How Weed Can Protect Us From Cancer and Alzheimer's
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 are 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.
Evidence also suggested that rimonabant could increase the likelihood of colon cancer. A study at the University of Texas published in August 2008, for example, found that mice treated with a CB1 receptor blocking drug—like rimonabant—had increases in the size and number of colon polyps, which are benign tumors that can become cancerous if not removed. Conversely, the study found that treatment with endocannabinoid activators—like THC from marijuana—decreased the number of polyps. In other words, while blocking the cannabinoid receptor increased the likelihood of colon polyps, stimulating it decreased that likelihood. Rimonabant and marijuana apparently have opposite effects on the likelihood of developing colon cancer. This suggests that it would be wise to conduct follow-up studies to assess the impact of rimonabant on increases in colon cancer. The damage already done by rimonabant may be beyond calculation. By 2007, before the EMEA suspended its approval, about 37,000 patients in the U.K. were using the drug. Even worse, although it is prohibited in both Europe and the U.S., rimonabant is still marketed over the Internet to unsuspecting consumers as a weigh-loss drug by Indian pharmaceutical companies.
The global policing organization INTERPOL states on its Web site that “member countries remain firmly committed to their enforcement efforts against the cultivation and trafficking of cannabis products.” Given what we know about the beneficial nature of cannabis and the harmful effects of cannabinoid-blocking drugs, it makes little sense that the eradication efforts of INTERPOL and other law enforcement organizations are more focused on marijuana than they are on drugs that are—like rimonabant—actually proven to be dangerous.
The suppression of the endocannabinoid system has been connected to numerous health-related problems, involving cognitive function, sleep cycles, digestion, sexual response, physical coordination, and overall happiness. In order to study the endocannabinoid system scientists have selectively bred mice with a specific genetic mutation that disables the CB1 receptors. Studies of these “CB1 knockout mice” have shown that an absence of activity at the CB1 receptor has devastating effects on the physical and mental health of these animals. These effects include:
Increased anxiety, increased susceptibility to the depressive effects of chronic stress
Reduced responsiveness to rewarding experiences
Reduced appetite and pronounced weight loss
Reduced ability to forget traumatic memories
Increased activity in the HPA axis, an area of the brain associated with stress and fear
Increased susceptibility to neurotoxins
Reduced ability to regenerate neurons in the hippocampus
Reduced amounts of trophic factors (biological compounds associated with cellular growth and healing) in response to damage
The CB1 Knockout mice also had a greater risk of developing neurological problems (such as seizures) and had a greater overall mortality. One group of researchers was somewhat mystified at the severity of the effects, going so far as to comment that “the CB1 knockout animals died suddenly without any obvious signs of disease." (It is also worth noting that taranabant, another cannabinoid-blocking diet drug, manufactured by Merck, has proven to have similar negative psychiatric and GI side effects as rimonabant.)
The side-effects of cannabinoid blockers and the results of experiments on CB1 knockout mice point to the existence of what we could call the “Cannabinoid Deprivation Syndrome.”
Cannabinoid researcher Ethan Russo, M.D., theorizes that endocannabinoid deficiency might well offer an “alternative biochemical explanation for certain disease manifestations.” It appears that a number of hard-to-treat diseases such as migraines headaches, fibromyalgia, and irritable bowel syndrome (IBS) may well be related to a lack of proper endocannabinoid activity—implying that supplemental cannabinoids derived from or based on marijuana could be of great value. Russo reasons that some people could be “endocannabinoid deficient” and has labeled the syndrome Clinical Endocannabinoid Deficiency (CECD). Cannabis won’t kill you, but a lack of cannabinoids could.
Let’s re-examine the evidence. Taking a drug that inhibits cannabinoid activity—like rimonabant—can cause agitation, anxiety, depression, vomiting, sleep disorders, suicidal tendencies, and an increase in accidents and injuries. On the other hand, drugs that increase the activity of the endocannabinoid system—like marijuana—result in euphoria, laughter, suppression of nausea, better sleep, resistance to cancer and dementia, and increased brain cell production. The implications are clear: When our cannabinoid receptors have an adequate supply of cannabinoids, we experience a heightened state of health. When they do not, we suffer from Cannabinoid Deprivation Syndrome. The rimonabant debacle and scientific studies have given us even more evidence that maintaining a well-nourished and active cannabinoid receptor system is vital to our health.