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Mainely Tipping Points

Posts Tagged ‘LDL cholesterol

Mainely Tipping Points 37: Statins: Profitable Toxins

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Mainely Tipping Points 37



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 28: Why We Get Fat

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Mainely Tipping Points 28:  WHY WE GET FAT


In WHY WE GET FAT (2011), Gary Taubes—a highly respected science researcher and writer, drives a scientific stake into the heart of the “calories in/calories out” paradigm that began developing in the 1950s and grew to become the medical orthodoxy we experience today.  Taubes explains the proven science behind why some people get fat—a question totally lost in the wilderness of the “energy balance” paradigm and its attendant low-fat/high carbohydrate diet.  The circular logic of this paradigm holds overweight people in a vicious, unscientific, damaging, deeply cultural  polarity:   either people of low character eat too much (gluttony) or exercise too little (sloth).  

Taubes traces the history of when research in nutrition and obesity “lost its way” and observes that these fields have “resisted all attempts” at correction.  Much understanding, Taubes writes, was lost after World War II with “the evaporation of the European community of scientists and physicians [particularly the Germans] that did the pioneering work” (ix).  Since that time, writes Taubes, “individuals involved in this research have not only wasted decades of time, effort, and money but have done incalculable damage….Their beliefs have remained impervious to an ever-growing body of evidence that refutes them while being embraced by public-health authorities and translated into precisely the wrong advice about what to eat and, more important, what not to eat if we want to maintain a healthy weight and live a long and healthy life” (ix). 

Taube’s earlier book GOOD CALORIES, BAD CALORIES (2008) is an extended, densely researched book written to start a conversation with “the experts.”  Taubes believes that it might take another lifetime to change this paradigm, but, meanwhile, he sees that the disease burden (obesity, diabetes, heart disease, and cancer) being created by eating the wrong foods is “overwhelming not only hundreds of millions of individuals but our health-care systems…” (x).  Taubes wrote WHY WE GET FAT so the lay person could understand what’s wrong and have the courage to take personal charge of his/her health rather than relying on “some of the misconceptions that pass for public-health and medical advice in this country” (xi).

So, why do some people get fat?  All real food, as compared to some of the chemical brews passed off as food today, is composed of fats, proteins, and/or carbohydrates.  In a nutshell, people have genetic tendencies toward fatness or thinness that combines with a hormonal chemical disorder caused by eating too many carbohydrates—which throws off the body’s ability to regulate fat accumulation appropriately in both fat and thin people. 

Here’s a gross simplification of Taube’s main explanation:  Fat accumulation is regulated by hormones, and the most important hormone is insulin.  Ideally, when our insulin levels are elevated, we accumulate fat in our fat tissue.  When insulin levels fall, fat is liberated from fat tissue and is burned for fuel.  However, easily digestible carbohydrates, like highly processed sugars and grains and starchy vegetables, make the body produce more insulin.  And, this insulin works to trap fat inside fat cells; it does not release them to burn for energy.  Thus, obesity is a hormonal imbalance, not a caloric imbalance.  Worse, this hormonal imbalance makes an overweight person hungrier because the body is growing larger, and it makes that person sedentary because all the food energy is being stored, not burned.  Gluttony and sloth are effects of this hormonal imbalance, not causes (10). 

Insulin, Taubes writes, works also with other hormones, like the sex hormones, and countless enzymes to partition fuel around the body.  This chemical process decides what food energy is burned, what is stored, and in which tissues it is stored (fat, muscle, liver).  An insulin disorder can partition a disproportionate amount of consumed calories into storage as fat, rather than having them used for energy by the muscles.  In lean people, the factors work to burn as fuel a disproportionate share of the consumed calories, which creates high energy levels (128).   

Some people, Taubes explains, develop insulin resistance, which means the body has to secrete higher and higher insulin levels in order to perform the same tasks—a “vicious cycle” intensified by eating easily digestible carbohydrates.  Next, these people start to manifest the precursor to heart disease, metabolic syndrome.  Body fat accumulates, especially around the waist; blood pressure rises; triglycerides levels rise; LDL cholesterol particles become small and dense; HDL cholesterol levels fall; and blood sugar becomes erratic (glucose intolerance).  Diabetes occurs when the pancreas can no longer secrete enough insulin to keep the body balanced.  And Alzheimer’s and most cancers are “associated with metabolic syndrome, obesity and diabetes” (195-198). 

Taubes’ subject is why we get fat, so he does not address the health effects on the lean, energetic person whose leanness is created by this hormonal disorder, which is, in turn, caused by eating too many of the wrong kinds of carbohydrates.  He does note that that as we age, our muscles become increasingly resistant to insulin and more energy gets partitioned into fat (130-131).   

There are generational components to these disorders.  Taubes notes that worldwide studies demonstrate that children born to a mother with hormonal imbalances that have created obesity are likely, also, to struggle with obesity.  The nutrients the mother’s body supplies to her baby affects his/her levels of glucose, which, in turn, affects the pancreas so that it develops more insulin-secreting cells, which, in turn, makes the baby fatter at birth.  These babies have a tendency both to oversecrete insulin and to become insulin-resistant (132).            

Exercise, Taubes demonstrates effectively, will not make one lose weight.  Indeed, for weight loss, exercise is counterproductive because it creates hunger (40-56).  And, undereating  does not work.  At some point one must return to eating normally, and the weight returns.  Taubes reports that the eight-year, billion-dollar National Institutes of Health initiative, the Women’s Health Initiative (WHI) of the 1990s, showed that a low-fat diet did not result in weight loss and “did not prevent heart disease, cancer, or anything else” (33-39). 

Taubes looks at many current studies, among them the 2007, two million dollar, government-funded A TO Z Weight Loss Study from Stanford University which compared four diets:  Atkins (low carbohydrate), LEARN (a traditional diet with 55-60 percent carbohydrates), Ornish (low fat), and the Zone diet.  The Atkins diet won, substantially and significantly, across the measured categories (weight loss, dropping triglyceride levels, dropping blood pressures, and improved cholesterol conditions)—prompting lead researcher Christopher Gardner, a twenty-five year vegetarian, to note that the results were, for him, a “`bitter pill to swallow’” (191-192). 

Taubes notes that Atkins diet participants were allowed to eat as much red meat and meat fat as they wanted (191-192).  And, that “since the 1960s, when it was first argued that animal products could be bad for our health because they contains saturated fat, nutritionists have typically refrained from pointing out that meat contains all the amino acids necessary for life, all the essential fats, and twelve of the thirteen essential vitamins in surprisingly large quantities.”  Meat, writes Taubes, “is a particularly concentrated source of vitamins A and E, and the entire complex of B vitamins.”  Indeed, “vitamins B12 and D are found only in animal products….”(176).

Vitamin C is the “one vitamin that is relatively scarce in animal products.”  But, “the more fattening carbohydrates we consume, the more of these vitamins we need.  We use B vitamins to metabolize glucose in our cells.  So, the more carbohydrates we consume, the more glucose we burn (instead of fatty acids), and the more B vitamins we need from our diets.”  When we eat carbohydrates, we “excrete vitamin C with our urine rather than retaining it” (176). 

Without carbohydrates in the diet, Taubes notes, “there’s every indication that we would get all the vitamin C we ever needed from animal products.”  Thus, Taubes concludes, “Carbohydrates are not required in a healthy human diet.”  And, “another way to say this (as proponents of carbohydrate restriction have) is that there is no such thing as an essential carbohydrate” (176).             

The solution to both obesity and leanness accompanied by excessive energy is actually pretty simple:  stop eating carbohydrates, especially the easily digestible ones, like, bread, pasta, potatoes, sweets, beer, fruit  juices, and sodas.  (I’d add cold breakfast cereals to this list.)  Taubes notes that before the 1960s, conventional wisdom recognized that these foods were “uniquely fattening.”  And, he notes that this message has been at the heart of an “unending string of often best-selling diet books” (11).  He also notes that “when physicians stopped believing it, a process that began in the 1960s and concluded in the late 1970s,” their change coincided “with the beginning of the current epidemics of obesity and diabetes” (150).     

Taubes does note that if the obesity has gone on too long, the body may not be able to reset its own chemistry (205).  And, that if one is taking medications to lower blood sugar or blood pressure, one should work closely with a doctor because following a low-carbohydrate diet lowers both so that a dangerous “double whammy” effect can occur (216). 

Taubes reproduces the Atkins-version diet used by Dr. Eric Westman of the Lifestyle Medicine Clinic at the Duke University Medical Center.  Westman has been working with this diet since 1998 (202).  And, Taubes points to four other doctors with similar clinical practices across the country (202).   

My only critique of this diet is that it allows artificial sweeteners and does not distinguish well between good fats and bad fats.  But, you can read Tipping Points 14 to understand how to sort those fats out for yourself.