Jump to content

Search the Community

Showing results for tags 'disease'.



More search options

  • Search By Tags

    Type tags separated by commas.
  • Search By Author

Content Type


Forums

  • Terms of service
    • Terms of service
  • Introductions Start Here!
    • Introductions
    • How To and Help Files
  • Conditions alleviated with cannabis
    • Conditions alleviated with cannabis
    • ALS / Lou Gehrig Disease
    • Alzheimer's / Cannabis / Cures
    • Diabetes
  • Resources
    • About the OMMP program
    • Community Resources
    • Cannabis Web Sites we Recommend.
    • Dispensaries We Recommend
  • Veterans Affairs
    • Veterans Issues
  • Disability
    • Disability
  • Healthy Living
    • Healthy Living
  • PIF Reviews
    • PIF Reviews
  • General
    • General
    • Important Announcements
    • PIF Contests
    • PIF (Private) Contests (Private members Only)
    • The Great Outdoors
    • Music
    • Pets
    • The latest Raves
    • Hobbies
    • Humor
    • The Writer's Block
    • Photos - Public
    • Photos - Private
    • Non Medicated Recipes
    • Cannabis Recipes
    • Succulents, trading, swapping & photos
  • Private Forums - for Private Members Only
    • Eugene, Central or Willamette Valley,
    • Med Requests
    • Private Transportation
    • Thank You!
    • Filled and Closed Requests
  • Spiritual Expression
    • Spiritual Expressions
    • Private room
    • Inspiration Repository
  • In The Garden
    • Growing Pot for Dummies 101
    • Cloning
    • Plant Hospital
    • Gardening Indoors
    • Gardening Outdoors
    • Hydroponics
    • Harvest & Curing
    • Organics
    • Pest Control
    • Private Grow Journals
    • Public Grow Journals
    • Flowers & Vegetables!
  • Cannabis Pest Control
    • Pest Control
  • Advanced Growing & Breeding
    • Advanced Growing Techniques
    • Breeding Cannabis
    • Tissue Culturing
    • Community Strain Reviews
    • Private Gardens
  • Indoor Garden Mechanics
    • Grow Room Design
    • DIY
    • The Electrical Conduit
  • Extraction & Purification - OLCC EXTRACTION PROCSEORS
  • Classifieds
    • Non-PIF Hosted Events
    • Member Owned Businesses
    • Wanted
    • For Sale or Barter
    • Free To Good Home
    • Anything Else
  • New in The News...
    • US legislation, News and More
    • Hemp
  • Cannabis News and Legislation
    • Cannabis News and Legislation
    • Activism
  • Downloads
  • Cannabis News
    • News by State
    • International News
    • US Federal News
    • Good News
    • Funny and amusing news
  • Mission Statement
  • CANNABIS SCIENCE
    • CANNABIS SCIENCE

Calendars

There are no results to display.

Blogs

  • Adiministrators's Blog
  • Cheri ♥'s Blog
  • Cheri ♥'s Blog
  • For what it's worth
  • ommppayitforward
  • Jack Mellow's Blog
  • Skunk Pharm Research LLC
  • OMMP PIF SPEAKS OUT
  • The Cannabis Think Tank
  • The Marijuana Re-legalization Front
  • Cannadad's Blog
  • Mom4Mj's Blog
  • The Cannabis Salvation Blog
  • HeavyMicroGrow's Blog
  • My first grow.... AKA "Oh my god it's working!"

Find results in...

Find results that contain...


Date Created

  • Start

    End


Last Updated

  • Start

    End


Filter by number of...

Joined

  • Start

    End


Group


AIM


MSN


Gmail


Website URL


ICQ


Yahoo


Jabber


Skype


Location


Interests

Found 41 results

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

    Diabetes

    Diabetes Diabetes is a condition wherein the body either produces inadequate amounts of insulin or fails to utilize available insulin properly. An estimated 1 million Americans suffer from Type 1 diabetes, which develops in childhood. Another 15 million suffer from Type 2 diabetes, also known as adult onset diabetes, which develops later in life. Symptoms generally include an imbalance of blood sugar levels and a high level of sugar excreted through the urine. Initial studies showed that cannabis has no effect on blood sugar levels. A recent test-tube study showed that very high doses of synthetic THC might aggravate diabetes, but that same research also indicates that continued use of cannabis creates a tolerance to the potential aggravation. [ii] No human studies have found that cannabis or synthetic cannabinoids contribute to symptoms of diabetes. At the same time, no human studies have been undertaken to prove or disprove the reports of long-term diabetics who claim that cannabis use causes an immediate lowering of abnormally high blood sugar levels. [iii] Some diabetics also claim that cannabis helps stabilize blood sugar levels and maintain mental stability, or correct mood swings caused by fluctuating blood sugar levels. [iv] Separating the apparent blood sugar response from the anti-anorexic properties of cannabis is currently a matter for further investigation. Diabetics are frequently instructed to refrain from alcohol use because of its high caloric content. Cannabis may provide a psychologically valuable alternative to alcohol in stress reduction, a major factor in managing the potentially life threatening symptoms of diabetes. Hence, cannabis may function in several ways to reduce and stabilize blood sugar levels for patients suffering from diabetes. However, regardless of mounting anecdotal evidence in medical practice, including medical testimony before a district court in California, [v] no scientific papers have been published on the effectiveness of cannabis in treating diabetes. While cannabis has been used as a replacement for insulin, diabetics are strongly advised to continue their physician’s prescribed treatment plan. Maugh, “Inhaled formed of insulin passes first test.” Los Angeles Times/Seattle Times, June 17, 1998 [ii] Hollister, “Health aspects of marijuana.” Pharmacological Review, Vol. 38, No. 1, 1986 [iii] Grinspoon, “Anecdotal surveys on diabetes.” The Forbidden Medicine Website, http://www.rxmarijuana.com [iv] Diabetic reports from Seattle and from the Sonoma Alliance for Medical Marijuana, 1998 [v] “Pot garden’s size brought case to court.” Sonoma Union Democrat (California), March 19, 1998 Drinking Chamomile Tea May Help Fight Complications Of Diabetes ScienceDaily (Sep. 16, 2008) — Drinking chamomile tea daily with meals may help prevent the complications of diabetes, which include loss of vision, nerve damage, and kidney damage, researchers in Japan and the United Kingdom are reporting. -------------------------------------------------------------------------------- The findings could lead to the development of a new chamomile-based drug for type 2 diabetes, which is at epidemic levels in this country and spreading worldwide, they note. Their study appears in the Sept. 10 issue of the ACS' Journal of Agricultural and Food Chemistry, a bi-weekly publication. In the new study, Atsushi Kato and colleagues point out that chamomile, also known as manzanilla, has been used for years as a medicinal cure-all to treat a variety of medical problems including stress, colds, and menstrual cramps. Scientists recently proposed that the herbal tea might also be beneficial for fighting diabetes, but the theory hasn't been scientifically tested until now. To find out, the researchers fed chamomile extract to a group of diabetic rats for 21 days and compared the results to a group of control animals on a normal diet. The chamomile-supplemented animals showed a significant decrease in blood glucose levels compared with the controls, they say. The extract also showed significant inhibition of both ALR2 enzymes and sorbitol, whose elevated levels are associated with increased diabetic complications, the scientists say. source: http://www.sciencedaily.com/releases/2008/...80915164519.htm Non-Psychoactive Cannabinoid Reduces Incidence Of Diabetes, Study Says Non-Psychoactive Cannabinoid Reduces Incidence Of Diabetes, Study Says - NORML Marijuana Compound May Help Stop Diabetic Retinopathy Marijuana Compound May Help Stop Diabetic Retinopathy Anticoagulant Effects of a Cannabis Extract in an Obese Rat Model Anticoagulant effects of a Cannabis extract in an obese rat model. Neuroprotective and Blood-Retinal Barrier-Preserving Effects of Cannabidiol Neuroprotective and Blood-Retinal Barrier-Preserving Effects of Cannabidiol in Experimental Diabetes -- El-Remessy et al. 168 (1): 235 -- American Journal of Pathology The Cannabinergic System as a Target for Anti-inflammatory Therapies http://www.ingentaconnect.com/conten...00013/art00008 Effect of tetrahydrocurcumin on blood glucose, plasma insulin and hepatic key enzymes Unbound MEDLINE | Effect of tetrahydrocurcumin on blood glucose, plasma insulin and hepatic key enzymes in streptozotocin induced diabetic rats. Journal article Cannabidiol reduces the development of diabetes in an animal study IACM-Bulletin Getting Eye On Cannabinoids Getting Eye On Cannabinoids: The Hempire - [cannabis, britain] Marijuana compound could prevent eye damage in diabetics Marijuana compound could prevent eye damage in diabetics: The Hempire - [cannabis, hemp] The synthetic cannabinoid HU-210 attenuates neural damage in diabetic mice Diabetes | Evolutionism | Dr. Bob Melamede Cannabidiol arrests onset of autoimmune diabetes in NOD mice CSA: Cannabis Research - Diabetes Cannabidiol attenuates high glucose-induced endothelial cell inflammatory response and barrier disruption Cannabidiol attenuates high glucose-induced endothelial cell inflammatory response and barrier disruption Biological effects of THC and a lipophilic cannabis extract on normal and insulin resistant 3T3-L1 adipocytes Unbound MEDLINE | Biological effects of THC and a lipophilic cannabis extract on normal and insulin resistant 3T3-L1 adipocytes. Journal article Beneficial effects of a Cannabis sativa extract on diabetes induced neuropathy and oxidative stress. Unbound MEDLINE | Beneficial effects of a Cannabis sativa extract treatment on diabetes-induced neuropathy and oxidative stress. Journal article Beneficial effects of a Cannabis sativa extract treatment on diabetes-induced neuropathy and oxidative stress. Unbound MEDLINE | Beneficial effects of a Cannabis sativa extract treatment on diabetes-induced neuropathy and oxidative stress. Journal article Happy reading!
  3. 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
  4. 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!
  5. 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
  6. 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. The agent that appears to be the furthest along is the selective androgen receptor modulator GTx-024 (Ostarine), developed by GTx Inc., based in Memphis, TN. In August, GTx launched two phase III clinical trials of the investigational agent, dubbed POWER1 and POWER2, for the prevention or treatment of cachexia in patients with advanced non-small cell lung cancer. More of their report here References_________________________________________________________________________________________________________________________________________________________________________________ 1. ^ http://www.merriam-w...ionary/Cachexia 2. ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. pp. 1169. ISBN 1-4160-2999-0. 3. ^ Lainscak M, Podbregar M, Anker SD (December 2007). "How does cachexia influence survival in cancer, heart failure and other chronic diseases?". Curr Opin Support Palliat Care 1 (4): 299–305. doi:10.1097/SPC.0b013e3282f31667. PMID 18685379. 4. ^ Bossola M, Pacelli F, Doglietto GB (August 2007). "Novel treatments for cancer cachexia". Expert Opin Investig Drugs 16 (8): 1241–53. doi:10.1517/13543784.16.8.1241. PMID 17685872. http://www.expertopi...3784.16.8.1241. 5. ^ Beck, Ivan T.; Bjertnaes, L (August 1964). "Treatment of Malabsorbtion Syndrome". Canadian Medical Association Journal 91 (6): 301–302. PMID 1927227. 6. ^ Garcia J.M., Garcia-Touza M., Hijazi R.A., Taffet G., Epner D., Mann D., Smith R.G., Cunningham G.R., Marcelli M. (May 2005). "Active ghrelin levels and active to total ghrelin ratio in cancer-induced cachexia". J. Clin. Endocrinol. Metab. 90 (5): 2920–6. doi:10.1210/jc.2004-1788. PMID 15713718. http://jcem.endojour...&pmid=15713718. 7. ^ a b Gagnon B, Bruera E (May 1998). "A review of the drug treatment of cachexia associated with cancer". Drugs 55 (5): 675–88. doi:10.2165/00003495-199855050-00005. PMID 9585863. 8. ^ Yavuzsen T., Davis M.P., Walsh D., LeGrand S., Lagman R. (November 2005). "Systematic review of the treatment of cancer-associated anorexia and weight loss". J. Clin. Oncol. 23 (33): 8500–11. doi:10.1200/JCO.2005.01.8010. PMID 16293879. 9. ^ Colomer R., Moreno-Nogueira J.M., García-Luna PP, et al. (May 2007). "N-3 fatty acids, cancer and cachexia: a systematic review of the literature". Br. J. Nutr. 97 (5): 823–31. doi:10.1017/S000711450765795X. PMID 17408522. 10. ^ Ryan A.M., Reynolds J.V., Healy L, et al. (2009). "Enteral nutrition enriched with eicosapentaenoic acid (EPA) preserves lean body mass following esophageal cancer surgery: results of a double-blinded randomized controlled trial". Ann. Surg. 249 (3): 355–63. doi:10.1097/SLA.0b013e31819a4789. PMID 19247018. 11. ^ J.R. Rigas et al (June 2010). [http:// http://www.asco.org/...bstractID=50646 "Affect of ALD518, a humanized anti-IL-6 antibody, on lean body mass loss and symptoms in patients with advanced non-small cell lung cancer (NSCLC): Results of a phase II randomized, double-blind safety and efficacy trial"]. J Clin Oncol 28 (1534). http:// http://www.asco.org/...stractID=50646. 12. ^ M.S. Steiner et al (June 2010). "Effect of GTx-024, a selective androgen receptor modulator (SARM), on stair climb performance and quality of life (QOL) in patients with cancer cachexia". J Clin Oncol 28 (1534). http://www.asco.org/...stractID=52947. 13. ^ G.S. Bhattacharyya et al (June 2010). "Phase II study evaluating safety and efficacy of coadministering propranolol and etodolac for treating cancer cachexia". J Clin Oncol 28 (1534). http://www.asco.org/...stractID=49474. 14. ^ Kung T et al (April 2010). "Novel treatment approaches to cachexia and sarcopenia: highlights from the 5th Cachexia Conference". Expert Opin Investig Drugs 19 (4): 579–585. doi:10.1517/13543781003724690. PMID 20367196. 15. ^ Zhou, Xiaolan; Wang, Jin Lin; Lu, John; Song, Yanping; Kwak, Keith S.; Jiao, Qingsheng; Rosenfeld, Robert; Chen, Qing; Boone, Thomas; Simonet, W. Scott; Lacey, David L.; Goldberg, Alfred L.; Han, H.Q. (2010). "Reversal of Cancer Cachexia and Muscle Wasting by ActRIIB Antagonism Leads to Prolonged Survival". Cell 142 (4): 531–43. doi:10.1016/j.cell.2010.07.011. PMID 20723755. 16. ^ http://www.hcup-us.a...nisoverview.jsp 17. ^ http://www.cdc.gov/nchs/ahcd.htm Yanovski SZ, Yanovski JA. Obesity. N Engl J Med 2002; 346: 591–602. | Article | PubMed | ISI | ChemPort | Schwartz MW, Woods SC, Porte Jr D, Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature 2000; 404: 661–671. | Article | PubMed | ISI | ChemPort | 2. Burstein S. Marijuana as a medicine. Nature 1997; 386: 320. | Article | PubMed | 3. Di Marzo V, Melck D, Bisogno T, De Petrocellis L. Endocannabinoids: endogenous cannabinoid receptor ligands with neuromodulatory action. Trends Neurosci 1998; 21: 521–528. | Article | PubMed | ISI | ChemPort | 4. Abel EL. Cannabis: effects on hunger and thirst. Behav Biol 1975; 15: 255–281. | Article | PubMed | ISI | ChemPort | 5. De Petrocellis L, Melck D, Bisogno T, Milone A, Di Marzo V. Finding of the endocannabinoid signalling system in Hydra, a very primitive organism: possible role in the feeding response. Neuroscience 1999; 92: 377–387. | Article | PubMed | ISI | ChemPort | 6. Porter AC, Felder CC. The endocannabinoid nervous system: unique opportunities for therapeutic intervention. Pharmacol Ther 2001; 90: 45–60. | Article | PubMed | ISI | ChemPort | 7. Gaoni Y, Mechoulam R. Isolation, structure and partial synthesis of an active constituent of hashish. J Am Chem Soc 1964; 86: 1646. | Article | ISI | ChemPort | 8. Matsuda LA, Lolait SJ, Brownstein MJ, Young AC, Bonner TI. Structure of a cannabinoid receptor and functional expression of the cloned cDNA. Nature 1990; 346: 561–564. | Article | PubMed | ISI | ChemPort | 9. Munro S, Thomas KL, Abu-Shaar M. Molecular characterization of a peripheral receptor for cannabinoids. Nature 1993; 365: 61–65. | Article | PubMed | ISI | ChemPort | 10. Howlett AC, Barth F, Bonner TI, Cabral G, Casellas P, Devane WA, Felder CC, Herkenham M, Mackie K, Martin BR, Mechoulam R, Pertwee RG. International Union of Pharmacology. XXVII. Classification of Cannabinoid Receptors. Pharmacol Rev 2002; 54: 161–202. | Article | PubMed | ISI | ChemPort | 11. Schlicker E, Kathmann M. Modulation of transmitter release via presynaptic cannabinoid receptors. Trends Pharmacol Sci 2001; 22: 565–572. | Article | PubMed | ISI | ChemPort | 12. Ameri A. The effects of cannabinoids on the brain. Prog Neurobiol 1999; 58: 315–348. | Article | PubMed | ISI | ChemPort | 13. Zimmer A, Zimmer AM, Hohmann AG, Herkenham M, Bonner TI. Increased mortality, hypoactivity, and hypoalgesia in cannabinoid CB1 receptor knockout mice. Proc Natl Acad Sci USA 1999; 96: 5780–5785. | Article | PubMed | ChemPort | 14. Marsicano G, Wotjak CT, Azad SC, Bisogno T, Rammes G, Cascio MG, Hermann H, Tang J, Hofmann C, Zieglgansberger W, Di Marzo V, Lutz B. The endogenous cannabinoid system controls extinction of aversive memories. Nature 2002; 418: 530–534. | Article | PubMed | ISI | ChemPort | 15. Ledent C, Valverde O, Cossu G, Petitet F, Aubert JF, Beslot F, Bohme GA, Imperato A, Pedrazzini T, Roques BP, Vassart G, Fratta W, Parmentier M. Unresponsiveness to cannabinoids and reduced addictive effects of opiates in CB1 receptor knockout mice. Science 1999; 283: 401–404. | Article | PubMed | ISI | ChemPort | 16. Devane WA, Hanus L, Breuer A, Pertwee RG, Stevenson LA, Griffin G, Gibson D, Mandelbaum A, Etinger A, Mechoulam R. Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science 1992; 258: 1946–1949. | Article | PubMed | ISI | ChemPort | 17. Felder CC, Joyce KE, Briley EM, Mansouri J, Mackie K, Blond O, Lai Y, Ma AL, Mitchell RL. Comparison of the pharmacology and signal transduction of the human cannabinoid CB1 and CB2 receptors. Mol Pharmacol 1995; 48: 443–450. | PubMed | ISI | ChemPort | 18. Felder CC, Nielsen A, Briley EM, Palkovits M, Priller J, Axelrod J, Nguyen DN, Richardson JM, Riggin RM, Koppel GA, Paul SM, Becker GW. Isolation and measurement of the endogenous cannabinoid receptor agonist, anandamide, in brain and peripheral tissues of human and rat. FEBS Lett 1996; 393: 231–235. | Article | PubMed | ISI | ChemPort | 19. Hanus L, Gopher A, Almog S, Mechoulam R. Two new unsaturated fatty acid ethanolamides in brain that bind to the cannabinoid receptor. J Med Chem 1993; 36: 3032–3034. | Article | PubMed | ChemPort | 20. Mechoulam R, Ben Shabat S, Hanus L, Ligumsky M, Kaminski NE, Schatz AR, Gopher A, Almog S, Martin BR, Compton DR. Identification of an endogenous 2-monoglyceride, present in canine gut, that binds to cannabinoid receptors. Biochem Pharmacol 1995; 50: 83–90. | Article | PubMed | ISI | ChemPort | 21. Sugiura T, Kondo S, Sukagawa A, Nakane S, Shinoda A, Itoh K, Yamashita A, Waku K. 2-Arachidonoylglycerol: a possible endogenous cannabinoid receptor ligand in brain. Biochem Biophys Res Commun 1995; 215: 89–97. | Article | PubMed | ISI | ChemPort | 22. Hanus L, Abu-Lafi S, Fride E, Breuer A, Vogel Z, Shalev DE, Kustanovich I, Mechoulam R. 2-arachidonyl glyceryl ether, an endogenous agonist of the cannabinoid CB1 receptor. Proc Natl Acad Sci USA 2001; 98: 3662–3665. | Article | PubMed | ChemPort | 23. Stella N, Schweitzer P, Piomelli D. A second endogenous cannabinoid that modulates long-term potentiation. Nature 1997; 388: 773–778. | Article | PubMed | ISI | ChemPort | 24. Di Marzo V, Fontana A, Cadas H, Schinelli S, Cimino G, Schwartz JC, Piomelli D. Formation and inactivation of endogenous cannabinoid anandamide in central neurons. Nature 1994; 372: 686–691. | Article | PubMed | ChemPort | 25. Dinh TP, Carpenter D, Leslie FM, Freund TF, Katona I, Sensi SL, Kathuria S, Piomelli D. Brain monoglyceride lipase participating in endocannabinoid inactivation. Proc Natl Acad Sci USA 2002; 99: 10819–10824. | Article | PubMed | ChemPort | 26. Mechoulam R, Feigenbaum JJ, Lander N, Segal M, Jarbe TU, Hiltunen AJ, Consroe P. Enantiomeric cannabinoids: stereospecificity of psychotropic activity. Experientia 1988; 44: 762–764. | PubMed | ChemPort | 27. Howlett AC, Johnson MR, Melvin LS. Classical and nonclassical cannabinoids: mechanism of action-brain binding. NIDA Res Monogr 1990; 96: 100–111. 28. Rinaldi-Carmona M, Barth F, Heaulme M, Shire D, Calandra B, Congy C, Martinez S, Maruani J, Neliat G, Caput D. SR141716A, a potent and selective antagonist of the brain cannabinoid receptor. FEBS Lett 1994; 350: 240–244. | Article | PubMed | ChemPort | 29. Lan R, Gatley J, Lu Q, Fan P, Fernando SR, Volkow ND, Pertwee R, Makriyannis A. Design and synthesis of the CB1 selective cannabinoid antagonist AM281: a potential human SPECT ligand. AAPS Pharm Sci 1999; 1: E4. 30. Rinaldi-Carmona M, Barth F, Millan J, Derocq JM, Casellas P, Congy C, Oustric D, Sarran M, Bouaboula M, Calandra B, Portier M, Shire D, Breliere JC, Le Fur GL. SR 144528, the first potent and selective antagonist of the CB2 cannabinoid receptor. J Pharmacol Exp Ther 1998; 284: 644–650. | PubMed | ISI | ChemPort | 31. Landsman RS, Makriyannis A, Deng H, Consroe P, Roeske WR, Yamamura HI. AM630 is an inverse agonist at the human cannabinoid CB1 receptor. Life Sci 1998; 62: L109–L113. 32. Beltramo M, Stella N, Calignano A, Lin SY, Makriyannis A, Piomelli D. Functional role of high-affinity anandamide transport, as revealed by selective inhibition. Science 1997; 277: 1094–1097. | Article | PubMed | ISI | ChemPort | 33. De Petrocellis L, Bisogno T, Davis JB, Pertwee RG, Di Marzo V. Overlap between the ligand recognition properties of the anandamide transporter and the VR1 vanilloid receptor: inhibitors of anandamide uptake with negligible capsaicin-like activity. FEBS Lett 2000; 483: 52–56. | Article | PubMed | ISI | ChemPort | 34. de Lago E, Fernandez-Ruiz J, Ortega-Gutierrez S, Viso A, Lopez-Rodriguez M, Ramos JA. UCM707, a potent and selective inhibitor of endocannabinoid uptake, potentiates hypokinetic and antinociceptive effects of anandamide. Eur J Pharmacol 2002; 449: 99–103. | Article | PubMed | ISI | ChemPort | 35. Lutz B. Molecular biology of cannabinoid receptors. Prostaglandins Leukot Essent Fatty Acids 2002; 66: 123–142. | PubMed | 36. Murphy LL, Munoz RM, Adrian BA, Villanua MA. Function of cannabinoid receptors in the neuroendocrine regulation of hormone secretion. Neurobiol Dis 1998; 5: 432–446. | Article | PubMed | 37. Pagotto U, Marsicano G, Fezza F, Theodoropoulou M, Grubler Y, Stalla J, Arzberger T, Milone A, Losa M, Di Marzo V, Lutz B, Stalla GK. Normal human pituitary gland and pituitary adenomas express cannabinoid receptor type 1 and synthesize endogenous cannabinoids: first evidence for a direct role of cannabinoids on hormone modulation at the human pituitary level. J Clin Endocrinol Metab 2001; 86: 2687–2696. | Article | PubMed | ISI | ChemPort | 38. Navarro M, Hernandez E, Munoz RM, del Arco I, Villanua MA, Carrera MR, Rodriguez de Fonseca F. Acute administration of the CB1 cannabinoid receptor antagonist SR 141716A induces anxiety-like responses in the rat. Neuroreport 1997; 8: 491–496. | PubMed | ISI | ChemPort | 39. Beilin M, Neumann R, Belkin M, Green K, Bar-Ilan A. Pharmacology of the intraocular pressure (IOP) lowering effect of systemic dexanabinol (HU-211), a non-psychotropic cannabinoid. J Ocul Pharmacol Ther 2000; 16: 217–230. 40. Calignano A, Katona I, Desarnaud F, Giuffrida A, La Rana G, Mackie K, Freund TF, Piomelli D. Bidirectional control of airway responsiveness by endogenous cannabinoids. Nature 2000; 408: 96–101. | Article | PubMed | ChemPort | 41. Wagner JA, Jarai Z, Batkai S, Kunos G. Hemodynamic effects of cannabinoids: coronary and cerebral vasodilation mediated by cannabinoid CB1 receptors. Eur J Pharmacol 2001; 423: 203–210. | Article | PubMed | ISI | ChemPort | 42. Wenger T, Ledent C, Csernus V, Gerendai I. The central cannabinoid receptor inactivation suppresses endocrine reproductive functions. Biochem Biophys Res Commun 2001; 284: 363–368. | Article | PubMed | ChemPort | 43. De Petrocellis L, Melck D, Bisogno T, Di Marzo V. Endocannabinoids and fatty acid amides in cancer, inflammation and related disorders. Chem Phys Lipids 2000; 108: 191–209. | Article | PubMed | ChemPort | 44. Munson AE, Harris LS, Friedman MA, Dewey WL, Carchman RA. Antineoplastic activity of cannabinoids. J Natl Cancer Inst 1975; 55: 597–602. | PubMed | ChemPort | 45. Bifulco M, Di Marzo V. Targeting the endocannabinoid system in cancer therapy: a call for further research. Nat Med 2002; 8: 547–550. | Article | PubMed | ISI | ChemPort | 46. Galve-Roperh I, Sanchez C, Cortes ML, del Pulgar TG, Izquierdo M, Guzman M. Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation. Nat Med 2000; 6: 313–319. | Article | PubMed | ISI | ChemPort | 47. Panikashvili D, Simeonidou C, Ben Shabat S, Hanus L, Breuer A, Mechoulam R, Shohami E. An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature 2001; 413: 527–531. | Article | PubMed | ISI | ChemPort | 48. Siler JF, Sheep WL, Bates LB, Clark GF, Cook GW, Smith WH. Marihuana smoking in Panama. Mil Surg 1933; 73: 269–280. 49. Tart CT. Marijuana intoxication common experiences. Nature 1970; 226: 701–704. | Article | PubMed | ChemPort | 50. Haines L, Green W. Marijuana use patterns. Br J Addict Alcohol Other Drugs 1970; 65 : 347–362. 51. Hollister LE. Hunger and appetite after single doses of marihuana, alcohol, and dextroamphetamine. Clin Pharmacol Ther 1971; 12: 44–49. 52. Abel EL. Effects of marihuana on the solution of anagrams, memory and appetite. Nature 1971; 231: 260–261. | Article | PubMed | ISI | ChemPort | 53. Gagnon MA, Elie R. Effects of marijuana and D-amphetamine on the appetite, food consumption and various cardio-respiratory variables in man. Union Med Can 1975; 104: 914–921. 54. Chopra RN, Chopra GS. The present position of hemp-drug addiction in India. Ind Med Res Mem 1939; 31: 1–119. 55. Greenberg I, Kuehnle J, Mendelson JH, Bernstein JG. Effects of marihuana use on body weight and caloric intake in humans. Psychopharmacology (Berl) 1976; 49: 79–84. 56. Foltin RW, Brady JV, Fischman MW. Behavioral analysis of marijuana effects on food intake in humans. Pharmacol Biochem Behav 1986; 25: 577–582. 57. Foltin RW, Fischman MW, Byrne MF. Effects of smoked marijuana on food intake and body weight of humans living in a residential laboratory. Appetite 1988; 11: 1–14. | Article | PubMed | ISI | ChemPort | 58. Mattes RD, Engelman K, Shaw LM, Elsohly MA. Cannabinoids and appetite stimulation. Pharmacol Biochem Behav 1994; 49: 187–195. 59. Kirkham TC, Williams CM. Endogenous cannabinoids and appetite. Nutr Res Rev 2001; 14: 65–86. | Article | ISI | ChemPort | 60. Williams CM, Kirkham TC. Anandamide induces overeating: mediation by central cannabinoid (CB1) receptors. Psychopharmacology (Berl) 1999; 143: 315–317. | Article | PubMed | ChemPort | 61. Koch JE. Delta(9)-THC stimulates food intake in Lewis rats: effects on chow, high-fat and sweet high-fat diets. Pharmacol Biochem Behav 2001; 68: 539–543. | Article | PubMed | ChemPort | 62. Gorter RW. Cancer cachexia and cannabinoids. Forsch Komplementarmed 1999; 6 (Suppl 3): 21–22. 63. Beal JE, Olson R, Lefkowitz L, Laubenstein L, Bellman P, Yangco B, Morales JO, Murphy R, Powderly W, Plasse TF, Mosdell KW, Shepard KV. Long-term efficacy and safety of dronabinol for acquired immunodeficiency syndrome-associated anorexia.J Pain Symptom Manage 1997; 14: 7–14. | Article | PubMed | ISI | ChemPort | 64. Gralla RJ. Cannabinoids and the control of chemotherapy-induced nausea and vomiting. In: Nahas GG, Sutin KM, Harvey DJ, Agurell S (eds). Marihuana and medicine. Humana Press: Totowa, NJ; 1999. pp 599–610. 65. Lanzotti VJ, Thomas DR, Boyle LE, Smith TL, Gehan EA, Samuels ML. Survival with inoperable lung cancer: an integration of prognostic variables based on simple clinical criteria. Cancer 1977; 39: 303–313. 66. Sallan SE, Zinberg NE, Frei III E. Antiemetic effect of delta-9-tetrahydrocannabinol in patients receiving cancer chemotherapy. N Engl J Med 1975; 293: 795–797. 67. Regelson W, Thomas DR, Boyle LE, Smith TL, Gehan EA, Samuels ML. 9-Tetrahydrocannabinol as an effective antidepressant and appetite-stimulating agent in advanced cancer patients. In: Brande MC, Szara S (eds). The pharmacology of marijuana. Raven Press: New York; 1976. pp 763–776. 68. Plasse TF, Gorter RW, Krasnow SH, Lane M, Shepard KV, Wadleigh RG. Recent clinical experience with dronabinol. Pharmacol Biochem Behav 1991; 40: 695–700. 69. Gorter R, Seefried M, Volberding P. Dronabinol effects on weight in patients with HIV infection. AIDS 1992; 6: 127. | PubMed | 70. Struwe M, Kaempfer SH, Geiger CJ, Pavia AT, Plasse TF, Shepard KV, Ries K, Evans TG. Effect of dronabinol on nutritional status in HIV infection. Ann Pharmacother 1993; 27: 827–831. | PubMed | ISI | ChemPort | 71. Beal JE, Olson R, Laubenstein L, Morales JO, Bellman P, Yangco B, Lefkowitz L, Plasse TF, Shepard KV. Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS. J Pain Symptom Manage 1995; 10: 89–97. | Article | PubMed | ChemPort | 72. Volicer L, Stelly M, Morris J, McLaughlin J, Volicer BJ. Effects of dronabinol on anorexia and disturbed behavior in patients with Alzheimer's disease. Int J Geriatr Psychiatry 1997; 12: 913–919. 73. Carlini EA, Kramer C. Effects of Cannabis sativa (marihuana) on maze performance of the rat. Psychopharmacologia 1965; 7: 175–181. 74. Dewey WL, Harris LS, Kennedy JS. Some pharmacological and toxicological effects of 1-trans- 8 and 1-trans- 9 -tetrahydrocannabinol in laboratory rodents. Arch Int Pharmacodyn Ther 1972; 196: 133–145. 75. Thompson GR, Fleischman RW, Rosenkrantz H, Braude MC. Oral and intravenous toxicity of delta9-tetrahydrocannabinol in rhesus monkeys. Toxicol Appl Pharmacol 1974; 27: 648–665. 76. Manning FJ, McDonough Jr JH, Elsmore TF, Saller C, Sodetz FJ. Inhibition of normal growth by chronic administration of delta-9-tetrahydrocannabinol. Science 1971; 174: 424–426. | PubMed | ChemPort | 77. Sjoden PO, Jarbe TU, Henriksson BG. Influence of tetrahydrocannabinols (delta8-THC and delta9-THC) on body weight, food, and water intake in rats. Pharmacol Biochem Behav 1973; 1: 395–399. 78. Fernandes M, Schabarek A, Coper H, Hill R. Modification of delta9-THC-actions by cannabinol and cannabidiol in the rat. Psychopharmacologia 1974; 38: 329–338. 79. Sofia RD, Barry III H. Acute and chronic effects of delta9-tetrahydrocannabinol on food intake by rats. Psychopharmacologia 1974; 39: 213–222. 80. Brown JE, Kassouny M, Cross JK. Kinetic studies of food intake and sucrose solution preference by rats treated with low doses of delta9-tetrahydrocannabinol. Behav Biol 1977; 20: 104–110. 81. McLaughlin CL, Baile CA, Bender PE. Cannabinols and feeding in sheep. Psychopharmacology (Berl) 1979; 64: 321–323. 82. Van Den Broek GW, Robertson J, Keim DA, Baile CA. Feeding and depression of abomasal secretion in sheep elicited by elfazepam and 9-aza-cannabinol. Pharmacol Biochem Behav 1979; 11: 51–56. 83. Williams CM, Rogers PJ, Kirkham TC. Hyperphagia in pre-fed rats following oral delta9-THC. Physiol Behav 1998; 65: 343–346. | Article | PubMed | ISI | ChemPort | 84. Anderson-Baker WC, McLaughlin CL, Baile CA. Oral and hypothalamic injections of barbiturates, benzodiazepines and cannabinoids and food intake in rats. Pharmacol Biochem Behav 1979; 11: 487–491. | Article | PubMed | ChemPort | 85. Trojniar W, Wise RA. Facilitory effect of delta 9-tetrahydrocannabinol on hypothalamically induced feeding. Psychopharmacology (Berl) 1991; 103: 172–176. 86. Arnone M, Maruani J, Chaperon F, Thiebot MH, Poncelet M, Soubrie P, Le Fur G. Selective inhibition of sucrose and ethanol intake by SR 141716, an antagonist of central cannabinoid CB1 receptors. Psychopharmacology (Berl) 1997; 132: 104–106. | Article | PubMed | ChemPort | 87. Gallate JE, McGregor IS. The motivation for beer in rats: effects of ritanserin, naloxone and SR 141716. Psychopharmacology (Berl) 1999; 142: 302–308. | Article | PubMed | 88. Freedland CS, Sharpe AL, Samson HH, Porrino LJ. Effects of SR141716A on ethanol and sucrose self-administration. Alcohol Clin Exp Res 2001; 25: 277–282. | Article | PubMed | ISI | ChemPort | 89. Simiand J, Keane M, Keane PE, Soubrie P. SR 141716, a CB1 cannabinoid receptor antagonist, selectively reduces sweet food intake in marmoset. Behav Pharmacol 1998; 9: 179–181. | PubMed | ISI | ChemPort | 90. Colombo G, Agabio R, Diaz G, Lobina C, Reali R, Gessa GL. Appetite suppression and weight loss after the cannabinoid antagonist SR 141716. Life Sci 1998; 63: L113–L117. | Article | 91. Freedland CS, Poston JS, Porrino LJ. Effects of SR141716A, a central cannabinoid receptor antagonist, on food-maintained responding. Pharmacol Biochem Behav 2000; 67: 265–270. | Article | PubMed | ISI | ChemPort | 92. Hao S, Avraham Y, Mechoulam R, Berry EM. Low dose anandamide affects food intake, cognitive function, neurotransmitter and corticosterone levels in diet-restricted mice. Eur J Pharmacol 2000; 392: 147–156. | Article | PubMed | ISI | ChemPort | 93. Gonzalez S, Manzanares J, Berrendero F, Wenger T, Corchero J, Bisogno T, Romero J, Fuentes JA, Di Marzo V, Ramos JA, Fernandez-Ruiz J. Identification of endocannabinoids and cannabinoid CB1 receptor mRNA in the pituitary gland. Neuroendocrinology 1999; 70: 137–145. | Article | PubMed | ISI | ChemPort | 94. Jamshidi N, Taylor DA. Anandamide administration into the ventromedial hypothalamus stimulates appetite in rats. Br J Pharmacol 2001; 134: 1151–1154. | Article | PubMed | ISI | ChemPort | 95. Di Marzo V, Goparaju SK, Wang L, Liu J, Batkai S, Jarai Z, Fezza F, Miura GI, Palmiter RD, Sugiura T, Kunos G. Leptin-regulated endocannabinoids are involved in maintaining food intake. Nature 2001; 410: 822–825. | Article | PubMed | ISI | ChemPort | 96. Spanagel R, Weiss F. The dopamine hypothesis of reward: past and current status. Trends Neurosci 1999; 22: 521–527. | Article | PubMed | ISI | ChemPort | 97. Gardner EL, Vorel SR. Cannabinoid transmission and reward-related events. Neurobiol Dis 1998; 5: 502–533. | Article | PubMed | ChemPort | 98. Hoebel BG. Brain neurotransmitters in food and drug reward. Am J Clin Nutr 1985; 42: 1133–1150. | PubMed | ChemPort | 99. Breivogel CS, Childers SR. The functional neuroanatomy of brain cannabinoid receptors. Neurobiol Dis 1998; 5: 417–431. | Article | PubMed | ISI | ChemPort | 100. Mechoulam R, Fride E. Physiology. A hunger for cannabinoids. Nature 2001; 410: 763–765. | Article | PubMed | 101. Kunos G, Batkai S. Novel physiologic functions of endocannabinoids as revealed through the use of mutant mice. Neurochem Res 2001; 26: 1015–1021. 102. Erickson JC, Clegg KE, Palmiter RD. Sensitivity to leptin and susceptibility to seizures of mice lacking neuropeptide Y. Nature 1996; 381: 415–421. | Article | PubMed | ISI | ChemPort | 103. Gallate JE, Saharov T, Mallet PE, McGregor IS. Increased motivation for beer in rats following administration of a cannabinoid CB1 receptor agonist. Eur J Pharmacol 1999; 370: 233–240. | Article | PubMed | ChemPort | 104. Chaperon F, Thiebot MH. Behavioral effects of cannabinoid agents in animals. Crit Rev Neurobiol 1999; 13: 243–281. | PubMed | ISI | ChemPort | 105. Bisogno T, Berrendero F, Ambrosino G, Cebeira M, Ramos JA, Fernandez-Ruiz JJ, Di Marzo V. Brain regional distribution of endocannabinoids: implications for their biosynthesis and biological function. Biochem Biophys Res Commun 1999; 256: 377–380. | Article | PubMed | ISI | ChemPort | 106. Hermann H, Marsicano G, Lutz B. Coexpression of the cannabinoid receptor type 1 with dopamine and serotonin receptors in distinct neuronal subpopulations of the adult mouse forebrain. Neuroscience 2002; 109: 451–460. | Article | PubMed | ISI | ChemPort | 107. Glass M, Dragunow M, Faull RL. Cannabinoid receptors in the human brain: a detailed anatomical and quantitative autoradiographic study in the fetal, neonatal and adult human brain. Neuroscience 1997; 77: 299–318. | Article | PubMed | ISI | ChemPort | 108. Berridge KC. Food reward: brain substrates of wanting and liking. Neurosci Biobehav Rev 1996; 20: 1–25. | Article | PubMed | ISI | ChemPort | 109. Di Marzo V, Berrendero F, Bisogno T, Gonzalez S, Cavaliere P, Romero J, Cebeira M, Ramos JA, Fernandez-Ruiz JJ. Enhancement of anandamide formation in the limbic forebrain and reduction of endocannabinoid contents in the striatum of delta9-tetrahydrocannabinol-tolerant rats. J Neurochem 2000; 74: 1627–1635. | Article | PubMed | ISI | ChemPort | 110. Vickers SP, Dourish CT, Kennett GA. Evidence that hypophagia induced by d-fenfluramine and d-norfenfluramine in the rat is mediated by 5-HT2C receptors. Neuropharmacology 2001; 41: 200–209. | Article | PubMed | 111. Rowland NE, Mukherjee M, Robertson K. Effects of the cannabinoid receptor antagonist SR 141716, alone and in combination with dexfenfluramine or naloxone, on food intake in rats. Psychopharmacology (Berl) 2001; 159: 111–116. | Article | PubMed | ChemPort | 112. Navarro M, Carrera MR, Fratta W, Valverde O, Cossu G, Fattore L, Chowen JA, Gomez R, del Arco I, Villanua MA, Maldonado R, Koob GF, de Fonseca FR. Functional interaction between opioid and cannabinoid receptors in drug self-administration. J Neurosci 2001; 21: 5344–5350. | PubMed | ISI | ChemPort | 113. Cooper SJ, Kirkham TC. Opioid mechanisms in the control of food consumption and taste preferences. In: Herz A, Akil H, Simon EJ (eds.) Handbook of experimental pharmacology. Springer-Verlag: Berlin; 1993. pp 239–263. 114. Kirkham TC, Williams CM. Synergistic effects of opioid and cannabinoid antagonists on food intake. Psychopharmacology (Berl) 2001; 153: 267–270. | Article | PubMed | ChemPort | 115. Williams CM, Kirkham TC. Reversal of Delta(9)-THC hyperphagia by SR141716 and naloxone but not dexfenfluramine. Pharmacol Biochem Behav 2002; 71: 333–340. | Article | PubMed | ISI | ChemPort | 116. Crawley JN, Corwin RL. Biological actions of cholecystokinin. Peptides 1994; 15: 731–755. | Article | PubMed | ISI | ChemPort | 117. Marsicano G, Lutz B. Expression of the cannabinoid receptor CB1 in distinct neuronal subpopulations in the adult mouse forebrain. Eur J Neurosci 1999; 11: 4213–4225. | Article | PubMed | ISI | ChemPort | 118. Wiesenfeld-Hallin Z, de Arauja LG, Alster P, Xu XJ, Hokfelt T. Cholecystokinin/opioid interactions. Brain Res 1999; 848: 78–89. 119. Beinfeld MC, Connolly K. Activation of CB1 cannabinoid receptors in rat hippocampal slices inhibits potassium-evoked cholecystokinin release, a possible mechanism contributing to the spatial memory defects produced by cannabinoids. Neurosci Lett 2001; 301: 69–71. | Article | PubMed | ISI | ChemPort | 120. Rodriguez de Fonseca F, Navarro M, Gomez R, Escuredo L, Nava F, Fu J, Murillo-Rodriguez E, Giuffrida A, LoVerme J, Gaetani S, Kathuria S, Gall C, Piomelli D. An anorexic lipid mediator regulated by feeding. Nature 2001; 414: 209–212. | Article | PubMed | ISI | ChemPort | 121. Huestis MA, Gorelick DA, Heishman SJ, Preston KL, Nelson RA, Moolchan ET, Frank RA. Blockade of effects of smoked marijuana by the CB1-selective cannabinoid receptor antagonist SR141716. Arch Gen Psychiatry 2001; 58: 322–328. | Article | PubMed | ISI | ChemPort | 122. Dhillo WS, Bloom SR. Hypothalamic peptides as drug targets for obesity. Curr Opin Pharmacol 2001; 1: 651–655. 123. Main navigation 124. Journal home 125. Advance online publication 126. About AOP 127. Current issue 128. Archive 129. Supplements 130. Press releases 131. Online submission 132. For authors 133. For referees 134. Contact editorial office 135. About the journal 136. For librarians 137. Subscribe 138. Advertising 139. Reprints and permissions 140. Contact NPG 141. Customer services 142. Site features 143. NPG resources 144. European Journal of Clinical Nutrition 145. International Journal of Impotence Research 146. Journal of Human Hypertension 147. Nature Reviews Endocrinology 148. Obesity 149. NPG Journals 150. by Subject Area 151. Chemistry 152. Chemistry 153. Drug discovery 154. Biotechnology 155. Materials 156. Methods & Protocols 157. Clinical Practice & Research 158. Cancer 159. Cardiovascular medicine 160. Dentistry 161. Endocrinology 162. Gastroenterology & Hepatology 163. Methods & Protocols 164. Pathology & Pathobiology 165. Urology 166. Earth & Environment 167. Earth sciences 168. Evolution & Ecology 169. Life sciences 170. Biotechnology 171. Cancer 172. Development 173. Drug discovery 174. Evolution & Ecology 175. Genetics 176. Immunology 177. Medical research 178. Methods & Protocols 179. Microbiology 180. Molecular cell biology 181. Neuroscience 182. Pharmacology 183. Systems biology 184. Physical sciences 185. Physics 186. Materials 187. by A - Z Index 188. Extra navigation 189. . 190. ARTICLE NAVIGATION - FULL TEXT 191. Previous | Next 192. Table of contents 193. Download PDF 194. Send to a friend 195. Rights and permissions 196. Order Commercial Reprints 197. Scopus lists 162 articles citing this article 198. Save this link 199. Abstract 200. Introduction 201. The endogenous cannabinoid system 202. Cannabinoid receptors 203. Endogenous cannabinoids 204. Cannabinoid receptor ligands 205. Roles of the endocannabinoid system 206. Cannabinoids and appetite in humans 207. Therapeutic use of cannabinoids in the control of food intake 208. Cannabinoid effects on food intake in animal models 209. Role of hypothalamus and reward circuitry in cannabinoid-induced hyperphagia 210. Cannabinoid antagonists in the therapy of obesity 211. References 212. Figures and Tables 213. Export citation 214. Export references 215. Papers by Cota 216. nature jobs 217. Postdoctoral Fellow - large-scale genetic analysis; ref. 80981 218. Wellcome Trust Sanger Institute 219. Postdoctoral Fellowships in the Earth, Environmental, and Ocean Sciences 220. Columbia University 221. More science jobs 222. Post a job for free 223. nature events 224. Disruptive Innovations in Clinical Trials 225. 15 September 2011 — 16 September 2011 226. 1200 Market Street, Philadelphia, PA, 19107, United States 227. Asia-Pacific Power and Energy Engineering Conference(APPEEC2012) 228. 26 March 2012 — 28 March 2012 229. Shanghai, China 230. More science events 231. ADVERTISEMENT 232. <div><a href="http://ad.doubleclick.net/jump/ijo.nature.com/homepage;type=;artid=;date=;pos=right;abr=!NN2;sz=160x600;ord=07893195?"><img src="http://ad.doubleclick.net/ad/ijo.nature.com/homepage;pos=right;abr=!NN2;sz=160x600;ord=07893195?" style="max-width:160px; height:600px; border:0;" alt="Advertisement" /></a> </div> 233. Top 234. International Journal of Obesity 235. ISSN: 0307-0565 236. EISSN: 1476-5497 237. About NPG 238. Contact NPG 239. RSS web feeds 240. Help 241. Privacy policy 242. Legal notice 243. Accessibility statement 244. Terms 245. Nature News 246. Nature jobs 247. Nature Asia 248. Nature Education 249. © 2011 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 250. partner of AGORA, HINARI, OARE
  7. 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
  8. 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!
  9. AMYOTROPHIC LATERAL SCLEROSIS Edit by Author, 1/15/2013 Some of the source links below are now dead. I was only allowed to take one third of the original content. And leave links. I give you permission to use one third also. Or search out the videos first and and take them from there. http://www.youtube.com/watch?v=Dp4q8YNF9o4 What Types of Nerves Make Your Body Work Properly? (from Living with ALS, Manual 1: What's It All About?) The body has many kinds of nerves. There are those involved in the process of thinking, memory, and of detecting sensations (such as hot/cold, sharp/dull), and others for vision, hearing, and other bodily functions. The nerves that are affected when you have ALS are the motor neurons that provide voluntary movements and muscle power. Examples of voluntary movements are your making the effort to reach for the phone or step off a curb; these actions are controlled by the muscles in the arms and legs. The heart and the digestive system are also made of muscle but a different kind, and their movements are not under voluntary control. When your heart beats or a meal is digested, it all happens automatically. Therefore, the heart and digestive system are not involved in ALS. Breathing also may seem to be involuntary. Remember, though, while you cannot stop your heart, you can hold your breath - so be aware that ALS may eventually have an impact on breathing. Although the cause of ALS is not completely understood, the recent years have brought a wealth of new scientific understanding regarding the physiology of this disease. Source Marijuana's Potential Exciting Researchers in Treatment of ALS, Parkinson's Disease A Legal Mood Lifter: Researchers are investigating a new antidepressant and pain reliever that works like cannabis (marijuana), without the illegal side effects. A decade ago, when Daniele Piomelli went to scientific conferences, he was often the only researcher studying cannabinoids, the class of chemicals that give marijuana users a high. His work often drew snickers and jokes, but no more. At the annual Society for Neuroscience conference recently, scientists here delivered almost 200 papers on the subject. Why the attention? Many scientists believe cannabis-like drugs might be able to treat a wide range of diseases, far beyond the nausea and chronic pain typically treated with medical cannabis. Researchers here presented tantalizing evidence that cannabinoid drugs can help treat amyotrophic lateral sclerosis, known as ALS or Lou Gehrig's disease, Parkinson's disease and obesity. Other researchers are studying whether the compounds can help victims of stroke and multiple sclerosis. Although the chemicals work on the same area of the nervous system, the new drugs are much more refined and targeted than cannabis, with few of its side effects. "Cannabinoids have a lot of pharmaceutical potential," said Piomelli, a neuroscientist at the University of California at Irvine. "A lot of people are very excited" Although the federal government opposes the use of medical marijuana, it generally doesn't restrict cannabinoid research, most of which doesn't involve the cannabis plant itself. Scientists who use Marinol, a legal but tightly regulated marijuana-like drug, do need government permission. Because the cannabinoid system wasn't discovered until the late 1980s, decades after serotonin, dopamine and other neurotransmitters, researchers still know relatively little about how it works. Like all neurotransmitter networks, the cannabinoid system consists of a series of chemical pathways through the brain and nervous system. Cannabis produces its effects by activating this pathway, primarily through the effects of tetrahydrocannabinol, or THC, the drug's main active ingredient. Over the past decade, researchers have been following these abundant trails to determine their real purpose. "You don't have them there to get stoned. So, there must be internal reasons," said Andrea Giuffrida, a neuroscientist at the University of Texas Health Sciences Center in San Antonio. Researchers have learned that endogenous cannabinoids, internal brain chemicals that activate the system, play a role in tissue protection, immunity and inflammation, among other functions. The cannabinoid system also appears to exert wide influence, modulating the release of dopamine, serotonin and other neurotransmitters. Giuffrida and others believe cannabinoids can treat degenerative disorders such as Parkinson's disease and ALS. At the conference, Giuffrida announced that a cannabinoid drug wards off Parkinson's-like effects in mice. The disorder, which afflicts more than 1 million Americans, destroys neurons in a key part of the brain, causing patients to lose control over movement. Giuffrida, with colleagues David Price and James Roberts, injected mice with a chemical called MPTP, which mimics Parkinson's damage. When some of the animals subsequently received a drug that blocks cannabinoid receptors, their nerve cells suffered far less damage than did the cells of the other mice. This was the first demonstration that a cannabinoid drug can have this effect. Although he is not sure how the anti-cannabinoid compound works, Giuffrida suspects it protects neurons by reducing inflammation, a key component in Parkinson's. Cannabinoids might also slow down ALS, which destroys neurons that control muscles until victims become paralyzed, unable to breathe on their own. Neuroscientist Mary Abood first became interested in cannabinoids after hearing about ALS patients who got some relief from smoking cannabis. So she began animal experiments at the California Pacific Medical Center in San Francisco. In her study, mice with a variant of ALS were given a combination of THC and cannabidiol, another compound found in cannabis. Both substances are cannabinoid agonists, chemicals that activate the cannabinoid system. Abood measured the course of the ailment by testing how long the mice could stand on a rod that was slowly rotating. The treatment delayed disease progression by more than seven days and extended survival by six days. In human terms, this would amount to about three years. That's a significant improvement over the only existing ALS drug, riluzole, which extends life by two months. "I was very excited when I got my initial results," Abood said. Also at the conference, researchers at the Institute of Neurology in London announced results that corroborated her findings. Cannabinoids have also helped some human ALS patients in one small trial, and Abood is trying to get funding for a larger one. If cannabinoids can shield human neurons from harm, researchers say, they might prove useful against other neurological diseases, including mental illness. Scientists are looking at whether cannabinoids can treat multiple sclerosis, epilepsy and Huntington's disease, while Giuffrida is beginning a study of their effect on schizophrenia. Advocates of medical cannabis have long argued that the drug can be useful for treating many conditions, particularly chronic pain, nausea and glaucoma (in the latter, cannabis works by temporarily decreasing pressure around the eye). Although they don't dispute this view, most researchers believe there are better, more precise ways to stimulate the cannabinoid system. They believe cannabis has too many negatives to be a truly effective drug, with side effects that include memory problems, decreased immunity and possibly addiction. (Some researchers dispute this "addictive" claim.) Cannabis has another drawback. From a scientific standpoint, Giuffrida says, it's "a very dirty drug." It contains more than 300 compounds, 60 of which affect the cannabinoid system. Scientists don't understand what most of these substances do or how they work together. This complexity makes it hard for researchers to pinpoint cannabis' effects. One cannabinoid, Marinol, is available legally. The compound, which contains THC in a pill form, is usually prescribed for nausea and for appetite loss among AIDS patients. But Marinol has the same psychoactive effects as cannabis. "So the key", Piomelli says, "is getting the effects without the side effects." To that end, Piomelli has developed a compound called URB597, which doesn't flood the body with cannabinoids, as Marinol and cannabis do. Instead, it slows the breakdown of the cannabinoids in the system. He thinks the drug may help treat pain, anxiety and even depression without making patients stoned and forgetful. He and others are testing it on animals. SOURCE http://www.illinoisn...ent/view/600/1/ http://www.youtube.com/watch?v=-qFSMXEYC3c Survey of Cannabis Use in Patients with Amyotrophic Lateral Sclerosis Dagmar Amtmann, PhD Patrick Weydt, Md Kurt L. Johnson, PhD Mark P. Jensen, PhD Gregory T. Carter, M.D. Abstract Cannabis (marijuana) has been proposed as treatment for a widening spectrum of medical condtions and has many properties that may be applicable to the management of amyotrophic lateral sclerosis (ALS). This study is the first, anonymous survey of persons with ALS regarding the use of cannabis. There were 131 respondents, 13 of whom reported using cannabis in the last 12 months. Although the small number of people with ALS that reported using cannabis limits the interpretation of the survey findings, the results indicate that cannabis may be moderately effective at reducing symptoms of appetite loss, depression, pain, spasticity, and drooling. Cannabis was reported ineffective in reducing difficulties with speech and swallowing, and sexual dysfuction. The longest relief was reported for depression (approximately two to three hours). Key words: pain, palliative care, cannabis, medicinal marijuana, amyotrophic lateral sclerosis. Introduction Amyotrophic lateral sclerosis (ALS), with an incident rate of five to seven per 100,000 population, is the most common form of adult motor neuron disease.1-3 ALS is a rapidly progerssive neuromuscular disease that destroys both upper and lower motor neurons, ultimately causing death, typically from respiratory failure. The vast majority of ALS is acquired and occurs sporadically. There is not yet a known cure for ALS. 4-6 ALS patients may present with any number of clinical symptoms, including weakness, spasticity, cachexia, dysarthria and drooling, and pain secondary to immobility, among others.7-8 Previous studies have reported both direct and theoretical applications for using cannabis to manage some of these ALS symptoms.9-11 Cannabis has easily observable clinical effects with rapid onset (e.g., analgesia, muscle relaxation, dry mouth). Moreover, some components of marijuana (not inhaled smoke) have been shown in laboratory studiues to have neuroprotective properties that may help prolong neuronal cell survival over extended time.12-16 Marijuana is a complex plant, containing over 400 chemicals.17 Approximately 60 are cannabinoids, chemically classified as 21 carbon terpenes.17,18 Among the most psychoactive of these is delta-9-tetrahydrocannabinol (THC).17,18 Because of this biochemical complexity, characterizing the clinical pharmacology of marijuana is difficult. The clinical pharmacology of marijuana containing high concentrations of THC may well differ from plant material containing small amounts of THC and higher amounts of the other cannabinoids. The bioavailability and pharmacokinetics of inhaled marijuana are also substantially different from those taken by ingestion. The cannabinoids are all lipid soluble compounds and are not soluble in water.19 Besides THC, which is the active ingredient in dronabinol, varying proportions of other cannabinoids, mainly cannabidiol (CBD) and cannabinol (CBN), are also present in marijuana and may modify the pharmacology of the THC as well as have distinct effects of their own. CBD is not psychoactive but has significant anticonvulsant and sedative pharmacologic properties and may interact with THC.20-21 The concentration of THC and other cannabinoids in marijuana varies greatly depending on growing conditions, plant genetics, and processing after harvest.21 In the usual mixture of leaves and stems distributed as marijuana, concentration of THC ranges from 0.3 percent to 4 percent by weight.21,22 However, specially grown and selected marijuana can contain 15 percent or more THC. Thus, one gram of marijuana might contain as little as three milligrams of THC or more than 150 mg.21 THC is a potent psychoactive drug, and large doses may produce mental and perceptual effects similar to hallucinogenic drugs.23,24 Despite this, THC and other cannabinoids have low toxicity, and lethal doses in humans have not been described.25,26 Despite risk for bronchitis, the main advantage of smoking is rapid onset of effect and easy dose titration. When marijuana is smoked, cannabinoids in the form of an aerosol in the inhaled smoke are rapidly absorbed and delivered to the brain, as would be expected of a highly lipid-soluble drug.27,28 However, smoking anything, including marijuana, carries health risks for the lungs and airway system. A healthier option is vaporization. Because the cannabinoids are volatile, they will vaproize at a temperature much lower than actual combustion.24 Heated air can be drawn through marijuana and the active compounds will vaporize, which can then be inhaled. This delivers the substance in a rapid manner that can be easily titrated to desired effect.29 Vaporization therefore removes most of the health hazards of smoking.27 The medicinal use of cannabis is better documented in multiple sclerosis (MS) than in other clinical conditions, although evidence tends to be anecdotal, and no controlled clinical trials of medicinal marujuana use in MS have been published.30-39 With respect to pain, the concominant use of cannabis with narcotics may be beneficial, because the cannabinoid receptor system appears to be discrete from that of opioids.40-45 In that regard, the antiemetic effect of cannabis may also help with the nausea sometimes associated with narcotic medications. Untoward effects of cannabis include potentially significant psychoactive properties, which may produce a sense of well-being or euphoria but can also induce anxiety, confusion, paranoia, and lethargy.46 To date there have not yet been any empirical studies to investigate the use of cannabis for medicinal purposes in ALS. The purpose of this survey was to gather preliminary data on the extent of use of cannabis among persons with ALS (PALS) and to learn which of the symptoms experienced by PALS are reported to be alleviated by the use of cannabis. Metohdology Participants in this survey were recruited from the ALS Digest (the Digest), an electronic discussion list published weekly to serve the worldwide ALS community, including patients, families, caregivers, and providers. The Digest serves as a forum for discussion of issues related to ALS and is not intended to provide medical advice on individual health matters. The Digest can be viewed at www.alslinks.com. Currently there are over 5,600 subscribers in 80 countries worldwide. However, the number of subscribers with ALS is not known. The editor is not a physician and the Digest is not peer reviewed. An e-mail invitation to participate was posted to the Digest four times over two months. The survey was available online from January 6 through March 2, 2003, approximately eight consecutive weeks. Any subscriber with ALS was invited to participate on a voluntary and anonymous basis. The sponsoring institution human subjects review board approved the study protocol. A Web-based survey tool developed by the University of Washignton was used to collect responses. The tool uses SSL encryption for transferred data, and all identifying information was stored in a code translation table separate from the actual data to protect the privacy of respondents. The University of Washington human subjects review board has approved this tool for research purposes. PALS who wanted to participate were given a Web site address that introduced the survey and provided a link to the survey site. The invitation to participate did not mention cannabis or marijuana, in order to discourage participation by individuals who do not have ALS but might otherwise be interested in promoting legalization of marijuana. The sruvey was titled "A survey of ALS Patients Who Use Alternative Therapies to Treat Symptoms." It was presumed by the investigatiors that the diagnostic information provided by the survey participants was accurate (i.e., no medical records were reviewed to confirm their diagnosis). In addition to a series of questions related to the ALS symptoms, the use of cannabis, and its effectiveness in alleviating the symptoms of ALS, participants were also asked to provide demographic and diagnostic information. The survey was anonymous and it is therefore impossible to conclusively determine whether all respondents were individuals with ALS. However, the first six questions of the survey asked about how and when the respondent was diagnosed with ALS and specifically asked those who were not diagnosed with ALS by a physician to not fill out the survey. The authors carefully studied the demographic and diagnostic information provided by each respondent for completeness, consistency, and plausiblity. Records with the diagnostic information missing were excluded from the analysis. Many participants offered extensive information about other alternative therapies they use, and the general comments appeared to reflect experiences of individuals living with ALS. Results A total of 137 responses were received. Four responses were excluded because of duplicate submission (i.e. the same person inadvertently submitting more than one survey by hitting the submit key more than once) and two because of failure to complete most of the questions of the survey. Eletronic logs of all submissions were inspected for repeated entries from the same Internet protocol (IP) address. None were found. A total of 131 responses were retained for analysis. The demographics of the sample are shown in Table 1. Seventy-five percent of the respondents were male and 90 percent were caucasian. The average age of participants was 54 years [standard deviation(sd)=11], with no significant difference between the genders [Mean(M) mean(m)=54 for=for males,=males, sd=12.5 m=53 females,=females,]. Eighty-four percent of the respondents were married or living with a significant other, 17 percent were employed (full time or part-time), 64 percent were unemployed or retired due to disability, and 18 percent were retired due to age. Respondents reported high levels of education, with only 13 percent with high school education or less and 62 percent with college education or higher. The time since ALS diagnosis ranged from one month to 24 years. The median time since diagnosis (i.e., duration) was three years, the mean duration was approximately four years (M=4.4, SD=4.0). About a half of the sample reported they used a wheelchair usually or always, and about 20 percent reported no restrictions in mobility. Eighty-one percent of the respondents filled out the survey independently while 19 percent reported that they required assistance from others. One-half of the participants were taking Riluzole. The majority of participants (69 percent) reported that they live in the Unted States, 8 percent in Canada, and 5 percent in Australia. Six percent of the participants live in Europe, while the rest (12 percent) of the respondents reported that they were from Africa, India, Israel, Brazil, Ecuador, Guatemala, or Argentina. Fifty-three participants (41 percent) reported drinking alcohol, 14 (11 percent) reported that they use tobacco, and four (3 percent) reported consuming both alcohol and tobacco. Use of cannabis Seventy-seven respondents (60 percent) reported that they never used cannabis, and 41 (31 percent) used cannabis in teenage or college years only. Thirteen respondents (10 percent) reported using cannabis in the last 12 months, and their demographics are outlined in Table 2. Those who reported using cannabis in the last 12 months were all male and all lived in the US. Ten of those who reported using cannabis in the last 12 months also responded affirmatively to the question that asked about the use of cannabis during the teenage, college, and adult years. All of those who reported using cannabis in the last 12 months also reported that they used cannabis at some point in their lives before they were diagnosed with ALS. Six of the cannabis users reported that they lived in a state where medical cannabis is legal, and four lived in a state where medical cannabis is illegal. The remaining three respondents were not sure whteher medical cannabis was legal in their state. There were no statistcally significant differences between the cannabis users and non-users (see Table 2) on any demographic variable (age, marital status, employment status, education level, time since diagnosis, mobility status). None of those who reported using cannabis in the past 12 months reported tobacco use, but all reported drinking alcohol. Eight cannabis users reported smoking cannabis in the last three months. Two respondents reported smoking cannabis infrequently (less often than once a month), one reported smoking one to two times a week, and three reported daily use. No respondents reported only breathing vaporized cannabis, although one participant reported using vaporized cannabis in addition to smoking and using medicinal cannabis. Two participants reported eating cannabis, one in addition to smoking it. Three respondents used medicinal cannabinoids (i.e., Dronabinol). Of the three respondents who used medicinal cannabinoids, one reported using only medicinal cannabinoids, one also smoked cannabis, and one both smoked as well as breathed vaporized cannabis. Symptoms The intensity of ALS-related symptoms was quantified by asking respondents to rate how much they experience each of the symptoms on a five-point scale ranging from "not at all" (0) to "very much" (4). The most frequent sympotm was weakness, followed by speech difficulties, drooling and swalowing difficulties. The intnesity of symptoms reported by respondents who did not use cannabis was not statistically significantly idfferent from the symptom intensity reported by the cannabis users [F(10, 120)=120) 1.07,=1.07, p=.39]. A summary of symptoms and their intensity is listed in Table 3. The ammount of relief attributed to cannabis use was assessed by asking the respondents to rate the degree to which cannabis alleviates each symptom on a five-point scale ranging from "not at all" (0) to "completely relieves the symptom" (4). Respondents reported that the use of cannabis helped moderately for depression, appetite loss, spasticity, drooling, and pain. All cannabis users who reported symptoms of appetite loss and depression also reported that cannabis reduced these symptoms. None of the cannabis users reported any reduction in difficulties with swallowing and speech or sexual dysfunction. The duration of symptom relief was measured on a scale from 0 (no relief) to 6 (more than nine hours). Respondents reported the most lasting relief (on average two to three hours) for depression. The loss of appetite, drooling, shortness of breath, spasticity, and pain were reported to be relieved on average for approximately one hour or less. Table 4 provides a summary of symptoms reported by the cannabis users. Level of relief was reported on a five-point scale ranging from "not at all" (0) to "completely relieves the symptom" (4). The duration of sumptom relief was measured on a scale from "no relief" (0), "less than one hour" (1), "two to three hours" (2), "four to five hours" (3), "six to seven hours" (4), "eight to nine hours" (5), "more than nine hours" (6). Discussion There is an increasing amount of research concerning the medicinal effects of cannabinoids. For example, cannabinoids have been reported to reduce chemotherapy-induced nausea and vomiting, lower intraocular pressure in patients with glaucoma, reduce anorexia in patients with cancer and AIDS-associated weight loss, and reduce pain and spasticity in MS.30-39 Cannabinoids, the active ingredients in marijuana, may also have properties that may be applicable to the management of ALS.9,10 However, to date no empirical studies of use and effectiveness of cannabis for symptom management by PALS have been published. Approximately 10 percent of the survey respondents reported using cannabis. This is a lower rate than the frequency of use reported by other patient populations, including MS, AIDS, and cancer patients.10,30,31 However, the pattern of symptom relief reported by the small number of PALS who reported using cannabis for symptom management by people with other conditions, including MS.30,35,36 Cannabis users reported that cannabis smoking was most effective at reducing depression, appetite loss, pain, spasticity, drooling, and weakness. The factor that most predicted current use of cannabis by PALS was reported previous use (presumably recreational). The survey had a number of limitations. First, the survey results reported here are based on a relatively small number of respondents (131) and on reports of 13 cannabis users, and may not be representative of the patterns of cannabis use in the ALS population by people with ALS in general. Second, 75 percent of the respondents were male, 25 percent were female. Men appear to be about 1.5 times more likely to be affected with ALS than women,7,8 so the percentage of female participants is slightly lower than expected in the general ALS population (about 33 percent). Published studies of Internet use consistently report that females are less likely to use the Internet for reasons that may be independent of income and estimate that only about one-third of Internet users are women.47,48 This may account for the lower than expected participation by women with ALS. A third limitation of the study is that a disproportionate number of the survey respondents were white (90 percent) and all cannabis users were white. There is some evidence that whites may be at higher risk for ALS though most researchers agree that ALS equally affects people of all races.49,50 Racial discrepancies in rates of ALS may be due to poorer access to healthcare for minority populations in the US, particularly access to tertiary referral centers, where the ALS diagnosis is often made. Published studies report that over 80 percent of Internet users are white;48 this is the most likely explanation for the disproportionate perticipation by Caucasians in this survey. Fourth, Internet users tend to be highly educated. Almost 60 percent repoert having at least one degree.48 Those with higher education are more likely to own computer equipment and to use it to connect to the Internet.51 The results of the survey we report here provide further evidence for this trend, with only 13 respondents (10 percent) reported having high school education or less. Finally, none of the participants from the countries where cannabis use is prevalent (India) or legal for medical uses (Australia, Canada) reported using cannabis. The most likely explanation for this finding is the small number of perticipants from these countries; only one respondent was from India, six from Australia, and eleven from Canada. In general, professionals with university degrees living in households with disposable incomes sufficient to purchase technology tools are likely to be over-represented in Internet surveys. Women, minorities, the elderly, those who liveon social assistance disability payments, or who earn minimum wages, are much less likely to participate.48,51 Privacy is a major issue associated with Web-based methodology. When the Internet is used for research, especially for research on sensitive issues (such as using substances that are illegal under federal law and most state laws), protecting the privacy of the participants is paramount. By making the survey anonymous, the authors protected the privacy of the respondents but gave up the ability to verify respondent' diagnoses or prevent repeated or malicious submittals. Although the records showed that no two responses were submitted from the same IP address, the IP address identifies the computer, not the user. Therefore, it cannot be conclusively determined that one respondent did not submit more than one response using different computers. The low response rate might be explained by many factors. First, we do not know how many participants in the electronic discussion list that was used to recruit participants have ALS. It is possible, even likely, that a large majority of the participants are family members, service providers, and advocates. Second, the respondents who do not use alternative therapies may have been less likely to respond. It is unclear what percentage of people with ALS use alternative therapies. A recent survey from Germany suggests that about half of the ALS patients there use complementary and alternative medicine.52 Some respondents who do not use alternative therapies such as vitamins and supplements, but do use cannabis to manage their symptoms may not have considered cannabis to be an "alternative therapy" and decided not to participate. Many respondents provided information on vitamins, supplements, and other alternative therapies in the write-in spaces of the survey even though they were nto asked about these therapies directly, probably because the respondents had anticipated the survey would gather informationon those topics. Third, even though the invitation as well as the introduction to the survey clearly stated that the survey was anonymous and there was no way for the researchers to associate a specific response with a specific respondent, many may have been individuals who are generally suspicious of providing information via the Internet and may have decided not to participate for this reason. Despite the limitations of this study noted above, these preliminary findings support the need for further research into the potential benefits of cannabis use for the clinical management of some ALS symptoms. These include pain, which was one of the symptoms identified in a recent study as not being sufficiently addressed in ALS.53 Further research is needed to see if the current findings can be confirmed using non-Internet-based survey methodology with a defined sample. It would also be informative to inquire about cannabis use within the context of subject beliefs about the efficacy of various alternative and complimentary approaches and their engagement and satisfaction with those approaches. Acknowledgements Funding for this research was provided by grants from the National Institute on Disability and Rehabilitation Research, Washington, DC and from the National Institutes of Health References 1. Norris F, Sheperd R, Denys E, Et al.: Onset, natural history and outcome in idiopathic adult motor neuron disease. J Neurol Sci. 1993; 118(1); 48-55. 2. Ringel SP, Murphy JR, Alderson MK, et al.: The natural history of amyotrophic lateral sclerosis. Neurology. 1993; 43(7): 1316-1322. 3. Neilson S, Tobinson I, Nymoen EH: Longitudinal analysis of amyotrophic lateral sclerosis mortality in Norway, 1966-1989: Evidence for a susceptible subpopulation. J Neurol Sci. 1994; 122(2): 148-154. 5. Eisen A: Amyotropic lateral sclerosis is a multifactorial disease. Muscle Nerve. 1995; 18(7): 741-752. 6. Eisen A, Schulzer M, MacNeil M, et al.: Duration of amyotrophic lateral sclerosis is age dependent. Muscle Nerve. 1993; 16: 27-32. 7. Carter GT, Miller RG: Comprehensive management of amyotrophic lateral sclerosis. Phys Med Rehabil Clin N Am. 1998; 9(1): 271-284. 8. Carter GT, Krivickas LS: Adult motor neuron disease. In Kirshblum S, Campagnolo DL, DeLisa JA, (eds.): Spinal Cord Injury Medicine. Philadelphia: Lippincott, Williams, and Wilkins, 2002. 9. Carter GT, Rosen BS: Marijuana in the management of amyotrophic lateral sclerosis. Am J Hosp Palliat Care. 2001; 18(4): 264-270. 10. Carter GT, Weydt P. Cannabis: Old medicine with new promise for neurological disorders. Curr Opin Investig Drugs. 2002; 3(3): 437-440. 11. Weydt P, Weiss MD, Moller T, et al.: Neuroinflammation as a therapeutic target in amyotrophic lateral sclerosis. Curr Opin Investig Drugs. 2002; 3(12): 1720-1724. 12. Hampson AJ, Grimaldi M, Axelrod J, et al.: Cannabidiol and (-)Delta9-tetrahydrocannabinol are neuroprotective antioxidants. Proc Natl Acad Sci USA 1998; 95(14): 8268-8273. 13. Hampson AH, Grimaldi M, Lolic M, et al.: Neuroprotective antioxidants from marijuana. Ann NY Acad Sci. 2000; 899: 274-282. 14. Nagayama T, Sinor AD, Simon RP, et al.: Cannabinoids and neuroprotection in global and focal cerebral ischemia and in neuronal cultures. J Neurosci. 1999; 19(8): 2987-2995. 15. Chen Y, Buck J: Cannabinoids protect cells from oxidative cell death: A receptor-independent mechanism. J Pharmacol Exp Ther. 2000; 293(3): 807-812. 16. Eshhar N, Striem S, Biegon A: HU-211, a non-psychotropic cannabinoid, rescues cortical neurones from excitatory amino acid toxicity in culture. Neuroreport. 1993; 5(3): 237-240. 17. Adams IB, Martin BR: Cannabid: Pharmacology and toxicoloty in animals and humans. Addiction. 1996; 91(11): 1585-1614. 18. Agurell S, Halldin M, Lindgren Je, et al.: Pharmacokinetics and metabolism of delta 1-tetrahydrocannabinol and other cannabinoids with emphasis on man. Pharmacol Rev. 1986; 38(1): 21-43. 19. Johansson E, Halldin MM, Agurell S, et al.: Terminal elimination plasma half-life of delta 1-tetrahydrocannabinol (delta 1-THC) in heavy users of Marijuana. Eur J Clin Pharmacol. 1989; 37(3): 273-277. 20. Thomas BF, Adams IB, Mascarella SW, et al.: Structure-activity analysis of anandamide analogs: Relationship to a cannabinoid pharmacophore. J Med Chem. 1996, 39(2): 471-497. 21. Mechoulam R, Davane WA, Breuer A, et al.: A random walk whrough a cannabis field. Special Issue: Pharmacological, chemical, biochemical and behavioral research on cannabis and the cannabinoids. Pharmacol Biochem Behav. 1991; 40(3): 461-464. 22. Conrad C: Hemp for Health: The Medicinal and Nutritional Uses of Cannabis Sativa. Rochester, Vermont: Healing Arts Press, 1997. 23. Jones RT: Drug of abuse profile: Cannabis. Clin Chem. 1987; 33(11 Suppl): 72B-81B. 24. Jones RT, Beonwitz NL, Herning RI: Clinical relevance of cannabis tolerance and dependence. J Clin Pharmacol.. 1981; 21: 143S-152S. 25. Polen MR, Sidney S, Tekawa IS, et al.: Health care use by frequent marijuana smokers who do not smoke tobacco. West J Med. 1993; 158(6): 596-601. 26. Pope HG, Yurgelun-Todd D: The residual cognitive effects of heavy marijuana use in college students. JAMA 1996; 275(7): 521-527. 27. Renn E, Mandel S, Mandel E: The medicinal uses of marijuana. Pharm Ther. 2000; 25(10: 536-524. 28. Gurley RJ, Aranow R, Katz M: Medicinal marijuana: A comprehensive review. J Psycho-active Drugs. 1998; 30(2): 137-147. 29. Voth EA, Schwartz RH: Medicinal applications of delta-9-tetrahydrocannabinol and marijuana. Ann Intern Med. 1997; 126(10): 791-798. 30. Cosroe P, Musty R, Rein J, et al.: The perceived effects of smoked cannabis on patients with multiple sclerosis. Eur Neurol. 1997; 38: 44-48 31. Beal JE, Olson DO, Laubenstein L, et al.: Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS. J Pain Symptom Manage. 1995; 10: 89-97. 32. Foltin RW, Fischman MW, Byrne MF: Effects of smoked marijuana on food intake and body weight of humans living in a residential laboratory. Appetite. 1988; 11: 1-14. 33. Greenberg I, Kuehnle J, Mendelson JH: Effects of marijuana use on body weight and caloric intake in humans. Psychopharmacology (Berl). 1976; 49: 79-84. 34. Nelson K, Walsh D, Deeter P, et al.: A phase II study of delta-9-tetrahydrocannabinol for appetite stimulation in cancer-associated anorexia. J Palliat Care. 1994; 10(1): 14-18. 35. Meinck HM, Schonle PW, Conrad B: Effects of cannabinoids on spasticity and ataxia in multiple sclerosis. J Neurol. 1989; 263(2): 120-122. 36. Greenberg HS, Weiness AS, Pugh JE: Short term effects of smoking marijuana on balance in patients with multiple sclerosis and normal volunteers. Clin Pharmacol Ther. 1994; 55: 324-328. 37. Renn E, Mandel S, Mandel E: The medicinal uses of marijuana. Pharm Ther. 2000; 25(10): 536-524. 38. Gurley RJ, Aranow R, Katz M: Medicinal marijuana: A comprehensive review. J Psychoactive Drugs. 1998; 30(2): 137-147. 39 Voth EA, Schwartz RH: Medicinal applications of delta-9-tetrahydrocannabinol and marijuana. Ann Intern Med. 1997; 126(10): 791-798. 40. Meng Id, Manning BH, Martin WJ, et al.: An analgesia circuit activated by cannabinoids. Nature. 1998; 395(6700): 381-383. 41. Noyes R, Brunk SF, Baram DA, et al.: Analgesic effect of delta-9-tetrahydrocannabinol. J Clin Pharmacol. 1975a; 15(2-3): 139-143. 42. Zeltser R, Seltzer Z, Eisen A, et al.: Suppression of neuropathic pain behavior in rats by a non-psychotropic synthetic cannabinoid with NMDA receptor-blocking properties. Pain. 1991; 47(1): 95-103. 43. Noyes R, Brunk SF, Avery DAH, et al.: The analgesic properties of delta-9-tetrahydracannabinol. Clin Pharmacol Ther. 1975b; 18(1):84-89. 44. Richardson JD. Cannabinoids modulate pain by multiple mechanisms of action. J Pain. 2000; 1(1): 1-20. 45. Carter GT, Butler LM, Abresch RT, et al.: Expanding the role of hospice in the care of amyotrophic lateral sclerosis. Am J Hosp Palliat Care. 1999; 16(6): 707-710. 46. National Institute on Drug Abuse. Reserach Report Series: Marijuana Abuse. Bethesda, MD: National Institutes on Health, 2003. 47. Edsworth SM: World Wide Web: Opportunities, challenges, and threats. Lupus. 1999; 8: 596-605. 48. Kehoe C, Pitkow J, Sutton K, et al.: Results of GVU's Tenth World Wide Web User Survey. Georgia Institute of Technology, Graphics Visualization and Usability Center, College of Computing, Atlanta, Georgia. Available at WWW.gvu.gatech.edu/user_surveys/survey-1998-10/tenthreport.html. Accessed May 14, 1999. 49. Leone M, Chandra V, Schoenberg BS: Motor neuron disease in the United States, 1971 and 1973-1978: Patterns of mortality and associated conditions at the time of death. Neurology. 1987; 37(8): 1339-1343. 50. Lilenfeld DE, Chan E, Ehland J, et al.: Rising mortality from motoneuron disease in the USA, 1962-84. Lancet. 1989; 1(8640): 710-713. 51. Kaye S: Computer and Internet Use Among People with Disabilities. Washington, DC: NIDRR, US Dept. of Education, 2000. 52. Wasner M, Klier H, Borasio GD: The use of alternative medicine by patients with amyotrophic lateral sclerosis. J Neurol Sci. 2001; 191(1-2): 151-154. 53. Mandler RN, Anderson FA, Miller RG, et al.: ALS C.A.R.E. Study Group. The ALS patient care database: insights in to end-of-life care in ALS. Amyotroph Lateral Scler Other Motor Neruon Disord. 2001; 2(4): 203-208 source: http://www.cannabism...rts/carter4.php Amyotrophic lateral sclerosis: delayed disease progression in mice by treatment with a cannabinoid. Raman C, McAllister SD, Rizvi G, Patel SG, Moore DH, Abood ME. Forbes Norris MDA/ALS Research Center, 2351 Clay Street, Suite 416, California Pacific Medical Center, San Francisco, CA 94115, USA. Effective treatment for amyotrophic lateral sclerosis (ALS) remains elusive. Two of the primary hypotheses underlying motor neuron vulnerability are susceptibility to excitotoxicity and oxidative damage. There is rapidly emerging evidence that the cannabinoid receptor system has the potential to reduce both excitotoxic and oxidative cell damage. Here we report that treatment with Delta(9)-tetrahydrocannabinol (Delta(9)-THC) was effective if administered either before or after onset of signs in the ALS mouse model (hSOD(G93A) transgenic mice). Administration at the onset of tremors delayed motor impairment and prolonged survival in Delta(9)-THC treated mice when compared to vehicle controls. In addition, we present an improved method for the analysis of disease progression in the ALS mouse model. This logistic model provides an estimate of the age at which muscle endurance has declined by 50% with much greater accuracy than could be attained for any other measure of decline. In vitro, Delta(9)-THC was extremely effective at reducing oxidative damage in spinal cord cultures. Additionally, Delta(9)-THC is anti-excitotoxic in vitro. These cellular mechanisms may underlie the presumed neuroprotective effect in ALS. As Delta(9)-THC is well tolerated, it and other cannabinoids may prove to be novel therapeutic targets for the treatment of ALS. source: http://www.ncbi.nlm....Pubmed_RVDocSum
  10. http://www.youtube.com/watch?v=yj72e5q61Fs Marijuana and ADD By: Kort E Patterson Year Written: 2000 Therapeutic uses of Medical Marijuana in the treatment of Attention Deficit Disorder --------------------------------- Note: The following research was part of a petition filed in 1999 to add Attention Deficit Disorder to the Oregon Medical Marijuana Act. The Oregon Health Division continues to refuse to add mental conditions such as ADD to the list of OMMA "covered conditions". The Health Division claims that medical marjuana isn't effective for mental conditions even though the primary justification for marijuana prohibition is its alleged psycho-active effectiveness. --------------------------------- At first glance it might seem counter-intuitive to use a medication that has a public perception of decreasing attention to treat a condition whose primary symptom is a deficit of attention. But just as taking stimulants often calms those with hyperactivity, medical marijuana improves the ability to concentrate in some types of ADD. Categorizing The Condition Attention Deficit Disorder (ADD) is a very broad category of conditions that share some symptoms but appear to result from different underlying causes. Most seem to involve, at least in part, imbalances in neural transmitter levels and functions. Some experts in the field expect that the broad category of ADD will be refined in the future, with many conditions that are now diagnosed as ADD being recognized as separate disorders. The particular type of ADD under consideration for treatment with medical marijuana might better be termed "Racing Brain Syndrome" (RBS). A useful analogy for this mental condition is that of a centrifugal pump that is being over-driven. As the pump speed increases, cavitation sets in and the pump's output decreases. The faster the pump is driven the greater the cavitation until a point is reached where large amounts of energy are being input but nothing is being output. Without medication there is a sensation that thoughts flash through the brain too fast to "think" them. Medical marijuana slows the brain down sufficiently to achieve impressive improvements in functionality. This syndrome probably only afflicts a small minority of all those diagnosed with ADD. The condition doesn't respond to the standard ADD medications, indicating that it results from different underlying processes than other forms of ADD. Individuals with types of ADD that do respond to the standard ADD medications also tend to have a far different reaction to medical marijuana than those with RBS. At this point in our limited understanding of the condition, it appears that RBS would make a good candidate to be redefined as a separate condition outside of the general diagnosis of ADD. Treating ADD/RBS With Medical Marijuana There is some evidence available that medical marijuana has been found to be an effective medication for some types of ADD by other researchers in the field.(1) Unfortunately, ADD encompasses such a variety of conditions that the limited amount of research in the field leaves many of the effective therapeutic mechanisms under-investigated. Considering the regulatory difficulties in researching the effects of medical marijuana, it isn't surprising that the information regarding medical marijuana and ADD is largely anecdotal(2). Individuals with RBS tend to have a very low tolerance for most stimulants, and report even caffeine aggravates their disorder. The one exception appears to be low doses of Dextrostat. While Dextrostat does have a calming effect, it fails to address the higher level mental functions needed for complex intellectual demands. Larger doses of Dextrostat tend to produce undesirable mental and physical stimulation, greatly limiting the level of medication that can be tolerated. Medical marijuana remains the only single medication that provides an adequate solution for RBS, and remains a necessary component in a multi-drug approach. Dextrostat does appear to reduce the amount of medical marijuana needed by individuals with RBS to achieve a functional mental state. This reduction probably justifies continuing with Dextrostat as a means of reducing the quantity of medical marijuana that must consumed, as well as allow those with RBS to gain the maximum benefit possible within the quantity limitations of the OMMA. The green leaves of certain strains of medical marijuana appear to provide the best therapeutic effects for RBS. Experiments with Marinol seem to indicate that THC is involved, but is not the primary therapeutic agent. The therapeutic agent(s) most useful in treating RBS appear to be present in relatively low concentrations in medical marijuana. As such those with this condition must consume a larger quantity of medical marijuana in order to ingest a sufficient dosage of the target agent(s). This would explain why dried low-THC green leaves appear to be the most effective treatment. The patient can consume enough of this low-THC marijuana to acquire the levels of the needed active agent(s) necessary to treat the condition without in the process consuming sufficient THC to become intoxicated. Underlying Cause of RBS It has long been suspected that RBS involved a deficit of one or more neural transmitters. It was observed as long ago as the 1970's that high levels of adrenaline had a residual therapeutic effect in those with RBS. The effect was first noted in those engaged in such activities as skydiving. Individuals with RBS reported that their mental functions were improved in the days following skydiving. It was first assumed that adrenaline stimulated the production of all neural transmitters - including those that were in deficit. It's now thought that while adrenaline initially acts as a stimulant of neural transmitter production, it has a secondary effect of depleting neural transmitters. The limited effectiveness of Dextrostat, as well as additional information about the secondary effects of adrenaline, suggests the possibility that at least part of the underlying cause of RBS may also be a surplus of one or more neural transmitters. The partial solution offered by Dextrostat also suggests that at least some part of the condition results from those neural transmitters and/or hormones that are influenced by both Dextrostat and medical marijuana. The failure of Dextrostat to provide a complete solution suggests two possible alternatives: (1) that the effects of Dextrostat and medical marijuana are additive - with both influencing the same neural transmitters and/or hormones, and together delivering the required level of therapeutic effect; or (2) that the condition is the result of multiple imbalances, some of which are unaffected by Dextrostat, but all of which appear to be affected by medical marijuana. Potential Beneficial Therapeutic Effects The research that has been done on the therapeutic effects of medical marijuana on other conditions provides a number of potential mechanisms that may be involved in RBS. The following are documented effects of medical marijuana that appear to have some potential for involvement. Perhaps the most obvious possibility is suggested by the fact that both Dextrostat and medical marijuana influence the release and/or functions of serotonin(3)(4). Since both Dextrostat and medical marijuana appear to decrease the apparent availability and effectiveness of serotonin, it would appear possible that a surplus of serotonin is involved in some way. There are over 60 cannabinoids and cannabidiols present in medical marijuana. The effect of most of these substances is at present largely unknown.(5) The discovery of a previously unknown system of cannabinoid neural transmitters is profound.(6) The different cannabinoid receptor types found in the body appear to play different roles in normal human physiology.(5) An endogenous cannabinoid, arachidonylethanolamide, named anandamide, has been found in the human brain. This ligand inhibits cyclic AMP in its target cells, which are widespread throughout the brain, but demonstrate a predilection for areas involved with nociception. The exact physiological role of anandamide is unclear, but preliminary tests of its behavioral effects reveal actions similar to those of THC.(7) Cannabinoid receptors appear to be very dense in the globus pallidus, substantia nigra pars reticulata (SNr), the molecular layers of the cerebellum and hippocampal dentate gyrus, the cerebral cortex, other parts of the hippocampal formation, and striatum - with the highest density being in the SNr. The Neocortex has moderate receptor density, with peaks in superficial and deep layers. Very low and homogeneous density was found in the thalamus and most of the brainstem, including all of the monoamine containing cell groups, reticular formation, primary sensory, visceromotor and cranial motor nuclei, and the area postrema. The hypothalamus, basal amygdala, central gray, nucleus of the solitary tract, and laminae I-III and X of the spinal cord showed slightly higher but still sparse receptor density.(5) While there are cannabinoid receptors in the ventromedial striatum and basal ganglia, which are areas associated with dopamine production, no cannabinoid receptors have been found in dopamine-producing neurons. According to the congressional Office of Technology Assessment, research over the last 10 years has proved that marijuana has no effect on dopamine-related brain systems.(6) However, cannabidiol has been shown to exert anticonvulsant and antianxiety properties, and is suspected by some to exert antidyskinetic effects through modulation of striatal dopaminergic activity.(3) It's been suggested that the cannabinoid receptors in the human brain play a role in the limbic system, which in turn plays a central role in the mechanisms which govern behavior and emotions. The limbic system coordinates activities between the visceral base-brain and the rest of the nervous system. Cannabis acts on memory by way of the receptors in the limbic system's hippocampus, which "gates" information during memory consolidation.(6) In addition, some effects of cannabinoids appear to be independent of cannabinoid receptors. The variety of mechanisms through which cannabinoids can influence human physiology underlies the variety of potential therapeutic uses for medical marijuana.(8) When the effects of cannabis on a "normal" brain are tracked on an electroencephalogram (EEG), there is an initial speeding up of brain wave activity and a reactive slowing as the drug effects wear off. The higher the dosage, the more intense the effects and longer the experience. There is an increase in mean-square alpha energy levels and a slight slowing of alpha frequency.(5) There is also an increase of beta waves reflecting increased cognitive activity. The distortion of time resulting from the "speeding up of thoughts" causes a subjective perception that there is a slowing of time.(9) As the cannabis effects wear off, stimulation gives way to sedation. The cognitive activity of the beta state gives way to alpha and theta frequencies. Theta waves are commonly associated with visual imagery. These images interact with thinking and disrupt the train of thought. Thinking can be distracted by these intrusions, with thought contents being modified to some extent depending on dose, expectations, setting, and personality.(9) Cannabis decreases emotional reactivity and intensity of affect while increasing introspection as evidenced by the slowing of the EEG after initial stimulation. Obsessive and pressured thinking is replaced by introspective free associations. Emotional reactivity is moderated and worries become less pressing.(10) Cannabis causes a general increase in cerebral blood flow (CBF). This increase in blood circulation is due to decreased peripheral resistance, which is in turn due to the dilation of the capillaries in the cerebral cortex. Changes in CBF affect the mental processes of the brain, with increases stimulating cognition, while decreases accompany sedation.(9) Relative Safety of Medical Marijuana "Marijuana is the safest therapeutically active substance known to man... safer than many foods we commonly consume." DEA Judge Francis L. Young, Sept. 6, 1988 "After carefully monitoring the literature for more than two decades, we have concluded that the only well-confirmed deleterious physical effect of marihuana is harm to the pulmonary system." Grinspoon M.D., James B. Bakalar, Medical Marijuana has been in use for thousands of years, and in spite of substantial efforts to find adverse effects, it remains the safest medication available for RBS. There has never been a single known case of lethal overdose. The ratio of lethal to effective dose for medical marijuana is estimated to be as 40,000 to 1. By comparison, the ratio is 3-50 to 1 for secobarbital and 4-10 to 1 for alcohol.(11) During the 1890s the Indian Hemp Drugs Commission interviewed some eight hundred people and produced a report of more than 3000 pages. The report concluded that "there was no evidence that moderate use of cannabis drugs produced any disease or mental or moral damage, or that it tended to lead to excess any more than the moderate use of whiskey."(12) The Mayor's Committee on Marihuana examined chronic users in New York City who had averaged seven marihuana cigarettes a day for eight years and "showed no mental or physical decline."(13) Several later controlled studies of chronic heavy use failed to establish any pharmacologically induced harm.(14) A subsequent government sponsored review of cannabis conducted by the Institute of Medicine, a branch of the National Academy of Sciences, also found little evidence of its alleged harmfulness.(15) Several studies in the United States found that fairly heavy marihuana use had no effects on learning, perception, or motivation over periods as long as a year.(16) Studies of very heavy smokers in Jamaica, Costa Rica, and Greece "found no evidence of intellectual or neurological damage, no changes in personality, and no loss of the will to work or participate in society."(17) The Costa Rican study showed no difference between heavy users (seven or more marihuana cigarettes a day) and lighter users (six or fewer cigarettes a day).(18) In addition, none of the studies involving prolonged and heavy use of medical marijuana have shown any effects on mental abilities suggestive of impairment of brain or cerebral function and cognition.(2) The inhalation of the combustion products of burning plant material is the cause of the only well-confirmed deleterious physical effects of medical marijuana. These adverse effects can be eliminated by using one of the non-combustion means of ingesting the mediation. Marijuana can be eaten in foods or inhaled using a vaporizer. The therapeutic agents in medical marijuana vaporize at around 190 degrees centigrade, while it takes the heat of combustion of around 560 degrees centigrade to generate the harmful components of marijuana smoke. A vaporizer heats the medical marijuana to the point where the therapeutic agents are released and can be inhaled, without getting the plant material hot enough to burn.(19) Cannabis And Blood Pressure Research Proposal 1. Possible Therapeutic Cannabis Applications for Psychiatric Disorders, Tod H. Mikuriya, M.D. 2. Marihuana, The Forbidden Medicine, Lester Grinspoon M.D., James B. Bakalar, Yale University Press, 1997 3. MARIJUANA AND TOURETTE'S SYNDROME, Journal of Clinical Psychopharmacology, Vol. 8/No. 6, Dec 1988 4. CANNABINOIDS BLOCK RELEASE OF SEROTONIN FROM PLATELETS INDUCED BY PLASMA FROM MIGRAINE PATIENTS, Int J Clin Pharm. Res V (4) 243-246 (1985), Volfe Z., Dvilansky A., Nathan I. Blood Research, Faculty of Health Sciences, Soroka Medical Center, Ben-Gurion University of the Negev, P.O. Box 151, Beer-Sheva 84101, Israel. 5. Nelson, P. L. (1993). A critical review of the research literature concerning some biological and psychological effects of cannabis. In Advisory Committee on Illicit Drugs (Eds.), Cannabis and the law in Queensland: A discussion paper (pp. 113-152). Brisbane: Criminal Justice Commission of Queensland. 6. Marijuana And the Brain, by John Gettman, High Times, March, 1995 7. Cannabis for Migraine Treatment: The Once and Future Prescription?: An Historical and Scientific Review; Ethan B. Russo, M.D. 8. Marijuana and Medicine, Assessing the Science Base, Janet E. Joy, Stanley J. Watson, Jr., and John A. Benson, Jr., Editors Division of Neuroscience and Behavioral Health, INSTITUTE OF MEDICINE 9. Marijuana Medical Handbook, by Tod Mikuriya, M.D. 10. Medicinal Uses of Cannabis, Tod H. Mikuriya, M.D. ©1998 11. Marihuana as Medicine: A Plea for Reconsideration; Lester Grinspoon M.D., James B. Bakalar; Journal of the American Medical Association (JAMA); June 1995 12. Report of the Indian Hemp Drugs Commission, 1893-1894, 7 vols. (Simla: Government Central Printing Office, 1894); D. Solomon, ed., The Marihuana Papers (Indianapolis: Bobbs-Merrill, 1966). 13. Mayor's Committee on Marihuana, The Marihuana Problem in the City of New York (Lancaster, Pa.: Jacques Cattell, 1944). 14. M. H. Beaubrun and F Knight, "Psychiatric Assessment of Thirty Chronic Users of Cannabis and Thirty Matched Controls," American journal of Psychiatry 130 (1973): 309; M. C. Braude and S. Szara, eds., The Pharmacology of Marihuana, 2 vols. (New York: Raven, 1976); R. L. Dombush, A. M. Freedman, and M. Fink, eds., "Chronic Cannabis Use," Annals of New Yorh Academy of Sciences 282 (1976); J. S. Hochman and N. Q. Brill, "Chronic Marijuana Use and Psychosocial Adaptation," American journal of Psychiatry 130 (1973):132; Rubin and Comitas, Ganja in Jamaica. 15. Institute of Medicine, Marijuana and Health (Washington, D.C.: National Academy of Sciences, 1982). 16. C. M. Culver and F W King, "Neurophysiological Assessment of Undergraduate Marihuana and LSD Users," Archives of General Psychiatry 31 (1974): 707-711; P.J. Lessin and S. Thomas, "Assessment of the Chronic Effects of Marijuana on Motivation and Achievement: A Preliminary Report," in Pharmacology of Marihuana, ed. Braude and Szara, 2:681-684. 17. Cognition and Long-Term Use of Ganja (Cannabis), Reprint Series, 24 July 1981, Volume 213, pp. 465-466 SCIENCE, Jeffrey Schaeffer, Therese Andrysiak, and J. Thomas Ungerleider Copyright 1981 by the American Association for the Advancement of Science 18. Rubin and Comitas, Ganja in Jamaica; W E. Carter, ed., Cannabis in Costa Rica: A Study of Chronic Marihuana Use (Philadelphia: Institute for the Study of Human Issues, 1980); C. Stefariis, J. Boulougouris, and A. I-iakos, "Clinical and Psychophysiological Effects of Cannabis in Long-term Users," in Pharmacology of Marihuana, ed. Braude and Szara, 2:659-666; P Satz, J. M. Fletcher, and L. S. Sutker, "Neurophysiologic, Intellectual, and Personality Correlates of Chronic Marihuana Use in Native Costa Ricans," Annals of the New York Academy of Sciences 282 (1976): 266-306. 19. Is Marijuana The Right Medicine For You?; Bill Zimmerman Ph.D., Rick Bayer M.D., and Nancy Crumpacker M.D.; (1998): pp. 125; Keats Publishing Inc. source: http://www.kortexplores.com/node/133 © International Association for Cannabis as Medicine1Case report Cannabis improves symptoms of ADHD http://66.218.69.11/...&...=1&.intl=us Cannabis as a medical treatment for attention deficit disorder "Why would anyone want to give their child an expensive pill... with unacceptable side effects, when he or she could just go into the backyard, pick a few leaves off a plant and make tea for him or her instead? Cannabinoids are a very viable alternative to treating adolescents with ADD and ADHD" WASHINGTON - As a California pediatrician and 49-year-old mother of two teenage daughters, Claudia Jensen says pot might prove to be the preferred medical treatment for attention deficit disorder - even in adolescents. While some wonder whether Jensen was smoking some wacky weed herself, the clinician for low-income patients and professor to first-year medical students at the University of Southern California said her beliefs are very grounded: The drug helps ease the symptomatic mood swings, lack of focus, anxiety and irritability in people suffering from neuropsychiatric disorders like ADD and attention deficit/hyperactivity disorder. "Cannabinoids are a very viable alternative to treating adolescents with ADD and ADHD.I have a lot of adult patients who swear by it." Under California state law, physicians are allowed to recommend to patients the use of cannabis to treat illnesses, although the federal government has maintained that any use of marijuana - medicinal or otherwise - is illegal. The federal courts have ruled that physicians like Jensen cannot be prosecuted for making such recommendations. Jensen said she regularly writes prescriptions recommending the use of cannabis for patients -particularly those suffering pain and nausea from chronic illnesses, such as AIDS, cancer, glaucoma and arthritis. She has also worked with one family of a 15-year-old - whose family had tried every drug available to help their son, who by age 13 had become a problem student diagnosed as suffering from ADHD. Under Jensen’s supervision, he began cannabis treatment, settling it on in food and candy form, and he has since found equilibrium and regularly attends school. But not everyone is so high on the idea of pot for students with neurological illnesses. Subcommittee Chairman Mark Souder, R-Ind., who invited Jensen to testify after reading about her ideas in the newspaper, was hardly convinced by her testimony. "I do believe that Dr. Jensen really wants to help her patients, but I think she is deeply misguided when she recommends cannabis to teenagers with attention deficit disorder or hyperactivity," he told Foxnews.com. "There is no serious scientific basis for using marijuana to treat those conditions, and Dr. Jensen didn’t even try to present one." Dr. Tom O’Connell, a retired chest surgeon who now works with patients at a Bay Area clinic for patients seeking medical marijuana recommendations, is working on it. He said cannabis not only helps pain, but also can treat psychological disorders. He is currently conducting a study of hundreds of his patients, whom he said he believes have been self-medicating with pot and other drugs for years, and he hopes to publish a paper on the subject soon. "My work with cannabis patients is certainly not definitive at this point, but it strongly suggests that the precepts upon which cannabis prohibition have been based are completely spurious," O’Connell said. Worse yet, he added, the prohibition has successfully kept certain adolescents away from pot who now turn to tobacco and alcohol instead. Jensen, who said she believes Souder invited her to testify to "humiliate me and incriminate me in some way," suggested that a growing body of evidence is being developed to back medical cannabis chiefly for chronic pain and nausea. She said it is difficult, however, for advocates like herself to get the funding and permission to conduct government-recognized tests on ADD/ADHD patients. "Unfortunately, no pharmaceutical companies are motivated to spend the money on research, and the United States government has a monopoly on the available cannabis and research permits," she told Congress. Studies done on behalf of the government, including the 1999 Institute of Medicine’s "Marijuana and Medicine: Assessing the Science Base," found that cannabis delivers effective THC and other cannabinoids that serve as pain relief and nausea-control agents. But these same studies warn against the dangers of smoking cannabis and suggest other FDA-approved drugs are preferable. "We know all too well the dangerous health risks that accompany (smoking)," said Rep. Elijah Cummings, D-Md., ranking member on the subcommittee, who like Souder, was not impressed by Jensen’s arguments. "It flies in the face of responsible medicine to advocate a drug that had been known to have over 300 carcinogens and has proven to be as damaging to the lungs as cigarette smoking," added Jennifer Devallance, spokeswoman for the White House Office of Drug Control Policy. The government points to Food and Drug Administration-approved Marinol, a THC-derived pill that acts as a stand-in for marijuana. But many critics say there are nasty side effects, and it’s too expensive for the average patient. On the other hand, Jensen and others say cannabinoids can be made into candy form, baked into food or boiled into tea. They say that despite the FDA blessing, giving kids amphetamines like Ritalin for ADD and other behavioral disorders might be more dangerous. "Ritalin is an amphetamine - we have all of these youngsters running around on speed," said Keith Stroup, spokesman for the National Organization for the Reform of Marijuana Laws. "Although it flies in the face of conventional wisdom, it’s nevertheless true that cannabis is far safer and more effective than the prescription agents currently advocated for treatment of ADD-ADHD," O’Connell said. Stroup said if Souder’s intention was to harangue Jensen, he was unsuccessful in the face of her solid and articulate testimony on April 1."It was a good day for her, and a good day for medical marijuana in Congress," he said. Nick Coleman, a subcommittee spokesman, said Souder doesn’t "try to humiliate people. "But to promote medical cannabis for teenagers with ADD... he does not feel that is a sound and scientific medical practice," Coleman said. While the issue of treating adolescents with medical marijuana is fairly new, the idea of using pot to treat chronically and terminally ill patients is not. Nine states currently have laws allowing such practices. A number of lawmakers on both sides of the aisle have added that they want the states to decide for themselves whether to pursue medical marijuana laws. Among those lawmakers are Reps. Ron Paul, R-Texas, a physician; Dana Rohrabacher, R-Calif.; and Barney Frank, D-Mass. "(Rep. Paul) believes there are some legitimate applications," like for pain and nausea, said spokesman Jeff Deist. "But the real issue is that states should decide for themselves." source: http://www.chanvre-i...-treatment.html Marijuana and ADD Therapeutic uses of Medical Marijuana in the treatment of Marijuana and ADD By Kort E Patterson Sam’s Story; Autism & Medical Marijuana Sam’s Story, Using Medical Cannabis to Treat Autism Spectrum Disorder ADD, ADHD & Medical Marijuana It was mentioned in the Portland newspaper that the Oregon Health Division is considering allowing medical marijuana to be used to treat Attention Deficit Disorder (ADD) under the Oregon Medical Marijuana Act. At first glance it might seem counter-intuitive to use a medication that has a public perception of decreasing attention to treat a condition whose primary symptom is a deficit of attention. But just as taking stimulants often calms those with hyperactivity, medical marijuana improves the ability to concentrate in some types of ADD. Categorizing The Condition Attention Deficit Disorder (ADD) is a very broad category of conditions that share some symptoms but appear to result from different underlying causes. Most seem to involve, at least in part, imbalances in neural transmitter levels and functions. Some experts in the field expect that the broad category of ADD will be refined in the future, with many conditions that are now diagnosed as ADD being recognized as separate disorders. The particular type of ADD under consideration for treatment with medical marijuana might better be termed "Racing Brain Syndrome" (RBS). A useful analogy for this mental condition is that of a centrifugal pump that is being over-driven. As the pump speed increases, cavitation sets in and the pump's output decreases. The faster the pump is driven the greater the cavitation until a point is reached where large amounts of energy are being input but nothing is being output. Without medication there is a sensation that thoughts flash through the brain too fast to "think" them. Medical marijuana slows the brain down sufficiently to achieve impressive improvements in functionality. This syndrome probably only afflicts a small minority of all those diagnosed with ADD. The condition doesn't respond to the standard ADD medications, indicating that it results from different underlying processes than other forms of ADD. Individuals with types of ADD that do respond to the standard ADD medications also tend to have a far different reaction to medical marijuana than those with RBS. At this point in our limited understanding of the condition, it appears that RBS would make a good candidate to be redefined as a separate condition outside of the general diagnosis of ADD. Treating ADD/RBS With Medical Marijuana There is some evidence available that medical marijuana has been found to be an effective medication for some types of ADD by other researchers in the field.(1) Unfortunately, ADD encompasses such a variety of conditions that the limited amount of research in the field leaves many of the effective therapeutic mechanisms under-investigated. Considering the regulatory difficulties in researching the effects of medical marijuana, it isn't surprising that the information regarding medical marijuana and ADD is largely anecdotal(2). Individuals with RBS tend to have a very low tolerance for most stimulants, and report even caffeine aggravates their disorder. The one exception appears to be low doses of Dextrostat. While Dextrostat does have a calming effect, it fails to address the higher level mental functions needed for complex intellectual demands. Larger doses of Dextrostat tend to produce undesirable mental and physical stimulation, greatly limiting the level of medication that can be tolerated. Medical marijuana remains the only single medication that provides an adequate solution for RBS, and remains a necessary component in a multi-drug approach. Dextrostat does appear to reduce the amount of medical marijuana needed by individuals with RBS to achieve a functional mental state. This reduction probably justifies continuing with Dextrostat as a means of reducing the quantity of medical marijuana that must consumed, as well as allow those with RBS to gain the maximum benefit possible within the quantity limitations of the OMMA. The green leaves of certain strains of medical marijuana appear to provide the best therapeutic effects for RBS. Experiments with Marinol seem to indicate that THC is involved, but is not the primary therapeutic agent. The therapeutic agent(s) most useful in treating RBS appear to be present in relatively low concentrations in medical marijuana. As such those with this condition must consume a larger quantity of medical marijuana in order to ingest a sufficient dosage of the target agent(s). This would explain why dried low-THC green leaves appear to be the most effective treatment. The patient can consume enough of this low-THC marijuana to acquire the levels of the needed active agent(s) necessary to treat the condition without in the process consuming sufficient THC to become intoxicated. Underlying Cause of RBS It has long been suspected that RBS involved a deficit of one or more neural transmitters. It was observed as long ago as the 1970's that high levels of adrenaline had a residual therapeutic effect in those with RBS. The effect was first noted in those engaged in such activities as skydiving. Individuals with RBS reported that their mental functions were improved in the days following skydiving. It was first assumed that adrenaline stimulated the production of all neural transmitters - including those that were in deficit. It's now thought that while adrenaline initially acts as a stimulant of neural transmitter production, it has a secondary effect of depleting neural transmitters. The limited effectiveness of Dextrostat, as well as additional information about the secondary effects of adrenaline, suggests the possibility that at least part of the underlying cause of RBS may also be a surplus of one or more neural transmitters. The partial solution offered by Dextrostat also suggests that at least some part of the condition results from those neural transmitters and/or hormones that are influenced by both Dextrostat and medical marijuana. The failure of Dextrostat to provide a complete solution suggests two possible alternatives: (1) that the effects of Dextrostat and medical marijuana are additive - with both influencing the same neural transmitters and/or hormones, and together delivering the required level of therapeutic effect; or (2) that the condition is the result of multiple imbalances, some of which are unaffected by Dextrostat, but all of which appear to be affected by medical marijuana. Potential Beneficial Therapeutic Effects The research that has been done on the therapeutic effects of medical marijuana on other conditions provides a number of potential mechanisms that may be involved in RBS. The following are documented effects of medical marijuana that appear to have some potential for involvement. Perhaps the most obvious possibility is suggested by the fact that both Dextrostat and medical marijuana influence the release and/or functions of serotonin(3)(4). Since both Dextrostat and medical marijuana appear to increase the apparent availability and effectiveness of serotonin, it would appear possible that a deficit of serotonin is involved in some way. There are over 60 cannabinoids and cannabidiols present in medical marijuana. The effect of most of these substances is at present largely unknown.(5) The discovery of a previously unknown system of cannabinoid neural transmitters is profound.(6) The different cannabinoid receptor types found in the body appear to play different roles in normal human physiology.(5) An endogenous cannabinoid, arachidonylethanolamide, named anandamide, has been found in the human brain. This ligand inhibits cyclic AMP in its target cells, which are widespread throughout the brain, but demonstrate a predilection for areas involved with nociception. The exact physiological role of anandamide is unclear, but preliminary tests of its behavioral effects reveal actions similar to those of THC.(7) Cannabinoid receptors appear to be very dense in the globus pallidus, substantia nigra pars reticulata (SNr), the molecular layers of the cerebellum and hippocampal dentate gyrus, the cerebral cortex, other parts of the hippocampal formation, and striatum - with the highest density being in the SNr. The Neocortex has moderate receptor density, with peaks in superficial and deep layers. Very low and homogeneous density was found in the thalamus and most of the brainstem, including all of the monoamine containing cell groups, reticular formation, primary sensory, visceromotor and cranial motor nuclei, and the area postrema. The hypothalamus, basal amygdala, central gray, nucleus of the solitary tract, and laminae I-III and X of the spinal cord showed slightly higher but still sparse receptor density.(5) While there are cannabinoid receptors in the ventromedial striatum and basal ganglia, which are areas associated with dopamine production, no cannabinoid receptors have been found in dopamine-producing neurons. According to the congressional Office of Technology Assessment, research over the last 10 years has proved that marijuana has no effect on dopamine-related brain systems.(6) However, cannabidiol has been shown to exert anticonvulsant and antianxiety properties, and is suspected by some to exert antidyskinetic effects through modulation of striatal dopaminergic activity.(3) It's been suggested that the cannabinoid receptors in the human brain play a role in the limbic system, which in turn plays a central role in the mechanisms which govern behavior and emotions. The limbic system coordinates activities between the visceral base-brain and the rest of the nervous system. Cannabis acts on memory by way of the receptors in the limbic system's hippocampus, which "gates" information during memory consolidation.(6) In addition, some effects of cannabinoids appear to be independent of cannabinoid receptors. The variety of mechanisms through which cannabinoids can influence human physiology underlies the variety of potential therapeutic uses for medical marijuana.(8) When the effects of cannabis on a "normal" brain are tracked on an electroencephalogram (EEG), there is an initial speeding up of brain wave activity and a reactive slowing as the drug effects wear off. The higher the dosage, the more intense the effects and longer the experience. There is an increase in mean-square alpha energy levels and a slight slowing of alpha frequency.(5) There is also an increase of beta waves reflecting increased cognitive activity. The distortion of time resulting from the "speeding up of thoughts" causes a subjective perception that there is a slowing of time.(9) As the cannabis effects wear off, stimulation gives way to sedation. The cognitive activity of the beta state gives way to alpha and theta frequencies. Theta waves are commonly associated with visual imagery. These images interact with thinking and disrupt the train of thought. Thinking can be distracted by these intrusions, with thought contents being modified to some extent depending on dose, expectations, setting, and personality.(9) Cannabis decreases emotional reactivity and intensity of affect while increasing introspection as evidenced by the slowing of the EEG after initial stimulation. Obsessive and pressured thinking is replaced by introspective free associations. Emotional reactivity is moderated and worries become less pressing.(10) Cannabis causes a general increase in cerebral blood flow (CBF). This increase in blood circulation is due to decreased peripheral resistance, which is in turn due to the dilation of the capillaries in the cerebral cortex. Changes in CBF affect the mental processes of the brain, with increases stimulating cognition, while decreases accompany sedation.(9) Relative Safety of Medical Marijuana "Marijuana is the safest therapeutically active substance known to man... safer than many foods we commonly consume." DEA Judge Francis L. Young, Sept. 6, 1988 "After carefully monitoring the literature for more than two decades, we have concluded that the only well-confirmed deleterious physical effect of marihuana is harm to the pulmonary system." Grinspoon M.D., James B. Bakalar, Medical Marijuana has been in use for thousands of years, and in spite of substantial efforts to find adverse effects, it remains the safest medication available for RBS. There has never been a single known case of lethal overdose. The ratio of lethal to effective dose for medical marijuana is estimated to be as 40,000 to 1. By comparison, the ratio is 3-50 to 1 for secobarbital and 4-10 to 1 for alcohol.(11) During the 1890s the Indian Hemp Drugs Commission interviewed some eight hundred people and produced a report of more than 3000 pages. The report concluded that "there was no evidence that moderate use of cannabis drugs produced any disease or mental or moral damage, or that it tended to lead to excess any more than the moderate use of whiskey."(12) The Mayor's Committee on Marihuana examined chronic users in New York City who had averaged seven marihuana cigarettes a day for eight years and "showed no mental or physical decline."(13) Several later controlled studies of chronic heavy use failed to establish any pharmacologically induced harm.(14) A subsequent government sponsored review of cannabis conducted by the Institute of Medicine, a branch of the National Academy of Sciences, also found little evidence of its alleged harmfulness.(15) Several studies in the United States found that fairly heavy marihuana use had no effects on learning, perception, or motivation over periods as long as a year.(16) Studies of very heavy smokers in Jamaica, Costa Rica, and Greece "found no evidence of intellectual or neurological damage, no changes in personality, and no loss of the will to work or participate in society."(17) The Costa Rican study showed no difference between heavy users (seven or more marihuana cigarettes a day) and lighter users (six or fewer cigarettes a day).(18) In addition, none of the studies involving prolonged and heavy use of medical marijuana have shown any effects on mental abilities suggestive of impairment of brain or cerebral function and cognition.(2) The inhalation of the combustion products of burning plant material is the cause of the only well-confirmed deleterious physical effects of medical marijuana. These adverse effects can be eliminated by using one of the non-combustion means of ingesting the mediation. Marijuana can be eaten in foods or inhaled using a vaporizer. The therapeutic agents in medical marijuana vaporize at around 190 degrees centigrade, while it takes the heat of combustion of around 560 degrees centigrade to generate the harmful components of marijuana smoke. A vaporizer heats the medical marijuana to the point where the therapeutic agents are released and can be inhaled, without getting the plant material hot enough to burn.(19) References: 1. Possible Therapeutic Cannabis Applications for Psychiatric Disorders, Tod H. Mikuriya, M.D. 2. Marihuana, The Forbidden Medicine, Lester Grinspoon M.D., James B. Bakalar, Yale University Press, 1997 3. MARIJUANA AND TOURETTE'S SYNDROME, Journal of Clinical Psychopharmacology, Vol. 8/No. 6, Dec 1988 4. CANNABINOIDS BLOCK RELEASE OF SEROTONIN FROM PLATELETS INDUCED BY PLASMA FROM MIGRAINE PATIENTS, Int J Clin Pharm. Res V (4) 243-246 (1985), Volfe Z., Dvilansky A., Nathan I. Blood Research, Faculty of Health Sciences, Soroka Medical Center, Ben-Gurion University of the Negev, P.O. Box 151, Beer-Sheva 84101, Israel. 5. Nelson, P. L. (1993). A critical review of the research literature concerning some biological and psychological effects of cannabis. In Advisory Committee on Illicit Drugs (Eds.), Cannabis and the law in Queensland: A discussion paper (pp. 113-152). Brisbane: Criminal Justice Commission of Queensland. 6. Marijuana And the Brain, by John Gettman, High Times, March, 1995 7. Cannabis for Migraine Treatment: The Once and Future Prescription?: An Historical and Scientific Review; Ethan B. Russo, M.D. 8. Marijuana and Medicine, Assessing the Science Base, Janet E. Joy, Stanley J. Watson, Jr., and John A. Benson, Jr., Editors Division of Neuroscience and Behavioral Health, INSTITUTE OF MEDICINE 9. Marijuana Medical Handbook, by Tod Mikuriya, M.D. 10. Medicinal Uses of Cannabis, Tod H. Mikuriya, M.D. ©1998 11. Marihuana as Medicine: A Plea for Reconsideration; Lester Grinspoon M.D., James B. Bakalar; Journal of the American Medical Association (JAMA); June 1995 12. Report of the Indian Hemp Drugs Commission, 1893-1894, 7 vols. (Simla: Government Central Printing Office, 1894); D. Solomon, ed., The Marihuana Papers (Indianapolis: Bobbs-Merrill, 1966). 13. Mayor's Committee on Marihuana, The Marihuana Problem in the City of New York (Lancaster, Pa.: Jacques Cattell, 1944). 14. M. H. Beaubrun and F Knight, "Psychiatric Assessment of Thirty Chronic Users of Cannabis and Thirty Matched Controls," American journal of Psychiatry 130 (1973): 309; M. C. Braude and S. Szara, eds., The Pharmacology of Marihuana, 2 vols. (New York: Raven, 1976); R. L. Dombush, A. M. Freedman, and M. Fink, eds., "Chronic Cannabis Use," Annals of New Yorh Academy of Sciences 282 (1976); J. S. Hochman and N. Q. Brill, "Chronic Marijuana Use and Psychosocial Adaptation," American journal of Psychiatry 130 (1973):132; Rubin and Comitas, Ganja in Jamaica. 15. Institute of Medicine, Marijuana and Health (Washington, D.C.: National Academy of Sciences, 1982). 16. C. M. Culver and F W King, "Neurophysiological Assessment of Undergraduate Marihuana and LSD Users," Archives of General Psychiatry 31 (1974): 707-711; P.J. Lessin and S. Thomas, "Assessment of the Chronic Effects of Marijuana on Motivation and Achievement: A Preliminary Report," in Pharmacology of Marihuana, ed. Braude and Szara, 2:681-684. 17. Cognition and Long-Term Use of Ganja (Cannabis), Reprint Series, 24 July 1981, Volume 213, pp. 465-466 SCIENCE, Jeffrey Schaeffer, Therese Andrysiak, and J. Thomas Ungerleider Copyright 1981 by the American Association for the Advancement of Science 18. Rubin and Comitas, Ganja in Jamaica; W E. Carter, ed., Cannabis in Costa Rica: A Study of Chronic Marihuana Use (Philadelphia: Institute for the Study of Human Issues, 1980); C. Stefariis, J. Boulougouris, and A. I-iakos, "Clinical and Psychophysiological Effects of Cannabis in Long-term Users," in Pharmacology of Marihuana, ed. Braude and Szara, 2:659-666; P Satz, J. M. Fletcher, and L. S. Sutker, "Neurophysiologic, Intellectual, and Personality Correlates of Chronic Marihuana Use in Native Costa Ricans," Annals of the New York Academy of Sciences 282 (1976): 266-306. 19. Is Marijuana The Right Medicine For You?; Bill Zimmerman Ph.D., Rick Bayer M.D., and Nancy Crumpacker M.D.; (1998): pp. 125; Keats Publishing Inc. source: http://www.onlinepot...cal/add&mmj.htm
  11. 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
  12. 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
  13. 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
  14. http://www.youtube.com/watch?v=7The1pjWO3g Kidney Disease: Cannabis Cream Effective Treatment for Pruritus IACM via BBSNews 2005-12-11 -- Researchers of the University of Wroclaw, Poland, investigated the effects of an ointment with structured physiological lipids and endocannabinoids in 21 patients with pruritus due to end- stage failure of kidney function. So-called uremic pruritus is still a common symptom in patients with end-stage renal failure. However, there is no effective treatment for this condition. All patients applied the tested cream twice daily for a period of three weeks. Global pruritus and dry skin were examined before the trial, on study visits at weekly intervals, and two weeks after completion of the study. After 3-week therapy pruritus was completely eliminated in 8 patients. Dry skin was significantly improved. Researchers noted that "it is very probable that the observed decrease of pruritus with the test product therapy was not only the result of dry skin improvement but that the addition of endocannabinoids may have also played a role." SOURCE: http://hightimes.com...s/ht_admin/2819 State OKs medical marijuana for chronic kidney failure By Carol M. Ostrom Seattle Times health reporter The state has added chronic kidney failure to the list of conditions for which medical marijuana is permitted under state law but has rejected petitions to add Alzheimer's and neuropathic pain. In approving chronic kidney failure, the state Medical Quality Assurance Commission said it was convinced that nausea caused by dialysis could be helped by marijuana. But it noted that using marijuana could also jeopardize a renal-failure patient's eligibility for transplant or have other adverse effects and that patients need to be informed of that when a provider authorizes them to use marijuana legally. That petition was brought by Kenneth Lachman, a dialysis patient. For neuropathic pain, the commission concluded that the term is so broad it might include some disorders that would already qualify, and others that don't. The request to include it was made by Dr. Sunil Aggarwal on behalf of the Cannabis Defense Coalition. For Alzheimer's disease, the commission said there was insufficient scientific or anecdotal evidence to support the contention of Kemp LaMunyon Sr., an Eastern Washington medical-marijuana advocate, that it could help prevent the disease in humans. For more information: www.doh.wa.gov/hsqa/medical-marijuana/default.htm. Medical Marijuana for kidney failure? just about a year ago( october 12 ) i was diagnosed with MPGN , a type of kidney failure.i i was in really bad shape i went from 180 pounds to 105 in about a month. had congestive heart failure and Ceedif, a type of stomachc virus,also have neuropathy which causes serious tingly, shocking spasms in my feet. i was malnurished because i couldnt eat. i was retaining water in my legs and my stomach. ( spelling is bad sorry ). but i strted smoking pot again in june and sincce then i have gainned back 50 pounds, and have been doing very well. ive been in remission ever since i strted back up again. I was just wondering that if i was to talk to my doctor , would i be qualified for a medical marijuana card.( nnow i live in Pennsylvania whichc i know they dont have but i would still like to know if i was. i looked it up online but i couldnt find anything on kidney problems). So if anyone is in my same position or knows if i coucld get it id appreciate some input . thanks more
  15. Can marijuana help treat Alzheimer's disease? General Reference (not clearly pro or con) The National Institute on Aging stated in its Mar. 2006 booklet Understanding Alzheimer's Disease: "Alzheimer's disease is an illness of the brain. It causes large numbers of nerve cells in the brain to die. This affects your ability to remember things and think clearly. Doctors don't know what causes the disease. They do know that it usually begins after age 60 and nearly half of people age 85 and older may have Alzheimer's. However, it is not a normal part of aging... There are medicines that can treat the symptoms of Alzheimer's. However, there is no cure. Some medicines keep your memory loss and other symptoms from getting worse for a time. These medicines work best if Alzheimer's disease is found early. Other medicines work to help you sleep better or feel less worried and depressed. These medicines don't directly treat the disease. They do help you feel more comfortable." more Stimulation of cannabinoid receptor 2 (CB2) suppresses microglial activation Background Activated microglial cells have been implicated in a number of neurodegenerative disorders, including Alzheimer's disease (AD), multiple sclerosis (MS), and HIV dementia. It is well known that inflammatory mediators such as nitric oxide (NO), cytokines, and chemokines play an important role in microglial cell-associated neuron cell damage. Our previous studies have shown that CD40 signaling is involved in pathological activation of microglial cells. Many data reveal that cannabinoids mediate suppression of inflammation in vitro and in vivo through stimulation of cannabinoid receptor 2 (CB2). Methods In this study, we investigated the effects of a cannabinoid agonist on CD40 expression and function by cultured microglial cells activated by IFN-γ using RT-PCR, Western immunoblotting, flow cytometry, and anti-CB2 small interfering RNA (siRNA) analyses. Furthermore, we examined if the stimulation of CB2 could modulate the capacity of microglial cells to phagocytise Ab1–42 peptide using a phagocytosis assay. Results We found that the selective stimulation of cannabinoid receptor CB2 by JWH-015 suppressed IFN-γ-induced CD40 expression. In addition, this CB2 agonist markedly inhibited IFN-γ-induced phosphorylation of JAK/STAT1. Further, this stimulation was also able to suppress microglial TNF-a and nitric oxide production induced either by IFN-γ or Ab peptide challenge in the presence of CD40 ligation. Finally, we showed that CB2 activation by JWH-015 markedly attenuated CD40-mediated inhibition of microglial phagocytosis of Ab1–42 peptide. Taken together, these results provide mechanistic insight into beneficial effects provided by cannabinoid receptor CB2 modulation in neurodegenerative diseases, particularly AD. more List of abbreviations Ab : Amyloid-b peptide CD40: CD40 receptor CD40L: CD40 ligand CNS: Central nervous system HIV: Human immunodeficiency virus IFN-γ : Interferon-gamma JAK: Janus kinase MHC II: Major histocompatibility complex II STAT1: Signal transducer and activator of transcription 1 TNF-a : Tumor necrosis factor-alpha Aloisi F, Penna G, Polazzi E, Minghetti L, Adorini L: CD40-CD154 interaction and IFN-gamma are required for IL-12 but not prostaglandin E2 secretion by microglia during antigen presentation to Th1 cells. J Immunol 1999, 162:1384-1391. PubMed Abstract | Publisher Full Text OpenURL Fischer HG, Reichmann G: Brain dendritic cells and macrophages/microglia in central nervous system inflammation. J Immunol 2001, 166:2717-2726. PubMed Abstract | Publisher Full Text OpenURL Aloisi F: Immune function of microglia. Glia 2001, 36:165-179. PubMed Abstract | Publisher Full Text OpenURL Tan J, Town T, Paris D, Placzek A, Parker T, Crawford F, Yu H, Humphrey J, Mullan M: Activation of microglial cells by the CD40 pathway: relevance to multiple sclerosis. J Neuroimmunol 1999, 97:77-85. PubMed Abstract | Publisher Full Text OpenURL Townsend KP, Town T, Mori T, Lue LF, Shytle D, Sanberg PR, Morgan D, Fernandez F, Flavell RA, Tan J: CD40 signaling regulates innate and adaptive activation of microglia in response to amyloid beta-peptide. Eur J Immunol 2005, 35:901-910. PubMed Abstract | Publisher Full Text OpenURL Gerritse K, Laman JD, Noelle RJ, Aruffo A, Ledbetter JA, Boersma WJ, Claassen E: CD40-CD40 ligand interactions in experimental allergic encephalomyelitis and multiple sclerosis. Proc Natl Acad Sci U S A 1996, 93:2499-2504. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL Laman JD, Maassen CB, Schellekens MM, Visser L, Kap M, de Jong E, van Puijenbroek M, van Stipdonk MJ, van Meurs M, Schwarzler C, Gunthert U: Therapy with antibodies against CD40L (CD154) and CD44-variant isoforms reduces experimental autoimmune encephalomyelitis induced by a proteolipid protein peptide. Mult Scler 1998, 4:147-153. PubMed Abstract | Publisher Full Text OpenURL Boon L, Brok HP, Bauer J, Ortiz-Buijsse A, Schellekens MM, Ramdien-Murli S, Blezer E, van Meurs M, Ceuppens J, de Boer M, et al.: Prevention of experimental autoimmune encephalomyelitis in the common marmoset (Callithrix jacchus) using a chimeric antagonist monoclonal antibody against human CD40 is associated with altered B cell responses. J Immunol 2001, 167:2942-2949. PubMed Abstract | Publisher Full Text OpenURL Howard LM, Neville KL, Haynes LM, Dal Canto MC, Miller SD: CD154 blockade results in transient reduction in Theiler's murine encephalomyelitis virus-induced demyelinating disease. J Virol 2003, 77:2247-2250. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL Tan J, Town T, Crawford F, Mori T, DelleDonne A, Crescentini R, Obregon D, Flavell RA, Mullan MJ: Role of CD40 ligand in amyloidosis in transgenic Alzheimer's mice. Nat Neurosci 2002, 5:1288-1293. PubMed Abstract | Publisher Full Text OpenURL Volicer L, Stelly M, Morris J, McLaughlin J, Volicer BJ: Effects of dronabinol on anorexia and disturbed behavior in patients with Alzheimer's disease. Int J Geriatr Psychiatry 1997, 12(9):913-9. PubMed Abstract | Publisher Full Text OpenURL Ramirez BG, Blazquez C, Gomez del Pulgar T, Guzman M, de Ceballos ML: Prevention of Alzheimer's disease pathology by cannabinoids: neuroprotection mediated by blockade of microglial activation. J Neurosci 25(8):1904-13. 2005 Feb 23 PubMed Abstract | Publisher Full Text OpenURL Wade DT, Makela P, Robson P, House H, Bateman C: Do cannabis-based medicinal extracts have general or specific effects on symptoms in multiple sclerosis? A double-blind, randomized, placebo-controlled study on 160 patients. Mult Scler 2004, 10(4):434-41. PubMed Abstract | Publisher Full Text OpenURL Zajicek J, Fox P, Sanders H, Wright D, Vickery J, Nunn A, Thompson A, UK MS Research Group: Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): multicentre randomised placebo-controlled trial. Lancet 362(9395):1517-26. 2003 Nov 8 PubMed Abstract | Publisher Full Text OpenURL Croxford JL, Miller SD: Immunoregulation of a viral model of multiple sclerosis using the synthetic cannabinoid R+WIN55,212. J Clin Invest 2003, 111(8):1231-40. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL Town T, Tan J, Sansone N, Obregon D, Klein T, Mullan M: Characterization of murine immunoglobulin G antibodies against human amyloid-beta1-42. Neurosci Lett 307(2):101-4. 2001 Jul 13 PubMed Abstract | Publisher Full Text OpenURL Tan J, Town T, Mullan M: CD45 inhibits CD40L-induced microglial activation via negative regulation of the Src/p44/42 MAPK pathway. J Biol Chem 2000, 275:37224-37231. PubMed Abstract | Publisher Full Text OpenURL Tan J, Town T, Paris D, Mori T, Suo Z, Crawford F, Mattson MP, Flavell RA, Mullan M: Microglial activation resulting from CD40-CD40L interaction after beta-amyloid stimulation. Science 1999, 286:2352-2355. PubMed Abstract | Publisher Full Text OpenURL Tan J, Town T, Saxe M, Paris D, Wu Y, Mullan M: Ligation of microglial CD40 results in p44/42 mitogen-activated protein kinase-dependent TNF-alpha production that is opposed by TGF-beta 1 and IL-10. J Immunol 1999, 163:6614-6621. PubMed Abstract | Publisher Full Text OpenURL Kitamura Y, Nomura Y: Stress proteins and glial functions: possible therapeutic targets for neurodegenerative disorders. Pharmacol Ther 2003, 97:35-53. PubMed Abstract | Publisher Full Text OpenURL Webster SD, Galvan MD, Ferran E, Garzon-Rodriguez W, Glabe CG, Tenner AJ: Antibody-mediated phagocytosis of the amyloid beta-peptide in microglia is differentially modulated by C1q. J Immunol 2001, 166:7496-7503. PubMed Abstract | Publisher Full Text OpenURL Wyss-Coray T, Loike JD, Brionne TC, Lu E, Anankov R, Yan F, Silverstein SC, Husemann J: Adult mouse astrocytes degrade amyloid-beta in vitro and in situ. Nat Med 2003, 9:453-457. PubMed Abstract | Publisher Full Text OpenURL Nguyen VT, Walker WS, Benveniste EN: Post-transcriptional inhibition of CD40 gene expression in microglia by transforming growth factor-beta. Eur J Immunol 1998, 28:2537-2548. PubMed Abstract | Publisher Full Text OpenURL Townsend KP, Shytle DR, Bai Y, San N, Zeng J, Freeman M, Mori T, Fernandez F, Morgan D, Sanberg P, Tan J: Lovastatin modulation of microglial activation via suppression of functional CD40 expression. J Neurosci Res 2004, 78:167-176. PubMed Abstract | Publisher Full Text OpenURL Nguyen VT, Benveniste EN: IL-4-activated STAT-6 inhibits IFN-gamma-induced CD40 gene expression in macrophages/microglia. J Immunol 2000, 165:6235-6243. PubMed Abstract | Publisher Full Text OpenURL Nguyen VT, Benveniste EN: Involvement of STAT-1 and ets family members in interferon-gamma induction of CD40 transcription in microglia/macrophages. J Biol Chem 2000, 275:23674-23684. PubMed Abstract | Publisher Full Text OpenURL Wei R, Jonakait GM: Neurotrophins and the anti-inflammatory agents interleukin-4 (IL-4), IL-10, IL-11 and transforming growth factor-beta1 (TGF-beta1) down-regulate T cell costimulatory molecules B7 and CD40 on cultured rat microglia. J Neuroimmunol 1999, 95:8-18. PubMed Abstract | Publisher Full Text OpenURL Delgado M: Inhibition of interferon (IFN) gamma-induced Jak-STAT1 activation in microglia by vasoactive intestinal peptide: inhibitory effect on CD40, IFN-induced protein-10, and inducible nitric-oxide synthase expression. J Biol Chem 2003, 278:27620-27629. PubMed Abstract | Publisher Full Text OpenURL Kim WK, Ganea D, Jonakait GM: Inhibition of microglial CD40 expression by pituitary adenylate cyclase-activating polypeptide is mediated by interleukin-10. J Neuroimmunol 2002, 126:16-24. PubMed Abstract | Publisher Full Text OpenURL Wallen-Ohman M, Larrick JW, Carlsson R, Borrebaeck CA: Ligation of MHC class I induces apoptosis in human pre-B cell lines, in promyelocytic cell lines and in CD40-stimulated mature B cells. Int Immunol 1997, 9:599-606. PubMed Abstract | Publisher Full Text OpenURL Chappel MS, Hough MR, Mittel A, Takei F, Kay R, Humphries RK: Cross-linking the murine heat-stable antigen induces apoptosis in B cell precursors and suppresses the anti-CD40-induced proliferation of mature resting B lymphocytes. J Exp Med 1996, 184:1638-1649. PubMed Abstract | Publisher Full Text OpenURL Aloisi F, De Simone R, Columba-Cabezas S, Penna G, Adorini L: Functional maturation of adult mouse resting microglia into an APC is promoted by granulocyte-macrophage colony-stimulating factor and interaction with Th1 cells. J Immunol 2000, 164:1705-1712. PubMed Abstract | Publisher Full Text OpenURL Magnus T, Chan A, Grauer O, Toyka KV, Gold R: Microglial phagocytosis of apoptotic inflammatory T cells leads to down-regulation of microglial immune activation. J Immunol 2001, 167:5004-5010. PubMed Abstract | Publisher Full Text OpenURL Chan A, Magnus T, Gold R: Phagocytosis of apoptotic inflammatory cells by microglia and modulation by different cytokines: mechanism for removal of apoptotic cells in the inflamed nervous system. Glia 2001, 33:87-95. PubMed Abstract | Publisher Full Text OpenURL Re F, Belyanskaya SL, Riese RJ, Cipriani B, Fischer FR, Granucci F, Ricciardi-Castagnoli P, Brosnan C, Stern LJ, Strominger JL, Santambrogio L: Granulocyte-macrophage colony-stimulating factor induces an expression program in neonatal microglia that primes them for antigen presentation. J Immunol 2002, 169:2264-2273. PubMed Abstract | Publisher Full Text OpenURL Monsonego A, Imitola J, Zota V, Oida T, Weiner HL: Microglia-mediated nitric oxide cytotoxicity of T cells following amyloid beta-peptide presentation to Th1 cells. J Immunol 2003, 171:2216-2224. PubMed Abstract | Publisher Full Text OpenURL Monsonego A, Weiner HL: Immunotherapeutic approaches to Alzheimer's disease. Science 2003, 302:834-838. PubMed Abstract | Publisher Full Text OpenURL Berdyshev EV: Cannabinoid receptors and the regulation of immune response. Chem Phys Lipids 2000, 108:169-190. PubMed Abstract | Publisher Full Text OpenURL Wagner AH, Gebauer M, Guldenzoph B, Hecker M: 3-hydroxy-3-methylglutaryl coenzyme A reductase-independent inhibition of CD40 expression by atorvastatin in human endothelial cells. Arterioscler Thromb Vasc Biol 2002, 22:1784-1789. PubMed Abstract | Publisher Full Text OpenURL Schonbeck U, Gerdes N, Varo N, Reynolds RS, Horton DB, Bavendiek U, Robbie L, Ganz P, Kinlay S, Libby P: Oxidized low-density lipoprotein augments and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors limit CD40 and CD40L expression in human vascular cells. Circulation 2002, 106:2888-2893. PubMed Abstract | Publisher Full Text OpenURL Mulhaupt F, Matter CM, Kwak BR, Pelli G, Veillard NR, Burger F, Graber P, Luscher TF, Mach F: Statins (HMG-CoA reductase inhibitors) reduce CD40 expression in human vascular cells. Cardiovasc Res 2003, 59:755-766. PubMed Abstract | Publisher Full Text OpenURL Becher B, Durell BG, Miga AV, Hickey WF, Noelle RJ: The clinical course of experimental autoimmune encephalomyelitis and inflammation is controlled by the expression of CD40 within the central nervous system. J Exp Med 2001, 193:967-974. PubMed Abstract | Publisher Full Text OpenURL Togo T, Akiyama H, Kondo H, Ikeda K, Kato M, Iseki E, Kosaka K: Expression of CD40 in the brain of Alzheimer's disease and other neurological diseases. Brain Res 2000, 885:117-121. PubMed Abstract | Publisher Full Text OpenURL Calingasan NY, Erdely HA, Altar CA: Identification of CD40 ligand in Alzheimer's disease and in animal models of Alzheimer's disease and brain injury. Neurobiol Aging 2002, 23:31-39. PubMed Abstract | Publisher Full Text OpenURL Benveniste EN, Nguyen VT, Wesemann DR: Molecular regulation of CD40 gene expression in macrophages and microglia. Brain Behav Immun 2004, 18:7-12. PubMed Abstract | Publisher Full Text OpenURL Yasukawa H, Sasaki A, Yoshimura A: Negative regulation of cytokine signaling pathways. Annu Rev Immunol 2000, 18:143-164. PubMed Abstract | Publisher Full Text OpenURL
  16. Researchers Tackle MRSA Using Cannabis Extracts Marijuana has long been associated with having potent anti-bacterial properties, but paradoxically, marijuana abuse has been associated with an increase in opportunistic infection. According to a new study, published August 6, 2008 in the Journal of Natural Products, cannabis has powerful antibiotic properties against several forms of MRSA strains, “of clinical relevance.” In the 1950’s, topical preparations from cannabis sativa were explored for treating skin and mouth infections and for tuberculosis treatment. Recent research shows that both psychotropic (THC) forms, as well non-psychotropic forms of cannabis might be used as antibiotic. The current researchers isolated THC, CBD, and CBG from three strains of cannabis sativa to produce a single major cannabinoid. Powder was extracted from the plant, heated, and the active ingredients were then extracted and purified. The researchers then used MRSA cultures to test the effectiveness of the purified cannabis extracts - “All compounds showed potent antibacterial activity, and the researchers saw “potent activity demonstrated against EMRSA-15 and EMRSA-16, the major epidemic methicillin-resistant S. aureus strains occurring in U.K. hospitals.” MRSA is not the only bacterium that has become drug-resistant. Concerns about extremely drug resistant strains of tuberculosis have also recently been in the spotlight. According to the current research authors, “plants are still a substantially untapped source of antimicrobial agents”, as “only one new class of antibacterial has been introduced in the last 30 years, … making C. sativa a potential source of compounds to address antibiotic resistance, one of the most urgent issues in antimicrobial therapy.” Large-scale studies are still needed, but the researchers write, “Given the availability of C. sativa strains producing high concentrations of nonpsychotropic cannabinoids, this plant represents an interesting source of antibacterial agents to address the problem of multidrug resistance in MRSA and other pathogenic bacteria. Furthermore, “Although the use of cannabinoids as systemic antibacterial agents awaits rigorous clinical trials and an assessment of the extent of their inactivation by serum, their topical application to reduce skin colonization by MRSA seems promising, since MRSA resistant to mupirocin, the standard antibiotic for this indication, are being detected at a threatening rate. … semipurified mixtures of cannabinoids could also be used as cheap and biodegradable antibacterial agents for cosmetics and toiletries, providing an alternative to the substantially much less potent synthetic preservatives, many of which are currently questioned for their suboptimal safety and environmental profile.” source: http://current.com/i...is_extracts.htmAccording to the Journal of the American Medical Association (JAMA), methicillin-resistant Staphylococcus aureus, colloquially known as MRSA or ‘the superbug,’ is now responsible for more annual US deaths than AIDS. Yet despite this sobering statistic, it’s unlikely that either JAMA or anyone in the mainstream US media will report on the findings of a forthcoming Italian study — you didn’t actually think I was going to say that this took place in America did you? — demonstrating that compounds in cannabis possess “exceptional antibacterial activity” against multi-drug resistant pathogens, including MRSA. “Although the use of cannabinoids as systemic antibacterial agents awaits rigorous clinical trials, … their topical application to reduce skin colonization by MRSA seems promising,” the study’s authors write. “Cannabis sativa … represents an interesting source of antibacterial agents to address the problem of multidrug resistance in MRSA and other pathogenic bacteria.” (You can read the full text ahead of publication here.) Ironically, the study notes that preparations from cannabis were “investigated extensively in the 1950s as highly active topical antiseptic agents.” Predictably — in yet another ‘victory’ for prohibition — authors declare that little, if any, research into this potential clinical application has taken place since. Several years ago, when I first began writing the booklet Emerging Clinical Applications for Cannabis and Cannabinoids, I mused about what sort of advancements in the treatment of disease may have been achieved over the past 70+ years had U.S. government chosen to advance — rather than stifle — clinical research into the therapeutic effects of cannabis. Now, more than ever, this is a question that our elected officials — both Republican and Democrat — must answer. source: http://pr.cannazine....a-superbug.html A New MRSA Defense Marijuana extracts kill antibiotic-resistant MRSA without a high. Substances harvested from cannabis plants could soon outshine conventional antibiotics in the escalating battle against drug-resistant bacteria. The compounds, called cannabinoids, appear to be unaffected by the mechanism that superbugs like MRSA use to evade existing antibiotics. Scientists from Italy and the United Kingdom, who published their research in the Journal of Natural Products last month, say that cannabis-based creams could also be developed to treat persistent skin infections. Cannabis has long been known to have antibacterial properties and was studied in the 1950s as a treatment for tuberculosis and other diseases. But research into using cannabis as an antibiotic has been limited by poor knowledge of the plant's active ingredients and by the controversy surrounding its use as a recreational drug. Now Giovanni Appendino of the Piemonte Orientale University, in Italy, and Simon Gibbons of the School of Pharmacy at the University of London, U.K., have revisited the antibiotic power of marijuana by systematically testing different cannabinoids' ability to kill MRSA. MRSA, short for methicillin-resistant Staphylococcus aureus, is a bacterium that can cause difficult-to-treat infections since it does not respond to many antibiotics. Many healthy people carry S. aureus on their skin, but problems arise when multi-drug-resistant strains infect people with weak immune systems through an open wound. In the worst cases, the bug spreads throughout the body, causing a life-threatening infection. To make matters worse, resistance to antibiotics is rapidly increasing, and some strains are now even immune to vancomycin, a powerful antibiotic that is normally used only as a last resort when other drugs fail. But when Appendino, Gibbons, and their colleagues applied extracts from five major cannabinoids to bacterial cultures of six strains of MRSA, they discovered that the cannabinoids were as effective at killing the bugs as vancomycin and other antibiotics. "The cannabinoids even showed exceptional activity against the MRSA strain that makes extra amounts of the proteins that give the bugs resistance against many antibiotics," says Gibbons. These proteins, he explains, allow the bacteria to "hoover up unwanted things from inside the cell and spit them out again." Conveniently, of the five cannabinoids tested by the researchers, the two most effective ones also happen to be nonpsychoactive, meaning that they cannot cause a high. "What this means is, we could use fiber hemp plants that have no use as recreational drugs to cheaply and easily produce potent antibiotics," says Appendino. In an attempt to discover how the cannabinoids kill MRSA, the team manipulated several chemical groups within the compounds. Most of the changes did not affect the antibiotic activity at all, and those that did seemed to influence only how well the cannabinoid is taken up by the bacterial cells. "Everything points towards these compounds having been evolved by the plants as antimicrobial defenses that specifically target bacterial cells," says Gibbons. "But the actual mechanism by which they kill the bugs is still a mystery. We've tested whether the cannabinoids affect common antibiotic targets like fatty acid synthesis or the [DNA-bending enzyme] DNA gyrase, but they don't. I really cannot hazard a guess how they do it, but their high potency as antibiotics suggests there must be a very specific mechanism." Appendino and Gibbons say that cannabinoids could quickly be developed as treatments for skin infections, provided the nonpsychoactive varieties are used. "The most practical application of cannabinoids would be as topical agents to treat ulcers and wounds in a hospital environment, decreasing the burden of antibiotics," says Appendino. Whether the cannabinoids could also be delivered in the form of an injection or in pills is less clear, the pair says, because they may be inactivated by blood serum. Frank Bowling of the University of Manchester, who has had success treating MRSA-infected wounds with maggots, says that "any alternative treatment that removes MRSA from the wound and prevents it from spreading into the body is fantastic and preferable to using antibiotics that have strong side effects and against which resistance is already developing." He cautions, however, that the researchers still need to show that the cannabinoids are safe to use. This is not something that Appendino is too concerned about: "The topical use of cannabis preparations has a long tradition in European medicine, and no allergies have been reported." Mark Rogerson of GW Pharmaceuticals, a U.K.-based company that develops cannabinoid-based drugs to treat severe pain caused by multiple sclerosis and cancer, says that the discovery that cannabinoids kill MRSA "really underlines the potentially great diversity of medical applications that cannabis-based medicine can have. You can almost think of the cannabis plant as a mini pharma industry in its own right." But Rogerson says that it is unlikely that existing cannabis-based medicines could be used to treat MRSA because the exact effect will depend on the correct combination and dosage of cannabinoids. Meanwhile, Appendino and Gibbons hope that antibacterial effectiveness could also make cannabinoids suitable preservatives for cosmetics and toiletries. "The golden standards of preservatives are parabens and chlorinated phenols," says Appendino, but these compounds do not degrade well in the environment and are strongly suspected to be hormonal modifiers. He also argues that, since all major cannabinoids are similarly effective, complete purification of a single compound isn't necessary. So semipurified cannabinoid mixtures extracted from nonpsychoactive plants could make a cheap and easy alternative to conventional preservatives. source: http://www.technolog.../Biotech/21366/ Cannabis plant extracts can effectively fight drug-resistant bacteria. Scientists Say Substances Derived From Cannabis Could Outdo Conventional Antibiotics In Killing Some Bacteria Substances harvested from cannabis plants could soon outshine conventional antibiotics in the escalating battle against drug-resistant bacteria. The compounds, called cannabinoids, appear to be unaffected by the mechanism that superbugs like MRSA use to evade existing antibiotics. Scientists from Italy and the United Kingdom, who published their research in the Journal of Natural Products last month, say that cannabis-based creams could also be developed to treat persistent skin infections. Cannabis has long been known to have antibacterial properties and was studied in the 1950s as a treatment for tuberculosis and other diseases. But research into using cannabis as an antibiotic has been limited by poor knowledge of the plant's active ingredients and by the controversy surrounding its use as a recreational drug. Now Giovanni Appendino of the Piemonte Orientale University, in Italy, and Simon Gibbons of the School of Pharmacy at the University of London, U.K., have revisited the antibiotic power of marijuana by systematically testing different cannabinoids' ability to kill MRSA. MRSA, short for methicillin-resistant Staphylococcus aureus, is a bacterium that can cause difficult-to-treat infections since it does not respond to many antibiotics. Many healthy people carry S. aureus on their skin, but problems arise when multi-drug-resistant strains infect people with weak immune systems through an open wound. In the worst cases, the bug spreads throughout the body, causing a life-threatening infection. To make matters worse, resistance to antibiotics is rapidly increasing, and some strains are now even immune to vancomycin, a powerful antibiotic that is normally used only as a last resort when other drugs fail. But when Appendino, Gibbons, and their colleagues applied extracts from five major cannabinoids to bacterial cultures of six strains of MRSA, they discovered that the cannabinoids were as effective at killing the bugs as vancomycin and other antibiotics. "The cannabinoids even showed exceptional activity against the MRSA strain that makes extra amounts of the proteins that give the bugs resistance against many antibiotics," says Gibbons. These proteins, he explains, allow the bacteria to "hoover up unwanted things from inside the cell and spit them out again." source: http://abcnews.go.co...=5787866&page=1 Chemicals in Marijuana May Fight MRSA Study Shows Cannabinoids May Be Useful Against Drug-Resistant Staph Infections By Caroline Wilbert WebMD Health News Reviewed by Louise Chang, MD Sept. 4, 2008 -- Chemicals in marijuana may be useful in fighting MRSA, a kind of staph bacterium that is resistant to certain antibiotics. Researchers in Italy and the U.K. tested five major marijuana chemicals called cannabinoids on different strains of MRSA (methicillin-resistant Staphylococcus aureus). All five showed germ-killing activity against the MRSA strains in lab tests. Some synthetic cannabinoids also showed germ-killing capability. The scientists note the cannabinoids kill bacteria in a different way than traditional antibiotics, meaning they might be able to bypass bacterial resistance. At least two of the cannabinoids don't have mood-altering effects, so there could be a way to use these substances without creating the high of marijuana. MRSA, like other staph infections, can be spread through casual physical contact or through contaminated objects. It is commonly spread from the hands of someone who has it. This could be in a health care setting, though there have also been high-profile cases of community-acquired MRSA. It is becoming more common for healthy people to get MRSA, which is often spread between people who have close contact with one another, such as members of a sports team. Symptoms often include skin infections, such as boils. MRSA can become serious, particularly for people who are weak or ill. In the study, published in the Journal of Natural Products, researchers call for further study of the antibacterial uses of marijuana. There are "currently considerable challenges with the treatment of infections caused by strains of clinically relevant bacteria that show multi-drug resistance," the researchers write. New antibacterials are urgently needed, but only one new class of antibacterial has been introduced in the last 30 years. "Plants are still a substantially untapped source of antimicrobial agents," the researchers conclude. source: http://www.webmd.com...-may-fight-mrsa Researchers Tackle MRSA Using Cannabis Extracts Marijuana has long been associated with having potent anti-bacterial properties, but paradoxically, marijuana abuse has been associated with an increase in opportunistic infection. According to a new study, published August 6, 2008 in the Journal of Natural Products, cannabis has powerful antibiotic properties against several forms of MRSA strains, “of clinical relevance.” In the 1950’s, topical preparations from cannabis sativa were explored for treating skin and mouth infections and for tuberculosis treatment. Recent research shows that both psychotropic (THC) forms, as well non-psychotropic forms of cannabis might be used as antibiotic. The current researchers isolated THC, CBD, and CBG from three strains of cannabis sativa to produce a single major cannabinoid. Powder was extracted from the plant, heated, and the active ingredients were then extracted and purified. The researchers then used MRSA cultures to test the effectiveness of the purified cannabis extracts - “All compounds showed potent antibacterial activity, and the researchers saw “potent activity demonstrated against EMRSA-15 and EMRSA-16, the major epidemic methicillin-resistant S. aureus strains occurring in U.K. hospitals.” MRSA is not the only bacterium that has become drug-resistant. Concerns about extremely drug resistant strains of tuberculosis have also recently been in the spotlight. According to the current research authors, “plants are still a substantially untapped source of antimicrobial agents”, as “only one new class of antibacterial has been introduced in the last 30 years, … making C. sativa a potential source of compounds to address antibiotic resistance, one of the most urgent issues in antimicrobial therapy.” Large-scale studies are still needed, but the researchers write, “Given the availability of C. sativa strains producing high concentrations of nonpsychotropic cannabinoids, this plant represents an interesting source of antibacterial agents to address the problem of multidrug resistance in MRSA and other pathogenic bacteria. Furthermore, “Although the use of cannabinoids as systemic antibacterial agents awaits rigorous clinical trials and an assessment of the extent of their inactivation by serum, their topical application to reduce skin colonization by MRSA seems promising, since MRSA resistant to mupirocin, the standard antibiotic for this indication, are being detected at a threatening rate. … semipurified mixtures of cannabinoids could also be used as cheap and biodegradable antibacterial agents for cosmetics and toiletries, providing an alternative to the substantially much less potent synthetic preservatives, many of which are currently questioned for their suboptimal safety and environmental profile. source: http://current.com/i...is_extracts.htm Pot Versus the 'Superbug' by Paul Armentano According to the Journal of the American Medical Association (JAMA), methicillin-resistant Staphylococcus aureus, colloquially known as MRSA or “the superbug,” is now responsible for more annual US deaths than AIDS. Yet despite this sobering statistic, it’s unlikely that either JAMA or anyone in the mainstream US media will report on the findings of a forthcoming Italian study – you didn’t actually think I was going to say that this took place in America did you? – demonstrating that compounds in cannabis possess “exceptional antibacterial activity” against multi-drug resistant pathogens, including MRSA. “Although the use of cannabinoids as systemic antibacterial agents awaits rigorous clinical trials, … their topical application to reduce skin colonization by MRSA seems promising,” the study’s authors write. “Cannabis sativa … represents an interesting source of antibacterial agents to address the problem of multidrug resistance in MRSA and other pathogenic bacteria.” Ironically, the study notes that preparations from cannabis were “investigated extensively in the 1950s as highly active topical antiseptic agents.” Predictably – in yet another “victory” for prohibition – authors declare that little, if any, research into this potential clinical application has taken place since. Several years ago, when I first began writing the booklet Emerging Clinical Applications for Cannabis and Cannabinoids, I mused about what sort of advancements in the treatment of disease may have been achieved over the past 70+ years had U.S. government chosen to advance – rather than stifle – clinical research into the therapeutic effects of cannabis. Now, more than ever, this is a question that our elected officials must be forced to answer. source: http://www.lewrockwe...entano-p36.html Methicillin-resistant Staphyloccus aureus (MRSA) Many bacterial infections possess multi-drug resistance. Arguably the most significant of these bacteria is methicillin-resistant Staphyloccus aureus, more commonly known as MRSA or ‘the superbug.’ This bacterium is resistant to standard antibiotics, including penicillin. According to the Journal of the American Medical Association, MRSA is responsible for nearly 20,000 hospital-stay related deaths annually in the United States.[1] Published data demonstrates that cannabinoids possess strong antibacterial properties. In 2008, investigators at Italy's Universita del Piemonte Orientale and Britain's University of London, School of Pharmacy assessed the germ-fighting properties of five separate cannabinoids against various strains of multidrug-resistant bacteria, including MRSA. They reported that all of the compounds tested showed “potent antibacterial activity,” and that cannabinoids were “exceptional” at halting the spread of MRSA.[2] A second study published that same year reported that non-cannabinoid constituents in the plant also possess antibacterial properties against MRSA and malaria.[3] Clinical trials regarding the use of cannabinoids for MRSA have been recommended, with some experts stating, “Cannabis sativa … represents an interesting source of antibacterial agents to address the problem of multidrug resistance in MRSA and other pathogenic bacteria.”[4] REFERENCES [1] Klevens et al. 2007. Invasive methicillin-resistant Staphylococcus aureus infections in the United States. Journal of the American Medical Association 298: 1763-1771. [2] Appendino et al. 2008. Antibacterial cannabinoids from cannabis sativa: a structure study. Journal of Natural Products 71: 1427-1430. [3] Radwan et al. 2008. Non-cannabinoid constituents from a high potency cannabis sativa variety. Phytochemistry 69: 26727-2633. [4]Appendino et al. 2008. op. cit. source: http://norml.org/ind...m?Group_ID=7787 You can fight Bacteria with…Marijuana ingredients ! Yes it is true, Marijuana may be something of a wonder drug but maybe not in the ways you might think. Some researchers from Italy and Britain ( on some wicked Bob Marley sounds ) have found that the main active ingredient in marijuana , the tetrahydrocannabinol or shortly THC, and related compounds may function as antibacterial agents, especially against microbial strains that are already resistant to several classes of drugs. We knew ( well, some of us anyway) for decades that Cannabis sativa has antibacterial properties and experiments in the 1950s tested various marijuana preparations against skin and other infections, but now Giovanni Appendino of the University of the Eastern Piedmont, looked at the antibacterial activity of the five most common cannabinoids. All of these compounds were found very effective against a few common multi-resistant bacterial strains. Researchers suggested that the nonpsychotropic cannabinoids might prove more promising for eventual use. They don’t know yet how the cannabinoids work, and if they would be effective as antibiotics then more research would have to be involved. But the compounds may prove useful sooner as a topical agent against MRSA ( is an infection caused by a strain of Staphylococcus aureus (S. aureus) bacteria that is highly resistant to antibiotics) to prevent the microbes from colonizing on the skin. source: http://www.techcurse...na-ingredients/ Cannabis plant extracts can effectively fight drug-resistant bacteria. Scientists Say Substances Derived From Cannabis Could Outdo Conventional Antibiotics In Killing Some Bacteria Substances harvested from cannabis plants could soon outshine conventional antibiotics in the escalating battle against drug-resistant bacteria. The compounds, called cannabinoids, appear to be unaffected by the mechanism that superbugs like MRSA use to evade existing antibiotics. Scientists from Italy and the United Kingdom, who published their research in the Journal of Natural Products last month, say that cannabis-based creams could also be developed to treat persistent skin infections. Cannabis has long been known to have antibacterial properties and was studied in the 1950s as a treatment for tuberculosis and other diseases. But research into using cannabis as an antibiotic has been limited by poor knowledge of the plant's active ingredients and by the controversy surrounding its use as a recreational drug. Now Giovanni Appendino of the Piemonte Orientale University, in Italy, and Simon Gibbons of the School of Pharmacy at the University of London, U.K., have revisited the antibiotic power of marijuana by systematically testing different cannabinoids' ability to kill MRSA. MRSA, short for methicillin-resistant Staphylococcus aureus, is a bacterium that can cause difficult-to-treat infections since it does not respond to many antibiotics. Many healthy people carry S. aureus on their skin, but problems arise when multi-drug-resistant strains infect people with weak immune systems through an open wound. In the worst cases, the bug spreads throughout the body, causing a life-threatening infection. To make matters worse, resistance to antibiotics is rapidly increasing, and some strains are now even immune to vancomycin, a powerful antibiotic that is normally used only as a last resort when other drugs fail. But when Appendino, Gibbons, and their colleagues applied extracts from five major cannabinoids to bacterial cultures of six strains of MRSA, they discovered that the cannabinoids were as effective at killing the bugs as vancomycin and other antibiotics. "The cannabinoids even showed exceptional activity against the MRSA strain that makes extra amounts of the proteins that give the bugs resistance against many antibiotics," says Gibbons. These proteins, he explains, allow the bacteria to "hoover up unwanted things from inside the cell and spit them out again." source: http://abcnews.go.co...=5787866&page=1 High ExpectationsResearch into medicinal marijuana grows up. By Amanda Schaffer This summer, British and Italian researchers found that in a laboratory plate, molecules in marijuana can slay the superbug methicillin-resistant staphylococcus aureus, which recently infected seven babies and four employees in a Yonkers, N.Y., maternity ward, heightening fears of outbreaks in schools and locker rooms, as well as in its more familiar breeding grounds, hospitals and nursing homes. In theory, compounds derived from the cannabis plant could someday serve in topical creams for patients with MRSA or other antibiotic-resistant infections. This isn't the first time marijuana has tantalized the world as a possible wonder drug. In recent years, compounds in cannabis or related molecules have been shown to slow the growth of lung tumors in mice, decrease hardening of the arteries in rats, and boost the egg-binding capability of tobacco smokers' sperm. Research on the receptors that THC and other cannabis compounds attach to—and the nitty-gritty mechanisms by which they exert their effects—has been booming. So has work on native molecules, called endocannabinoids, that bind to the same sites. These molecular interactions affect a wide range of functions, from appetite to inflammation to the perception of pain. The onslaught of basic science has helped to separate cannabis from an association with hippies and recreational pot smokers. It has also spurred hopes that these molecules (or similar ones) might prove therapeutic for traumatic brain injury, inflammatory bowel disease, allergic contact dermatitis, atherosclerosis, osteoporosis, and Alzheimer's disease, among others. For all the razzle-dazzle, though, potential treatments frequently seem stuck in perpetual adolescence. Research on traumatic brain injury seemed promising but got mixed results in human clinical trials, while most of the others simply haven't gotten very far in the experimental process. Still, a few prospects show signs of inching toward adulthood. The most enticing are aimed at lessening pain associated with nerve damage and improving some symptoms of multiple sclerosis. Between 2007 and this summer, several randomized clinical trials have found that smoking marijuana can relieve pain in patients with nerve degeneration caused by HIV or other disorders. Compounds in cannabis also seem to reduce nerve pain and possibly decrease spastic movements in people with MS. A drug called Sativex—which delivers two cannabis compounds in a spray under the tongue—is now in late-stage clinical trials in Europe for MS patients. Much as we've heard the hype before, these findings deserve some notice even from the jaded. Studying the upside of marijuana can be a bureaucratic nightmare. In 1970, Congress deemed it a Schedule 1 drug, meaning that it has a high potential for abuse and "no currently accepted medical use"—making research on possible benefits a tough sell. In the 1980s, the Food and Drug Administration approved Marinol, an oral formulation of THC, the most psychoactive ingredient in cannabis, to treat nausea and vomiting associated with chemotherapy. Later, it also approved Marinol to boost the appetites of people with AIDS. But Marinol was never fully accepted by patients, says Donald Abrams, a professor of clinical medicine at the University of California-San Francisco. It took effect more slowly than smoked marijuana and was also more psychoactive. (When THC enters the bloodstream from the digestive tract, it is broken down by the liver into even more psychoactive molecules.) Nor has Marinol been approved in the United States to treat pain. Those who wished to push research further—whether by studying smoked marijuana, developing better formulations, or testing cannabis for other conditions—got no love from the federal government. Some did get a boost, however, from the state of California, which paid for the recent work on cannabis smoking and pain. In 2000, the state funded the University of California's Center for Medicinal Cannabis Research, which vets research proposals with an NIH-style review process, pays for projects, and helps scientists navigate state and federal regulations. The center helps researchers obtain cannabis cigarettes, for instance, and deal with federal rules for record-keeping and security—like making sure the safe in which the drug is stored is properly bolted to the floor, says director Igor Grant. The work has moved slowly, but it's finally paying off with a handful of publications. The first clinical-trial-based paper, which appeared in Neurology in 2007, was a randomized study of 50 patients with HIV-related nerve damage, which can cause discomfort often described as aching, painful numbness, or burning. Those who smoked cannabis each day reported a 34 percent decrease in chronic pain—an effect that's on par with medications often used for this condition, like anti-convulsants and antidepressants, says Abrams. Two other randomized clinical trials, published in June and August, found similarly clear benefits. The June study focused on patients with pain related to a range of neurological conditions, including spinal cord injury. The August paper focused again on HIV-related symptoms. Both found that patients who smoked cannabis reported significantly less pain than those who used dummy cigarettes. These studies were relatively small, but cumulatively they are persuasive. Other recent research suggests that cannabis can relieve MS-related pain and may be able to help other symptoms, too. Sativex, which contains THC and cannabidiol, a nonpsychoactive compound, and is absorbed through the mouth, is already approved in Canada for cancer-related pain and nerve pain associated with MS. In 2007, this randomized clinical trial of 189 MS patients found that those who took Sativex self-reported a significant decrease in involuntary muscle spasms. (The study was funded by GW Pharmaceuticals, the British company that developed the drug.) Researchers are now conducting a late-stage clinical trial of Sativex in MS patients across five European countries. The company has also begun a Phase II/III clinical trial in the United States for patients with cancer-related pain. Sativex may offer particular advantages because it is neither smoked nor swallowed: It does not introduce toxins to the lungs, as smoking does. It enters the bloodstream rapidly but does not pass initially to the liver, as oral formulations do, which prevents it from getting broken down as quickly and may make it less psychoactive. (GW Pharmaceuticals says that patients who take Sativex tend not to experience psychoactive side effects at normal dosage levels.) source: http://www.slate.com/id/2203922/ Study Says Cannabinoids Show Exceptional Antibacterial Activity Against MRSA Video http://www.liveleak...._1241032173&c=1 Cannabis Science, Inc. (OTCBB: GFON). Dr. Robert Melamede, PhD., Director and Chief Science Officer, reported to the Board on the current state of research into the use of natural plant cannabinoids to reduce the spread of drug-resistant bacteria, including methicillin-resistant Staphyloccus aureus (MRSA), and the prospects for development of topical whole-cannabis treatments. Acco More..rding to studies published in the Journal of the American Medical Association and by the Center for Disease Control in 2007, MRSA is responsible for more than 18,500 hospital-stay related deaths each year, and increased direct healthcare costs of as much as $9.7 billion. Dr. Melamede stated, “Research into use of whole cannabis extracts and multi-cannabinoid compounds has provided the scientific rationale for medical marijuana’s efficacy in treating some of the most troubling diseases mankind now faces, including infectious diseases such as the flu and HIV, autoimmune diseases such as ALS (Lou Gehrig’s Disease), multiple sclerosis, arthritis, and diabetes, neurological conditions such as Alzheimer’s, stroke and brain injury, as well as numerous forms of cancer. One common element of these diseases is that patients often suffer extended hospital stays, risking development of various Staphyloccus infections including MRSA. Read the rest here: http://govaporize.co...ant-infections/ Cannabis Compounds Reduce Multi-Drug Resistant Infections Study Says Cannabinoids Show "Exceptional" Antibacterial Activity Against MRSA SAN FRANCISCO--(BUSINESS WIRE)--Cannabis Science, Inc. (OTCBB: GFON). Dr. Robert Melamede, PhD., Director and Chief Science Officer, reported to the Board on the current state of research into the use of natural plant cannabinoids to reduce the spread of drug-resistant bacteria, including methicillin-resistant Staphyloccus aureus (MRSA), and the prospects for development of topical whole-cannabis treatments. According to studies published in the Journal of the American Medical Association and by the Center for Disease Control in 2007, MRSA is responsible for more than 18,500 hospital-stay related deaths each year, and increased direct healthcare costs of as much as $9.7 billion. Dr. Melamede stated, “Research into use of whole cannabis extracts and multi-cannabinoid compounds has provided the scientific rationale for medical marijuana’s efficacy in treating some of the most troubling diseases mankind now faces, including infectious diseases such as the flu and HIV, autoimmune diseases such as ALS (Lou Gehrig’s Disease), multiple sclerosis, arthritis, and diabetes, neurological conditions such as Alzheimer’s, stroke and brain injury, as well as numerous forms of cancer. One common element of these diseases is that patients often suffer extended hospital stays, risking development of various Staphyloccus infections including MRSA. A topical, whole-cannabis treatment for these infections is a functional complement to our cannabis extract-based lozenge.” Investigators at Italy's Universita del Piemonte Orientale and Britain's University of London, School of Pharmacy reported in the Journal of Natural Products that five cannabinoids - THC, CBD, CBG, CBC, and CBN - "showed potent antibacterial activity" and "exceptional" antibacterial activity against two epidemic MRSA occurring in UK hospitals. The authors concluded: "Although the use of cannabinoids as systemic antibacterial agents awaits rigorous clinical trials, … their topical application to reduce skin colonization by MRSA seems promising. … Cannabis sativa … represents an interesting source of antibacterial agents to address the problem of multidrug resistance in MRSA and other pathogenic bacteria." About Cannabis Science, Inc. Cannabis Science, Inc. is at the forefront of medical marijuana research and development. The Company works with world authorities on phytocannabinoid science targeting critical illnesses, and adheres to scientific methodologies to develop, produce, and commercialize phytocannabinoid-based pharmaceutical products. In sum, we are dedicated to the creation of cannabis-based medicines, both with and without psychoactive properties, to treat disease and the symptoms of disease, as well as for general health maintenance. source: http://www.businessw...amp;newsLang=en How Cannabis Could Save Your Life The list of medical uses for marijuana (Cannabis Sativa) continues to grow. The Journal of Natural Products recently published a paper outlining the newly isolated antibiotic effects of the class of molecules known as cannabanoids. This group includes the non-psychoactive cannabichromene, cannabigerol, and cannabidiol but also includes the well-known and definitely psychotropic tetrahydrocannabinol (THC). Researchers believe that the powerful antibiotic effects of cannabanoids can be enlisted in the increasingly difficult fight against MRSA (Methicillin-Resistant Staphylococcus Aureus) and other ’superbugs’ that have evolved resistances to most modern antibiotics. MRSA is perhaps the best known of these superbugs, often running rampant in hospitals, with estimates of up to 1.2 million hospital patients becoming infected and possibly over 100,000 patients dying each year in the United States due to lack of effective medicines against them. The known effectiveness of cannabanoids and the fact that they have not been used before, and therefore no bacteria has yet developed a resistance to them, could prove to be a very valuable tool in the arms race against these constantly changing bacterial strains. In some ways the notion of cannabis having antibiotic effects is counterintuitive. This is because it has been proven that the act of smoking marijuana actually increases vulnerability to infections. This vulnerability however seems to be a result of inhaling marijuana smoke or even smoke in general and likely has little to do with the presence or absence of cannabanoids. Contrastingly, cannabis sativa itself, when not smoked, has been known since the 1950s to have strong antibacterial properties. However, as the technology of looking into how molecules are structured and how they interact was in its infancy at the time, the researchers were unable to determine which marijuana compounds were actually causing the antibacterial effects. As the social and research climates started to grow increasingly hostile to the investigation of black-listed substances in the US and around the world, antibiotic cannabis studies were soon shelved and ignored until they were finally picked up again fairly recently by modern science. With all of the advances in chemical analysis made since the fifties, the new batch of scientists studying cannabis related antibiotics were now able to pinpoint the basic backbone structure that is common to all cannabanoids, to be the active component in killing off bacteria. Now that the bio-active section of the cannabanoid molecules has been identified, researchers and drug makers are busy developing and testing antibiotic drugs as well as considering potential uses for cannabanoids in various soaps and cleaning products. At present they are focusing their efforts on the derivatives of the non-psychoactive cannabanoids. This is presumably because the US FDA, and other governing bodies world-wide, might have a hard time with people getting high in order to cure a bacterial infection; not to mention getting high by just washing their hands. source: http://www.environme...-save-life/2712
  17. Gordon Wiltsie / Getty ImagesA compound found in marijuana can treat schizophrenia as effectively as antipsychotic medications, with far fewer side effects, according to a preliminary clinical trial. Researchers led by Markus Leweke of the University of Cologne in Germany studied 39 people with schizophrenia who were hospitalized for a psychotic episode. Nineteen patients were treated with amisulpride, an antipsychotic medication that is not approved in the U.S., but is comparable to other medications that are. The rest of the patients were given cannabidiol (CBD), a substance found in marijuana that is thought to be responsible for some of its mellowing or anxiety-reducing effects. Unlike the main ingredient in marijuana, THC, which can produce psychotic reactions and may worsen schizophrenia, CBD has antipsychotic effects, according to previous research in both animals and humans. Neither the patients nor the scientists knew who was getting which drug. At the end of the four-week trial, both groups showed significant clinical improvement in their schizophrenic symptoms, and there was no difference between those getting CBD or amisulpride. (MORE: The Complex Link Between Marijuana and Schizophrenia) “The results were amazing,” says Daniel Piomelli, professor of pharmacology at the University of California-Irvine and a co-author of the study. “Not only was [CBD] as effective as standard antipsychotics, but it was also essentially free of the typical side effects seen with antipsychotic drugs.” Antipsychotic medications can potentially cause devastating and sometimes permanent movement disorders; they can also reduce users’ motivation and pleasure. The new generation of antipsychotic drugs also often leads to weight gain and can increase diabetes risk. These side effects have long been known to be a major obstacle to treatment. In the German study, published online in March by the journal Translational Psychiatry, weight gain and movement problems were seen in patients taking amisulpride, but not CBD. “These exciting findings should stimulate a great deal of research,” says Dr. John Krystal, chair of psychiatry at Yale University School of Medicine, who was not associated with the research. He notes that CBD not only had fewer side effects, but also seemed to work better on schizophrenia’s so-called “negative symptoms,” which are notoriously hard to treat. Negative symptoms include social withdrawal, blunting of pleasure and lack of motivation, which commonly occur in schizophrenia. Since current antipsychotic medications can themselves cause the same problems, however, it wasn’t clear whether CBD was better than amisulpride at treating these symptoms, or whether CBD simply caused fewer side effects to begin with. (MORE: Stoned Driving Nearly Doubles the Risk of Fatal Car Crash) Nevertheless, the new research helps elucidate the intricate complexities of the brain’s natural cannabinoid system and how CBD may work to alleviate symptoms of schizophrenia. Years ago, Piomelli and his colleagues discovered that people with schizophrenia have elevated levels of anandamide — a neurotransmitter that activates the same receptor activated by THC — in their cerebrospinal fluid, suggesting that they also had higher levels of it in the brain. The difference was huge: anandamide levels were nine times higher in schizophrenic people than in mentally healthy controls, Piomelli says. The researchers theorized that these radically high levels would correlate with hallucinations and delusions: the more anandamide bathing patients’ brains, the worse their disease would be. The thinking was, in essence, that people with schizophrenia are constantly high on their own natural THC. But what the researchers actually found was the opposite. “What you get is not a positive correlation, but a negative one. The higher the levels of anandamide, the lower the symptoms,” Piomelli says. It didn’t seem to make much sense at first, but research in both animals and humans now shows that anandamide is a natural stress reliever and antipsychotic. Piomelli thinks that the high levels seen in people with schizophrenia aren’t the cause of the problem, but the result of the brain’s attempts to solve it. (MORE: Study: Smoking Marijuana Not Linked with Lung Damage) The new study confirmed that as CBD relieved patients’ symptoms, anandamide levels rose in concert. “It looks like anandamide is a signaling molecule that has evolved to help us cope with stress,” Piomelli says. “In the brain, everything it does seems to be related to ways of relieving stress. It can relieve anxiety and reduce the stress response. It is involved in stress-induced analgesia [when you stop feeling pain while fighting or fleeing]. These are all mechanisms to help us prevent [negative outcomes related to stress],” says Piomelli. “If Dr. Piomelli is right, then the brain is exquisitely sensitive to changes in anandamide levels,” says Krystal. This raises another question, however. THC itself mimics anandamide. If high levels of anandamide are helpful for schizophrenia, why does marijuana smoking intensify psychotic states? Here’s where it gets complex. THC mimics not only anandamide, but also another cannabinoid, 2-AG, which fits the same receptors and is far more common. “There is 200 times more 2-AG than anandamide in the brain,” Piomelli says. “At the end of the day, the complexity is such that 2-AG has a whole cluster of effects. Anandamide has completely different effects, sometimes even opposite effects. That is why with THC you get a big mess.” (MORE: Marijuana May Both Trigger and Suppress Psychosis) Complicating matters further, when chronic marijuana smokers build up a tolerance to THC, it may down-regulate the entire system, making it harder for anandamide to have its positive effects. This may be why some studies find that people with schizophrenia who smoke marijuana get worse. So, where does CBD fit in? It doesn’t attach to a receptor like THC, or fool the brain into thinking that it’s getting extra anandamide or 2-AG. “What CBD seems to be doing is preventing anandamide from being destroyed,” says Piomelli. That allows the substance to exert its stress-reducing and antipsychotic effects on the brain longer, without the negative effects of THC. If replicated, the results suggest that CBD may be at least as effective as existing drugs for the treatment of schizophrenia, without the severe side effects that make patients reluctant to take medication. The catch: “The real problem with CBD is that it’s hard to develop for a variety of silly reasons,” says Piomelli. Because it comes from marijuana, there are obvious political issues surrounding its use. Extracting it from the plant is also expensive. But the biggest barrier may be that CBD is a natural compound, and therefore can’t be patented the way new drugs are. That means that despite the possibility that it could outsell their current blockbuster antipsychotic drugs, pharmaceutical companies aren’t likely to develop it — a particularly striking fact when you consider that every major manufacturer of new generation antipsychotics in the U.S. has so far paid out hundreds of millions or billions of dollars in fines for mismarketing these drugs. Yet they still reaped huge profits. (MORE: The Case Against the Ban on ‘Bath Salts’ and Fake Marijuana) Piomelli and others are working to develop synthetic versions of CBD that would avoid such hurdles. “We have one and are hoping to move forward in the near future,” he says. For people with schizophrenia and their families, of course, it is likely to be infuriating that non-scientific issues like marijuana policy and patenting problems could stand in the way of a treatment that could potentially be so restorative. While it’s possible that these study results may not hold up or that researchers could discover problems related to long-term use of CBD, it’s hard to imagine that they could be any worse than what patients already experience. Maia Szalavitz is a health writer for TIME.com. Find her on Twitter at @maiasz. You can also continue the discussion on TIME Healthland’s Facebook page and on Twitter at @TIMEHealthland. Read more: http://healthland.time.com/2012/05/30/marijuana-compound-treats-schizophrenia-with-few-side-effects-clinical-trial/#ixzz1wblOwaHI
  18. Impulsive Behavior Regulated By Cannabinoid 2 Receptors Main Category: Psychology / Psychiatry Also Included In: Schizophrenia; Bipolar Article Date: 11 Mar 2012 - 0:00 PST A new study lead by the Neuroscience Institute of Alicante reveals how manipulating the endocannabinoid system can modulate high levels of impulsivity. This is the main problem in psychiatric illnesses such a schizophrenia, bipolar disorder and substance abuse. Spanish researchers have for the first time proved that the CB2 receptor, which has modulating functions in the nervous system, is involved in regulating impulsive behaviour. "Such a result proves the relevance that manipulation of the endocannabinoid system can have in modulating high levels of impulsivity present in a wide range of psychiatric and neurological illness," explains SINC Jorge Manzanares Robles, a scientist at the Alicante Neuroscience Institute and director of the study. Carried out on mice, the study suggests the possibility of undertaking future clinical trials using drugs that selectively act on the CB2 and thus avoid the psychoactive effects deriving from receptor CB1 manipulation, whose role in impulsivity has already been proven. However, the authors of the study published in the British Journal of Pharmacology remain cautious. Francisco Navarrete, lead author of the study, states that "it is still very early to be able to put forward a reliable therapeutic tool." The study assessed the actions of two cannabinoid drugs that stimulate and block CB2 in the mouse strain showing high levels of impulsivity. The scientists then analysed whether these drugs were capable of modulating impulsive behaviour and the cerebral modifications associated with this change in behaviour. The authors concluded that CB2 receptor activity modulation reduced impulsive behaviour in mice, depending on the patterns that governed the administration of each drug. Furthermore, the genetic expression levels of CB2 tended to return to normal, leaning towards strains that had little impulsivity. The Endocannabinoid System
  19. Does Cannabis help with Parkinson's? Answer: Improve YES, Nearly half of Parkinson's disease patients who have tried marijuana say the drug helped relieve their symptoms, according to a survey of patients with the degenerative neurological disorder. Dr. Evzin Ruzicka, an attending neurologist at Charles University in Prague in the Czech Republic, reported the findings here at the Movement Disorders Society's Seventh International Congress of Parkinson's Disease and Movement Disorders. Ruzicka is also a consultant at the Prague Movement Disorders Center. "It's difficult to directly study the medical effects of cannabis in the Czech Republic, where we conducted our research, because of its illegal status," Ruzicka told Reuters Health. "Therefore, we had to conduct anonymous surveys. To our knowledge, this is the first study to assess the effect of cannabis on Parkinson's disease, and our findings suggest it may alleviate some symptoms." Ruzicka and his colleagues chose to investigate marijuana's effects on Parkinson's disease after hearing from several patients that they had tried the drug and it had helped them. The investigators asked all patients who were treated for Parkinson's disease at their center to complete a questionnaire that asked about cannabis use and about several Parkinson's disease symptoms, including overall symptoms; tremor while at rest; bradykinesia, or slow movement; muscle rigidity; and dyskinesias, or involuntary movements. Dyskinesias are caused by levodopa, the mainstay medication in Parkinson's treatment. Among the 630 patients to whom the investigators sent questionnaires, 339 (54%) returned them. The responders' average age was about 66, and they had had Parkinson's disease for an average of roughly 9 years. Among the responders, 25% reported that they had used cannabis. Most had used it orally, either as fresh or dried leaves. Within this group, 39 patients (46%) reported that their Parkinson's disease symptoms in general were relieved after they started using cannabis. In terms of specific symptoms, 26 (31%) reported an improvement in tremor while at rest, and 38 (45%) experienced a relief of bradykinesia. Relief of muscle rigidity was reported by 32 (38%), and 12 (14%) said they had an improvement in levodopa-induced dyskinesias. The respondents reported that the improvement in symptoms occurred an average of 1.7 months after they had started using cannabis. Patients who used it for at least three months were more likely to experience symptom relief than those with shorter experience, the investigators reported. This delay between the beginning of cannabis use and the relief of symptoms made it unlikely that the respondents were having a placebo effect, Ruzicka said. A placebo effect can occur when the individual taking a treatment experiences a benefit even if the "treatment," such as a sugar pill, contains no active ingredients. They found no relationship between the length of cannabis use and the effect on involuntary movements. However, daily marijuana users reported more improvement in their dyskinesias than those using it less often. The investigators speculated that the effect of cannabis on Parkinson's disease symptoms may be due to interaction among cannabis, certain brain receptors that respond to cannabis and endogenous cannabinoids or cannabis-like substances within the body. He and colleagues plan to investigate a relationship between cannabis use and relief of Parkinson's disease symptoms by collaborating in further studies with investigators in the United Kingdom, Ruzicka told Reuters Health. Read more: http://wiki.answers....e#ixzz1umRR3dgN Parkinson’s Disease and the THCV in cannabis. New British and Spanish research on one of cannabis’ cannabinoids show its great potential for treating Parkinson’s disease. The cannabinoid is the lesser known but hugely interesting THCV, aka Delta-9-tetrahydrocannabivarin. The molecule is present to varying decrees in different strains of cannabis, from trace amounts to a hefty proportion. Unlike your own body’s cannabinoid anandamide, or its phyto(plant based)-cannabinoid cousin, THC, THCV does not activate CB1 receptors in your endocannbinoid regulatory system. Activation of these CB1 receptors, found mainly on nerve cells, is responsible for most of THC’s psychoactive effects and medical benefits. THC also activates CB2 receptors, found more on immune cells and thought responsible for some of cannabis’ beneficial effects on some autoimmune disorders. Like THC, THCV also binds with and activates these CB2 receptors. Like THC, THCV is a powerful antioxidant, capable of sopping up cell-killing free radicals. Unlike THC, THCV does not activate CB1 receptors. Instead, it blocks (serves as an antagonist to) the activation of the CB1 system. It may play a major role in future treatments of cardiometabolic diseases and obesity. Posted by Don Fitch under anandamide, cannabinoids, phytocannabinoids Parkinson’s disease Spanish and British researchers investigated the effects of Delta-9- tetrahydrocannabivarin (THCV) in an animal model of Parkinson’s disease. They concluded that “given its antioxidant properties and its ability to activate CB2 but to block CB1 receptors, Delta-9-THCV has a promising pharmacological profile for delaying disease progression in PD and also for ameliorating parkinsonian symptoms.” (Source: García C, et al. Br J Pharmacol. 2011 Feb 16. [in press]). What is THCv? Tetrahydrocannabivarin— abbreviated in THCv— is a cannabinoid substance that occurs in the plant known to the scientific community as Cannabis Sativa, from which marijuana is made. THCv originally grew in Central Asia and on the Indian Subcontinent, where it may have been a component in the drug known as soma; an archeologist discovered traces of it in a Zoroastrian temple. (The drug of the same name in "Brave New World" is quite different.) Then, as now, the medicinal potential of cannabis was was widely recognized. THCV is what scientists call a CB1 receptor antagonist— that is, it inhibits the release of the psychoactive THC, which is a partial agonist on the CB1 and CB2 receptors on the central nervous and immune systems respectively. CB1 contributes to certain types of hypotension and also plays a role in pain transmission. CB2 appears to have a part in the functions of white blood cells. Another cannabinoid substance, called THCa (trans- 4- hydroxycrotonic acid), is commonly used for scientific research. Its molecular structure is considerably less complex than that of THCv. Raw cannabis consists primarily of this ingredient, which, like THCv, is being promoted for its medicinal properties: Some research has shown can be used to treat cancer by inhibiting the growth of tumorous cells. It can also be used as an antispasmodic. THCa is known, in fact, to be responsible for both the good and the bad effects that marihuana has on people-- it gives the drug its medicinawl value, but also causes its intense high. Both compounds are non- psychoactive. Hemp does not produce THCa. THCV is what scientists call a CB1 receptor antagonist— that is, it inhibits the release of the psychoactive THC, which is a partial agonist on the CB1 and CB2 receptors on the central nervous and immune systems respectively. CB1 contributes to certain types of hypotension and also plays a role in pain transmission. CB2 appears to have a part in the functions of white blood cells. Another cannabinoid substance, called THCa (trans- 4- hydroxycrotonic acid), is commonly used for scientific research. Its molecular structure is considerably less complex than that of THCv. Raw cannabis consists primarily of this ingredient, which, like THCv, is being promoted for its medicinal properties: Some research has shown can be used to treat cancer by inhibiting the growth of tumorous cells. It can also be used as an antispasmodic. THCa is known, in fact, to be responsible for both the good and the bad effects that marihuana has on people-- it gives the drug its medicinawl value, but also causes its intense high. Both compounds are non- psychoactive. Hemp does not produce THCa. My link http://www.youtube.com/watch?v=cvHTSAGqxXQ Cannabis Use, Effect And Potential Therapy For Alzheimer's, MS and Parkinson's ScienceDaily (Oct. 14, 2007) — Cannabis (marijuana) is the most widely produced plant-based illicit drug worldwide and the illegal drug most frequently used in Europe. Its use increased in almost all EU countries during the 1990s, in particular among young people, including school students. Cannabis use is highest among 15- to 24-year-olds, with lifetime prevalence ranging for most countries from 20--40% (EMCDDA 2006) Recently there has been a new surge in the level of concern about potential social and health outcomes of cannabis use, although the available evidence still does not provide a clear-cut understanding of the issues. Intensive cannabis use is correlated with non-drug-specific mental problems, but the question of co-morbidity is intertwined with the questions of cause and effect (EMCDDA 2006). Prevention is of importance in adolescents, which is underlined by evidence that early-onset cannabis-users (pre- to mid-adolescence) have a significantly higher risk of developing drug problems, including dependence (Von Sydow et al., 2002; Chen et al., 2005). The illegal status and wide-spread use of cannabis made basic and clinical cannabis research difficult in the past decades; on the other hand, it has stimulated efforts to identify the psychoactive constituents of cannabis. As a consequence, the endocannabinoid system was discovered, which was shown to be involved in most physiological systems -- the nervous, the cardiovascular, the reproductive, the immune system, to mention a few. One of the main roles of endocannabinoids is neuroprotection, but over the last decade they have been found to affect a long list of processes, from anxiety, depression, cancer development, vasodilatation to bone formation and even pregnancy (Panikashvili et al., 2001; Pachter et al., 2006). Cannabinoids and endocannabinoids are supposed to represent a medicinal treasure trove which waits to be discovered. Raphael Mechoulam will tell the discovery story of the endocannabinoid system. His research has not only helped us to advance our understanding of cannabis use and its effects, but has also made key contributions with regard to understanding "neuroprotection," and has opened the door for the development of new drugs. My link Marijuana-like chemicals in the brain may point to a treatment for the debilitating condition of Parkinson's disease. In a study published in Nature, researchers from the Stanford University School of Medicine report that endocannabinoids, naturally occurring chemicals found in the brain that are similar to the active compounds in marijuana and hashish, helped trigger a dramatic improvement in mice with a condition similar to Parkinson's. "This study points to a potentially new kind of therapy for Parkinson's disease," said senior author Robert Malenka, MD, PhD, the Nancy Friend Pritzker Professor in Psychiatry and Behavioral Sciences. "Of course, it is a long, long way to go before this will be tested in humans, but nonetheless, we have identified a new way of potentially manipulating the circuits that are malfunctioning in this disease." Malenka and postdoctoral scholar Anatol Kreitzer, PhD, the study's lead author, combined a drug already used to treat Parkinson's disease with an experimental compound that can boost the level of endocannabinoids in the brain. When they used the combination in mice with a condition like Parkinson's, the mice went from being frozen in place to moving around freely in 15 minutes. "They were basically normal," Kreitzer said. But Kreitzer and Malenka cautioned that their findings don't mean smoking marijuana could be therapeutic for Parkinson's disease. This work was supported by a Ruth L. Kirchenstein Fellowship, the National Institutes of Health and the National Parkinson Foundation. Neither researcher has financial ties to Kadmus Pharmaceuticals. Stanford University Medical Center integrates research, medical education and patient care at its three institutions - Stanford University School of Medicine, Stanford Hospital & Clinics and Lucile Packard Children's Hospital at Stanford. For more information, please visit the Web site of the medical center's Office of Communication & Public Affairs at http://mednews.stanford.edu/.
  20. NaturalNews) Relax! It's just chemo... In an enlightening study in Molecular Cancer Research, researchers found that anyone who gets stressed out before chemotherapy (and who wouldn't...) can awaken the stress protein HSF-1, or heat shock factor-1. This one "side effect" of chemotherapy alone makes the treatment worse than the disease by allowing cancer cells to repair themselves in spite of the poisonous chemo. Even when used "correctly", toxic chemotherapy drugs can kill you, destroy your digestive tract, immune system, vascular system, and cause other cancers later on with the impaired immune system and genetic damage. Most chemotherapeutic drugs are cytotoxic and work by impairing mitosis (cell division), and targeting fast-dividing cells for destruction. Chemotherapy is supposed to kill fast-growing cancer cells but it also targets the body's white blood cells that also grow quickly. This destruction also targets the rapidly growing healthy cells in your hair, digestive system, and bone marrow (where blood cells are produced). Unfortunately, in older tumors and in the center of solid tumors, cell division has already ceased, making them insensitive to chemotherapy even if the chemotherapeutic agent does somehow reach the core of the tumor. Learn more: http://www.naturalne...l#ixzz1vWwe2saM Surviving chemotherapy is not about quality of life Learn more: http://www.naturalnews.com/035902_chemotherapy_toxicity_survival_rates.html#ixzz1vWwjyzle The "double standard" of conventional medicine
  21. Fascinating documentary exposes cancer industry's death agenda: Cut Poison Burn (NaturalNews) As free as many Americans might think they are, there are certain glaring aspects of American life for which individuals are not free to make their own choices, and cancer treatment is one of them. In the sobering documentary Cut Poison Burn, filmmaker Wayne Chesler brings to light the sinister nature of the multi-billion dollar cancer industry, its suppression of any real pursuit of a cure, and its stranglehold on medicine that restricts individuals from choosing their own personalized, alternative forms of treatment. Learn more: http://www.naturalnews.com/035926_cancer_industry_poison_documentary.html#ixzz1vWvzbGQr Cancer is big business for drug companies and the federal government Thomas is not the only victim of the cancer industry, of course -- millions of Americans, including many children, have died on the altar of Big Pharma's cancer machine, and many more will follow unless the People wake up and take their freedoms back. And in order to wake people up to the truth, they need to hear and see the truth as it is plainly laid out in films like Cut Poison Burn. Be sure to watch the official trailer for Cut Poison Burn at the following link, where you can also purchase a DVD or downloadable copy of the film: http://cutpoisonburn.com/ Learn more: http://www.naturalnews.com/035926_cancer_industry_poison_documentary.html#ixzz1vWvv0Tqe
  22. FDG-PET/CT image the article source The Image of Psoriasis By Cliff Collins Despite many recent advances by specialists in understanding psoriasis, too many people, including some doctors, still believe that it is merely a skin problem. So says Dr. Nehal N. Mehta, whose latest research provides further evidence that psoriasis is more than skin deep. Mehta, a preventive and nuclear cardiologist with the University of Pennsylvania Perelman School of Medicine, was lead author of a groundbreaking study, funded by the National Psoriasis Foundation, that used a sophisticated, highly advanced imaging technology to detect areas of inflammation in people with psoriasis. As the researchers expected, the images did show inflamed skin and inflammation in blood vessels. But they were surprised to observe inflammation in other organs and joints in the patients with psoriasis, one of whom also had psoriatic arthritis. The evidence impressed Mehta and his associates, who believe the study provides further evidence that psoriasis and other inflammatory diseases are linked. The images showed inflammation in the liver, joints, tendons and aorta, even though the study participants had no symptoms or apparent risk factors for diseases that affect those organs. The participants who did not have psoriasis did not show any increased inflammation in any of these locations. The study, published in the Archives of Dermatology, adds to a growing body of evidence that people with psoriasis are at a higher risk for heart, joint and liver disease, even when they do not have any symptoms. Mehta was especially interested to discover inflammation in the liver. "For the first time, a study showed liver inflammation is much higher in psoriasis patients when looking in real time," he said. This finding suggests why patients with psoriasis may have high cholesterol and blood sugars, as well as trouble with certain drugs, such as methotrexate or commonly used statin medications for cholesterol, which are metabolized by the liver. 'Seeing' inflammation For the study, Mehta's research team used a highly sensitive imaging technique called fluorodeoxyglucose positron emission tomography—computed tomography, or FDG-PET/CT, which produces images that detect the metabolic activity of tissues within the body. The study's purpose was to learn whether this technique could capture an image of inflammation beyond the skin in patients who have moderate to severe psoriasis to better understand why patients with psoriasis may be at higher risk for heart disease and diabetes. The study produced two main findings. First, it showed that psoriasis as a disease affects the whole body, not just the skin (denoted by the arrows in the image on the previous page). It also showed that FDG-PET/CT imaging is effective for identifying inflammation in the blood vessels, joints and liver, as well as the skin of patients with psoriasis who have not yet shown symptoms of problems in these areas. Mehta explains that FDG-PET/CT combines nuclear medicine—the branch of medicine that uses radiation and radioactive materials to diagnose and treat diseases—with two imaging technologies, PET and CT scans. It most frequently has been used for cancer imaging because this technique is able to show images of cancer cells, which are highly active, with great precision. "This was a pilot study, meaning that it was the first attempt to test whether FDG-PET/CT can be used to detect inflammation in psoriasis and to understand if severe psoriasis affects critical organs beyond the skin," Mehta explained. "We have to keep in mind that the findings we report are based on a single study, and, thus, additional studies are necessary to confirm and extend our findings." Help the National Psoriasis Foundation fund more early-stage research projects like Dr. Nehal Mehta's that could lead to better treatments and a cure for psoriasis and psoriatic arthritis. Support research today » Commenting in Archives of Dermatology, University of Michigan researchers Drs. Johann E. Gudjonsson and Abhishek Aphale noted that, as one of the first studies to show objective evidence of inflammation in the blood vessels and liver of patients with psoriasis, Mehta's research "may eventually lead to earlier and more aggressive treatments and closer monitoring of patients with psoriasis." Mehta says his next step in the research will be to test whether treating psoriasis with certain biologic drugs or with ultraviolet B phototherapy—treatments that reduce psoriasis inflammation—can also help calm inflammation throughout the body. He wants to understand whether these treatments will improve traditional and emerging risk factors for heart disease and diabetes. He also hopes his research will raise awareness among medical providers who still consider psoriasis a cosmetic disease, and demonstrate the need to look beyond skin when confronting the disease. Cliff Collins is a Portland, Ore.-based freelance writer and a regular contributor to Psoriasis Advance.
  23. (NaturalNews) Researchers have reported that when healthy cells were placed in a sample dish with the human immunodeficiency virus (HIV), along with a dose of cannabinoids, the cells, which normally would rather quickly become infected, simply denied entry to the virus, and responded as if it were not a threat at all. Not a replacement for an immune system, but an extra set of hands keeping the wall up READ MORE http://www.naturalne..._marijuana.html
×