lead, cadmium, barium, chromium, mercury and selenium. [7] These metals are normally present in the natural environment at low levels. However when they are found in larger amounts they may impose additional risks to the body. Humans normally acquire these metals through ingestion, drinking, eating, and breathing or inhalation. Of course, many people have acquired mercury through mercury amalgam dental fillings. Sufficient mercury is picked up through fish consumption for there to have been warnings about over-consumption of certain types of fish. People living / working in industrial areas where these metals are utilized, or those who reside in areas where these metals are disposed improperly, also have a risk for exposure. source When exposed to larger quantities of these metals, humans tend to experience various symptoms which include vomiting, nausea, increase in blood pressure, breathing difficulties, muscle weakness, diarrhea, and abdominal cramps. Some victims also tend to have runny nose, asthma, cough, nose ulcers, wheezing, allergic reactions, and shortness of breath. Heavy metal poisoning is serious stuff: In the worst cases, victims may suffer from changes in heart rhythm, liver and kidney damage, high blood pressure, paralysis, bronchitis, damage to blood vessels, dementia and even death. In pregnant women, overexposure to these harmful elements may even trigger miscarriage. Here’s the good news: We’ve found an amazing all-natural, super-delicious cilantro pesto recipe that may be able to aid you in dealing with heavy metals. Aside from being inexpensive it is easy to make. for best results, please use organic ingredients! Also known as coriander, cilantro is considered to have numerous amazing healing and medicinal properties. In addition to its crisp taste, cilantro is packed with nutritious constituents that are thought to offer unique protection to the body against a wide range of diseases. What have you got to lose with this wonderful cilantro pesto? Here, then, is the link to the full recipe, with much additional valuable information: http://ybertaud9.wordpress.com/2012/04/07/cilantro-pesto-removes-heavy-metals-health-benefits/ References / further studies: [1] http://www.ncbi.nlm.nih.gov/pubmed/8686573 [2] http://www.ncbi.nlm.nih.gov/pubmed/8914687 [3] Aga, et al. (2001) Preventive effect of Coriandrum sativium on localized lead deposition in ICR mice. Journal of Ethnopharmacology, vol. 77, no. 2-3, pp. 203–208, 2001. [4] http://www.ncbi.nlm.nih.gov/pubmed/15721537 [5] http://www.planetaryherbals.com/publications/controlled/102273 [6] Carr, et al, (1998) Characterization of the Cadmium-binding Capacity of Chlorella vulgaris. Bulletin of Environmental Contamination and Toxicology. 60: 433-440. [7] http://www.osha.gov/SLTC/metalsheavy/
  13. 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
  14. 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!
  15. Killing bacteria with cannabis Pharmacists and chemists have found another use for the multipurpose cannabis as a source of antibacterial chemicals for multidrug resistant bacteria. Ironically, inhaling cannabis is known to damage the lung's ability to fend off invading pathogens, but the ingredients in cannabis, particularly the cannabinoids, have antiseptic properties. Although scattered research has been conducted since the 1950s, no comprehensive study existed that relates the structure of cannabinoids with antibacterial activity. Giovanni Appendino, Simon Gibbons, and coworkers attempted to remedy that problem by examining the activity of five common cannabinoids and their synthetic derivatives. Five of the most common cannabinoids. All five cannabinoids (THC, CBD, CBG, CBC, and CBN) were potent against bacteria. Notably, they performed well against bacteria that were known to be multidrug resistant, like the strains of MRSA that plagued U.K. hospitals. CBD and CBG have the most potential for consumer use because they are nonpsychotropic. Besides identifying antibacterial capability, the researchers wanted to figure out why these cannabinoids are so good at killing bacteria. They obviously are very effective at specifically targeting some vital process in the bacteria. Unfortunately, even after extensive work at modifying the cannabinoids and comparing their activities, that targeting mechanism remains a mystery. The scientists were able to figure out that the position of the n-pentyl chain (orange) relative to the terpenoid moiety (blue) serves to control lipid affinity. These cannabinoids are promising enough to warrant rigorous clinical trials. They are applicable as topical antiseptics, biodegradable antibacterial compounds for cosmetics, and systematic antibacterial agents. J. Nat. Prod., 2008. DOI: 10.1021/np8002673 Marijuana (Cannabis sativa) has long been known to contain antibacterial cannabinoids, whose potential to address antibiotic resistance has not yet been investigated. All five major cannabinoids (cannabidiol (1b), cannabichromene (2), cannabigerol (3b), Δ9-tetrahydrocannabinol (4b), and cannabinol (5)) showed potent activity against a variety of methicillin-resistant Staphylococcus aureus (MRSA) strains of current clinical relevance. Activity was remarkably tolerant to the nature of the prenyl moiety, to its relative position compared to the n-pentyl moiety (abnormal cannabinoids), and to carboxylation of the resorcinyl moiety (pre-cannabinoids). Conversely, methylation and acetylation of the phenolic hydroxyls, esterification of the carboxylic group of pre-cannabinoids, and introduction of a second prenyl moiety were all detrimental for antibacterial activity. Taken together, these observations suggest that the prenyl moiety of cannabinoids serves mainly as a modulator of lipid affinity for the olivetol core, a per se poorly active antibacterial pharmacophore, while their high potency definitely suggests a specific, but yet elusive, mechanism of activity. Several studies have associated the abuse of marijuana (Cannabis sativa L. Cannabinaceae) with an increase in opportunistic infections,(1) and inhalation of marijuana has indeed been shown to interfere with the production of nitric oxide from pulmonary macrophages, impairing the respiratory defense mechanisms against pathogens and causing immunosuppression.(2) The association of C. sativa with a decreased protection against bacterial infections is paradoxical, since this plant has long been known to contain powerful antibacterial agents.(3) Thus, preparations from C. sativa were investigated extensively in the 1950s as highly active topical antiseptic agents for the oral cavity and the skin and as antitubercular agents.(3) Unfortunately, most of these investigations were done at a time when the phytochemistry of Cannabis was still in its infancy, and the remarkable antibacterial profile of the plant could not be related to any single, structurally defined and specific constituent. Evidence that pre-cannabidiol (1a) is a powerful plant antibiotic was, nevertheless, obtained,(4) and more recent investigations have demonstrated, to various degrees, antibacterial activity for the nonpsychotropic cannabinoids cannabichromene (CBC, 2),(5) cannabigerol (CBG, 3b),(6) and cannabidiol (1b),(7) as well as for the psychotropic agent Δ9-tetrahydrocannabinol (THC, 4b).(7) These observations, and the inactivity of several noncannabinoid constituents of C. sativa as antibacterial agents, suggest that cannabinoids and their precursors are the most likely antibacterial agents present in C. sativa preparations.(8) However, differences in bacterial strains and end-points make it difficult to compare the data reported in these scattered studies, and the overall value of C. sativa as an antibacterial agent is therefore not easy to assess. There are currently considerable challenges with the treatment of infections caused by strains of clinically relevant bacteria that show multidrug-resistance (MDR), such as methicillin-resistant Staphylococcus aureus (MRSA) and the recently emerged and extremely drug-resistant Mycobacterium tuberculosis XDR-TB. New antibacterials are therefore urgently needed, but only one new class of antibacterial has been introduced in the last 30 years.(9) Despite the excellent antibacterial activity of many plant secondary metabolites(10) and the ability of some of them to modify the resistance associated with MDR strains(11) and efflux pumps,(12) plants are still a substantially untapped source of antimicrobial agents. These considerations, as well as the observation that cross-resistance to microbial and plant antibacterial agents is rare,(10) make C. sativa a potential source of compounds to address antibiotic resistance, one of the most urgent issues in antimicrobial therapy. To obtain structure−activity data and define a possible microbiocidal cannabinoid pharmacophore, we investigated the antibacterial profile of the five major cannabinoids, of their alkylation and acylation products, and of a selection of their carboxylic precursors (pre-cannabinoids) and synthetic positional isomers (abnormal cannabinoids). Results and Discussion The antibacterial cannabinoid chemotype is poorly defined, as is the molecular mechanism of its activity. Since many simple phenols show antimicrobial properties, it does not seem unreasonable to assume that the resorcinol moiety of cannabinoids serves as the antibacterial pharmacophore, with the alkyl, terpenoid, and carboxylic appendices modulating its activity. To gain insight into the microbiocidal cannabinoid pharmacophore, we have investigated how the nature of the terpenoid moiety, its relative position compared to the n-pentyl group, and the effect of carboxylation of the resorcinyl moiety are translated biologically, assaying the major cannabinoids and a selection of their precursors and regioisomeric analogues against drug-resistant bacteria of clinical relevance. Within these, we have selected a panel of clinically relevant Staphylococcus aureus strains that includes the (in)famous EMRSA-15, one of the main epidemic methicillin-resistant strains,(13) and SA-1199B, a multidrug-resistant strain that overexpresses the NorA efflux mechanism, the best characterized antibiotic efflux pump in this species.(14) SA-1199B also possesses a gyrase mutation that, in addition to NorA, confers a high level of resistance to certain fluoroquinolones. A macrolide-resistant strain (RN4220),(15) a tetracycline-resistant line overexpressing the TetK efflux pump (XU212),(16) and a standard laboratory strain (ATCC25923) completed the bacterial panel. Δ9-Tetrahydrocannabinol (THC, 4b), cannabidiol (CBD, 1b), cannabigerol (CBG, 3b), cannabichromene (CBC, 2), and cannabinol (CBN, 5) are the five most common cannabinoids.(17) They could be obtained in high purity (>98%) by isolation from strains of C. sativa producing a single major cannabinoid (THC, CBD, CBG), by total synthesis (CBC),(6) or by semisynthesis (CBN).(18) Their antimicrobial properties are listed in Table 1. All compounds showed potent antibacterial activity, with MIC values in the 0.5−2 μg/mL range. Activity was exceptional against some of these strains, in particular the multidrug-resistant (MDR) SA-1199B, which has a high level of resistance to certain fluoroquinolones. Also noteworthy is the potent activity demonstrated against EMRSA-15 and EMRSA-16, the major epidemic methicillin-resistant S. aureus strains occurring in U.K. hospitals.(13, 19) These activities compare highly favorably with the standard antibiotics for these strains. The potent activity against strains possessing the NorA and TetK efflux transporters suggests that cannabinoids are not substrates for the most common resistance mechanisms to current antibacterial agents, making them attractive antibacterial leads. Table 1. MIC (μg/mL) Values of Cannabinoids and Their Analogues toward Various Drug-Resistant Strains of Staphylococcus aureusab compoundSA-1199BRN-4220XU212ATCC25923EMRSA-15EMRSA-161a2222221b1110.51122212223a4244243b1111213f64c64ccc4a8484844b211120.5511111c61111117210.512c8323216161632106464641286464norfloxacin321410.5128erythromycin0.2564>1280.25>128>128tetracycline0.250.251280.250.1250.125oxacillin0.250.251280.12532>128 a Compounds 1c−g, 3c−e, 3g, and 9 exhibited MIC values of >128 μg/mL for all organisms in which they were evaluated. b Compound 11 exhibited MIC values of >256 μg/mL for all organisms in which they were evaluated. c Not tested. Given their nonpsychotropic profiles, CBD (1b) and CBG (3b) seemed especially promising, and were selected for further structure−activity studies. Thus, acetylation and methylation of their phenolic hydroxyls (compounds 1c−e and 3c−e, respectively) were both detrimental for activity (MIC >100 μg/mL), in accordance with the essential role of the phenolic hydroxyls in the antibacterial properties. However, in light of the potent activity of the monophenols CBC (2), THC (4b), and CBN (5), it was surprising that monomethylation of the diphenols CBD (1b) and CBG (3b) was so poorly tolerated in terms of antibacterial activity. Cannabinoids are the products of thermal degradation of their corresponding carboxylic acids (pre-cannabinoids).(17) Investigation of the antibacterial profile of the carboxylated versions of CBD, CBG, and THC (compounds 1a, 3a, and 4a, respectively) showed a substantial maintenance of activity. On the other hand, methylation of the carboxylic group (compounds 1f and 3f, respectively) caused a marked decrease of potency, as did esterification with phenethyl alcohol (compounds 1g and 3g, respectively). This operation is associated with a potentiation of the antibacterial properties of phenolic acids, as exemplified by phenethyl caffeate (CAPE), the major antibacterial from propolis, compared to caffeic acid.(20) Remarkably, the synthetic abnormal cannabinoids abn-CBD (6)(21) and abn-CBG (7)(22) showed antibacterial activity comparable to, although slightly less potent than, their corresponding natural products, while olivetol (10) showed modest activity against all six strains, with MICs of 64−128 μg/mL, and resorcinol (11) did not exhibit any activity even at 256 μg/mL. Thus, the pentyl chain and the monoterpene moiety greatly enhance the activity of resorcinol. Taken together, these observations show that the cannabinoid antibacterial chemotype is remarkably tolerant to structural modification of the terpenoid moiety and its positional relationship with the n-pentyl chain, suggesting that these residues serve mainly as modulators of lipid affinity, and therefore cellular bioavailability. This view was substantiated by the marked decrease of activity observed when the antibacterial activity of CBG (3b) was compared to that of its polar analogue carmagerol (8).(23) The results against the resistant strains confirm this suggestion, and it is likely that the increased hydrophilicity caused by the addition of two hydroxyls greatly reduces the cellular bioavailability by substantially reducing membrane permeability. Conversely, the addition of a further prenyl moiety, as in the bis-prenylated cannabinoid 9,(21) while increasing membrane solubility, may result in poorer aqueous solubility and therefore a lower intracellular concentration, similarly leading to a substantial loss of activity. A single unfunctionalized terpenyl moiety seems therefore ideal in terms of lipophilicity balance for the antibacterial activity of olivetol derivatives. The great potency of cannabinoids suggests a specific interaction with a bacterial target, whose identity is, however, still elusive. This article references 30 other publications. 1. Caiffa, W. T., Vlahov, D., Graham, N. M. H., Astemborski, J., Solomon, L., Nelson, K. E., and Munoz, A. Am. J. Resp. Crit. Care Med. 1994 150 1593 1598 2. Roth, M. D., Whittaker, K., Salehi, K., Tashkin, D. P., and Baldwin, G. C. J. Neuroimmunol. 2004 147 82 86[CrossRef], [PubMed], [CAS] 3. (a) Krjci, Z. Lekarske Listy 1952 7 500 503 ; Chem. Abstr. 1952, 48, 78326 [PubMed] ( Ferenczy, L., Gracza, L., and Jakobey, I. Naturwissenschaften 1958 45 188[CrossRef], [CAS] © Krejci, Z. Pharmazie 1958 13 155 156[PubMed], [CAS] (d) Rabinovich, A. S., Aizenman, B. L., and Zelepukha, S. I. Mikrobiol. Zh 1959 21 40 48 (PubMed ID 14435632) [PubMed] (e) Turner, C. E., Elsohly, M. A., and Boeren, E. G. J. Nat. Prod. 1980 43 169 243[ACS Full Text ], [PubMed], [CAS] 4. Schultz, O. E., and Haffner, G. A. Z. Naturforsch. 1959 14b 98 100[CAS] 5. Turner, C. E., and Elsohly, M. A. J. Clin. Pharmacol. 1981 21 283S 291S[PubMed], [CAS] 6. Elsohly, H. N., Turner, C. E., Clark, A. M., and Elsohly, M. A. J. Pharm. Sci. 1982 71 1319 1323[CrossRef], [PubMed] 7. Van Klingeren, B., and Ten Ham, M. Lab. Chemother. Natl. Inst. Public Health 1976 42 9 12 ; Chem. Abstr. 1976, 85, 14622 [CAS] 8. Molnar, J., Csiszar, K., Nishioka, I., and Shoyama, Y. Acta Microb. Hung. 1986 33 221 231[PubMed], [CAS] 9. Barrett, C. T., and Barrett, J. F. Curr. Opin. Biotechnol. 2003 14 621 626[CrossRef], [PubMed], [CAS] 10. Gibbons, S. Nat. Prod. Rep. 2004 21 263 277[CrossRef], [PubMed], [CAS] 11. Stavri, M., Piddock, L. J. V., and Gibbons, S. J. Antimicrob. Chemother. 2007 59 1247 1260[CrossRef], [PubMed], [CAS] 12. Smith, E. C. J., Kaatz, G. W., Seo, S. M., Wareham, N., Williamson, E. M., and Gibbons, S. Antimicrob. Agents Chemother. 2007 51 4480 4483[CrossRef], [PubMed], [CAS] 13. Richardson, J. F., and Reith, S. J. Hosp. Infect. 1993 25 45 52[CrossRef], [PubMed], [CAS] 14. Kaatz, G. W., Seo, S. M., and Ruble, C. A. Antimicrob. Agents Chemother. 1993 37 1086 1094[PubMed], [CAS] 15. Ross, J. I., Farrell, A. M., Eady, E. A., Cove, J. H., and Cunliffe, W. J. J. Antimicrob. Chemother. 1989 24 851 862[CrossRef], [PubMed], [CAS] 16. Gibbons, S., and Udo, E. E. Phytother. Res. 2000 14 139 140[CrossRef], [PubMed], [CAS] 17. (a) Mechoulam, R., McCallum, N. K., and Burstein, S. Chem. Rev. 1976 76 75 112[ACS Full Text ], [CAS] ( Elsohly, M. 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L., Louie, L., Watt, C., Ofner-Agostini, M., Gravel, D., Mulvey, M., Loeb, M., McGeer, A., Bryce, E., and Matlow, A. Antimicrob. Agents Chemother. 2007 51 3880 3886[CrossRef], [PubMed], [CAS] 27. McGrath, K. G. Eur. J. Cancer Prev. 2003 12 479 485[CrossRef], [PubMed], [CAS] 28. Hazekamp, A., Peltenburg, A., Verpoorte, R., and Giroud, C. J. Liq. Chromatogr. Rel. Technol. 2005 28 2361 2382[CrossRef], [CAS] 29. Vailancourt, V., and Albizati, K. F. J. Org. Chem. 1992 57 3627 3631[ACS Full Text ] 30. Mechoulam, R., and Gaoni, Y. Tetrahedron 1965 21 1223 1229[CrossRef], [PubMed], [CAS] My link
  16. 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. 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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
  17. 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
  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. Marijuana compound may stop deadly cancer metastasis We've known about medical applications of cannabis (or marijuana) for years, but the research findings of two scientists studying it have the potential to change the deadliness of cancer forever. A cannabis compound known as cannabidiol can stop metastasis in many types of aggressive cancers, found the researchers from California Pacific Medical Center in San Francisco. Cannabidiol (CBD) is a non-toxic, non-psychoactive chemical found in the cannabis plant, that had already been effective in relieving convulsion, inflammation, anxiety and nausea, and in treating schizophrenia and dystonia. For the 2007 study, Sean McAllister, who was specifically studying the effects of cannabidiol, collaborated with Pierre Desprez, who for the last 10 years has been studying the ID-1 gene in cancer that causes metastasis. Metastasis is when a cancer spreads from the primary tumor area to other parts of the body, typically using the bloodstream or lymphatic system, and is one of the hallmarks of a tumor becoming malignant. "What we found was that his Cannabidiol could essentially 'turn off' the ID-1," Desprez told The Huffington Post. "We likely would not have found this on our own," he added. "That's why collaboration is so essential to scientific discovery." more
  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. http://www.sharecare.com/quizzes/vaccine-smarts#cmpid=mlqz001
  22. Mission Statement Welcome to OMMP pay it forward; (PIF) Our Goal here, is to provide you with a welcoming and helpful community . In which all members feel free to express themselves in any way they like so long as it does not infringe on other members enjoyment of the site, Also we simply ask that you treat each other with the respect we all deserve . Any issues may be brought up to a staff member. Ommp Pay It Forward is a OMMP community, and therefore abides by all OMMP laws, and we DO ask that you do the same, as per our (TOS) As staff here we work for you , to keep things clean, and running smoothly. We accept suggestions and constructive criticism. We hope that you find our forums helpful and informative, and that we can help you learn and then you in turn, can teach someone else. This is how we really pay it forward, by teaching others. Driving, talking ,being here to support others, are all ways to pay it forward. Our goal is self sufficiency, and we would like to see each patient achieve that, thank you for choosing Freemygreenpdx.com and enjoy our forums. What you will find after you join: •Seasoned cultivators will share secrets to successful harvests. •Retired Scientists/Patients who are willing to share their medication, tips on how to produce quality medication every harvest. •Mentoring by experienced growers. •Grow room tips and DIY advice by our professional installers. •Oregon carded members will gain access to our private forums. •You’ll find cannabis legislation and more. •OMMP Pay it forward is a community of compassionate people willing to offer help today. •All free! PIF is about Peace, Love and actually caring about one and another! We teach Paying it Forward, by how we help those in need. There are many sick and dying people here, are goal is to lesson the stress for the sick. We are not trying to be all about "RULES" but because of our society there will be humans that will take advantage of that and we are aware of this. Our Administrators have experienced first hand how others take advantage of situations, We have all known one and another for several years and trust each others opinions and decisions. When or if we see a situation arise we are on top of it, we have no intentions of causing any hardships or stress for our members. ©EKJ
  23. 10 Health Benefits That Legitimize Legalization source "There are no deaths from cannabis use. Anywhere. You can't find one," said Dr. Lester Grinspoon, professor emeritus at Harvard Medical School. Believe it: In 10,000 years of known use of cannabis, there's never been a single death attributed to marijuana. "I've heard you have to smoke something like 15,000 joints in 20 minutes to get a toxic amount of delta-9 tetrahydrocannibinol," said Dr. Paul Hornby, a biochemist and human pathologist who also happens to be one of the leading authorities on cannabis research. "I challenge anybody to do that." Alzheimer's disease - In 2006, the Scripps Research Institute in California discovered that delta-9-tetrahydrocannabinol (THC), the active ingredient in marijuana, can prevent an enzyme called acetylcholinesterase from accelerating the formation of "Alzheimer's plaques" in the brain, as well as protein clumps that can inhibit cognition and memory, more effectively than commercially marketed drugs. Epilepsy - A study performed by researchers at Virginia Commonwealth University discovered that ingredients found in natural marijuana "play a critical role in controlling spontaneous seizures in epilepsy." Dr. Robert J. DeLorenzo, professor of neurology at the VCU School of Medicine, added that "Although marijuana is illegal in the United States, individuals both here and abroad report that marijuana has been therapeutic for them in the treatment of a variety of ailments, including epilepsy." Multiple sclerosis- It's long been believed that smoking pot helps MS patients, and a study published as recently as May provided yet another clinical trial as evidence of marijuana's impact on multiple sclerosis patients with muscle spasticity. Even though the drug has been known to cause dizziness and fatigue in some users, most MS patients report marijuana not only helps ease the pain in their arms and legs when they painfully contract, but also helps them just "feel good." How many prescription drugs can say their side effects include "happiness"? Hepatitis C - A 2006 study performed by researchers at the University of California at San Francisco found that marijuana helps improve the effectiveness of drug therapy for hepatitis C, an infection that roughly 3 million Americans contract each year. Hepatitis C medications often have severe side effects like loss of appetite, depression, nausea, muscle aches and extreme fatigue. Patients that smoked marijuana every day or two found that not only did they complete the therapy, but that the marijuana even made it more effective in achieving a "sustained virological response," which is the gold standard in therapy, meaning there was no sign of the virus left in their bodies. Cachexia Aids (Hiv) & Aids Wasting Parkinson’S Disease Read more Marijuana: Why Is It Illegal Again? This is too big of a question to answer in just one single article, but looking at cannabis through the lens of its medical properties, there seem to be few, if any, reasons to keep marijuana off the market. It doesn't kill, and while it may not be as effective as other treatments, it doesn't seem to get in the way much. When Mikuriya was asked if there was a product out there today - anything - that has as many benefits as medical marijuana, he said simply: "No." Medical marijuana may be beneficial for everyone's health, but it's not very healthy for the pockets of the pharmaceutical companies. And unfortunately for Americans in need of a cheap, all-natural alternative medicine, the pharmaceutical industry is the biggest industry in America with powerful connections in high places. And they don't like marijuana. At all. "It's unlimited," Hornby said of marijuana. "Grow more, get more medicine. Pharmaceutical companies don't want you growing your own medicine." The idea of legalizing a cheap, all-natural medicine that grows out of the dirt is a threat to the pharmaceutical industry's bottom line.