Medicinal Information

TetrahydrocannabinolThere are marked differences in the knowledge on the medical uses of cannabis and cannabinoids in different diseases. For nausea and vomiting associated with cancer chemotherapy, anorexia and cachexia in HIV/AIDS, spasticity in multiple sclerosis and spinal cord injury there is strong evidence for medical benefits. For many other indications, such as epilepsy, movement disorders and depression there is much less available data.

Clinical studies with single cannabinoids or, less often with whole plant preparations (smoked marijuana, encapsulated cannabis extract) have often been inspired by positive anecdotal experiences of patients employing crude cannabis products. The anti-emetic, the appetite enhancing, relaxing effects, analgesia, and therapeutic use in Tourette's syndrome were all discovered in this manner.

Incidental observations have also revealed therapeutically useful effects in a study with patients with Alzheimer's disease wherein the primary issue was an examination of the appetite- stimulating effects of THC. Not only appetite and body weight increased, but disturbed behaviour among the patients also decreased. The discovery of decreased intraocular pressure with THC administration in the beginning of the 1970s was also serendipitous. For this reason, more surveys have been conducted in the past decade questioning individuals that use cannabis therapeutically.

Does cannabis use cause heart attacks?


Technical terms:
- Angina = Feeling of discomfort in the chest or chest pain due to heart disease
- Beta-blockers = class of drugs used for the treatment of high blood pressure and heart diseases
- Coronary = with regard to the arteries of the heart
- Coronary disease (coronary heart disease) = narrowing of the arteries of the heart
- CRP (C-reactive protein) = indicator of inflammation
- Exercise time = Time in a stress test that tests heart function
- Longitudinal epidemiological studies = studies that follow a certain group of people (often several hundreds or thousands) for a long period of time to discover differences in subgroups, for example in dependency of life style and habits
- Myocardium = heart muscle
- Myocardial = with regard to the heart muscle
- Myocardial infarction = heart attack

(Murray A. Mittleman and colleagues):
We interviewed 3882 patients (1258 women) with acute myocardial infarction an average of 4 days after infarction onset. (...) Of the 3882 patients, 124 (3.2%) reported smoking marijuana in the prior year, 37 within 24 hours and 9 within 1 hour of myocardial infarction symptoms. (...) The risk of myocardial infarction onset was elevated 4.8 times over baseline (95% confidence interval, 2.4 to 9.5) in the 60 minutes after marijuana use. The elevated risk rapidly decreased thereafter. Conclusion: Smoking marijuana is a rare trigger of acute myocardial infarction.
Mittleman MA, Lewis RA, Maclure M, Sherwood JB, Muller JE. Triggering Myocardial Infarction by Marijuana. Circulation 2001;103(23):2805-2809.

(Lindesmith Center (USA)):
An analysis of the research methods used [in the study of Mittleman and colleagues] reveals glaring flaws. The sample size is statistically insignificant, no casual relationship has been established, and the study itself has never been replicated. (...) Out of 3,882 patients who had heart attacks, 124 were current marijuana smokers and 9 had smoked within an hour of their heart attack. Based on this minuscule, self-selected sample, Dr. Mittleman concludes that the risk of a heart attack is 4.8 times higher after smoking marijuana. The sample size alone renders the results meaningless. Assuming that Dr. Mittleman's conclusions are correct, the fact that heart attack risk for an otherwise healthy 50-year-old man is about 10 in 1 million highlights the sensationalism of the widespread publicity the study is receiving.
Lindesmith Newsletter. Junk Science Makes Headlines. Questionable Study Links Marijuana Smoking and Heart Attacks. June 15, 2001.

(L.A. Gottschalk and colleagues):
In view of associated findings that marijuana smoking decreased myocardial oxygen delivery, decreased exercise time until the onset of anginal pain, and increased myocardial oxygen demand in anginal patients, the use of marijuana by such patients is clearly inadvisable. Gottschalk LA, Aronow WS, Prakash R. Effect of marijuana and placebo-marijuana smoking on psychological state and on psychophysiological cardiovascular functioning in anginal patients.
Biol Psychiatry 1977;12(2):255-266.

(Franjo Grotenhermen):
The overall effect of cannabis use on the frequency of heart attacks is unknown. This can only be ascertained in longitidudinal epidemiological studies. There are some studies and case reports that support the assumption that cannabis use may be harmful in people with coronary disease and may trigger a heart attack. However, this seems to be a very rare event. Cannabis will not cause a heart attack in a healthy person.
There are some pharmacological effects of cannabis that may act preventive and some that may be damaging.

Factors that may be damaging:
- The decrease of oxygen delivery to the heart (only if cannabis is smoked), due to the production of carbon monoxide.
- The increase of heart rate of about 45% on average in the first hour after smoking. Thus a normal heart rate of 70 may increase to about 100. This increases labour and thus oxygen demand (or oxygen need) of the heart muscle.
- Changes of blood pressure. Cannabis may cause the blood pressure to increase when the person is lying down, and to decrease when the person stands up.

Factors that might be preventive:
- If the angina is based on a spastic contraction of the coronary arteries, cannabis may relax the spasm.
- Cannabinoids reduce platelet aggregation, thus they may reduce the tendency of the blood to form clots.
- Cannabinoids act anti-inflammatory. Inflammation measured as the level of CRP is associated with a higher risk of heart attack.
In coronary disease the heart attack risk of cannabis use may be as high as going for a walk or having sex. So if you feel chest pain while walking or if you know that you have a severe coronary disease you should better not take cannabis or only in low doses that do not significantly increase heart rate. These low doses are often high enough for the therapeutic effectiveness of cannabis. You can measure your heart rate yourself and find out how it changes in reaction to cannabis. In case of an accidential overdose you can prevent the increase of heart rate by taking a beta-blocker.

Can cannabis be helpful in gastric ulcers?


(Franjo Grotenhermen):
There are no clinical studies with cannabinoids in gastric ulcers. However, THC and other substances that bind to the cannabinoid-1-receptor (CB1 receptor agonists) inhibited the gastric acid production in humans and the formation of ulcers in animals.

(Roger Pertwee):
The nervous system of the bowel of several species, including the mouse, rat, guinea pig and humans, contains cannabinoid CB1 receptors that depress motility of stomach and intestine. (...)
Gastric acid secretion is also inhibited in response to CB1 receptor activation, although the detailed underlying mechanism has yet to be elucidated. Cannabinoid receptor agonists delay gastric emptying in humans as well as in rodents and probably also inhibit human gastric acid secretion. (...)
The extent to which the effects on gastrointestinal function of cannabinoid receptor agonists or antagonists/inverse agonists can be exploited therapeutically has yet to be investigated as has the extent to which these drugs can provoke unwanted effects in the gastrointestinal tract when used for other therapeutic purposes.
Modified according to: Pertwee RG. Cannabinoids and the gastrointestinal tract. Gut 2001;48(6):859-867.

(Adami et al.):
In anaesthetized rats the non selective CB-receptor agonist WIN 55,212-2 and the selective CB(1)-receptor agonist HU-210 dose-dependently decreased the acid secretion. (...) Our results indicate that the antisecretory effects of cannabinoids on the rat stomach are mediated by suppression of the activity of the vagus nerve on the stomach through activation of CB1 receptors.
Modified according to: Adami M, et al. Gastric antisecretory role and immunohistochemical localization of cannabinoid receptors in the rat stomach. Br J Pharmacol 2002;135(7):1598-1606.

(Sofia et al.):
Delta-9-tetrahydrocannabinol (THC) inhibited ulcer formation in the rat. However, this antiulcer activity of THC was substantially less than for tridihexethyl chloride.
Modified according to: Sofia RD, et al. Evaluation of antiulcer activity of delta9-tetrahydrocannabinol in the Shay rat test. Pharmacology 1978;17(3):173-177.

(Nalin et al.):
In 90 volunteers participating in a vaccine-development programme consumption of beer more than 3 days a week was linked with high stomach acid output, and smoking of cannabis greater than 2 days a week was linked with low acid output.
Source: Nalin DR, et al. Cannabis, hypochlorhydria, and cholera. Lancet 1978;2(8095):859-862.

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