Drugs  
comments_image Comments

How Weed Can Protect Us From Cancer and Alzheimer's

Hardly the harmful intoxicant that many once thought it was, cannabis is a nourishing plant that actually improves and prolongs life.
 
 
Share
 
 
 

The following is an excerpt from MARIJUANA: GATEWAY TO HEALTH—How Cannabis Protects Us from Cancer and Alzheimer’s Disease. 

For thousands of years cannabis has been used as a medicine for a remarkably broad range of ailments. Opponents of medical marijuana have claimed that nothing works on so many diverse illnesses and that the only relief offered was one of stupor from being stoned. But in 1988, the first cannabinoid receptor was discovered and since then researchers have learned that there are two types of cannabinoid receptors which are distributed throughout our bodies and that we make chemicals within our bodies—endocannabinoids—that a re similar to the cannabinoids made by the cannabis plant. Both plant and human cannabinoids bind to and influence these receptors in order to discourage the rise and progression of numerous disease processes.

The discovery of the cannabinoid receptor system has changed our entire understanding of cannabis and its effects. In fact, from the inception of the anti-marijuana campaign of the 1930s and its subsequent prohibition until today, almost everything we believed about it was wrong. Hardly the harmful intoxicant that many once thought it was, cannabis is a nourishing plant that can improve and prolong life.

We have recently learned that cannabinoids can help bring our bodies and nervous systems into balance, but what happens when certain compounds block the interaction between endocannabinoids and their receptors, effectively depriving our bodies of sufficient cannabinoids?

It is well known that one of marijuana’s most notable effects is appetite stimulation, or what is colloquially referred to as the “munchies,” a compelling drive to eat and snack. Researchers studying the endocannabinoid system have found that this phenomenon is linked to the activation of the CB1 receptor in the part of the brain that regulates appetite. With the increasing incidence of obesity becoming a public health crisis, scientists have begun to explore the effect of cannabinoids on the regulation of appetite. Researchers working for the international pharmaceutical company Sanofi-Aventis, for example, began looking for chemical agents that effectively block CB1 receptor activity (known as CB1 receptor antagonists), which they reason could help suppress appetite and reduce compulsive eating. The company eventually developed a compound called rimonabant, which appeared to effectively inhibit the ability of cannabinoids to activate the CB1 receptor.

The European Medicines Agency (EMEA) approved rimonabant for use in Europe in mid-2006, and it was soon available in Great Britain as an over-the-counter drug available without prescription.By early 2008, the drug was available in 56 countries. The Food and Drug Administration (FDA), however, refused to approve it for distribution in the United States due to concerns about its possible side effects. This decision was based on the recommendation of an FDA review panel, which in mid-2007 unanimously concluded that rimonabant was associated with unacceptable increases in the risk of adverse psychiatric events, suicidality, neurological problems, nausea, vomiting, and more. Then, in late 2008, the EMEA decided to review the drug’s post-marketing data. Agreeing with the FDA’s belief that the risks of rimonabant outweighed its benefits, the European regulators revoked its previous approval and suspended Sanofi-Aventis’ marketing authorization for the drug.

The first cannabinoid-blocking drug turned out to be a disastrous failure. An alarming number of research subjects in clinical trials around the world (which included 16,000 subjects in the U.S. alone) experienced severe neuropsychiatric side-effects including anxiety, depression, panic attacks, sleep disorders, amnesia, and psychomotor agitation leading to contusions, concussions, falls, traffic accidents, and whiplash injuries. Others had gastrointestinal symptoms and erectile dysfunction at a rate three times higher than those who had not received the drug. One patient experienced an increase in multiple sclerosis symptoms and another developed optic neuritis. Two committed suicide. Rimonabant also appeared to promote the development of neurodegenerative illnesses such as Alzheimer’s disease, ALS, Parkinson’s disease, and Huntington’s disease.