Statin cholesterol drugs are for bread-eaters

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Much of the $23 billion spent each and every year on statin drugs is really targeting the treatment of “high cholesterol”—but actually unhealthy distortions in lipoproteins—created by consuming grains.

Most people, unfortunately, continue to focus on fat consumption, especially saturated fat, as the cause for high cholesterol and have been led to believe that cutting saturated fat and statin drugs are the solution. So let me try and clear up this somewhat confusing issue and show you that 1) there is no real benefit to cutting saturated fat, 2) grains and sugars cause distortions that increase cardiovascular disease, and 3) statin drugs do not fully address the causes of cardiovascular disease, accounting for their relatively trivial benefits.

Here is a typical panel of someone who consumes grains:

Triglycerides 170 mg/dl
LDL cholesterol (calculated) 150 mg/dl
HDL cholesterol 40 mg/dl
Total cholesterol 224 mg/dl

In other words, HDL cholesterol is lowish, triglycerides high, LDL cholesterol and total cholesterol high. What does this mean? Let’s take each, one by one. It’s a bit complex, but stick with it and you will emerge smarter than 95% of doctors who “treat” high cholesterol.

Triglycerides are the byproduct of two digestive processes: 1) De novo lipogenesis or the liver’s conversion of the amylopectin of grains and other sugars into triglyceride-rich VLDL particles that enter the bloodstream, and 2) absorption of dietary fats (which are triglycerides themselves). De novo lipogenesis dominates triglyceride levels in the bloodstream, far outstripping consumption of fat as a determinant of triglyceride levels. This simple fact was only identified recently, as the rise in triglycerides that occurs after consuming fats and oils develops within 2-4 hours, but the much larger rise in triglycerides from carbohydrate-to-triglyceride conversion starts 6-8 hours later, a fact not uncovered in older studies that failed to track this far out in time. (And, in certain genetic types, such as apo E2, the rise from carbohydrates in grains and sugars can last for days to weeks.)

LDL cholesterol is calculated, not measured. The Friedewald calculation, developed in the early 1960s to provide an easy but crude means of estimating the quantity of cholesterol in the low-density lipoprotein fraction of the blood applied several basic assumptions: 1) that everyone consumes an average diet of average macronutrient composition, and 2) that the triglyceride content of all lipoproteins remained constant from person to person (which is not true, but is wildly variable), and 3) that all LDL particles are the same (also not true, as LDL particles vary in size, conformation, surface characteristics, etc.).

Grain consumption, thanks to the process of de novo lipogenesis, increases blood levels of triglycerides and VLDL particles. VLDL particles interact with LDL particles, enriching LDL particle triglyceride content and reducing cholesterol content. This leads to a process of LDL particle “remodeling” that creates small LDL particles–glycation-prone, oxidizable, adherent to inflammatory blood cells, and persistent in the bloodstream for 7 days, rather than the 24 hours of more benign large LDL particles. Grains thereby trigger the process creating persistent and damaging small LDL particles; fats trigger the process that does not.

When we cut out grains and sugars, the Friedewald calculation is therefore no longer valid, as the assumptions–-weak to begin with–-are disrupted. LDL cholesterol, this crude, surrogate effort to indirectly quantify LDL particles, is therefore completely useless—the calculation of LDL cholesterol is INVALID. This has not, unfortunately, dampened enthusiasm among my colleagues nor the drug industry for trying to treat this number with statin drugs to the tune of $23 billion per year.

Better ways to quantify LDL particles: NMR LDL particle number (which includes quantification of small and large LDL particles) or an apoprotein B. (Each LDL particle contains one apo B, which thereby provides a virtual count of LDL particles, but no breakdown into small vs. large.) Lipoprotein testing has been around for over 20 years, is inexpensive and available—but requires an informed doctor to interpret.

HDL cholesterol is, unlike LDL cholesterol, a measured and reliable value. Ironically, it is among the most ignored. Grain-consuming humans tend to have low HDL because the high triglyceride/VLDL particles interact in the bloodstream with HDL particles, enriching HDL particles in triglycerides and reducing cholesterol content. This leads to a reduction in HDL size and HDL quantity, thus low HDL cholesterol values. The lower the HDL, the higher the cardiovascular risk.

Total cholesterol is the sum of all three values: LDL cholesterol + HDL cholesterol + triglycerides/5. (More accurately, LDL cholesterol is the calculated value: LDL = total chol – HDL – trg/5.)

Given the mix of values, total cholesterol is therefore essentially useless. A large increase in HDL, for instance–-a GOOD thing–-will raise total cholesterol; a large reduction in HDL–-a BAD thing–-will reduce total cholesterol: the opposite of what you would think. Total cholesterol can indeed yield useful prognostic information when applied to a population, though the relationship is weak. But it is useless when applied to an individual.

If we reject the silly and simple-minded notions of cholesterol panels, and apply the greater insights provided by advanced lipoprotein analysis, several nutritional observations can be made:

–Saturated fat increases HDL, shifts HDL to larger, more protective, particles, and triggers formation of large LDL particles.
–The amylopectin carbohydrates of grains trigger higher triglycerides, thereby providing more VLDL particles to interact with HDL and LDL particles, the process that leads to triglyceride enrichment and smaller ineffective HDL and smaller atherogenic LDL (heart disease-causing).
–Given the unusual persistence time of small (7 days) vs large (1 day) LDL particles, grain consumption is FAR worse than fat consumption.

You can begin to appreciate how overly simplistic this notion of “reducing cholesterol” using statin drugs really is. You can also appreciate that the real situation is a bit more complicated and beyond the reach of most busy primary care physicians, while being outside the interests of most cardiologists, obsessed as they are with revenue-producing activities like heart catheterizations, stent and defibrillator implantation.

A typical response in the cholesterol panel of someone who has eliminated all wheat, grains, and sugars would look something like this:

Triglycerides 50 mg/dl
LDL cholesterol (calculated) — mg/dl
HDL cholesterol 70 mg/dl
Total cholesterol 200 mg/dl

I left the LDL cholesterol blank because it can do just about anything: go up, go down, remain unchanged—but it doesn’t matter, because it is inaccurate, unreliable, invalid. If you were to measure advanced lipoproteins, however, you would see a dramatic reduction or elimination of small LDL particles and reduction of the total count of LDL particles (since the small LDL component has been reduced or eliminated) with large LDL particles remaining.

Common distortions of cholesterol panels can be easily explained by the chain of events that emerge from a diet rich in “healthy whole grains.” The relatively trivial benefits of statin cholesterol drugs (about a 1% reduction in real risk, not the inflated “relative risks” quoted in ads and statistically-manipulated studies) should come as no surprise, since high cholesterol is not the cause for cardiovascular disease.

Written By: Dr. William Davis

Article Source: http://www.wheatbellyblog.com/2016/02/statin-cholesterol-drugs-are-for-bread-eaters/

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The Best Predictor for Heart Disease

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Cholesterol has been blamed for just about every case of heart disease for the last 20 years, when in reality, you need the good cholesterol (HDL) in order to be healthy. Your body uses cholesterol for cell membranes, hormones, neurotransmitters and overall nerve function. 

Your total cholesterol number isn’t the best  indicator of heart disease risk. One of the most important tests you can get to determine your risk is the NMR lipoprofile, which measures your LDL particle number. This test also has other markers that can help determine if you have insulin resistance, which is a primary cause of elevated LDL particle number and increased heart disease risk 

 If you’ve had your cholesterol levels checked, your doctor most likely tested your total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. But the newest research shows those are not accurate predictors for cardiovascular disease risk. A much more accurate predictor is testing your LDL particle number.  

 Imagine your bloodstream’s like a river, the LDL particles are like the boats that carry the cholesterol and fats around your body. The cholesterol and fats are like cargo in the boats. Right now doctors are usually measuring the amount of cargo or cholesterol in the LDL particles. But what we should be measuring is the number of LDL particles, or the number of boats in the river, so to speak, because that’s a much more accurate risk factor for heart disease.” 

 Therefore, it’s possible to have a normal total or LDL cholesterol level, yet have a high number of LDL particles.  

Fortunately, there are now ways to test for your LDL particle number and Core Medical Group is offering this test. The results of this test will help determine if you truly need a statin medication, and which treatment modality is the most beneficial.  

For more information and appointments, please contact Clinic Director Charlie Blaisdell at CBlaisdell@CoreNewEngland.com

BTP/CORE New England
www.BostonTestosterone.com
CBlaisdell@CORENewEngland.com
Clinic: 781-269-5953

Do Cholesterol Drugs Have Men By Their Gonads?

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Cholesterol-lowering agents in the statin drug class have long been linked with erectile dysfunction and low testosterone — effects that compromise more than just a man’s general sense of well-being and physical health, but his ego as well.

Now, a new study on statins and male fertility has found for the first time that this cholesterol-lowering class of drugs may be causing significant and lasting damage to men’s testicles and sperm, and by implication, possibly the health of future generations.

The new study published in Reproductive Biology and Endocrinology titled, “Evaluation of atorvastatin efficacy and toxicity on spermatozoa, accessory glands and gonadal hormones of healthy men: a pilot prospective clinical trial,” evaluated the effects of 10 mg daily of Lipitor (atorvastatin), daily, for 5 months, in 17 normal men with normal plasma lipid and standard semen parameters.

Sperm health parameters, accessory gland markers, semen lipid levels and blood levels of testicular hormones were evaluated before Lipitor intake, during the treatment, and 3 months after its withdrawal.

The alarming results were reported as follows:

  • Atorvastatin treatment significantly decreased circulating low-density lipoprotein cholesterol (LDL-C) and total cholesterol concentrations by 42% and 24% (p < 0.0001) respectively, and reached the efficacy objective of the protocol.”
  • “During atorvastatin therapy and/or 3 months after its withdrawal numerous semen parameters were significantly modified, such as total number of spermatozoa (-31%, p < 0.05), vitality (-9.5%, p < 0.05), total motility (+7.5%, p < 0.05), morphology (head, neck and midpiece abnormalities, p < 0.05), and the kinetics of acrosome reaction (p < 0.05). Seminal concentrations of acid phosphatases (p < 0.01), alpha-glucosidase (p < 0.05) and L-carnitine (p < 0.05) were also decreased during the therapy, indicating an alteration of prostatic and epididymal functions.”
  • “Moreover, we measured at least one altered semen parameter in 35% of the subjects during atorvastatin treatment, and in 65% of the subjects after withdrawal, which led us to consider that atorvastatin is unsafe in the context of our study.”

They concluded:

“Our results show for the first time that atorvastatin [trade name Lipitor] significantly affects the sperm parameters and the seminal fluid composition of healthy men.”

Why Are We Taking Statin Drugs If They Harm The Heart?

Statin drugs are purported to have cardioprotective properties because they reduce the production of low-density lipoprotein (LDL) – colloquially known as, and falsely equated with, ‘cholesterol‘ (there are actually hundreds of lipid species in the human liposome) – despite the fact the drug class itself has been found to be cardiotoxic to the heart muscle in several ways:

On the Greenmedinfo.com Statin Research database we have cataloged over 15 studies from the National Library of Medicine indicating the heart-damaging properties of this class of supposedly ‘heart friendly’ drugs.  View our professional data page here, or if you are not a member, view the open access reference page for public view and linking here.

Statins do not only reduce lipoprotein production but have so-called pleoitropic properties, which include immune system down-regulating and anti-inflammatory properties, which is why they are believed to have a small benefit in reducing the inflammatory burden caused by autoimmune processes in the artery that can precipitate myocardial infarction (heart attack) in some individuals — but not without having the unintended, adverse effect of increasing cancer risk (at all sites) and contributing to congestive heart failure, effectively cancelling out the small, mostly theoretical benefit of reduced heart attack risk. For instance, it has been estimated that “…at least 23,000 low-risk people would have to take statins for five years to prevent one death from heart disease.” [Source]

Statins are also clearly diabetogenic, increasing the risk of type 2 diabetes by about 50% in some populations, with the FDA now requiring drug manufacturers to include a warning of diabetes risk on statin drug labels. Considering morbidity and mortality from type 2 diabetes is caused not by the elevated blood sugar in and of itself, but the damage glycated sugar does to the vascular system and the subsequent cardiovascular harm it produces, the case against using statins for primary and secondary prevention of heart disease seems clear as day.

Moreover, cardiovascular harm is not the only concern. Statin drugs have been linked to over 300 adverse health effects. We issued a consumer alert on the topic several years ago. For the more technically minded, here is the database page on Statin drugs listing 300+ adverse health effects based on 465 published studies.

Heart Disease Is Not Caused By A Lack of A Drug

Should we be surprised to find so much research on this drug class’s adverse health effects? After all, cholesterol is fundamental for the health of each cell in the human body, and low cholesterol has been found to cause a wide range of health problems, including psychiatric states such as violence against self and other. The food and drug industries have used cholesterol phobia to manipulate health professionals and the lay public into believing that the cause of heart disease is genetic, and can only be addressed through the use of synthetic, patented, essentially toxic chemicals, i.e. pharmaceuticals, or eating semi-synthetic ‘low fat,’ ‘low cholesterol’ foods with very little nutritional value.

This latest study speaks to why we must exercise the precautionary principle when considering taking a patented chemical – technically a xenobiotic alien to human physiology – for suppressing a symptom of a much deeper and more complex problem. While oxidized cholesterol forms a significant part of the problem of atherosclerotic build-up in the arteries, it is not the primary cause of the damage to the inner lining of the arteries (endothelium), and the pre-existing endothelial dysfunction that can go on for many decades silently in the background. Ox-LDL deposits in atheromatous lesions have been viewed as an epiphenomenon, generated as part of a cascade of immune-mediated events the body activates in order to attempt to heal arterial damage. In certain respects, cholesterol deposits in the arteries at the site of damage can be likened to a Band-Aid. Do we blame the Band-Aid for causing the injury upon which it is placed?

It is important to point out that oxidized cholesterol (ox-LDL) can be toxic and harmful to the vascular system, but the problem with modern blood testing for ‘cholesterol’ is that it does not take into the quality of the lipoproteins, only their quantitative dimensions.  Depending on one’s diet, environmental factors, and overall bodily health, LDL particles will oxidize at different rates. If you are eating an antioxidant rich diet, full of healthy fats, phytocompounds, etc., your properly functioning LDL will be less susceptible to conversion to ox-LDL.  On the other hand, eating a diet full of non-essential, oxidized fats, deficient in phytonutrients, antioxidants, etc. – and adding in environmental toxins and toxicants, e.g. smoking – will produce more ox-LDL, rendering it artherogenic. Obviously, therefore, diet and lifestyle form the basis for a sound preventive approach if the ‘lipid hypothesis‘ of cardiovascular disease is even deemed truly relevant. [For more research on natural substances which inhibit cholesterol oxidation, view our database on the topic: Prevent Cholesterol Oxidation.]

Furthermore, there are many ways to address underlying vascular pathologies without suppressing the production of a vital building block and signaling molecule, which is what cholesterol is. Pomegranate, chocolate, and many other natural substances, have been confirmed in research to have profound heart disease preventive and reversing properties. You can explore our database sections relevant to the topic within our Heart Health guide, to find hundreds of studies proving this point. Basic nutritional incompatibilities, including the consumption of wheat which has cardiotoxic properties in genetically susceptible individuals, and excessive consumption of omega-6 versus omega-3 fats can profoundly increase the risk of heart disease. One groundbreaking study published last year, in fact, indicates that statins actually reduce the health benefits of omega-3 fats in the diet – adding another mechanism by which statin drugs exert heart disease promoting effects.

Beyond the Pharmaceutically-Driven Medical Paradigm

If statin drugs are toxic to human sperm, and if the men within whom this statin-induced damage is occurring are of reproductive age, the implications of this latest study on statins and fertility are potentially devastating to the health of future generations. Changes in our species germlines – sperm or egg – are carried on to future generations, possibly forever. With recent research indicating that even changes to somatic cells in this lifetime are capable of transferring information to the sperm, what we do here and now – our chemical exposures, our nutritional status, and even our psychospiritual and mental orientation (which gear into real physiological and genetic/epigenetic processes – can have critical and irreversible affects on our offspring.

Clearly, the time has come both to re-evaluate the role of pharmaceuticals in ‘preventive’ health care, as well as the effects these novel new chemical compounds will have on the next generation, and the next.

For alternatives to lipid lowering chemicals, take a look at the following, evidence-based natural interventions:

Source: http://www.greenmedinfo.com/blog/do-cholesterol-drugs-have-men-their-gonads

For more information and appointments, please contact Clinic Director Charlie Blaisdell at CBlaisdell@CoreNewEngland.com

BTP/CORE New England
www.BostonTestosterone.com
CBlaisdell@CORENewEngland.com
Clinic: 781-269-5953