Is the Cholesterol Theory Completely Wrong?

High Cholesterol may make you live longer

A couple of unheralded research papers claim that it’s actually low LDL cholesterol that’s bad and that statins should be discontinued.

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Cholesterol Science: There is Something Off

Let me tell you a story about cholesterol. It involves my mother.

She was suffering from the terrible trio of radiation, lung cancer, and chemotherapy. I tried to convince her to eat high-calorie foods and anything else to keep from starving. She refused to listen and continued to nibble at her food. Why? Because she was concerned about her cholesterol.

The poor woman was given only two years to live. She was more concerned about the potential effects that high cholesterol might have on her heart and lungs than she was about the cancer in her lungs.

That’s how much the medical community has made us fear cholesterol. What makes my mother’s death possibly even more tragic is that there’s apparently some evidence that having low total cholesterol actually makes one more susceptible to cancer and other diseases.

For now, forget about that. I’m personally at a crossroads here. I inherited high cholesterol from my mother and father, and, despite all my efforts, despite all I know about health, I haven’t been able to solve it.

Granted, my total cholesterol isn’t that bad compared to some. It usually hovers around 220 with an LDL of between 130 and 140, but my doc doesn’t like it. The American Heart Association doesn’t agree. The doc wants me to take a statin, especially since I’ve got that familial hypercholesterolemia (FH) thing going on.

However, I find more answers the more I study it. I’ve suspected something’s wrong with cholesterol science for a long time and even touched on this topic a few years ago, but a couple of relatively unnoticed reviews of the current research makes a hugely compelling case that we know very little about the effects cholesterol – specifically low-density lipoprotein cholesterol (LDL-C) – has on cardiovascular health.

They believe that the current cholesterol hypothesis is based on misleading statistics and lots of ignored contradictory data, as well as the passing over of unsuccessful trials. Worse, these contrarians believe what we think we know is virtually the opposite of what’s true.

The first paper was published by a somewhat obscure (more later) journal. “Expert Review of Clinical Pharmacology,” presents their argument on the alleged dangers of high LDL-C largely in an easily accessible question-and-answer format, which I’ve mimicked below.

Do High Cholesterol Levels Cause Atherosclerosis? This is the build-up cholesterol and fats in the artery walls.

The authors start their answer by stating the obvious. If high total cholesterol (TC), causes atherosclerosis in people, then people with high TC should have greater atherosclerosis than those with lower TC. Researchers Lande and Sperry discovered that people with low TC were as likely to develop atherosclerosis as those with high TC in 1936. While it’s easy to dismiss research from 1936 as possibly flawed, their observation has been confirmed by at least a dozen studies.

The authors admit that there have been a few studies showing a weak relationship between atherosclerosis (TC) and TC. However, those studies did not include patients admitted to hospitals. Therefore, they could have included FH patients, which might have introduced a bias.

Is High TC a Cause of Cardiovascular Disease (CVD).

According to the authors, TC could be a major contributor to CVD. People with high TC should therefore die sooner from CVD. They argue this by referring to the Framingham Heart study, which was started in 1960 and has followed for 30 years the health of Framingham residents in England.

The 30-year follow-up was a frightening revelation. According to it, each 1 mg/dl decline in TC per a year (e.g. TC dropping from 135 into 134) resulted in an 11% increase in mortality and coronary risk. Holy crap!

Three years later, American Heart Association and U.S. National Heart, Lung, and Blood Institute published joint summaries that included the findings of the Framingham report. “a one percent reduction in an individual’s TC results in an approximate two percent reduction in CHD risk.”

Huh? How could this happen? Is it possible that the AHA and Heart, Lung and Blood Institute misinterpreted the results or cherry-picked them to avoid causing any damage to the cardiovascular apple cart?

It was too bizarre, so I searched for the Framingham study. I didn’t have to go past the abstract to find the following damning statement:

“There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels).”

Granted, this statement was, according to the study, only true for people over 50, but since most people over 50 are routinely prescribed statins, even for mild hypercholesterolemia, it raises a whole bunch of questions about cholesterol science in general.

How strong is the relationship between TC & CVD?

The authors of the contrarian report assert that numerous studies have found that high TC isn’t associated with future CD, of which the strongest evidence of this lack of correlation is found in old people. The authors cite a 2004 Austrian study which followed for many years the health of 67.413 men, and 82.237 women.

They found that TC was weakly associated with CD mortality in men, except for those between 50 and 64 – the age group for whom it’s supposedly the biggest concern. It was not associated with CD mortality for women over 50 years old, but it was weakly related to CD mortality in women younger than 50.

While this doesn’t perfectly support the argument of the contrarians, it’s an example of how current cholesterol science is horribly imprecise at best.

Atherosclerosis: Can high levels of LDL-C cause it?

LDL-C cholesterol may cause “hardening of the arteries,” Then it makes sense that people with higher LDL-C levels have more atherosclerosis than those with lower LDL.

They did however find that LDL-C was significantly higher in people with subclinical atherosclerosis. They claim, however, that “association does not prove causation,” It is important to note that LDL-C readings can be affected by simple mental stress. They can drop as high as 10% to 50% in as little as half an hour. This alone makes nearly all clinical measurements of TTC suspect.

Atherosclerosis can also be caused by mental stress, such as high blood pressure and platelet aggregation.

Can High LDL C Cause CVD

A large American study discovered that the LDL cholesterol of 140,000 patients suffering from acute myocardial damage was lower than usual upon admission to the hospital. The authors of another study who discovered the same thing decided to take it one step further: They intervened and lowered the patients’ LDL-C even further. Unfortunately, three years later, the mortality rate for patients with lower LDL levels was twice that of those with higher LDL levels, even after correcting for confounding variables.

Are Older People With High LDL-C Live Longer?

The authors cite a recent review of 19 cohorts (studies that track people for several years) which found that those over 60 with the highest LDL levels lived longer than those who were on statins.

What about people with FH? Are they more likely to die earlier?

According to cholesterol contrarians, it appears not. They point out the Simon Broome registry which provides diagnostic criteria to determine if genetically influenced hypercholesteemia is occurring based on familial, genetic, and clinical history.

This registry allegedly found that only a small percentage of FH people die at an early age, and the mortality among old patients with high LDL-C doesn’t differ from those of the general population.

If the Contrarians Are Right, How Would High LDL C Prolong Life?

If what the cholesterol theory contrarians are saying is true – that there’s an inverse relationship between LDL-C and mortality, what’s the possible explanation?

It could also be related to the unheralded and important role LDL cholesterol plays in the function of the immune systems. LDL-C binds to and inhibits many microorganisms, as well as their toxic byproducts. This theory supports the idea that patients with low LDL cholesterol have an increased chance of developing infectious diseases or cancer.

They suggest that infections may play a role in heart disease development, as well as high LDL-C.

The majority of the preceding applies to older people. What about LDL-C and young people?

Many studies have shown a correlation between CVD and high HDL.

Contrarians believe it could be due to a failure to account for many CVD-promoting variables like inflammation, mental strain, coagulation factor, infections, and endothelial sensitivity, all of which are closely connected to abnormalities of LDL receptors.

As mentioned earlier, mental stress can increase TC in minutes. This is because cholesterol is required to produce cortisol, and other stress hormones. In other words, high TC can fuel the production of epinephrine (which are key players) and hypercoagulation (clotting which can lead to stroke or heart attack).

Contrarians believe that high TC is a risk factor for both young and old because mental stress is often more common in the young working-age than in the older generation.

Let’s sum up:

• CVD could be caused by high stress and high TC in young people.
• High TC and no stress mean they aren’t at great risk for CVD.

How well do statins work?

As you might have guessed, the anti-cholesterol theory authors aren’t too keen on the use of statins to treat high LDL-C. For one thing, they think they’re mitotoxic. They believe statins cause mitochondrial damage (in the cells in the heart and elsewhere in the body).

In turn, this damage to mitochondria leads to decreased oxidative phosphorylation, which, it stands to reason, isn’t good for the heart or any other part of the human body, for that matter.

Then there’s the myopathy issue associated with the use of statins. Contrarians refers to a study which found that muscle myopathy was only linked with 0.01% in treated patients (Collins, and al. 2016,). It seems that myopathy is only detected in statin studies when creatine kinase (a marker for muscle destruction) is higher than 10x normal. Yikes.

They also reference a study of 22 statin-treated professional sportsmen, 17 of whom ended treatment due to adverse muscular symptoms.

Statins, they write, are also linked to cataracts, hearing loss, suicidal ideation, peripheral neuropathy, depression, Parkinson’s, interstitial cystitis, herpes, and diabetes. Cholesterol is a vital substance for the renewal of all cells, so they feel it’s inevitable that they lead to a slew of unfortunate side effects like the ones just listed.

They even tie the use of statins to heart attacks they’re supposed to prevent. They block production of important molecules. Coenzyme Q10 is one example. This is crucial for energy production in both the muscles and the heart. As such, they suspect the extensive use of statins might have led to epidemics of heart failure in countries where they’re widely prescribed.

(One adverse effect of statins that the contrarians didn’t bring up was the fact that they inhibit the synthesis of vitamin K, which is vital for the prevention of vascular calcification. That means that if statin users don’t supplement with vitamin K, they could, ironically, be hastening the development of the very disease they’re trying to prevent.)

Contrarians have concluded that clinicians should stop using statins, along with other anti-statin drugs, PCSK-9 inhibits. “and instead identify and target the actual causes of CVD.”

Potential Problems with the Contrarian Cholesterol Position Paper

Researchers from the University of South Florida, Japan Institute of Pharmacovigilance and other institutions in Japan, Sweden and the USA wrote the paper.

It needs to be pointed out that four of the authors have written books that are critical of the cholesterol hypothesis and that nine of the authors, at least, are members of THINCS – The International Network of Cholesterol Skeptics, an organization that opposes the theory that animal fat and cholesterol play a role in heart disease.

That, however, isn’t necessarily damning. It might be proof of pre-existing bias, but on the other hand, it tells us they’ve spent a lot of time studying and thinking about the topic. I mean, we didn’t automatically dismiss Einstein’s papers and lectures on relativity because he had previously written a book about it.

Another legitimate criticism, as pointed out by a physician friend of mine, is that the paper was published in a somewhat obscure pharmacology journal, which he suggests they didn’t meet the publication standards of the more well-known journals, “who would love a good article that challenges current theory.”

That’s true, but another group, consisting of mostly the same authors, wrote a similar paper that was accepted and published in the British Medical Journal (BMJ), which is widely known and respected.

As far as his point about journals liking articles that challenge current theory, that’s probably true, at least in most cases. Now, I’m hardly a conspiracy theorist, but I wonder if there’s just too much money and too much influence directly involved in statins. Numerous doctors make fun of statins being added to drinking water. However, this is a common joke given the large number of statin-using people in the world.

Finally, statin and cholesterol beliefs may be so deeply rooted in the medical community that it is impossible to argue against them. This might be the case for cholesterol believers. “Semmelweis reflex,” This is a reflexive approach to information that conflicts with established norms.

However, I should point out that there have been other studies that show a link between TC, heart disease and TC. One such study was published in The Lancet by Lewington et al (2008), which involved almost a million people. Despite the fact that it was unable to prove TC and heart disease, the results did not show a link between stroke mortality and TC.

What can we make of this mess?

This is the most bizarre thing about these papers and their damning evidence. Virtually no one has paid any attention. I only stumbled on them because someone in T Nation’s forum I posted a link.

It’s difficult to know what to believe. It’s maddening, frankly. These papers were written by contrarians. Or are they also trapped by confirmation biases and unable to discern legitimate research?

Or, are they correct? Tens of thousands upon thousands of medical and research personnel ignored all the contradictory data and blamed cholesterol for CVD. This has ironically caused damage to the health of millions.

I don’t know, but hell if I did. We need to do more research without preconceived notions or bias.

FOR WHAT IT’S WORTH, HERE’S WHAT I BELIEVE

Inflammation may be the true villain in heart disease, and if statins do prolong life, as some studies seem to indicate, they probably do so because they’re powerful anti-inflammatories.

An excess intake of saturated fats, as well as a diet that is low in omega-3 and omega-6 fatty oils are all factors that can cause inflammation. It is important to maintain optimal blood pressure for heart health. The keys to this are exercise and stress reduction.

Supplements can also be very beneficial. To combat inflammation further, I also take supplements. Flameout® You should also eat sardines every day. micellar curcumin.

As an insurance against clotting and to supplement with other medications, I take 12 hours apart, two baby aspirin per day (despite the current recommendations). vitamin K Coenzyme Q10 is used to prevent calcium formation in blood vessels. magnesium (which controls heart contractions and other functions).

I’ve also chosen to compromise on the statin issue. Most of the side effects, if they’re true, probably come from the use of higher dosages (up to 80 mg. a day). With that in mind, I’ve opted to take one relatively tiny 5 mg. rosuvastatin (Crestor) pill twice a week. While the dosage is minuscule, there’s research to support such a protocol (if it can be believed).

Lastly, I don’t worry about cholesterol in foodBecause there is little evidence that it can affect blood cholesterol levels, I do not recommend it. As I mentioned above, I monitor my saturated fat intake. Contrary to popular opinion, I don’t eat too much saturated fat. egg A combination of two or more is good for your heart because it is high in cholesterol and low in saturated fat.

However, I could be wrong on a number of counts. I could be wrong on a few counts, as could the contrarians. It doesn’t matter if you believe the current cholesterol theory, there may be better ways of treating CVD than what is being currently practiced.

Whatever you do, don’t stop taking statins based on anything you read in this article. Contrarians can be wrong. Talk to your doctor before you decide to stop taking medication. This article is intended to answer some questions.

References

References

1. Ravnskov U et al. LDL-C doesn’t cause cardiovascular disease: A review of all the relevant literature. Expert Rev Clin Pharmacol. 2018 Oct;11(10):959-970. PubMed.
2. Ravnskov U et al. A systematic review of the association between low-density cholesterol and mortality in the older: An inverted or absent association BMJ Open. 2016 Jun 12;6(6):e010401. PubMed.

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Whats sad is we still don’t know who to believe

Cardiologists and most personal doctors agree that high cholesterol can kill you.

So, with whom is it possible to believe?

It can be difficult to understand the differences between CVD and CHF. My cardiologist, along with a few nurses, told me that it’s primarily genetic. Lifestyle factors can also play a significant role.

I’m a lightning rod for side effects of statins. After suffering a severe heart attack at the age of 47 (now 50), I began taking atorvastatin. It worked for about one year but then it backfired with mild rhabdomyolysis. Next came rosuvastatin, which made my spine feel like it was crackling peanut butter brittle. Although I have found pravastatin to be very effective, it is difficult to discern the effects of statins from the damage to my heart from the initial stemi. There was also another blockage that formed after the first one was cleared and stented.

I don’t worry about cholesterol in food much either, but I also stick mainly to fats like evo, etc. and I don’t go nuts with them either. It’s the liver’s job, and it is where blood fats are converted, regulated, or dysregulated.

It’s good advice. Since this began, Ive heard every rationale under the sun for not taking the prescribed medications, from a lot of people I wouldn’t really even have expected it from.

It was a very long recovery period after a heart attack. My doctor asked me about a time frame. He was honest (facetiously). “You can stop taking them any time you want. I work out of the ER, and I’ll be there when you come back.”.

Ask anyone with homozygous familial hypercholesterolemia who is over the age of 30 whether cholesterol matters…

Except they’re all dead.

There’s a difference between mild dyslipidemia and congenital familial hypercholesterolemia.

One can have mildly elevated lipids, low trigs and decent particulate counts and it doesn’t matter all that much.

FH patients tend to have shitty subfractions of lipids, which are all associated with higher all-cause cardiovascular mortality rates.

You’d be hard pressed to find someone of a healthy body composition without FH who has seriously out of whack lipids from diet alone.

An independent association exists between low HDL and higher CVD burden. Ditto for poor trig/hdl rates, high subclass B blood ldl, and an increased cardiovascular risk.

Pushing cholesterol below the floor can pose some risks. Target lipid levels can vary from one person to the next.

The prescribing of statins seems very aggressive in America. In Australia you aren’t getting statins unless LDL is at least 150 unless you are deemed high risk i.e type 2 diabetic, overweight smoker with hypertension etc.

FH patients are still at 2.85x greater risk of dying from CV-related causes than non FH patients. Statistics generally indicate those with FH who are never treated with statins or pcsk9 inhibitors die on average 20 or so years earlier than those who don’t have FH.

Statins have very few side effects such as suicidal ideation and rhabado. Many medications can have dangerous side effects.

Metformin can cause lactic acidosis, SSRI’s can cause serotonin syndrome… doesn’t mean its likely to happen.

There are several levels of heterozygous FH.

You might have an LDL of 145, HDL of 40 (mild case) with poor subfractions… or you might have an LDL of 350, LDL of 50 with poor sub fractions.

If he leads a healthy lifestyle, the former guy may not have to deal with any serious problems until his 70s. The second person is in serious need of treatment.

Most healthy guys on t nation with normal or mildly elevated lipids likely don’t need statins. Guys taking boatloads of gear should consider it if they have seriously out of whack lipids (there’s no way HDL of 20 and LDL of 170 is healthy etc), and people with FH confirmed with genetic testing should take them… or pcsk-9 inhinitors.

FH is rare. It affects approximately 1/250 people. People with high levels of cholesterol need to lose weight.

Thank you for your valuable feedback.

Thank you for that!

There is an a “new” Highly credentialed guy who is also a triathlete/meathead and showing up everywhere now. -Dr. Peter Attia.

He’s a big proponent of statins, says he has 80% of his 45+ yrs old patients on statins (or/plus another drug I’ve never heard of ). On a loong podcast with Andrew Huberman, has Huberman thinking about statins; also saw Layne Norton recently talking about the same thing, didn’t listen to that full podcast, but I’m betting he was influenced by Attia since he was on one of Attia’s podcasts.

Thoughts? @TC_Luoma

Layne Norton, as far as I remember, had a CAC score of 99th percentile. This infers out of 100 men his age, he probably has more calcified plaque in his arteries than 99 of them…

His cholesterol has been high since childhood.

This is an example of someone who would take statins for a reason. You can’t compare him to a normal person, because most men in their 40s don’t have a CAC of 200+ (his CAC was 212 if I recall correctly).

Statins are a popular choice among doctors. And statistics show that they do prolong life, but as I wrote in the article, I suspect it may because they’re powerful anti-inflammatories and heart disease is first and foremost a disease of inflammation. But I could be wrong. They could be right. That’s the point. It’s so murky. And the other drug they spoke of? It’s probably Ezetimbe (sp?). It functions in the same way as fiber. “sops up” cholesterol.

I refused to have the CAC score taken. It showed the least amount of calcification so I refused to have my CAC score taken. Every time my heart started racing from exercise, I’d get paranoid. The CAC score can also lead to unnecessary followup treatments, which I think is a problem. That’s just me, though. Clearly, though, it hasn’t curtailed Norton’s activities.

A low CAC score that’s above zero isn’t something to be heinously concerned about unless you are young though?

Layne Norton was a 99th percentile CAC

Lets say yours is 65th percentile… not a big deal. 99th percentile can be a huge deal

Is there cause for concern? Are there any family history of strokes or heart attacks when you were young?

To prevent blood clots from occurring, TC should investigate nattokinase. This enzyme is known to clear arteriosclerosis and prevent blood clots. Many studies. It is safer and better than aspirin.

No. No.

I’m only peripherally aware of it, but I’ll look into it. Thanks!

A good book to learn the cholesterol myth by Dr Sinatra and Bowden

The 220-230 range is the maximum limit for life if you only look at total cholesterol. A range they’d put you on a statin to lower. It’s also worth noting that the slope is steeper on the lower side than on the upper side. A total cholesterol of less than 160 is likely to make you more susceptible to death than a score of 300. We know cholesterol is critical for fighting infectious disease and regulating hormones, in addition to relationships to cancer/mental health/etc… But doctors only ever look at risk factors in isolation when all risks should be considered.

Spot on! We do know that both the govt. and the big pharma sets the clinical ranges. Follow the money… I was raised to trust the medical community but as I have gotten older I have formed a very. You may have a different opinion.

Who has read The Great Cholesterol Myth. A few years ago, my trainer gave me a copy. It was very interesting, especially the section about the sugar industry and its connection to big government. The same trainer also trained a local cardiologist and gave him a copy. The doctor was hesitant to read the book.

Was lucky to have my HRT doc recommend a CAC test after blood work showed some wonky lipids, which weren’t the norm over the past two decades.

Result 1700 Calcium score

Got in to see a leading cardiac doc @ John’s Hopkins. Echo cardio gram stress test…kicked it’s ass at 13+ minutes. Zero symptoms. Doc stated that he’s seen many marathon runners and athletes with high CAC scores. Possible calcification at the exterior of vessels.

Moving to FL. Mayo hospital gave me a cardiac doctor. Tan same tests. Physically kicked again. Zero symptoms. Doc said you’re good. You can take statins if necessary. Vascpea prescription. Doc said that I have more questions than answers. Do we need to run an angiogram? Said ok. Let’s do it.

Laying on table…watching them snake through coronary arteries…doc said …LAD (widow maker) 90% blockage @ age 48.

Insist on the stenting. Zero symptoms. Feel great. Great cholesterol and lipids. Never were bad.

Genetics can be very frustrating. After years of heart issues, a biological father died at 62.

Get your shit checked. Be proactive…or you may not be around tomorrow to do so. These are my two cents.

Hey TC didn’t you also point out in an earlier article that some people are genetically predisposed to atherosclerosis when taking statins? This article is both fascinating and informative.