Interesting Information: December 30, 2015
Here’s a post that kind of got lost in the holidays.
But it’s never to late to post this one…
MY LOW COUNTRY ADVENTURE
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).