September 14, 2007
Dear Reader,
I hope you had a great summer! September is a time of new beginnings, especially the school year. Cholesterol class is back in session. Enjoy!
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--Chris Masterjohn
In This Issue
Site Updates
Special Report: Thyroid Toxins
Best of the 'Net
Research Watch
Copyright and Disclaimer
Search
Feedback
Site Updates
Cholesterol Synthesis and the Activation of Rho
Much of the illusion that cholesterol causes disease may have to do with an enzyme called Rho. Inflammation increases it, cholesterol correlates with it, and statins inhibit it. Read more here.
Ron Paul for President 2008 -- Protect Our Health Freedom!
Ron Paul is the only candidate running for president who has a consistent record of standing up to the FDA for our freedom to pursue health and true information about health. He is also Congress's most outspoken opponent of the National Animal Indentification System (NAIS) -- the gravest current threat to the liberty of our farmers and all who wish to buy quality food from small, local farms. Dr. Paul is an outstanding and principled spokesman for liberty, for the rule of law, and for fidelity to the Constitution of the United States. And he has my wholehearted endorsement!
Special Report: Thyroid Toxins
Wondering how to avoid the goitrogens in soy, millet, crucifers, and fruits and nuts in the Rosacea family? Confused about how cooking, fermenting, and other processing methods affect these chemicals? This 25-page report will answer all your questions. It contains six figures, one table and 66 references. It provides quantitative information about what proportion of the goitrogenic activity of cruciferous vegetables various cooking methods -- microwaving, steaming, boiling -- destroy. It explains that, contrary to popular belief, fermentation increases the goitrogenicity of crucifers. Traditional soaking and fermenting destroy the goitrogenicity of foods containing cyanogenic glycosides but increase the goitrogenicity of millet and soy. In fact, even cooking increases the goitrogenicity of millet. This is information you do not want to miss.
To order the individual report for $15, click here.
To subscribe to Special Reports for one year (four reports) for $30, click here.
Best of the 'Net
The Future of Food
We used to be a nation of farmers. But that was the past. Who will control the future of food?
In 1975, a conference of pioneers in genetic engineering met to discuss how to approach the safety risks of the new technology. The majority vote was against a moratorium on its use, but the members vowed to keep it safely within the bounds of the tightly controlled environment of the laboratory. Unlike some of the life-saving medical technologies that have been produced in these laboratories, genetically engineered plants cannot be contained: once they invade the environment, they become part of it. During the first Bush Administration, the FDA strongly opposed steamrolling the use of genetic engineering in agriculture. Vice President Dan Quayle had a solution: Monsanto Senior Counselor Michael Taylor became the FDA Deputy Commissioner for Food Policy. In 1992, the "no regulation" method of regulation that Taylor developed became national policy for "regulating" genetically engineered foods.
Meanwhile, the pesticide industry bought the seed industry. Monsanto spent $8 billion buying seed companies. By the 1990s, corporations were not only patenting genetically engineered seeds but any seeds that simply had not been patented before. In 1996, 3.7 million acres in the US were devoted to genetically engineered canola, soy, corn, cotton and soy. By 2003, this number had multiplied by a factor of 27 to 100 million acres. Unless we do something about it, the answer to the question -- who will control the future of food? -- is a bleak one indeed.
Two thirds (about 53 of 88 minutes) of this movie are available for free on YouTube as seven clips: Part 1, Part 2, Part 3, Part 4, Part 5, Part 6, and Part 7. Parts 2 and 4 may have some trouble loading.
You can purchase the two-disc DVD at Whole Foods or on the movie's official web site.
Mae-Wan Ho: Making the World GM-Free and Sustainable
In her keynote address from the 2006 Wise Traditions conference of the Weston A. Price Foundation, geneticist Mae-Wan Ho presented a different vision of the future of food: a model for an integrated zero-emission, zero-waste farm that runs at high productivity without the need for fossil fuels. She calls it Dream Farm 2.
She doesn't neglect to first state the crisis. She reveals recent research out of Moscow showing that genetically modified soy severely stunts the growth of rats and increases mortality when it is given as a supplement to rat pellets instead of non-genetically modified soy or no supplement -- and she has pictures to prove it.
But, according to Dr. Ho, there are real global energy and food crises from which this technology cannot safely save us. World grain yield is falling; aquifers are suffering chronic depletion in the world's bread baskets; global warming is a real threat. Dr. Ho presents her "Dream Farm" model as a solution to these problems.
Considering the daunting and depressing vision of the future of food we must face, any and all ideas are welcome.
FDA/USDA: Raw Milk 10 Times Less Dangerous Than Deli Meats
The FDA is waging a vigorous propaganda campaign against raw (unpasteurized) milk. It concludes, "Raw milk is inherently dangerous and should not be consumed. . . . FDA encourages everyone charged with protecting the public health to prevent the sale of raw milk to consumers and the operation of so-called 'cow-sharing' schemes. To do otherwise would be to take a backwards step with public health protection."
So far the FDA has, in conjunction with the USDA, produced one comprehensive report comparing the risk of food-borne illness between different foods -- this report covers the bacterium Listeria monocytogenes. It should come as no surprise that the absolute number of illnesses attributable to raw milk is very low: there are 515 times as many illnesses attributable to deli meats, 29 times as many attributable to pasteurized milk and 10 times as many attributable to hot dogs that have not been reheated. The more interesting question, however, is how dangerous raw milk is on a per serving basis. In other words, let's say in a hypothetical situation that as many people drink raw milk on a regular basis as eat deli meats on a regular basis. Which would be more dangerous? That's where the report gets interesting: Table 4 on page 17 of the report (click here to read it in html) shows that deli meats are ten times more dangerous than raw milk on a per serving basis!
Where are the FDA's charges that deli meats are "inherently dangerous and should not be consumed"? Where is FDA's exhortation to "everyone charged with protecting the public health" to "prevent the sale of deli meats to consumers"? They simply do not exist.
Let us eagerly await more revelations from forthcoming comparative risk assessments. This should get interesting.
Fluoride and the Brain: Dr. Phyllis Mullenix
We know fluoride for its ability to stave off tooth decay. But what is its effect on the developing brain of an infant and child?
Dr. Phyllis Mullenix is a pharmacologist and toxicologist who studied at Johns Hopkins School of Hygeine and Public Health and has been affiliated with Harvard School of Medicine, Boston Children's Hospital and the Forsyth Dental Infirmary for Children. In the 1990s, she developed the first computer pattern recognition system to monitor animal behavior and pick out abnormal patterns without the subjectivity and error of human assessment. She worked with Dr. Harold Hodge, a world expert on fluoride chemistry and toxicology, a founding father of the Society of Toxicology, and the chief pharmacologist on the Manhattan Project, to study the effect of fluoride on behavior. After finding in 1995/1996 that moderate doses of fluoride accumulated in the brain and caused marked effects on behavior in laboratory animals, they presented their findings to the National Institute of Dental Research. The response was less than welcoming.
After Hodge passed away, the government declassified Manhattan Project documents showing that Hodge himself had made similar discoveries decades ago, though he never told Mullenix about them. She first discovered a 1949 document reporting marked behavioral effects in two separate incidents of accidental exposure to large amounts of fluoride. Later, she discovered an April, 1944 document attributing central nervous system (CNS) effects to the fluoride component of uranium hexafluoride. The document proposed animal experiements to study the effects of fluoride on the CNS. A budget and protocol was approved for the experiments to go forward. Less than six months later, another secret document ordered that if the experiments had not yet been started they stay that way, and if they had been started they come to an immediate end.
Promised funding for further research since Mullenix's first paper has yet to materialize.
The YouTube presentation comes in three parts: Part 1, Part 2, Part 3.
You can also read an interview with Dr. Mullenix here. She will be speaking at the 2007 Wise Traditions conference this November.
Neanderthals Brushed Their Teeth, Paleontologists Find
"Two molar teeth of around 63,400 years old show that Neanderthal predecessors of humans may have been dental hygiene fans, the Web site of newspaper El Pais reported on Tuesday." Read more.
It's the Vitamin E, not the Fatty Acids
The Journal of the American College of Cardiology published my letter responding to the August, 2006 study by Nicholls, et al. claiming to show that just one meal high in saturated fat destroys the functioning of blood vessels. In it, I briefly stated my hypothesis that the effects exerted by isolated HDL particles on the expression of inflammatory molecules by the endothelial cells with which they were incubated was due to the relative vitamin E concentrations of the two oils used in the study -- coconut and safflower -- rather than the relative saturation of their fatty acids. In my original article on this site, I presented the hypothesis in much more detail.
My letter was accepted on August 28, 2006 but was not published until May 1, 2007. The journal was planning to publish the authors' response with my letter. The authors, however, apparently chose not to respond.
Research Watch
Periodontal Disease, Rheumatoid Arthritis, and Atherosclerosis
Researchers from the University of Alexandria, Egypt published a study in the Annals of the New York Academy of Sciences this June highlighting the inflammatory nature of heart disease. They examined the prevalence of periodontal disease in 100 patients with rheumatoid arthritis, 50 of whom had coronary artery disease and 50 of whom did not, and compared them to 50 healthy controls. Periodontal disease -- the leading cause of tooth loss in adults -- and rheumatoid arthritis are both inflammatory diseases with an autoimmune component. They involve the production of high levels of proinflammatory chemicals such as tumor necrosis factor alpha (TNF-alpha), interleukin 1 (IL-1) and C-reactive protein (CRP), which are also associated with atherosclerosis.
Periodontal disease (PD) was seven times more prevalent in rheumatoid arthritis (RA) patients than in controls, and was more prevalent and more severe in patients who had both RA and coronary artery disease (CAD) than in patients who had RA alone. Missing teeth, an indirect indicator of PD, was six times more prevalent among RA patients without CAD than controls, and almost eight times more prevalent among RA patients with CAD than controls. Gingival bleeding was 7.5 times more prevalent among patients with RA alone than controls and 10.5 times more prevalent among RA patients with CAD than controls. Among RA patients altogether, the presence of PD increased the risk of CAD by 3.5 times.
The authors suggested that the inflammatory burden of PD and RA can both contribute to CAD, and the combined presence of each contributes an even greater inflammatory burden. Total cholesterol levels were 13 percent higher among RA patients than among controls. One of the mechanisms by which inflammation contributes to atherosclerosis is likely to be the activation of Rho, which indirectly increases cholesterol levels.
Low Cholesterol and Suicide in Schizoaffective Disorder
Researchers from the University Hospital Zagreb in Zagreb, Croatia published a paper this August in the journal, Progress in Neuro-Psychopharmacology & Biological Psychiatry, demonstrating once again a correlation between low cholesterol and the risk of suicide. Forty male patients with schizoaffective disorder -- a combination of schizophrenia and either mania or depression -- 20 of whom were suicidal and 20 of whom were not were compared to 20 healthy age- and sex-matched controls. Total cholesterol levels were 27 percent lower in suicidal patients than in the other two groups -- 170 compared to 230. LDL levels were 26 percent lower in suicidal patients than in the other two groups -- 105 compared to 140. HDL levels were 19 percent lower in the suicidal group than in the group of non-suicidal schizoaffective patients and 25 percent lower in the suicidal group than in the healthy controls -- 40 compared to 50 and 55. (I rounded the figures to the nearest 5.) Total cholesterol levels also had a continuous negative correlation with the severity of suicidality.
In attempting to offer an explanation for the findings, the authors referred back to a 1992 paper published in Lancet suggesting that low cholesterol levels decrease the functioning of serotonin receptors in the membranes of nerve cells.
This paper is consistent with one I reported on in Issue #009 of this newsletter connecting low brain cholesterol levels to violent suicide and one I reported on the section on my web site, Is Dietary Cholesterol Essential?, showing that people who carry the gene for Smith-Lemli-Opitz Syndrome (SLOS), which results in a low cholesterol level, are three times more likely to have attempted suicide than controls.
Cholesterol and Survival in the Elderly
Researchers from the Nagoya University Graduate School of Medicine in Nagoya City, Japan, published a paper this month entitled, "Nitric Oxide Metabolites Are Associated with Survival in Older Patients," in the Journal of the American Geriatrics Society. The authors followed 150 elderly men and women with an average age of 82 for just under three years. At the beginning of the study and at regular intervals afterwards, they measured the patients' blood levels of cholesterol and other lipids, inflammatory chemicals, and breakdown products ("metabolites") of nitric oxide, and determined the correlations between these measurements and the rate of survival over the course of the study. They published the paper primarily about nitric oxide, but the correlations with cholesterol are easier to interpret and more interesting.
Nitric oxide is a gas that dilates and relaxes blood vessels, increases blood flow, stops the adhesion of white blood cells to the lining of blood vessels, stops the migration of smooth muscle cells to the sites of atherosclerotic lesions, and decreases the tendency of the blood to clot. The nitric oxide produced by the lining of the blood vessels -- called the vascular endothelium -- is highly protective against heart disease and stroke. Exercise and the amino acid L-arginine increase endothelial nitric oxide levels; free radicals, insufficient oxygen, oxidized LDL and inflammation (via the activation of Rho) decrease endothelial nitric oxide levels. One would expect any indicator of endothelial nitric oxide levels to be associated with a lower risk of heart disease and total mortality.
This study found the opposite -- breakdown products of nitric oxide were associated with decreased survival. There are a few problems with this finding, however. First, because nitric oxide only lasts for a few seconds in the blood before it breaks down, the researchers had to measure various breakdown products such as nitrite and nitrate instead of nitric oxide itself. Nitrites and nitrates from the diet could have influenced this level. Second, measuring nitric oxide or nitric oxide metabolites in the plasma cannot distinguish between nitric oxide produced by the endothelium -- which is protective -- and other nitric oxide. Inflammatory cells such as macrophages and T cells -- both of which are involved in atherosclerosis -- produce their own nitric oxide. So while inflammation hurts the endothelium's ability to make its own protective nitric oxide, the inflammatory process itself can increase the total amount of nitric oxide produced and the breakdown products released into the blood.
Thankfully we don't have these interpretive problems when measuring cholesterol levels. So what is interesting in this study is that patients who survived had higher total and LDL cholesterol levels. LDL cholesterol was 13 percent higher among patients who survived than those who died -- 129 compared to 114. Total cholesterol was 17 percent higher among survivers than non-survivors -- 210 compared to 179.
As the authors put it, ". . . it was reported recently that elderly individuals with low cholesterol constitute a heterogeneous group with regard to health characteristics and mortality risk."
In other words, it is high cholesterol levels that are supposed to kill you, not low ones. And elderly people don't follow the rules.
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Please take notice that the contents of this newsletter and Cholesterol-And-Health.com are copyright of Chris Masterjohn, 2007, and that this information is not to be construed or understood as any form of advice. Please visit my disclaimer page here.