Study estimates Fukushima radiation-caused deaths, cancers.

The first study to estimate the global health impact of the release of radiation from the Fukushima nuclear disaster concluded that it might eventually cause 130 deaths and 180 cases of cancer, mostly in Japan, though the range of possibilities varied widely.

While the number seems small relative to the scope of the disaster, the study focused only on the radiation and excluded the immediate, actual deaths that occurred during the initial earthquake and tsunami.

And the analysis contradicts previous claims, such as by the United Nations Science Committee on the Effects of Atomic Radiation, that the nuclear disaster would cause no deaths.

The study, conducted by Stanford University PhD graduate John Ten Hoeve and Stanford civil engineering professor Mark Z. Jacobson, is to be published in the July 17 issue of Energy and Environmental Science.

How the study was conducted

The researchers used a 3-D global atmospheric model to predict how the radioactive material would move over earth and a health-effects model to see how humans would be exposed to radioactivity.

The possible death toll ranged widely from 15 to 1,300 dead; the best estimate was 130. The number of cancer cases also varied widely, from 24 to 2,500 with 180 being the best estimate.

The models showed that most of the ill health effects would be felt in Japan, with a few small effects noticeable in mainland Asia and North America; as many as 12 deaths and 30 cancer cases could show up in the United States.

The number of people exposed to the radiation was relatively contained, because only 19% of the released radioactive material fell over land; the rest was dumped in the Pacific.

Another reason for the contained health effects is that the Japanese government responded more rapidly than the Soviets did after the Chernobyl nuclear disaster. For instance, the Japanese government evacuated the 20-kilometer around the plant and stopped cultivation of crops whose radiation exposure exceeded a certain threshhold.

Update, July 17, 2012, 10:45pm EST: The original version of this post said this study excluded the immediate deaths that occurred during the “catastrophe.” It has been updated to clarify that the catastrophe referenced was the precipitating earthquake and tsunami.

Source: Stanford News Service



Are genetically modified mosquitoes coming to America?

To control dengue fever, one biotech has developed genetically modified mosquitoes whose offspring die before they can spread the disease.

These mosquitoes have already been released in Brazil, Malaysia, and the Cayman Islands. In Key West, Florida, the disease reappeared 3 years ago, after an absence of over 70 years.

And the US Food and Drug Administration is currently reviewing an application from the UK-based Oxitec. Florida residents are gathering names for a petition.
Nature News explains:

  1. Their mosquitoes (known as OX513A) are an engineered version of Aedes aegypti, the main transmitter of dengue fever, which infects at least 50 million people a year.
  2. The modified males carry a lethal gene kept in check only by a special diet.
  3. They survive to mate with wild females, but the offspring die.
  4. In field tests conducted in Juazeiro, Brazil, the engineered insects shrank the A. aegypti population in an 11-hectare area by 85% over a year.

The Florida Keys Mosquito Control District (FKMCD) in Stock Island is a taxpayer-funded operation that spends more than $1 million a year to control A. aegypti in Key West with insecticides.

In 2010, the FKMCD asked Oxitec if it would do a field trial with its mosquitoes in Key West. The next year, the company applied for FDA approval. A media report that very month suggested that officials were hoping for a mosquito release as early as January 2012, prompting concerns among residents.

The petition raises prospects of unintended consequences, such as the emergence of a deadlier dengue virus that gets around the absence of A. aegypti. And residents in Key West say they don’t want to be tested like “guinea pigs” and “I don’t want my family being used as laboratory rats for this.” Michael Specter writes in The New Yorker:

There is, of course, another theoretical catastrophe to consider: a dengue epidemic in Key West. So far the city has largely been spared, but the region, as Oxitec’s chief scientist Luke Alphey told me when I spoke with him for my article, is “living in a sea of dengue.”

When Oxitec opened up Moscamed, a mosquito-production facility, earlier this month in Juazerio, residents cheered. But the University of Sao Paula team engaged the community before seeking approval for their trial from Brazil’s agency for biotechnological safety, CTNBio.

Source: Nature.

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.

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.

Clint Werner is a journalist and medical marijuana advocate, and is the author of Marijuana: Gateway to Health – How Cannabis Protects us from Cancer and Alzheimer’s Disease.

Source: galactic free press