The western medicine paradigm’s, diet-heart disease belief (that consumption of saturated fat and cholesterol foods raises blood cholesterol and triggers the heart disease process), oversimplifies and totally distorts the true causes and processes that have led to the current heart disease epidemic. In reality the true causal risk factors of heart disease are oxidation and inflammation in the blood stream, a situation that is caused by poor eating and lifestyle habits.

Most interestingly there is no correlation between the intake of foods that are high in cholesterol and saturated fats and the risk of heart disease. Saturated fats have been the preferred form of energy source throughout our evolutionary history. The familiar offender when it comes to the accepted western medicine paradigm concerning the diet-heart disease hypothesis – LDL Cholesterol – is only problematic when present simultaneously with a high insulin-producing diet or other risk factors that compromise the effective clearance of oxidized LDL from the blood stream.

The actual heart disease process develops as follows:

  • Excess consumption of processed carbohydrates (grains and sugars) promotes excess insulin production and high triglycerides in the blood…
  • Coupled with consumption of easily oxidized industrialized polyunsaturated oils…
  • Combine that with a lifestyle of excess stress (not enough sleep, not enough sun and chronic exercise)…
  • This dietary eating pattern promotes a state of oxidation and inflammation in the blood stream…
  • Under these circumstances cholesterol in the blood stream can turn dangerous…
  • As small, dense LDL molecules can become lodged on arterial walls and sustain oxidative damage…
  • This elicits an immune response further promoting inflammation, the formation of plaque on arterial walls and an eventual heart attack or stroke.

Are Statins the Wonder Drugs They’re Made Out to Be?

Statins have been hailed by many in the conventional medical establishment as wonder drugs, with some physicians going as far as suggesting they should be added to the water supply.(The doctor that made that particular suggestion is named John Reckless—I kid you not.) But are statins really the wonder drugs they’ve been made out to be?

Before we dive in to what the statistics on statins say, I need to briefly explain the difference between relative and absolute risk reduction. Researchers and pharmaceutical companies often use relative risk statistics to report the results of drug studies. For example, they might say, “In this trial, statins reduced the risk of a heart attack by 30 percent.” But what they may not tell you is that the actual risk of having a heart attack went from 0.5 percent to 0.35 percent. In other words, before you took the drug you had a one in two hundred chance of having a heart attack; after taking the drug you have a one in two hundred eighty-five chance of having a heart attack. That’s not nearly as impressive as using the 30 percent relative risk number, but it provides a more accurate picture of what the actual, or “absolute,” risk reduction is.

Another important concept to understand when discussing the efficacy of statins is that they don’t have the same effects in all populations across the board. For example, a young woman with no prior history of heart disease will not get the same benefit as a middle-aged man who has recently had a heart attack.

The number needed to treat (NNT) is an important metric because it provides information about a drug’s usefulness and practicality in a clinical setting. The NNT reports the number of patients that would have to be treated to prevent one outcome, such as a heart attack or a death, measured in a study. For example, if a study looking at the efficacy of statins in reducing heart attacks reports an NNT of thirty for five years, that means you’d need to treat thirty people for five years to prevent one heart attack.

With this in mind, let’s take a closer look at the efficacy of statins in two broad groups of people: those with pre-existing heart disease and those without pre-existing heart disease. In the medical literature, these groups are referred to as “primary prevention” and “secondary prevention,” respectively.

Secondary prevention (those with pre-existing heart disease)

An analysis by Dr. David Newman in 2010, which drew on large meta-analyses of statins, found that for those with pre-existing heart disease that took statins for five years:

  • 96 percent saw no benefit at all
  • 2 percent (1 in 83) had their lifespan extended (were saved from a fatal heart attack)
  • 6 percent (1 in 39) were helped by preventing a repeat heart attack
  • 8 percent (1 in 125) were helped by preventing a stroke
  • 6 percent (1 in 67) were harmed by developing diabetes
  • 10 percent (1 in 10) were harmed by muscle damage

Even in the population for which statins are most effective—those with pre-existing heart disease—eighty-three people have to be treated to extend one life, and thirty-nine people have to be treated to prevent a repeat heart attack. But these results do not apply to all populations across the board. Most studies have shown that while statins do reduce cardiovascular disease (CVD) events and deaths from CVD in women, they do not reduce the risk of death from all causes (“total mortality”).

Nor do these results apply to men or women over the age of eighty. Statins do reduce the risk of heart attack and other CVD events in men over the age of eighty, and at especially at this age, these events can have a significant negative impact on quality of life. However, the bulk of the evidence suggests that statins don’t extend life in people over eighty years of age, regardless of whether they have heart disease, and the highest death rates in people over eighty are associated with the lowest cholesterol levels.

Primary prevention (those without pre-existing heart disease)

Statins do reduce the risk of cardiovascular events in people without pre-existing heart disease. However, this effect is more modest than most people assume. Dr. Newman also analysed the effect of statins given to people with no known heart disease for five years:

  • 98 percent saw no benefit at all
  • 6 percent (1 in 60) were helped by preventing a heart attack
  • 4 percent (1 in 268) were helped by preventing a stroke
  • 5 percent (1 in 67) were harmed by developing diabetes
  • 10 percent (1 in 10) were harmed by muscle damage

These statistics present a more sobering view on the efficacy of statins in people without pre-existing heart disease.

Adverse effects

If statins were harmless and free, then it wouldn’t matter how many people need to be treated to prevent a heart attack or extend someone’s lifespan. But statins are not free, nor are they harmless. Statin use has been associated with a wide range of side effects, including myopathy (muscle pain), liver damage, cataracts, kidney failure, cognitive impairment, impotence, and diabetes.

Unfortunately, studies show that physicians are more likely to deny than affirm the possibility of statin side effects, even for symptoms with strong evidence in the scientific literature. Assuming that physicians would likely not report the adverse reaction in these circumstances, it’s probable that the incidence of statin side effects is much higher than the reported rates.

One of the most troubling side effects of statins that has only recently become apparent is their potential to increase the risk of diabetes, especially in women. A study by Dr. Naveed Sattar and colleagues published in The Lancet in 2010 examined thirteen randomized clinical trials involving more than 90,000 patients taking statins. They found that statin use was associated with a 9 percent increased risk in developing diabetes. Note that this is a relative risk, so the absolute risk of developing diabetes while taking a statin is very low. That said, observational data from the Women’s Health Initiative found a 48 percent increased risk of diabetes in healthy women taking statins after adjusting for other risk factors

The Ancestral Health movement states that a blanket strategy of reducing total cholesterol levels through use of deadly statin medication is problematic for several reasons.

LDL Particle Size: Critical patient care decisions are commonly made based on the total LDL reading instead of testing and considering the levels of each LDL type. Evaluating the big picture of heart disease risk factors – triglycerides, LDL particle sizes, HDL, systemic inflammation markers and other advanced blood tests – is a more effective approach than the current trend of prescribing statins to millions of patients based on total cholesterol readings or total LDL readings.

Oxidation and Inflammation: Reducing heart disease risk down to a single number on a blood test may allay fears and anxieties held by both patient and doctor – “take this pill, lower your LDL and be fully protected from any cardio or cerebro-vascular event” – but predominant risk factors will be overlooked in the process. For example, even relatively small amounts of ‘small, dense LDL’ can still be problematic when other risk factors are present, such as insufficient HDL and high stress, pro-inflammatory lifestyle practices.

Side Effects: Statins reduce the production of cholesterol in the liver, producing lower blood level of all types of lipoproteins including the highly protective and beneficial HDL. Since cholesterol is critical to many important functions in the body, artificially suppressing all cholesterol production through artificial pharmaceutical means can interfere with healthy serotonin balance (less energy and alertness and potential mood alterations), hampered vitamin D synthesis, dysfunctional regulation of blood sugar, disturbances in regulation of inflammation and disturbances in an array of important hormonal processes.

Statins have been shown to cause inflammation in the liver and also deplete cellular levels of an important energy substrate – Co-Enzyme Q10 (CoQ10). CoQ10 is essential for the mitochondria to produce energy in your cells. Depletion of this critical co-enzyme can cause fatigue, muscle pain and other indicators of muscle dysfunction. Furthermore CoQ10 deficiency can hamper the cells ability of all cells to fight free radicals and moderate inflammation. This state of cellular depletion can lead to adverse lifestyle practices such as insufficient exercise (prompted by the lack of energy and muscle pain side effects) and elevated oxidative damage in cells whose normal energy production mechanisms are compromised.

On top of all the above, statins do not positively affect high triglyceride levels (blood fat) or LDL (so-called bad cholesterol) particle size! Numerous studies including a long term study published three times in the New England Journal of Medicine, showed that people taking multiple cardiac medications (including a statin), have a 40 percent higher risk of mortality after four years, than those taking no medication.

“Statin Use Comes With Serious Side Effects And Fails To Address The Proximate Causes Of Heart Disease – Inflammation And Oxidation!”


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