Cholesterol is a word that strikes fear into the heart. But does it also strike disease? Because here’s the curious thing: having a high cholesterol level is associated with living a longer life, especially if you have heart disease. Confused? Of course you are! Welcome to the cholesterol paradox.
The term “cholesterol paradox” was coined as early as 2006 (if not before), when a study of data collected from 24 countries, involving nearly 11,000 patients with heart disease, found that “Low cholesterol levels were associated with worse prognosis in patients with acute heart failure.”
That was just the start of it. Since then, many studies have been published that discuss this baffling observation, one that has been replicated many times.
Indeed, raised total cholesterol has been shown to be a predictor of survival — in a study of 114 patients with chronic heart failure, the chances of survival increased by 25% for each mmol/l increment in total cholesterol. Similarly, it has been found that most — nearly 75% — of people who are admitted to hospital with heart attack have normal cholesterol levels.
How is it possible to make sense of all this? Easy. Just call it a paradox and ignore the cognitive dissonance.
Nobody argues that cholesterol is essential to life. This fat-like substance, made in the liver, is present in every cell of the body. It is needed to make hormones and to make vitamin D. It is a component of the cell membrane and plays a key role in the immune system. The brain has the highest concentration of cholesterol in the body, where it is involved in nerve transmission and memory recall. So vital is it that the brain makes its own supply.
Drugs designed to reduce cholesterol in the body — statins — are among the most prescribed in the world. In 2019, Atorvastatin was the most widely prescribed drug in both the UK and US.
“The recently presented ACCELERATE trial dumbfounded many experts by failing to demonstrate any cardiovascular benefit of evacetrapib (cholesterol-lowering medication) despite dramatically lowering low-density lipoprotein cholesterol and raising high-density lipoprotein cholesterol in high-risk patients with coronary disease.”
Unpacking the paradox
One way to decipher this enigma is to talk about “good” and “bad” cholesterol. Yet this too is misleading. There is only one type of cholesterol, and it’s called cholesterol. There are, however, different types of cholesterol transport systems.
Cholesterol is transported around the body by different protein carriers, known as lipoproteins. There are several types, the main ones being high density lipoprotein (HDL), low density lipoprotein (LDL) and very low-density lipoprotein (VLDL).
HDL is assumed to be “good” because it transports cholesterol away from the arteries and to the liver, for disposal.
LDL is assumed to be “bad” because it transports cholesterol from the liver to the rest of the body — including the arteries, where it is a component of arterial plaques. That is why cholesterol is vilified as the enemy of heart health. (Plaques contain, among other things, calcium, but nobody suggests you avoid calcium.)
Arterial plaques can build up, causing narrowing of the arteries and a condition called atherosclerosis. Eventually a clot can break off, blocking flow to the heart and causing a heart attack.
So far, so neat and tidy. It’s only when you delve deeper that it all starts to get rather messy.
Even though LDL is the one with the bad reputation, low levels of LDL are linked to higher overall mortality in patients with heart failure. If you want to survive, you might be better off with high levels of not-so-bad-after-all LDL cholesterol.
Similarly, people with high cholesterol, including high LDL cholesterol, are less likely to have atrial fibrillation. Atrial fibrillation (AF) is irregular, sometimes rapid heart rhythm, which can cause blood clots in the heart. It also increases the risk of stroke and heart failure.
“This research adds to the body of evidence which suggests an inverse relationship between cholesterol levels and AF — the “cholesterol paradox” for AF.”
It’s all about the ratio…
Lowering LDL cholesterol has no substantial effect on reducing heart attacks or death. Which is not to say that cholesterol doesn’t matter; it does.
The key issue is the ratio of total cholesterol to HDL. This is now considered to be a more important, stronger predictor of heart attack in both men and women, even though “the clinical use of the ratio is often overlooked”.
How do you calculate your ratio? Simple — just divide your total cholesterol figure by your HDL figure. The optimal range is 1.0–4.8. These days test results usually include the all-important ratio. When you next get tested, be sure to ask about this.
…..and the fat
While you’re about it, ensure also that you have your triglycerides measured; triglycerides are a strong risk for cardiovascular disease. Serum triglyceride is the fat circulating in your blood and high levels (over 1.68mmol/L) increase your risk of coronary heart disease and stroke.
Where diet comes in
And here’s another paradox to scramble your brain. Eating saturated fat does not raise blood fat. It does increase both LDL and HDL cholesterol, but without changing the ratio of total cholesterol to HDL.
Despite the lack of evidence to indict it, the fear of saturated fat persists. To resolve this contentious issue once and for all, the Journal of the American College of Cardiology published, in 2020, a thorough, “state-of-the-art” review into the relationship between saturated fat consumption and cardiovascular disease.
The researchers discovered that most analyses and trials found that not only was there no benefit in reducing saturated fat to minimise the risk of cardiovascular disease, it was actually protective against stroke. The conclusion of this review was:
“The recommendation to limit dietary saturated fatty acid (SFA) intake has persisted despite mounting evidence to the contrary.”
So what does increase levels of triglycerides, and therefore risk of heart disease?
The answer is carbohydrate.
The best way to lower your risk of heart disease and early death is to reduce your intake of carbohydrates, especially sugar and refined carbohydrates.
When you eat a low carbohydrate, high fat diet, your triglyceride level goes down. This is exactly what you want. Do the opposite — eat a high carbohydrate, low fat diet — and your blood fat rises and your HDL decreases. That is the effect of insulin, or rather insulin resistance.
Insulin resistance is a pre-diabetic state, where the body is no longer able to respond adequately to all the glucose circulating in the blood.
“…the conventional dietary advice on lowering cholesterol by reducing saturated fat intake is not just wrong, but has also likely worsened the risk of heart disease by fuelling the single most important root cause of coronary artery disease and heart attacks: insulin resistance.” (Dr Aseem Malholtra: A Statin-Free Life.)
A review of the evidence surrounding sugar consumption and its role in the development of coronary heart disease found “relatively consistent evidence” of an association between sugar intake and the risk of developing cardiovascular disease.
“To reduce the burden of CHD, guidelines should focus particularly on reducing intake of concentrated sugars, specifically the fructose-containing sugars like sucrose and high-fructose corn syrup in the form of ultra-processed foods and beverages.”
These are the foods that increase your risk of developing insulin resistance. Diabetic patients are more likely to have coronary atherosclerosis than non-diabetics and more likely to die from heart disease. But even without diabetes, insulin resistance puts you at greater risk.
There are so many “paradoxes” in nutrition that they are becoming the norm. Perhaps you’ve heard of the French paradox — the observation that the French have one of the highest consumption rates of saturated fat in Europe, but a relatively low rate of heart disease.
However you view all these contradictions, something clearly isn’t working, because “The global campaign to lower cholesterol by diet and drugs has failed to thwart the developing pandemic of coronary heart disease around the world.”
Indeed it has. A re-examination of entrenched beliefs about diet, heart disease and longevity is surely long overdue.
As I mention above, cholesterol is essential for brain health. Deficiency is linked to a number of diseases, including dementia.
For decades, statins—the most common cholesterol-lowering medications—have been recognized as a lifesaver for those with heart disease. While statins have revolutionized heart health in a positive way, some studies highlight the lesser-known concerns of the medication: energy-sapping, increased diabetes risk, and, for many people, muscle pain.
The Puzzling Link Between Statins and Insulin Resistance
A recent systematic review of 11 epidemiological studies with nearly 47 million participants found associations between statin use and decreased insulin sensitivity, as well as insulin resistance—both significant factors for developing Type 2 diabetes. Additionally, statins were found to reduce glycemic control and elevate fasting glucose levels.
Experts are uncertain about the precise mechanism through which statins might impact insulin resistance, considering their advantages, such as lowering inflammation, decreasing oxidative stress, and enhancing endothelial function—all of which actually improve insulin sensitivity rather than diminish it.
A 2021 study published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology also found that statins can increase the risk of Type 2 diabetes, but how was unclear. In weighing the potential risks of statins, however, most researchers and health care professionals still believe them to be more beneficial than harmful.
“It is generally viewed that the strengths of lower cholesterol by a lot outweigh a modest increase in insulin resistance,” Michael Snyder, a genetics professor and chair of the Genetics Department at Stanford University School of Medicine, told The Epoch Times.
But the double-sided nature of statins remains unclear to researchers, added Dr. Snyder, who has coauthored multiple studies investigating the correlation between statin usage and insulin intolerance.
Lifestyle factors like obesity also play a major role in insulin resistance. Insulin resistance is often associated with high body weight, which individuals can reduce to potentially offset statins’ effects, Dr. Snyder said.
Why Do Statins Drain Energy?
Fatigue and muscle pain seem to be common with statin use. A study of over 350 statin users found that 93 percent reported muscle pain and fatigue, while 85 percent reported weakness.
“This is of no surprise because of the well-documented effects that statins have on Coenzyme Q-10 (CoQ10), which is a primary cofactor for mitochondrial function,” Dr. Node Smith, a board-certified naturopathic physician, told The Epoch Times. Mitochondria create energy for the entire body at the cellular level. Therefore, in practical terms, statins can deplete the body’s cellular energy by depleting CoQ10, he added.
A letter to the editor published in the British Journal of Clinical Pharmacology noted that people taking statins who also supplemented with CoQ10 were less likely to experience chronic fatigue.
Dr. Smith said many of his patients who have taken statins long-term have reported experiencing persistent muscle pain, weakness, fatigue, and brain fog. “Some of these patients are avid athletes and simply are confused why they can no longer work out,” he added. “If I see this presentation in someone on a statin medication, I will almost always assume the statin is at least a contributing factor and discuss with the patient its removal and replacement with another therapy.”
Is Vitamin B3 an Alternative to Statins?
Statins are commonly used alongside niacin (vitamin B3), recommended for over 40 years to prevent heart disease due to the vitamin’s positive impact on lipid levels.
Niacin is the most common and effective treatment that replaces statins, according to Dr. Smith. “Of all the pharmaceutical medications I’ve helped people get off of, statins are the easiest, least concerning, and patients typically have the best results with—because it is not uncommon for them to feel almost instantly better.”
Niacin decreases LDL cholesterol, which can build up plaque in arteries when levels are too high. It also increases HDL cholesterol, which absorbs other forms of cholesterol in the bloodstream and carries it back to the liver for removal, according to a clinical trial of over 300 people. Additionally, niacin lowers triglycerides, a type of fat in the blood.
Optimized niacin therapy costs patients $15 to 30 per month and is worth trying before statins, Dr. Smith added.
Studies have found that combining niacin and statins may outperform statins alone. Dr. Smith has observed similar results in his practice, although some studies suggest otherwise.
Niacin fell out of favor due to the side effect of niacin flushing, which produces a slight prickly heat sensation for about 30 minutes and can be quite concerning and uncomfortable for some people, he said.
About 15 years ago, wax-coated niacin tablets were developed. They allow high doses of niacin to be delivered while reducing flushing for most people, according to Dr. Smith. Side-effect management methods like taking niacin with food or baking soda can also help.
However, Dr. Smith cautioned that people with familial hypercholesterolemia, a genetic disorder, may need more aggressive therapies, potentially including statins.
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