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by Clint Werner July 19, 2012 from AlterNet Website
- How Cannabis Protects Us
from Cancer and Alzheimer’s Disease -
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.
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.
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,
...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.
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.
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.
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.
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:
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,
(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.)
It appears that a number of hard-to-treat diseases such as,
...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.
Taking a drug that inhibits cannabinoid activity - like rimonabant - can cause,
On the other hand, drugs that increase the activity of the endocannabinoid system - like marijuana - result in,
The implications are clear:
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.
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