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Mainely Tipping Points

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Mainely Tipping Points 37: Statins: Profitable Toxins

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Mainely Tipping Points 37

STATINS:  PROFITABLE TOXINS

 

Stephanie Seneff is a senior research scientist in the EECS (Electrical Engineering, Computer Science) department at the Massachusetts Institute of Technology (MIT).  Her degrees–a B.S. in biology, and an M.S., E.E., and Ph.D. in EECS—were awarded by MIT.  She researches within the interdisciplinary intersections of medicine, computer science, and electrical engineering, or the highly-respected biomolecular discipline.   

Seneff’s article, “Cholesterol:  The Essential Molecule–and The Adverse Effects and Overuse of Statins” (Well Being Journal, November/December 2011, 13-24), is the most complete, chemical explanation I have read of why statins are not a solution to the prevention of heart attacks. Statins, Seneff explains, create a situation where muscles are destroyed and where, eventually, the whole body is seriously at risk. 

Once again, drug industry researchers and medical doctors only looked at one piece of an illness puzzle—prevention of heart attacks–without understanding the actual causes and without acknowledging the long-term impact of their drug (statins) solution.  (Surely they know the harm statins do and are ignoring this harm because statins are so profitable.)  After exhaustive research, Seneff says the following:  “I will…make the bold claim that nobody qualifies for statin therapy, and that statin drugs can best be described as toxins” (13).  And, “I would in fact best characterize statin therapy as a mechanism to allow you to grow old faster” (22).

In addition, the drug industry and doctors have played a game I think of as “medical math.”  Seneff notes that a meta-study reviewing seven drug trials and 42,848 patients over a three- to five-year period did show a 29 percent decreased risk of a major cardiac event.  But as heart attacks were “rare among this group, what this translates to in absolute terms is that 60 patients would need to be treated for an average of 4.3 years to protect one of them from a single heart attack.  However, essentially all of them would experience increased frailty and mental decline….” (14).       

Seneff’s article describes the chemical components within the body when cholesterol is fully present and when it has been compromised.  Her explanations are clear and fully understandable, but complicated.  If you are taking statins or are contemplating them, I urge you to read Seneff’s article.  Meanwhile, I will do my best to synthesize the high points so that you can understand why it is so dangerous to use statins to reduce cholesterol in your body. 

Furthermore, many, many studies—some of them long-term studies—clearly show that people—and especially women–with high cholesterol counts live longer than those with low cholesterol counts.  This information is readily available, and it is a mystery to me why our doctors continue to ignore it.

 Statins interfere with the synthesis of cholesterol, a nutrient, explains Seneff, that has been demonized by the drug industry and doctors, but which is essential to human health.   “Cholesterol is absolutely essential to the cell membranes of all our cells, where it protects the cell not only from ion leaks but also from oxidation damage to membrane fats” (14).  Reducing cholesterol “places a much bigger burden on the body to synthesize sufficient cholesterol to support the body’s needs, and it deprives us of several essential nutrients” (14).       

Further, Seneff notes, “there are three distinguishing factors that give animals an advantage over plants:  a nervous system, mobility, and cholesterol.”  Cholesterol, which is “absent from plants, is the key molecule that allows animals to have mobility and a nervous system” (14). In a nutshell, when statins reduce cholesterol, they force the body to jerry-rig alternative chemical systems that lead eventually to body-wide damage (20).

One mythology today is that elevated serum levels of LDL (low density lipoprotein) cholesterol is a problem.  But, Seneff explains, “LDL is not a type of cholesterol, but… [is] a container that transports fats, cholesterol, vitamin D, and fat-soluble anti-oxidants to all the tissues of the body.”  Because these nutrients are not water-soluble, they “must be packaged up and transported inside LDL particles in the blood stream.”  Thus, “if you interfere with the production of LDL you will reduce the bioavailability of all these nutrients to your body’s cells” (15).

The LDL package, explains Seneff, is “vulnerable to attack by glucose and other blood sugars, especially fructose.”  If “gummed up” by sugars, “the LDL particles become less efficient in delivering their contents to the cells,” they “stick around longer in the bloodstream,” and the “measured serum LDL level goes up” (15).  But, worse, after the LDL particles have delivered their contents, they “become small dense LDL particles, remnants that would ordinarily be returned to the liver to be broken down and recycled.”  However, “the attached sugars interfere with this process…so the task of breaking them down is assumed instead by macrophages in the artery wall and elsewhere in the body.”  These “small dense LDL particles become trapped in the artery wall so that the macrophages can salvage and recycle their contents, and this is the basic source of atherosclerosis” (15). 

The liver, explains Seneff, produces the LDL particles.  Statin therapy “greatly impacts the liver, resulting in a sharp reduction in the amount of cholesterol it can synthesize.”  Also, the liver breaks down fructose and converts it into fat.  So, when there is a lot of fructose in the system, the liver becomes burdened with the task of converting it to fat and cannot “keep up with the cholesterol supply.”  Both conditions mean that “fats cannot be safely transported”(16).

Additionally, as the liver is burdened with handling the fructose, “it produces low quality LDL particles” (16).  So, harmful chain reactions begin to occur, such as the following:  fructose builds up in the blood stream, which causes more damage; the skeletal muscle cells are severely affected; and the brain, which houses 25 percent of the body’s cholesterol, is impaired.  Diabetes and arthritis are also associated with statin therapy (19, 21).   

When overburdened, the liver shifts the processing of excess fructose to the muscle cells, explains Seneff.  The muscle cells themselves begin to use an alternative fuel source that requires an abundance of fructose and which allows the production of lactate, which is a high-quality fuel for the heart.  This desperate production of lactate is why statin therapy can lead to a “reduction in heart attack risk.” (17).

But, continues Seneff, “the muscle cells get wrecked in the process” (17).  In effect, the muscles “can no longer keep up with essentially running a marathon day in and day out.”  The muscles “start literally falling apart, and the debris ends up in the kidney, where it can lead to the rare disorder rhabdomyolysis, which is often fatal” (20).  The drug industry readily admits to muscle pain and weakness with statin use (17).

The dying muscles also “expose the nerves that innervate them to toxic substances, which then leads to nerve damage such as neuropathy, and ultimately amyloid lateral sclerosis (ALS), also known as Lou Gehrig’s disease, a very rare, debilitating, and ultimately fatal disease that is now on the rise due (I believe) to statin drugs” (20).

Also, as the cells struggle with ion leaks caused by insufficient cholesterol, they begin to replace a potassium/sodium system with a calcium/magnesium-based system.  The result is the “extensive calcification of artery walls, heart valves, and the heart muscle itself.”  Indeed “research has shown that statin therapy leads to increased risk of diastolic heart failure” (20). 

Seneff is very interested in the role of cholesterol sulfate.   Cholesterol sulfate is “very versatile.  It is water soluble, so it can travel freely in the blood stream, and it enters cell membranes ten times as readily as cholesterol, so it can easily resupply cholesterol to cells” (24).

Cholesterol sulfate, explains Seneff, is produced by the skin in large quantities with sun exposure.  Seneff  thinks that “the natural tan that develops upon sun exposure offers far better protection from skin cancer than the chemicals in sunscreens.”  And, Seneff thinks we should eat foods “rich in both cholesterol and sulfur”—“eggs are an optimal food, as they are well supplied with both of these nutrients” (24).     

To avoid heart disease, Seneff suggests cutting back on fructose intake, eating whole foods instead of processed foods, and eating foods which are good sources of lactate (sour cream, yogurt, and milk products in general).  (One can use goat-milk products if cow’s milk is a problem.)  Strenuous physical exercise helps “get rid of any excess fructose and glucose in the blood, with the skeletal muscles converting them to the much coveted lactate” (23) 

Seneff further advises:  “spend significant time outdoors; eat healthy cholesterol-enriched, animal-based foods like eggs, liver, and oysters; eat fermented foods like yogurt and sour cream; eat foods rich in sulfur like onions and garlic.  And, finally say `no-thank-you’ to your doctors when they recommend statin therapy” (24).

Mainely Tipping Points 13: The Failure of the Low-Fat, High-Carbohydrate American Diet

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(Oops!  Read TP 12 first; it’s part of a series in the essays) 

Tipping Points 13

The Failure of the Low-Fat, High-Carbohydrate American Diet

 

 When Luise Light and her team of experts attempted to scientifically formulate the 1980 USDA Food Guide, they accepted two current dietary ideas as truth:  fat should be no more than 30 percent of the diet, and since the end of World War II, and especially in the 1960s, Americans had been experiencing “rising rates of heart disease, high blood pressure, stroke, and diabetes” (13, Luise Light, WHAT TO EAT:  THE TEN THINGS YOU REALLY NEED TO KNOW TO EAT WELL AND BE HEALTHY).

Current historians show us that the low-fat premise that has governed the American diet for the past fifty years sprang from belief, not science, and became part of American cultural and economic practices when the stars aligned around a constellation that included the political power of a congressional committee, media acceptance of its recommendations, and the firmly-held beliefs of a handful of people.

Science writer Gary Taubes, in his myth-exploding article “The Soft Science of Dietary Fat,” published in “Science” magazine in March 2001, questioned the idea that there ever was an epidemic of heart disease after World War II (http://www.nasw.org/awards/2001/The%20soft%20science.pdf).  When Taubes interviewed Harry Rosenberg, Director of the National Center for Health Statistics (NCHS), Rosenberg said a heart disease epidemic never existed.  First, in 1949 the International Classification of Diseases (ICD) added arteriosclerotic heart disease as a new category under the general category of heart diseases.  Between 1948-1949, the new category appeared to raise coronary disease death rates about 20 percent for males and 35 percent for females. 

Again, In 1965, the ICD added a category for coronary heart disease, which added more deaths to the statistical data as physicians began using the new categories.  Furthermore, Rosenberg explained, by the 1950s, Americans were healthier, so more were living to be 50-year-olds who would go on to die of chronic diseases like heart disease, which physicians were now listing on death certificates under the new categories.  Taubes reports that Rosenberg said that, in actuality, risk rates of dying from a heart attack remained unchanged.

Taubes also discussed the fact that between 1989 and 1992, three independent research groups (Harvard Medical School; The University of California, San Francisco, funded by the U.S. Surgeon General’s Office; and McGill University, Montreal) used computer models to work out added life expectancy for a person eating a low-fat diet that controlled saturated fats.  All three models agreed, but their conclusions have been ignored by media. 

The Harvard study showed that if a person’s total fat consumption was less than 30 percent of their daily total calories and if their saturated fat consumption was 10 percent of that 30 percent, a healthy nonsmoker might add from 3 days to 3 months of life.  The latter two studies showed net increase of life expectancy would be from three to four months.  Taubes noted that the U.S. Surgeon General’s office tried to prevent the University of California study from being published in “The Journal of the American Medical Association (JAMA), but JAMA published it in June 1991.

The Lipid Hypothesis is the “scientific” paradigm calling for a low-fat diet.  The Lipid Hypothesis is the premise that ingested fat, especially saturated fat, raises blood cholesterol levels, and high cholesterol levels cause chronic heart disease (CHD).  Yet, many, many scientists now have argued that these cause-and-effect links have never been proven and, in fact, cannot be proven.  More recently than Taubes, Michael Pollan, in IN DEFENSE OF FOOD (2008), traces this history and current thinking on dietary fats in a section entitled “The Melting of the Lipid Hypothesis” (40-50). 

So how did the Lipid Hypothesis and the low-fat paradigm get installed with scant scientific data to support it?  Biochemist Ancel Keys is a key player.  In the mid 1950s, Keys (University of Minnesota) claimed that his epidemiological Seven Countries Study showed a correlation between the consumption of dietary fat and heart disease.  But, an epidemiological study cannot control or eliminate variables, and correlation is not proved causation.  Furthermore, many now, among them Taubes and Uffe Ravnskov, claim that Keys eliminated countries whose statistics did not fit his hypotheses, like France, Holland, Switzerland, Norway, Denmark, Sweden, and West Germany, where national populations ate 30 to 40 percent of their calories as fat and whose death rates from CHD were half that of the United States.  Nevertheless, in 1961, the American Heart Association began advocating low-fat diets for men with high cholesterol levels.

Also in the 1950s, Nathan Pritkin, was diagnosed with heart disease.  Though he had no college degree and no scientific training, Pritkin created and published a low-fat, aerobic exercise regime that sold millions of copies.  Pritkin also suffered from leukemia, and it began causing complications and pain in the early 1980s.  Pritkin committed suicide in 1985.        

In 1977, the Congressional Select Committee on Nutrition and Human Needs, chaired by Senator George McGovern, promoted the low-fat hypothesis—despite objections by scientists expert in the field.  Taubes determines that “a handful of McGovern staffers…almost single-handedly changed nutritional policy in this country” by initiating “the process of turning the dietary fat hypothesis into dogma” (4).

In 1976, Taubes reports, after two days of testimony, this committee turned “the task of researching and writing the first `Dietary Goals for the United States’” over to Nick Mottern, a labor reporter with “no experience writing about science, nutrition, or health” (5).  Mottern relied on Harvard School of Public Health nutritionist Mark Hegsted’s low-fat beliefs.  Hegsted, unlike E. H. Ahrens, whose laboratory at the Rockefeller University in New York City was doing seminal research on fat and cholesterol metabolism, saw no risks associated with such a major change to the American diet.  Ahrens, as early as 1969, was concerned that eating less fat or changing the proportions of saturated to unsaturated fats could have profound and harmful effects on the body (3-6).  Nevertheless, the Select Committee published Mottern’s dietary guidelines. 

Next, Taube relates, Carol Tucker Foreman, a political appointee at USDA who later forms a public relations and lobbying firm whose clients have included Phillip Morris, Monsanto (bovine growth hormone), and Procter and Gamble (fake fat Olestra), hired Hegsted to produce “Using the Dietary Guidelines for Americans,” which supported the McGovern Committee Report.  Foreman hired Hegsted despite the fact that Philip Handler, National Academy of Sciences (NAS) President and an expert on metabolism, had told her that Mottern’s Dietary Goals were “`nonsense’ “ (6).

When NAS released its own dietary guidelines a few months later (watch your weight and everything else will be all right), the media criticized the NAS for having industry connections.  Hegsted later returned to Harvard where his research was funded by Frito-Lay.

So, a consensus was achieved, oneTaube says is “continuously reinforced by physicians, nutritionists, journalists, health organizations, and consumer advocacy groups such as the Center for Science in the Public Interest” (1).  And, science was “left to catch up” (7).

 Only, science never has.  And, what has emerged is that all calories are not equal and substituting carbohydrates for fat has caused weight gain and diabetes.  And, according to lipid biochemist Mary Enig, substituting highly-processed fats for time-honored, traditional fats is causing chronic heart disease.   

Pollan notes that in a 2001 review of the relevant research and report by “prominent nutrition scientists” at the Harvard School of Public Health, “just about every strut supporting the theory that dietary fat causes heart disease” was removed, except for consuming trans fats and consuming fats that alter ratios of omega 3 to omega 6 fatty acids (41-42).  Pollan notes the Harvard scientists stated the following in their report’s second paragraph:  “`It is now increasingly recognized that the low-fat campaign has been based on little scientific evidence and may have caused unintended health consequences’ “ (43).    

Pollan assesses that the low-fat ideology of nutritionism has been nutrition’s “supreme test and, as now is coming clear, its most abject failure” (41).