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Your Doctor is NOT Responsible for Your Health—YOU Are! Recommended Reading to Open Your Mind and Ask the Right Questions, Because Your Life Depends On It

What follows are my views, developed over years.

No doctor can know everything, because no one can do that. Nor do many doctors have cross-discipline knowledge (take just nutrition for starters!) or knowledge outside their field which many nonetheless have direct bearing on medical solutions. At the least, doctors are under time pressure, and many simply do not keep up with the latest medical information. Time passes and a grueling workload means that many doctors are badly out of date. Some think they know it all, by experience, when in fact at least a few of their beliefs are false.

Worse, few doctors give consideration to nutrition based on real data—too many still repeat the awful health-damaging official guidelines that were issued under political pressure, and still are. And organizations like the American Heart Association will endorse just about anything, for enough money.

But it is far worse than that: doctors also are under tremendous pressure to conform, lest they risk medical board, licensing board and insurer threats up to and including loss of license. Few are willing to take on that gut-wrenching hassle. Many doctors will not speak out due to these pressures, and so they just go along with dubious guidelines which are fundamentally a financial and political thing, NOT solid medical practice subject to frequent and regular scrutiny.

The gullible and uninformed are at big risk for all these reasons. And our medical system is far removed from an open intellectual process.

My own recent direct experience shows me that risk assessment is just not done for things like statinsguidelines are so easy to follow and no one gets in trouble for following them—so so easy to rationalize. It is deeply troubling when the most highly relevant study I could find for myself was unknown to two of my doctors, both recommending statins to me. That is unacceptable.

So.. it is your job to learn as much as you can, and ask probing questions. A doctor that gets upset or angry at questioning is one you need to fire—lazy and incompetent because at the least, patient concerns should be the #1 priority and patients can frequently provide 80% of the diagnostic clues, if only the doctor listens well.

Books

This book confirms many of my pet theories. A few things I disagree with based on hard data of my own, namely the calories in/out thing for extreme athletes, though I do not dispute it for ordinary exercise.

Lies My Doctor Told Me Second Edition: Medical Myths That Can Harm Your Health, by Ken D. Berry MD, FAAFP

The Truth about Statins is shocking in revealing the intellectual fraud, financial conflicts of interest, shoddy studies, of the $30B statin industry. Statins are in effect a slow-acting poison on every system in the body. The original Ansel Keys cholesterol claims were such an intellectual fraud as to beggar belief. About 70% of side effects are dismissed and never reported by doctors, thus statins are “safe” (ask MD and astronaut Duane Graveline about that!).

All while diet has been proven to be superior to a statin for most people, and with numerous beneficial effects and no negative effects. A fact suppressed and ignored by nearly all of the medical establishment.

The Truth about Statins, by Barbara H Roberts, MD

This book is in a similar vein:

The Great Cholesterol Myth: Why Lowering Your Cholesterol Won't Prevent Heart Disease - and the Statin-Free Plan That Will, by Jonny Bowden Ph.D, C.N.S and Stephen Sinatra, M.D., F.A.C.C.

This is not about doctors, but highly relevant to health and productivity:

When: The Scientific Secrets of Perfect Timing, by Daniel H. Pink


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Southern Inyo Double Double Century

Legal disclaimer: since we are not doctors, do NOT follow anything based on health-related topics on this or related sites without first consulting with your doctor or other trusted health professional. This is NOT medical advice and we are not qualified in any way to offer medical advice.

A double double century (over two days)... can I do it? Sure! Well, if everything works. I look at my brain and body as tools that sometimes work and sometimes don’t, damned wet computers and non-repairable hardware. At 55, I am doing pretty well, but it aint’ 47 or 36.

Of course, giving money and power to government is like giving whiskey and car keys to teenage boys*.

Oh, where was I... with some brain problems lately, seemingly a disrupted sleep cycle occuring every few months a problem since my concussion, I’ve had a tough time the last 2 weeks (extreme fatigue, wanting to fall asleep on my bike in the middle of the day). But today I rode a fast ascent with hardly any acclimatization to Tioga Pass, a rare treat in early March and a bad-ass performance (for me) this early in the season... heck any time of the season.

The Southern Inyo Double Century is March 7th, with the “double double” part on Sunday March 8. I am keen to to do both having not been up to it last year. And to do it twice more this year (three double double centuries!), a unique challenge and the only such opportunity for self-flagellation in the country AFAIK. Crazy dumb-ass idea I suppose, from most people’s perspective, but few people pause to examine their own motivations, and I know what motivates me.

* PJ O'Rourke, “A Parliament of Whores”.

Gate to Tioga Pass: heart rate, power in watts
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The Awful Side Effects of Statins

Legal disclaimer: since we are not doctors, do NOT follow anything based on health-related topics on this or related sites without first consulting with your doctor or other trusted health professional. This is NOT medical advice and we are not qualified in any way to offer medical advice.

I’ve now made it through The Truth About Statins by Barbara H Roberts, MD. Read this book if you are considering a statin or taking one—your quality of life or your life itself may depend on it. Women in particular should take a keen interest.

Many doctors routinely ignore side effects of statins, let alone report them*. Even doctors receptive to feedback are often too busy to take the time to report side effects. Failure to abide by “standards of practice” for cardiac disease means that millions of people get statins because doctors are under pressure to push statins to larger and larger numbers of people, when lifestyle changes would be a risk free and superior treatment

In my view, a doctor recommending a statin who has not read and carefully considered this book (including looking hard at the sorry state of the research whatever the time it takes) is engaging in medical malpractice concurrent with an unacceptable intellectual and ethical laziness.

There is a surely a justification for some people (very few) to take a statin. But it is now a multi-billion dollar business with surely many billions of additional dollars spent dealing with the side effects and tests required when taking statins.

* My personal experience with Metronidazole makes me skeptical that side effects are regularly reported. I would say it is far more likely for most side effects to go unreported, with only severe side effects to be reported. In my case, the side effects were severe, and not reported—the doctor never called me back, all I got was a nurse ignorant of the risks and I suffered further damaged as a result of a two-day delay just to hear from the nurse. That idea that hyper overloaded doctors would have the time to report mild or even moderate side effects with statins is laughable, particularly in the context of the dogmatic idea that statins are very safe.

Summarizing my take-aways from this book.

Dietary note: red rice yeast contains lovostatin and has been banned by the FDA as having the risk of muscle damage, yet this same drug is regularly prescribed!

NOT the author’s words, these are MY statements summarizing the take-aways as I understand them:

The Truth About Statins
by Barbara H Robers M.D.
  • The evidence for the benefit of statins is deeply flawed and IMO totally corrupt. It does not qualify as even bad science!. For example, the JUPITER study is severely flawed, had severe financial conflicts of interest, assessment flaws, was terminated prematurely just as it was beginning to reverse the trend. Data was suppressed/withheld, yet it was used to justify vastly expanded use of statins. Vomit inducing stuff.
  • There is zero or near-zero evidence for women that a statin is beneficial, but with serious side-effects risks approaching 20% and some of those are life-damaging, physically and cognitively.
  • Willy-nilly recommendations for statins by physicians seeking only to cover their ass from a liability standpoint.
  • Confirmation bias and cognitive commitments stemming from recommended care guidelines coupled with the threat of failing to treat per guidelines surely prevent most physicians from objectively assessing statins, even if they had the time. Physicians are like anyone else—busy and with no time to critically read studies.
  • Statin side effects are often not diagnosed properly or at all, causing suffering and financial harm and damaging lives to the point of hardly being livable. How many people have been damaged by statins, at huge financial and pyschological cost and how many ever got it figured out by doctors incompetent to figure it out, having cognitive commitments to statins being safe?
  • Statins degrade cognitive performance along with greatly increased risk of neuropathy. Attention, psychomotor control, memory disfunction, learning, altered areas of the brain to be engaged are all degraded by statins. Studies are just not there on such effects for use of statins over years.
  • Nerve damage can be caused by many things and there are very few treatments for nerve damage and it takes time to recover, if ever. Since statins impede the body’s ability to process cholesteral needed for nerve/brain myelination, should it surprise that nerve damage could occur? Danish researchers found that statin users were 14.2 times more likely to have polyneuropathy, climbing to 26.4 times more likely after two years, with possible diseases like ALS (Lou Gherig’s disease) resulting from statin use. What happens after 3/4/5/10/15 years of statin use? It is quite likely that diagnoses of such problems would not be attributed to statins!
  • Simply eating foods like grapefruit or pomegranate can spike statin blood levels and precipitate severe physical or cognitive damage, which could be permanent.
  • Blood tests for muscle damage are not reliable. Yet many physicians take the blood test as gospel, telling their patients that the statin is not responsible (to call this cruel and irresponsible is an understatement!). Yet normal blood tests following by muscle biopsies prove that damage occurs. That’s confirmation bias and cognitive blindness at work and guess who suffers? Not the doctor.
  • Risks of statins escalate rapidly as the dose increases. What might have been minor muscle pain could suddenly be life altering damage or death at a higher dose. A “higher dose” can result from drug interactions or simply by eating grapefruit or pomegranate.
  • There is a substantial possibility that a decade from now, statins will be seen to have done more harm than good. And even at their best, statins achieve a ridiculously marginal risk reduction, presented in a way designed to deliberately mislead (relative risk reduction based on very small numbers),
  • Statins damage the operation of mitochondria (tiny energy factories in cells), which are vital to operation of every cell in the body. Many devastating diseases stem from mitochondrial defects, yet here we are pushing statins on millions of people—and statins damage mitochondria by suppressing key chemicals like co-enzyme Q10.
  • Simply changing diet/lifestyle can achieve a greater risk reduction that taking a statin.
  • The great majority of athletes are unable to tolerate statins.
  • The side effects of statins can be severe, life changing, and sometimes fatal.
  • There are special cases in which statins surely are appropriate (e.g., genetics that cause extremely high cholesterol).
  • Fatal liver injury is rare, but it occurs with statins. Abnormal liver function occurs in up to 3% of statin users. What does that mean long term with the liver under assault like this?
  • Rhabdomyolysis (severe muscle damage which can result in kidney failure and death) is not very common with statins, but it happens, and lower levels of muscle damage are very common. Tendonitis and tendon rupture are also seen in women. Osteoarthritis risk rises as well.
  • Diabetes risk escalates by up to 300% relative risk. Compare that to 0% to (giggle) 36% relative risk reduction for statins and observe that a person most at risk of cardiac events is probably a very high risk for diabetes propensity!
  • Attorneys, physicians, and other professionals leading useful lifes have had their physical and cognitive abilities destroyed by statins, leaving them crippled and unable to work or function.

How good is the evidence for statins?

First of all there is zero or near-zero hard science done! It’s all correlation and data analysis. This does not even qualify as science in my view.

  • Corrupt medical associations and doctors. Doctors running studies usually have direct financial interest in seeing a drug trial succeed, which means showing benefit while minimizing or not looking for risks. Is it objectionable to call it “corrupt” when doctors have a direct financial interest in studies they run? Not in my ethical book! The drug business is driven by money. These are NOT disinterested parties. Side effects and alternatives are ignored or suppressed or not investigated. Even if the trial is double blind, analysis is subject to bias from these interests. No one in their right mind should trust any study with such conflicts which means that nearly all studies are suspect.
  • Drug companies offer bribes to doctors that come in many forms: luxury trips, lucrative speaking enagements (censored to drug company topics/slides), etc. Even simple freebies like pens and knick-knacks are PROVEN in research to influence doctor decisions (even though doctors will vehemently deny being influenced). If you were born yesterday, you can ignore these points. UPDATE: as of 2020 (sometime earlier) “regular clinicians are now effectively banned by the FDA from receiving any freebies from drug or device companies” according to a doctor who wrote me on thi who continues, saying “investigators are paid handsomely for their roles in 'Advisory Councils' and 'Speakers Bureaus' for the drug companies”. And of course stock interest or patents or similar are far more lucrative. Which should make anyone extremely skeptical of any “science” these days, at scientific studies are bullshit 75% of the time. Add in financial incentives and it’s hard to have any faith at all in the results. Even if a study is reasonable, what was omitted that might argue against it for various reasons?
  • Clinical trials last only a few years, but side effects can take years to appear. Yet the damage accumulates steadily until the day you’re life is ruined, perhaps permanently.
  • Risk reduction achieved by taking a statin is modest at best, and presented in a highly misleading manner for cardiac disease (“50%” not “5% vs 10%”) while NOT being stated in those terms for severe life-changing risks, such as diabetes, neuropathy, muscle damage, cognitive damage, et—whose risk escalation can be up to 2600% greater, and those risks are NOT presented in relative terms. This is intellectually and ethically despicable.
  • Risk reduction figures are often quoted from barely statistically significant figures and cited devoid of absolute figures. Does a risk reduction of 10% reduction sound good to you? How about 1% vs 0.9%
  • Participation in the treatment or control group just by starting the study is included even after opt-out! Some studies have as many as 50% of participants ending participation early. Yet these opt-out participants are still computed into the data! This is GIGO (garbage-in = garbage-out).
  • Patients taking other medications are usually excluded, so that severe and even deadly drug interactions are not detected. You are a guinea pig!
  • Women are not men with breasts! Yet the medical community has long treated women as such after studying men. With statins, the response of women is not at all like men!
  • The history of statin testing is a sordid tale of harm for too many unlucky guinea pigs. Some of this was from specific statins, but all statins share the same core operating mechanism of suppressing critical physiological processes. Statins are a poison you take every day in hope of a benefit greater than the risks—but the chances of having some kind of damage escalates with continued use and/or with increased dose.
  • Studies are almost always short-term, thus leaving out the ongoing and escalating side effects risks which escalate 10X or even 100X in relative terms—compare that to a 15% relative risk reduction for cardiac events!
  • “Hard” endpoints (death) are straightforward. “Soft” study endpoints are subject to manipulation and interpretation in the way they are reported.
  • Try finding a study that compares statin usage versus a Mediterranean diet as in the LYON study, which showed results as good as statins in health outcomes, with no side effects and with numerous other greatly increased health benefits far greater in the relative risk reduction of statins for cardiac events.
  • Some trials of statins have been ended due to premature death of some statin-taking participants... meaning DEATH much higher with the statin users. No one ever talks about these studies!
  • There are grotesequely unethical financial conflicts of interest in a cabal of “expert” doctors with personal financial interests in statin companies.
  • Drug companies fund drug trials, collect data, contractally prohibit researchers from using the data freely. Drug companies approve or disapprove study results for publication up to and including making sure studies that do not make their drugs look good are never published. You do not get tenure for going against the grain!
  • Organizations like the American Heart Association (AHA) are driven by MONEY, not by health. These are the same corrupt who surely harmed millions of people by recommending low-fat diets for decades.
  • Vast majority of clinical trial participants were men, with very few women. Statins behave very differently in women including all the risks and no benefit for most women.
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Mayo Clinic: Extreme Physical Activity May Increase Coronary Calcification, But Fitness Still Prevails

Legal disclaimer: since we are not doctors, do NOT follow anything based on health-related topics on this or related sites without first consulting with your doctor or other trusted health professional. This is NOT medical advice and we are not qualified in any way to offer medical advice.

Nick M writes:

...On a loosely related note, the same cardiologist did advocate caution with endurance sport, specifically with high intensity exercise of longer than two hours or so (largely due to the inflammatory response that gets triggered). He referred me to a book written by a cardiologist (and keen cyclist) called ’The Haywire Heart’ (by John Mandrola and Chris Case) which you might be interested in.

WIND: my primary comment is that I’m going to live. That means doing things I love, which means endurance cycling and all-day hikes, and feeling fantastic because of it.

I am not afraid to die, but I am very much afraid of not living, and no one can tell anyone else what that means—so if “crazy Lloyd” wants to ride double centuries... well other people have far more damaging passions (or no passions or meaningless passions).

Cardiologists are spot-on in expressing some concern about the issue of extreme exercise—they would be remiss not to. But the research is still in its infancy. My best is that extreme exercise carries some risks (why wouldn’t it?) but a risk analysis has to weight that against the benefits, which are physical, psychological, hormonal, and spiritual. No medical study will ever do that properly.

To speak to the research, there is evidence that endurance athletes incur hard plaques from their excess activity. But these hard plaques have a much lower cardiac risk than soft plaques and recent research finds that there is NO INCREASED RISK of cardiovascular events.

Mayo Clinic Proceedings: Extreme Physical Activity May Increase Coronary Calcification, But Fitness Still Prevails.

CRF = cardiorespiratory fitness
  PA = physical activity

...high levels of PA and CRF are extremely protective against CVD events and mortality, making it possible for individuals to perform high doses of running and exercise safely even with high CAC and "hearts of stone."

Reader Comment: Heart Health and Diet

Legal disclaimer: since we are not doctors, do NOT follow anything based on health-related topics on this or related sites without first consulting with your doctor or other trusted health professional. This is NOT medical advice and we are not qualified in any way to offer medical advice.

Nick M writes:

I’ve been interested by your recent posts touching on heart health and diet. I became interested in the topic of diet a few years ago when a prominent South African sports scientist, Tim Noakes, came out strongly in favour of a low carb, high fat diet for general health (and not least heart health). This was a 180 degree shift for Noakes who had been involved in driving the popularity of sports drinks in South Africa some years ago. His position was that having spent a couple of years reviewing the scientific literature he felt that the evidence pointed towards the ‘conventional wisdom’ of the past 60-70 years being wrong (ie pro carb and anti fat, especially saturated fats). Noakes has been vilified by much of the conventional medical establishment, but has stood firm with his position.

I adopted a non-obsessive low carb, high fat diet and have found it has helped me regulate my blood sugar very significantly. But after growing up hearing the high carb, low fat story, I remained slightly concerned about which of the opposing ’truths’ to believe. At a routine visit to a cardiologist a couple of years ago, I made the point that as a layman I have found it hard to know what to believe, but have found success with the low carb, high fat approach. His response was interesting! In essence he said that the science is clear and strongly in support of low carb, high fat. He went on to say that he made a decision some years ago to stop going to cardiology conferences since his experience was that they were peddling a story based on questionable research sponsored in large part by the (processed) food and pharmaceutical industries.

There is obviously lots of literature on all this stuff. The challenge is that much of it is conflicting - hence, my question to the cardiologist. I did read a couple of the more ‘populist’ books on the subject. The one that made the most sense to me overall - despite finding the writing style rather painful - was ’The Primal Blueprint’ by Mark Sisson. The book does lay out the case for low carb, high fat in layman’s terms and it makes suggestions around diet and exercise.

On a loosely related note, the same cardiologist did advocate caution with endurance sport, specifically with high intensity exercise of longer than two hours or so (largely due to the inflammatory response that gets triggered). He referred me to a book written by a cardiologist (and keen cyclist) called ’The Haywire Heart’ (by John Mandrola and Chris Case) which you might be interested in.

WIND: as far as I can tell, the whole cholesterol vs cardiac health thing is one huge scam based on no hard science (hard science shows direct links by varying one factor while holding others fixed). Instead we see mass statistical data correlations masquerading as science. The reason that statins lower reduce heart attack risk modestly has NOT been proven to result from lowering LDL. It is almost certainly an incorrect assumption, the body being far more complex.

That’s right—the reason is NOT known—it’s just a correlation. And there things sit stopped in their tracks as “knowledge” when even the basics remain unknown, such as whether (making up an example) putting 1000 people on a strict Mediterranean diet can not just beat a statin for CVD events, but improve health and avoid all the nasty side effects of statins. The state of this medical pseudo science is pathetic to any objective outside observer.

The only good hard science I have found so far is by a layman—a non-medical person, an engineer like myself, who correctly points out that what passes for science in medicine wouldn’t pass muster in engineering. And directly refutes the accepted link between a high fat diet and LDL cholesterol.

Low carb

In general, “low carb” makes a lot of sense (30% or less seems about right, less when not active perhaps) and I’d agree with it. I suspect that it will be shown to be harmful over time to aim for 5% or less carbs (Keto diet) as this almost certainly has negative aspects coming from the failure to eat fruits and vegetables and the incorporation of a lot more saturated fat. The body did NOT evolve to subsist that way and there is real risk of nutrient deficiency.

My guess is that much of “low carb” craze (fad) results from the reduction or elimination of excess quantities of poor food choices, e.g., lots of bread/pasta/etc—those largely SUCK and yet such bad choices drive fads/fanatic diets. Throwining the baby out with the bathwater: it makes no sense to stop eating moderate amounts of oranges/strawberries/blueberries/bananas/etc in pursuit of fad diets like Keto—fruits like that are full of nutrition. Ditto for vegetables, especially kohlrabi, cabbage, cauliflower, bell peppers, radishes, carrots, kale, etc.

I’m a believer in moderation, which is to say I enjoy lots of fruits and vegetables (mostly carbs) and See’s candy (mostly nuts but a good amount of carbs) and very limited amounts of bread and sweet potatoes and ric. But zero soft drinks, no fruit juice, very little processed food, no fast food, I rarely eat out, etc.

Athletes and carbs

As an athlete, my favorite competitor is someone on a Keto diet which guarantees poor performance because the multiple energy pathways of the body cannot be used when the required effort rises. You MUST be able to create energy from glucose, and it is literally DANGEROUS if glucose gets low (brain fade). Ride 50 double centuries as I have and learn that fat metabolism is the primary energy source, BUT failure to take in carbs like Tailwind will result in horribly slow and unpleasant day.

Worse, those on a Keto diet are subject to catabolic muscle loss. During a double century for example, the body will eat its own muscle tissue to the tune of 10% to 15% of required energy. That equates to 1/3 to 1/2 POUND of muscle “eaten” as an energy source. Those on a Keto diet might see much higher losses, with the body deprived of adequate carbohydrate stores. Seems like a dumb move to me.

When I complete the Southern Inyo Double Century on March 7, I will burn about 7000 calories. Probably at least another 1000 calories are needed for repair. I will need to take in at least 2000 calories, mostly carbohydrate, from 5 PM to 5 AM before I do the Sunday March 8 double century.

Carbohydrate and 10% to 15% protein together are essential for athletic recovery, for driving the carbs into muscles to be stored as glycogen together with the protein for repair. The Keto diet maniac will NOT recover properly or repair muscle even if doing my paltry baseline 1000 calorie per day ride (7000 calories or 100 MET-hours per week), unless tht pace is kept low.

Tere are times when my athletic recovery cries out for carbs, I go on a binge eating day, which I have found to be effective in losing body fat and dropping weight, believe it or not. Limiting this to one day per week seems about right and highly effective in keeping the body from trying to make itself more and more calorie efficient.

Try riding 60 miles a day for two weeks and see how much cabs matter! An excellent binge day is a bottle of champagne and a half pound of dark chocolate caramel pecan clusters—works wonders and I have had some of my best workouts following that!

High intensity exercise of longer than two hours

See Mayo Clinic: Extreme Physical Activity May Increase Coronary Calcification, But Fitness Still Prevails.

Heart Health and Diet: Medical Malpractice Going Straight to a Statin vs a Mediterranean Diet Proven to be Just as Effective with No Risks

Legal disclaimer: since we are not doctors, do NOT follow anything based on health-related topics on this or related sites without first consulting with your doctor or other trusted health professional. This is NOT medical advice and we are not qualified in any way to offer medical advice.

See prior posts on arteriosclerosis.

First, do no harm

Swearing a modified form of the Hippocratic oath remains a rite of passage for medical graduates in many countries. Its simplified form is:

First do no harm.

Medicine paint-by-numbers

Statins have numerous risks, some severe and life-changing so much so as to destroy lives. Professors, attorneys, etc have had their lives destroyed by statins, as discussed in The Truth About Statins by Barbara H Roberts, MD. So we are not talking about some internet tripe, but actual experiences seen by a cardiologist. And there are numerous other sources of such adverse reaction issues. Numerous risks whose odds ratio rises dramatically with statin use, increasing over time.

Yet I have had two primary care physicians and one cardiologist recommend a statin to me in the past two years. The cardiologist might have briefly discussed diet, but the main thing I remember is the statin recommendation.

In my view, these doctors all have violated their oath because they all went right to a statin that raises the odds ratio for numerous risks, some severe and debilitating. In my case, the recommendations are particularly egregious given multiple risk factors: (1) history of neuropathy (2) concussion and brain issues, (3) extreme exercise which greatly increases the risk of muscle damage and liver and kidney issues. How the hell can a body under physical duress repair itself properly when a key system function is suppressed? How can suppressing a key biological function for one single-minded goal (suppressing LDL) be a tenable proposition?

By what metric is it not medical malpractice to recommend a statin to a patient without first insisting that a patient follows a Mediterranean diet for at least a year?

In my view, doctors who to not first demand their patients change diet and lifestyle for at least two years are in fact violating the “do no harm” oath directly. At best, this is ethically and professionally dubious. It places the doctor first (“who can blame me, I followed the guidelines”) versus the patient (risk-free alternatives).

There are studies showing that a Mediterranean diet can work as well as a statin, with numerous other benefits and no risk. But who will pay for good studies showing diet vs statins? Big Pharma won’t! When there isn’t money to be made, the money-making alternative wins, hands down.

Odds ratios, flawed studies, poor followup, financial corruption

Statistical data analysis measures are irrelevant to any individual and particularly an out-of-bounds individual like me. No doctor can tell any particular patient if a statin will have any benefit whatsoever. But it is highly likely that at least one side effect will emerge. And how many patients get liver tests, cognitive tests, muscle biopsies, etc as follow up? In other words, the side effects are largely ignored unless they stand out in obvious life-changing ways.

Using a statin causes the odds ratio to spike dramatically for numerous risks, some of which are debilitating, some less obvious (cognitive) or just suffering (constant muscle pain). Oh, if you are pregnant, how about a severely deformed newborn?

As just one example, if my risk of neuropathy rises by 2600% over a few years of statins, is that worth reducing my risk of cardiac events over ten years from 4% to 3% ( a relative risk reduction of 25%)? Along with greatly increased risk of numerous other problems? What about the cost of all the tests for liver malfunction and the costs of the statin, the psychological toll when something feels wrong, etc?

Look at the actual real risk reduction for statins—it’s a joke. Then consider all the hugely heightened risks in other areas.

Severely flawed and financially corrupt research

The alleged benefits of statins are poorly understood—we have data analysis studies showing reduced cardiac events, but the studies have so many obvious flaws that even a layperson of average intelligence could understand the ridiculous bias involved:

  • Assuming that women are little more than men with breasts and different gonads. Women respond very differently and may in fact take on all the risks of statins with ZERO benefit.
  • Including those who drop out of studies in study results. In computers this is known as GIGO (garbage in = garbage out).
  • Assuming that certain types of endpoint results (death or serious issues) are relevant.
  • Assuming that certain “soft” endpoints are the same as “hard” like death.
  • Assuming that the reduction in LDL is what drives the lower cardiac event profile. No science actually proves that key supposition! All we have is correlation by data analysis, not causation. Real science on this matter should give anyone pause.
  • Failing to perform risk analysis for all sorts of debilitating side effects.
  • Minimizing, ignoring, or just not looking for side effects.
  • Trials lasting two years or less, when there is strong evidence that statin damage can occur years later.
  • Failure to disclose all study data to interested parties (Jupiter study).
  • HUGE financial incentives in play (billions of dollars), with studies funded by Big Pharma, data collected and controlled by Big Pharma, lead doctors for the study having financial conflicts of interest, an FDA that colludes with Big Pharma and is subject to political influence.

Deeply flawed studies* funded and run by drug companies driven by data analysis are junk science. Financial incentives always corrupt.

We will see in a decade or so just how badly public health was damaged by statin use, in two ways: (1) first, in not using superior approaches like dietary intervention that improve health in myriad ways without side effects and (2) in saving lives from cardiac events better than a statin. That is the real shame here, which doctors should take to heart: the emphasis on statins is damaging people and taking lives. Shame on everyone who toes the line on statins.

Guinea pigs

The American Heart Association (AHA) recommended a low fat “heart healthy” diet for years, damaging untold millions of people. Yet a high fat Mediterranean diet is proven to have numerous benefits including heart health. You cannot trust these “experts”, who have a financial and authoritative axe to grind*.

Why does the FDA issue a statement calling red rice yeast “harmful to health” (!!!) for its potentially serious side effects when the active ingredient is a statin (lovastatin)? Perhaps because it *is* dangerous, and drug companies have poison to peddle for profit. But in a food, that’s bad and it needs to be outlawed?

We are told to take statins as some sort of risk-free miracle pill. And now the drug industry and the medical establishment are pushing statins on healthy women, who take on all the risks but in most all cases get zero benefit. Outrageous drug pushers.

Statins are recommended for lifelong use, yet side effects can take months or years to emerge and can then be so damaging as to render a person incompetent to lead a useful life. How can dishing out statins willy-nilly like Halloween candy before demanding dietary interventions be considered anything but a grotesque perversion of medicine?

Doctors have no skin in the game in the right way. The liability of a doctor for failing to prescribe a statin violates guidelines and thus makes the doctor a target of litigation. A doctor who prescribes a statin that causes pain and suffering and life-damaging events has essentially no liability (“I just followed the guidelines”). This is an ethical cesspool.

* The evidence for statins is poor, with short-term studies used as the basis for major public health conclusions. This is so corrupt—statin usage risks clearly grow with time. For example, the Jupiter study was cut short and has so many flaws it’s a bad joke. It was funded by a statin maker, data was collected by a statin maker, data was withheld from interested parties, the data for women is radically different than for men. Worst of all, it was cut short just as it was showing signs that were unfavorable to the statin maker. Yet the FDA moved ahead with it and it is a done deal. No objective person can look at that study and how it was handled and have confidence in it.

Under-reporting of side effects, minimal research

Statin risks guaranteed to be under-reported for several reasons. First, too often they will simply not be diagnosed as related to the statin, for all sorts of obvious reasons. Second, there is huge financial and professional pressure to toe the line. Third and perhaps most important: no one gives a damn: very little research money is going to pop up to show just how bad statins are—who would pay for that?

This in spite of life-destroying side effects that can occur with statins and many less significant but still damaging risks, those risks growing in relative terms far more than any relative risk reduction for a single risk (cardiac events).

Reader Comments

Anon physician writes:

I am a physician in a specialty that sees the effects of statin use but does not prescribe them. As an ophthalmologist retina specialist I see tons of very elderly patients with macular degeneration. Over the decades of my practice I am seeing a larger and larger number of these elderly patients. They just don’t die like they used to. Yes, they depart eventually, but I am convinced it’s the statins and improvement in cardiac care that keeps these folks going on for virtually forever. The quality of life often isn’t so good, though. Something eventually does eventually get them: cancer, dementia, diabetes, COPD, pneumonia, influenza, stroke, etc.

I have seen the side effects of statin use and I agree they seem to get swept under the rug. Understand that statins are a multi-billion dollar global business and that business will do anything to keep this profit machine going. Advertise the Hell out of the product to patients. Advertise to physicians, sponsor the studies, kill the studies that show adverse results. No, it’s not 100% control but with the proverbial thumb on the scale you can tip the business in your favor.

Also understand that population-based statin recommendation is a macro phenomenon. If you look at a population of a million and put half of them on statins statistically you will see the reduction in cholesterol, reduction in plaque and drop in atherosclerotic events. But prescribing statins by an individual physician is a micro phenomenon. The individual prescriber, if they are tuned in to their patients, will see the variable anti-cholesterol effect and they will also see the side effects. The challenge is that not all patients are going to have a given statin side effect. But when they do, then it becomes a project to explain to the patient the pros and cons, the “are you willing to put up with this in exchange for that.” Or can we try a different drug or a different dose in order to minimize the side effects while maximizing the benefit.

And of course in the background are all the studies showing global statin benefits that make it harder and harder for a physician to ignore the pressure to prescribe. And in many areas of practice, treatment of heart and atherosclerotic disease now follows protocols. As a doc, if you follow the protocol and an adverse event ensues, you’re covered. The other way around and you are potentially screwed. The pressure to simply follow the protocol is enormous.

And on top of this you have to consider the fact that all of this is based on statistical data and the quality and granularity of the results depends enormously on the quality and granularity of the study. Since drug companies and researchers are under enormous pressure to achieve “positive” results as quickly as possible, most studies are as nongranular as possible. If there is money and time, the granular parsing of data may come later. But it may ever come at all.

Has anyone ever done an in-depth study on statin use in top drawer aerobic-sport male athletes and looked at longevity, serious adverse events (stroke, heart attack, etc) and also compiled data on side effects, including effects on performance, etc? I seriously doubt it for two reasons. First, the study may not show what you the sponsoring drug company want it to show. Second, the number of subjects you would be able to enroll would be really limited and may not be enough to demonstrate statistical significance. There just aren’t enough of you folks out there.

And I think it is folly to try to extrapolate mass study data results to small subsets of patients without actually doing a study. A doc can certainly quote the results of the mass study to their patient and forget to mention that it may have little or no bearing on you, the individual. Ultimately, you need to have a really good physician who understands the data and its pitfalls and who understands you and your needs.There are a few of them out there, but not many. Good luck finding one. And when you do find one, stick with them.

WIND: longer life can be a cruel thing, especially if it is degraded by pain and suffering.

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Statins: Systemic Poison that Damages Virtually Every System in the Body

Legal disclaimer: since we are not doctors, do NOT follow anything based on health-related topics on this or related sites without first consulting with your doctor or other trusted health professional. This is NOT medical advice and we are not qualified in any way to offer medical advice.

See prior posts on arteriosclerosis.

Americans love an easy pill solution, but the more I learn about statins the more I think that 40 million Americans taking statins are just guinea pigs in a huge and damaging experiment.

What a statin does

Statins damage a key function of the body: the ability of the body to use cholesterol effectively. Cholesterol is vital for metabolism, nerve and brain function, liver function, and much more.

Yet here we are, severely impacting the body’s ability to use cholesterol for all its necessary functions. Doctors would have us believe that stomping on a key biological bodily function is worry free.

Would you accept a 2600% increased risk of neuropathy for a 25% reduction in risk of a cardiac event? More on that below!

Statins damage just about everything

The Truth About Statins
by Barbara H Robers M.D.

Consider that it is a certainty than many adverse reactions are not reported at all, or never properly investigated and reported.

Consider a few points I picked up from The Truth About Statins by Barbara H Roberts, MD. You can find numerous studies backing up all this stuff; do your own reading. It doesn’t matter if any particular area is more or less risk; the key point here is that statins affect just about every key area in the body, and that this damage can appear early or later and if you’re unlucky, it can be permanent.

You can count on there being very little money for research on any of these issues—no one has an interest in funding it and the FDA and Big Pharma and experts making money from this stuff have no interest in making an issue of it.

  • WOMEN ARE NOT MEN — studies have shown women often get zero (ZERO) benefit from statins. Drugs get approved tested largely on men. That situation is just outrageously irresponsible. Yet the drug pushers push statins on women too, increasingly so.
  • Polyneuropathy (damage to multiple nerves) — this is near and dear to me because it took me two years to recover from peripheral neuropathy from the antibiotic Metronidazole. What would a statin do to myelination of my nerves and to my brain function, finally (mostly) recovered from concussion?
    Statins have been shown to increase the "odds ratio" to 14.2 times higher for polyneuropathy in short term use to 26.4 times for 3+ years. For perspective, being severely obese vs being of normal weight has an odds ratio of 7! Since statins are a lifelong medication, what does that mean 5 or 10 years out? How many cases of ALS cases (Lou Gherig’s disease) or similar issues result from statin use, and how would they even be diagnosed as such?
  • Tendonities and tendon rupture —hundreds of cases. What the hell happens to an athlete putting tendons under far greater stress vs the general population?
  • Rhabdomyolosis, severe muscle damage, muscles aches —muscle aches are very common. What happens year after year and one day you have grapefruit juice and end up in the hospital with your kidneys about to fail?
  • Mitochondrial damage — damage to mitochondria which are essential not just in muscles, but in nerves and the brain too.
  • Cancer — increased risk of some cancers (think colon polyps), possible lower risk of others.
  • Congenital birth defects — babies with neurological and other problems from mothers who take stations.
  • Diabetes — with 40 million Americans taking statins, the estimate is that 146,000 of them might develop diabetes due to statin use.
  • Cognitive decline — statin users don’t learn or remember as well and may suffer serious problems like memory loss. What does this mean after 20 years of a statin for dementia and similar declines?!
  • Liver damage — liver inflammation can cause all sorts of issues.
  • Stroke — potentially lower risk of some mild strokes but higher risk of severe strokes because cell walls might be damaged by statins.

Doctors get the squeeze

There is considerable pressure on doctors to recommend statins, since the guidelines say they should. In other words, a doctor who fails to recommend a statin is at risk of being sued. Yet a doctor who prescribes a statin has no liability for that damage, no skin in the game. That in itself is a grotesquely flawed system.

Accordingly, most doctors go along with the dogma which has little or no actual cause-effect science to back up its claims. Data analysis for millions of people is not real science, it is only the basis for hypotheses to be tested. Yet statins are the recommendation stemming from this data analysis and in a contexte which fails badly from a total risk analysis perspective (the numerous side effects and how those risks escalate over time). We don’t know what we don’t know and those things known to be side effects are poorly studied, particularly over time.

If you don’t look for things you won’t find them, and that’s largely the story of statins. Sadly, the case is largely closed on statins. The FDA and Big Pharma consider the matter a nice solid done deal, they are NOT going to fund basic research to prove or disprove out the various assumptions on diet vs cholesterol and cholesterol vs heart disease, let alone go looking hard at the downsides. No one today can make any statement about individual risk, yet it is individuals being treated!

Intellectually and ethically bankrupt government-medical establishment

At 8% body fat I was borderline obese. That’s all you need to know about the intellectual rigor of modern medical “science”, whether it is BMI or cholesterol. The same data analytics approach gives rise to the same mass guidelines that any statistician will tell you are inapplicable to single data points (e.g., a human being).

This intellectually bankrupt approach is used for cholesterol levels to recommend to individual patients to take on all the risks, for an unknown benefit, a mere statistical probability.=

Are we really so clueless as to have a fixed cutoff value of a “safe” level of LDL, stating that regardless of genetics, epigenetics, gut biome, diet, activity level, family history, gender, etc—that everyone should have an LDL under 100? Such a guideline is profoundly anti-intellectual, yet that’s all most doctors will even look at.

In light of research showing the exact opposite assumed relationship between fat intake and LDL and a reliance on gross data analysis, the whole cholesterol thing is worm-holed structure of rotten wood. We don’t really even know why statins lower cardiac events—only that there is a correlation between their use and fewer events. It might have nothing to do with LDL!

I go on record here as saying that within 10-15 years, we will look back and find that statins incurred far more damage than benefit, and that some of those damaged will be severe for for some, and millions will have needlessly suffered an impaired quality of life for all the years they take statins.

Furthermore, the risks rise over time, so as millions of people continue to use statins the risk rises. Eat that grapefruit and (maybe) you suddenly one of those with a severe problem up to and including death.

Patently misleading claims: relative risk reduction

It reads like a sales pitch to me, virtually a scam: when speaking to benefits, a relative risk reduction is used.

If I told you that you could reduce a 4% risk to a 3% risk (a 25% risk reduction) over ten years , would you accept a 2600% higher risk of neuropathy? Along with numerous other hugely increased risks? Risks that almost certainly rises each year as never and brain and other body organs are under continuous assault by the statin.

IMO, you have to be a fool to accept odds like that (barring some overriding extreme factors).

Don’t expect your doctor to be reliable or even rational here. They will be off in fantasy land relying on experts. They don’t have time to go study up on the huge number of risks and they don’t have time to take a serious look at risk vs benefits. You’re going to get a quick “take your pill and see you in 6 months” recommendation from most doctors. Managed care, but not managed for your benefit.

The Dynamic Influence of a High Fat Diet on Cholesterol Variability: Dave Feldman’s Nerd Research on Diet vs Cholesterol

Legal disclaimer: since we are not doctors, do NOT follow anything based on health-related topics on this or related sites without first consulting with your doctor or other trusted health professional. This is NOT medical advice and we are not qualified in any way to offer medical advice.

See prior posts:

As far as I can tell, Dave Feldman (an engineer like myself!), has a better mind for research on dietary fat vs cholesterol than the entire medical research community! Fresh eyes of an engineer free of dogmatic thinking and free of cognitive commitments and cognitive dissonance go a long, long way.

What follows is what I can grok from Feldman’s presentation. If you are an MD, watch it and tell me where I got it wrong, if I did. The main point here is that accepted “knowledge” looks to have a huge gaping hole in its understanding.

Feldman gets right down to showing a direct inverse correlation of dietary fat vs LDL-C/LDL-P cholesterol, showing that large changes can be seen in just a few days (HDL is a direct correlation). And he claims a 100% success rate across more than two dozen individuals in repeating the same inverse correlation.

The correlations and inverse correlations are so predictable and so strong that some of his study participants used the findings to “get their doctor off their backs” and/or to reduce life insurance premiums!

Dave Feldman’s graph of dietary fat vs inverted LDL-C level
===> MORE FAT = LOWER LDL-C

Feldman’s findings are so transparently presented and so contradictory to what the medical establishment regards as correct that it ought to flummox you if you are a doctor, that is, if you can avoid severe cognitive dissonance.

I am not surprised. Research on how diet actually affects cholesterol for an individual* is so absent in showing the link between diet and cholesterol that at best it makes the whole thing seem a farce. Not to mention a host of other factors*.

My hunches on my own cholesterol vs diet vs how good I feel fall right in line with what Feldman is showing (though I don’t follow a Keto diet due to extreme exercise load, I have a very high aerobic capacity which means I am adapted to using fat for energy).

Feldman’s data is persuasive because a direct mathematical correlation in an individual and consistent across individuals is as close to a proof as you are going to get. Compare that to averaging millions of people with dozens of confounding variables—the 8.873% pregnant pseudo-science stuff.

Seems to me that Feldman is doing science as science should and must be done to be persuasive: formulating a hypothesis, directly testing the hypothesis while varying the hypothetical causal factor, and repeating the results with more and more subjects.

Medical establishment claims that cholesterol takes months to change meaningfully is refuted directly in Dave’s research, showing that cholesterol levels not only can change dramatically in just a few days , but those levels are strongly and inversely correlated with high fat diets (the opposite of accepted thinking).

The data Feldman presents is so compelling with such strong and repeatable correlations that one has to presume that extreme cognitive dissonance must be in place in the medical establishment. Or more likely, willful ignorance driven by money—you find what you look for so don’t look for other stuff since the funding isn't there.

Bottom line from what I can tell: medical establishment thinking on cholesterol is fundamentally ignorant of actual physiological response. At least in the short term. That calls into question the entire body of claims about diet vs cholesterol. I see only a huge pool of ignorance out there, trying to give advice based on averaging millions of people over dozens of variables—research hubris. The medical community needs to get down to basics and prove (or disprove) the link between dietary fat and cholesterol, as Feldman shows so persuasively.

See also Podcast: Dave Feldman & Alan Flanagan – Debating LDL Causality & the “Lipid Triad.

* Actual diet, genetics, epigenetics, gene activation, exercise, etc are all just averaged away for a net total effect that is an absurd mass average finding.


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How important is Dietary Management in Hypercholesterolemia?

Legal disclaimer: since we are not doctors, do NOT follow anything based on health-related topics on this or related sites without first consulting with your doctor or other trusted health professional.This is NOT medical advice and we are not qualified in any way to offer medical advice.

See prior posts:

Everyone loves a pill: doctors love prescribing statins (“nobody can blame me!”) and patients love taking them (“awesome, I am absolved of taking responsibility”). More or less, most of the time, and not that I blame doctors much given the harried dysfunctional state of medicine today in terms of total health management. Everyone is happy, ain’t that great?

Statins be damned until I prove for myself that diet won’t do as well or better and with far more attendant benefits that come from diet.

The single-bullet statin epidemic of pill taking stems from an epidimiological “forest without trees” approach to medicine. Generic statistical risk management without a full risk assessement is intellectually bankrupt for an individual, what with all its attendant risks of damage to body and brain for some percentage of those taking.

Just the muscle pain or the fact that the large majority of pro athletes cannot tolerate a statin ought to give pause to any active person—it’s a huge guinea pig experiment, and where is the risk analysis for those harmed in mostly small but sometimes large ways (e.g., diabetes, nerve damage, liver damage)? What about productivity losses from cognitive impairment? Money to fund such research is not exactly readily available. Wherever money is a factor, fraud and cognitive dissonance and cognitive bias are unavoidable and inherent. And if you’re in the unlucky few percent, it’s all “on you” for the downsides—no skin in the game for doctors.

Diet and cholesterol

When I collect more dietary data, I may find a way to aggregate it for an average daily look at what I’ve ingested. I predict here that I will be able to drop my 250 cholesterol (HDL of 111) to close to 190 by diet an exercise alone within 4 months.

With the exception of my whole fat yogurt binge of the past 5 months (for good reasons, mainly massive caloric burn in the cold while traveling), I already follow a diet in line with recommendations:

How important is Dietary Management in Hypercholesterolemia?

I don’t agree with “margarines” (very bad idea IMO), or soy (potential hormonal issues from phytoestrogens), but these recommendations seems on target otherwise. Emphasis added.

The cholesterol-lowering supple- ments include margarines, dairy products and other foods enriched with gram doses of phytosterols or stanols; soluble fiber products, such as psyllium, pectin and guar gum; soy protein and red yeast rice. Virgin olive oil, the culi- nary fat preferentially used in the Mediterranean diet, is a pure ‘juice’ of olives containing both the fat (mainly oleic acid) and the minor bioactive components of olives, such as phytosterols, tocopherols and phenolic compounds, and has recently emerged as another cardioprotective food, with both cholesterol-lowering and HDL-raising properties.

A bold approach to dietary cholesterol-lowering is to use a combination of these foods. The portfolio diet described by Jenkins and colleagues comprised four key components:

  • Foods rich in soluble fiber „
  • Soy protein„„
  • Plant sterols
  • Almonds

Their combined effect resulted in a 29% LDL-cholesterol reduction, comparable with that observed with a small dose of a statin.

Yesterday’s diet and exercise as one example.

Diet for one day, to the gram, with fat and protein content
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Relationship Between Lifelong Exercise Volume and Coronary Atherosclerosis in Athletes

Legal disclaimer: since we are not doctors, do NOT follow anything based on health-related topics on this or related sites without first consulting with your doctor or other trusted health professional.This is NOT medical advice and we are not qualified in any way to offer medical advice.

This article below bears directly on previous discussions on coronary atherosclerosis including my recent post Can an Extreme Endurance Athlete Have an Early Heart Attack?.

METs are a measure of oxygen consumption, with one MET corresponding to about 70 KCal. My caloric burn per hour when training intensively is about 740 calories per here, let»s round that down to 10 METs when rounded. During a double century, that typically drops to 650 to 680 KCal/hour depending on the course and how good I am feeling.

The last 4 days alone I have expended 8200 KCal* ~= 117 MET-hours. If I have that correct, than that is 117 * 60 = ~7000 MET-min, which far exceeds the study’s cutoff of 2000 MET-min/week—and the week has 3 days left. Having done this for years, it would surely explain my CT coronary calcium score.

* According to my highly accurate SRM power meter. Right now I am having problems with my SRM PC8 connecting to the computer and it may need to be fixed, but I plan to show an entire week’s overload-cycle spring training.

Relationship Between Lifelong Exercise Volume and Coronary Atherosclerosis in Athletes

Participants in the >2000 MET-min/wk group had a higher prevalence of CAC and atherosclerotic plaques. The most active group, however, had a more benign composition of plaques, with fewer mixed plaques and more often only calcified plaques. These observations may explain the increased longevity typical of endurance athletes despite the presence of more coronary atherosclerotic plaque in the most active participants.

The key take-aways from the article are:

  • Physically highly active individuals may have substantial, asymptomatic coronary atherosclerosis.
  • The plaque types of the most active group are more benign calcified plaques and need more study to understand the implications.
  • The relationship between high exercise volume and coronary artery calcification and plaque is as yet poorly understood.
  • The more calcified plaques in high volume athletes may offset calcification scores and contribute to superior life expectancy of athletes.
  • ...possible that it is not the duration of exercise that is most important in the development of coronary atherosclerosis but the intensity of exercise.
  • Underlying mechanisms for higher prevalence of CAC/plaque and increased calcification in athletes with the highest exercise volume and intensity are unknown.

This adds yet more context to the relatively context-free paint-by-numbers evaluation of heart disease favored in doctor’”s offices. Also, the data does not seem to have distinguished runners from cyclists, and runners take much more of a beating/pounding, which could affect the health of arteries.

See also

Various Interesting Health Findings in Science Daily: Exercise and Hidden Fat, Extreme Exercise and Heart Disease, Fasting, Brain and Fasting, Peripheral Neuropathy

MESA 10-Year CHD Risk With Coronary Artery Calcification

ACCEL: Detecting CAD in Older Athletes and What to Recommend When You Find

Expert Opinion: "Crazy for Ketones" – The Ketogenic Diet in Athletes: Variable Effects on Athletic Performance with Potential for Cardiovascular Harm

Expert Opinion: Fat for Thought – Any Role for the Ketogenic Diet in Athletic Training?

Coronary Atherosclerosis in Masters Athletes: Mechanisms and Implications for Cardiovascular Disease Risk

Association of All-Cause and Cardiovascular Mortality With High Levels of Physical Activity and Concurrent Coronary Artery Calcification


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Can an Extreme Endurance Athlete Have an Early Heart Attack? CT Coronary Calcium Scan, HDL Cholesterol, LDL Cholesterol, Statins, etc (UPDATE with a cardiologist viewpoint)

Legal disclaimer: since we are not doctors, do NOT follow anything based on health-related topics on this or related sites without first consulting with your doctor or other trusted health professional.This is NOT medical advice and we are not qualified in any way to offer medical advice.

A new challenge: reversing early arteriosclerosis. I think I may have to get down to 5% body fat to see if it can be done. There is no consensus on whether getting body fat that low can reverse arterial plaque. My working theory is that the body will scavenge soft plaque), but I do know that when I was at 8% body fat with only 1 pound of visceral fat (!), my cholesterol was the lowest it had ever been over a period of 22 years—see the graph.

The core problem I face in researching this issue is that as a layman, sorting through conflicting expert opinions is difficult. What is clear is that the evidence for heart disease root causes is exceedingly weak, and based on epidemiological studies of large numbers of mostly obese people who never exercised and ate garbage all their lives (e.g. Americans—just go visit Walmart one day!).

Worse, the link to diet is weak to say the least, let alone the role of the microbiome, exercise, genetics, epigenetics, etc. Given the fiascoes in nutrition revealed in recent years by new research, it is very hard to accept any recommendations as having merit. Heck, medical science can’t even figure out trivially simple (by comparison) glycemic index, which varies hugely for the same food for different people.

23 year cholesterol history: total cholesterol, HDL, LDL, triglycerides

Background

Just under two years ago in late March of 2018 I had a CT Coronary Calcium Scan which showed arteriosclerosis placing me in the 81st percentile for my age (mid 50's), the 99th percentile being the worst, 0th the best. Meaning that out of 100 men, 88 or so would have less arterial plaque for my age.

Visual assessment of the coronary arteries shows moderate coronary artery calcification centered within the LAD. Quantitative calcium score provided by the 3D Lab is 91.2, which places the patient in the 81st percentile for age and gender.

Heart: normal in size, no significant valvular calcification.
Pericardium: no pericardial effusion.
Pulmonary arteries: not enlarged.
Thoracic aorta: no significant abnormality.

That was a shocker, given my exercise and diet, but I seem to have inherited a genotype or have had epigenetic triggers or a gut microbiome that is unfavorable for cholesterol. See my 22 year cholesterol chart further below, which suggests that it’s pretty much the way my body works.

The CT calcium scan is not very helpful, so I am looking into a heartflow scan. Do I have 10% blockage, 30%, what? No meaningful risk assessment can be made with such vague information IMO, particularly in weighing against all the potential downsides of statins, which appear to be much higher than the medical industry wants to acknowledge, and such risks are always framed in epidemiological terms which means mainly high risk people who never exercised much or at all, and ate badly as a life habit. And... maybe it is all about inflammation and sugar and has nothing to do with dietary cholesterol.

I’m willing to do what it takes to halt and hopefully reverse arteriosclerosis, but the more questions I ask, the more I find that doctors have no idea how to do that! Meaning it’s all vague recommendations that on average might help. But the more I learn about the gut microbiome, the more I think that much of that is averaged-out epidemiological bullshit for any particular individual. Basically, the science is crap when it comes to an individual cases and there isn’t even agreement on the side effect profile. So how do I assess if I’m going to collapse and die of a heart attack in five or ten years and weigh that against the risks that no one can properly assess?

Seems like one huge guinea pig experiment: New Study Adds to Debate Over Statin Use to Prevent CVD

The authors consistently found that the harms outweighed the benefits until 10-year CVD risk thresholds substantially exceeded those recommended in current guidelines... anywhere from 50 to 200 people who don’t have CVD must take a statin to prevent just 1 heart attack over 5 years. Meanwhile, many of these patients will develop muscle pains and they are also at higher risk of developing type 2 diabetes.

Moreover, studies I’ve found suggest that the majority of pro athletes cannot tolerate statins. What does that say for me, doing double centuries and the training for it? Moreover, statins can attenuate fitness gains and fitness gains can offset the risks from high LDL.

Worse, how does one make intelligent choices without monthly lipid profiles to see what works and what doesn’t? Good science means changing one variable and seeing if it helps (e.g., using psyllium husk or oatmeal or whatever for a month, or dropping 10 pounds of body fat, etc). I have had exceptional dietary discipline before (recording food to the gram, etc), but more than a month is discouraging without feedback.... are the changes working for me or not? That is the massive flaw in the whole system.

Data for 2020-02-14 shows HDL (good) cholesterol level of 111 mg/dL, which is sort of off the charts. While HDL is called “good cholesterol” for its scrubbing of LDL cholesterol, the latest science now ponders if too much HDL may be associated with increased risk of heart attack and death:

...more research is needed to elucidate the mechanisms of this paradoxical association. "While the answer remains unknown, one possible explanation is that extremely elevated HDL cholesterol may represent 'dysfunctional HDL' which may promote rather than protect against cardiovascular disease," he said.

I know that my HDL rises the more I lose body fat, while LDL decreases. This seems paradoxical, just as the above states. But could my latest HDL of 111 (extremely high) be associated with LDL, sort of rising in tandem? That would violate past patterns in which HDL rise is associated with LDL decrease. Go figure.

23 year cholesterol history: total cholesterol, HDL, LDL, triglycerides

Statin?

Last week my internist said I would likely have a heart attack within 7 years if I did not get my LDL cholesterol down (further buildup). ALL other tests are poster-perfect including blood pressure of 116/68.

All of my doctors say I should be on a statin. A statin is a medication that reduces cholesterol with alleged reductions of 24% to 36% reduced risk of heart attack, which is not much IMO and why the hell the wide range? Seems sketchy at best.

I am loathe to take a statin because the “rare” side effects are likely not so. I know from personal experience with Metronidazole that doctors DO NOT report adverse effects properly, or at all. So statistics on side effects are almost certainly total bullshit. And for those in poor health (most), side effects are both less important and less noticed and maybe a reasonable tradeoff.

My specific concerns with taking a statin are :

  • Risk of nerve inflammation. After severe nerve damage from Metronidazole that took two years to recover from, the least thing I want in my body is anything that carries any risk of nerve damage.
  • Cognitive impairment—years from now maybe we’ll find that dementia and similar are made worse by statins. Statins can affect cognitive function (“reversible cognitive impairing effect in some patients”, “clinical trials were not originally designed to detect cognitive impairment”) but science is in doubt as to benefit or impairment. And with my brain finally mostly back in order after a concussion, the last thing I want is to fuck it up with a statin or find out that “reversible” is really a lie from big pharma—big money means bigger lies.
    A double blind placebo-controlled trial of lovastatin’s effect on cognitive functioning and mood showed detrimental effects on cognitive performance on four neuropsychological tests assessing attention, working memory, and overall mental efficiency... Post-marketing surveillance has continued to uncover case reports of cognitive effects associated with statin use since the FDA report
  • 100% to 200% increased risk of diabetes with some statins.
  • Risk of life threatening muscle damage with some statins; rare but one drug was withdrawn from the market for that reason. Or just muscle aches and pains, a total non-starter for me as an athlete.
  • Liver inflammation—what does a statin do to the liver during extreme stress such as in a double century? I doubt there is any science at all on such things.

Scientific studies

Scientific studies are so dubious these days: there is disconcerting evidence of sloppy work or money involved 75% of the time. So call me a skeptic on statins and the $billions involved in selling statins to millions of obese sedentary people, versus someone like myself doing double centuries and exercising 10 times as much every day as most of those statistical people do in a week.

While every doctor I’ve seen (two internists and a cardiologist) have recommended a statin to me, no doctor has ever offered a credible risk assessment of the side effects of statins, or even brought the issue up. That’s a huge red flag, a “halfpinion”—it’s bad science, bad medicine, bad risk management to offer a “solution” without also considering the negatives.

No one is an epidemiological statistic. A recommendation that works on average—that’s like saying every woman is 13.7% pregnant, which is obviously idiotic. Some people are damaged by some medications, sometimes fatally. What I want is a tailored personal recommendation based on my lifestyle, my genetics along with my current gut microbiome, my diet. But that doesn’t exist AFAIK with regards to arteriosclerosis.

Every person responds differently to medications, as I learned the hard way. PLUS, I am an extreme outlier with respect to epidemiological statistics for arteriosclerosis, as follows:

  • I am an ultra endurance athlete.
  • I have been active nearly all my life.
  • I regularly take my body fat to 10% or so, sometimes lower.
  • I have an off-the-chart HDL cholesterol of 111 out of a 250 total cholesterol. Medical science cannot agree on how protective this “good” HDL cholesterol is, but I am certainly several standard deviations away from any normal.
  • Both my parents are at or near 80, and have never had a heart attack or stroke. My mother has high cholesterol, my father’s is very good.
  • I eat a far healthier diet than most Americans. my diet being 100% free of cheeseburgers and sodas and processed foods and the garbage that most people eat. I eat the good stuff. My main dietary failing is having eaten 2-3 quarts of full-fat Greek yogurt the past 5 months, a great travel food when burning an extra 2000 calories a day in the cold.

How I plan to handle it

I am strongly averse to a statin, which aside from the risk discussed above, seems like a bad idea without first making all reasonable efforts on diet and body fat, which do not carry risks.

  • Reduce body fat by 10 pounds to get to 8% body fat. I have done this before, so it can be done.
  • (stretch goal) Get to 5% body fat in hopes that this will REVERSE arteriosclerosis.
  • Increase consumption of psyllium husk, oatmeal. Add 4000 mg omega 3. Continue olive oil and similar friendly oils, avocado, etc. These items together in theory could cut blood cholesterol by 20% or more.
  • Reduce consumption of whole fat yogurt to no more than one quart per week.
  • Continue with favorable diet for gut microbiome including

Based on past assessments, achieving 8% body fat should drop total cholesterol to 190 or so (2011-05-20 in graph). Since I cannot maintain that low level of body fat, I will have to rely on diet for most of the year.

See also

MESA 10-Year CHD Risk With Coronary Artery Calcification

ACCEL: Detecting CAD in Older Athletes and What to Recommend When You Find

Expert Opinion: "Crazy for Ketones" – The Ketogenic Diet in Athletes: Variable Effects on Athletic Performance with Potential for Cardiovascular Harm

Expert Opinion: Fat for Thought – Any Role for the Ketogenic Diet in Athletic Training?

Coronary Atherosclerosis in Masters Athletes: Mechanisms and Implications for Cardiovascular Disease Risk

Association of All-Cause and Cardiovascular Mortality With High Levels of Physical Activity and Concurrent Coronary Artery Calcification

Cardiologist viewpoint

Emphasis added.

From Jon L (a recently retired academic cardiologist).

“Can endurance athletes die of premature heart attack?”
The answer is yes.  Perhaps the most notable case is that of the runner Jim Fixx.  From Wikipedia: 
          “Fixx died on July 20, 1984 at age 52 of a fulminant heart attack, during his daily run on Vermont Route 15 in Hardwick.[1] The autopsy, conducted by Vermont's chief medical examiner, Dr. Eleanor McQuillen, revealed that atherosclerosis had blocked one coronary artery 95%, a second 85%, and a third 70%.[4] (His father Calvin Fixx had died of a second heart attack at age 43.[5])
        “In 1986 exercise physiologist Kenneth Cooper published an inventory of the risk factors that might have contributed to Fixx's death.[6] Granted access to his medical records and autopsy, and after interviewing his friends and family, Cooper concluded that Fixx was genetically predisposed - his father died of a heart attack at 43 after a previous one at 35, and Fixx himself had a congenitally enlarged heart - and had an unhealthy life: Fixx was a heavy smoker before beginning running at age 36, had a stressful occupation, had undergone a second divorce, and his weight before he took up running had ballooned to 214 pounds (97 kg).[7] Medical opinion continues to uphold the link between moderate exercise and longevity.[8]

At issue is what risk any individual has for developing atherosclerotic vascular disease (ASVD).  Risk is assessed using data from population studies (“derived from pooled cohort estimates”).  As you suggest, endurance athletes are poorly represented in these pooled cohorts.  Given the fact that exercise is generally accepted as reducing risk of ASVD, risk assessed using these tools may overestimate risk for endurance athletes.  Although it is generally accepted that moderate exercises reduces cardiovascular risk, there is evidence that this benefit diminished with the highest levels of exercise (most notably in marathon runners). 

In contrast to Fixx, the estimate of your risk, based on the data you have provided (age, gender, cholesterol levels, negative family history of premature disease, etc,) would be on the order of 2% which is considered low.  Even adding your coronary calcium score, (which would not be recommended in your case given the low basal risk), your risk would still be considered low (3.8% with ≤ 5% considered low risk). 

The presence of coronary calcification indicates the presence of atherosclerosis.  Recent studies suggest that the prevalence of coronary calcification is higher in endurance athletes, and that coronary calcification scores may be elevated in response to vigorous exercise.  These studies are not large enough to clearly establish whether the increased coronary calcium was associated with an increase in ASVD events.  See DeFina et al, JAMA Cardiol, 2019;4(2):174-181.  Association of All-Cause and Cardiovascular Mortality With High Levels of Physical Activity and Concurrent Coronary Artery Calcification.  Additional studies with CT angiography suggest that these lesions are more densely calcified, thought to be more stable, and less likely to rupture and cause an event. 

You correctly point out that our understanding of the pathogenesis of ASVD remains incomplete.  There is good evidence to support the presence of diabetes, hypertension, chronic kidney disease, unfavorable cholesterol levels, smoking and family history as major risk factors for premature ASVD.  Current research is focused on the role of the gut microbiome, inflammation and other factors.  The role of gut microbiome is being addressed by informatics and analysis of large datasets (stool DNA analysis) where the role of artificial intelligence may come to into play.

As regards your high levels of total cholesterol, the significance is offset by the high HDL cholesterol, normal LDL cholesterol and triglycerides.  

You raise the question of what further tests might be considered to refine further your individual risk of premature ASVD.  Assessment of coronary blood flow by myocardial perfusion imaging would be of limited value given your low pre-test likelihood and excellent exercise tolerance.  Elevation of high-sensitivity C-reactive protein (hs-CRP) has been used as a marker of subclinical inflammation and has been considered to provide additional information as to risk.  Asymptomatic individuals with elevated hs-CRP have been shown to benefit from statin therapy with a reduction in ASVD events (Jupiter trials).  This finding has not been assessed in endurance athletes

The next question is how would the results of additional testing change the approach to further risk reduction.  Some authorities would recommend statins.  However, given your overall low risk, the benefit of statins might be expected to be low.  Moreover, as you correctly point out, statins are not well tolerated in athletes.  Similarly, aspirin which has proven benefit in patients with manifest ASVD events, would not be indicated for you given that the risk of increased bleeding would outweigh any potential benefit (particularly if you had another bike crash while cycling!).

All of the aforementioned discussions are predicated on the information you have provided.  As indicated in the 2019 AHA/ACC Guidelines for Primary Prevention of ASVD, shared decision making between you and your doctors should determine the best strategies top reduce your risk.  Your case is further complicated by the lack of clear data for high endurance athletes.  Moreover, our current health care systems do not provide physicians the time to have detailed discussion of the relative risks and benefits of interventions with their patients (and may in fact penalize the physician if they “…spend too much time…” with a patient.  Many patients are looking for a pill to fix their problem and they are rewarded with a statin.  The patient is happy because he got a pill and the physician is happy because he has done something to meet the patient’s expectations.  Additionally, should the patient have an atherosclerotic event, the physician would not be faced with the question “Why didn’t you start the patient on a statin?”.

For now, the most important thing would be to watch for unexplained changes in your exercise tolerance, shortness of breath or the development of new chest tightness.  The onset of new symptoms or decrease in exercise tolerance should prompt further cardiac evaluation.  Continued extreme exercise does carry some risk of a cardiac event, but there is little compelling evidence to suggest how that risk might be reduced further.  Again, these recommendations should be considered relatively unique to your situation and not necessarily appropriate for other endurance athletes.

WIND: I felt vigorous at 14252' elevation (4344m) just last August, along with weeks spent at 10K to 12K feet last fall and hiking faster with a load than most people half my age... that the low partial pressure of oxygen would have a high likelihood of flushing out a heart blockage issue, particularly at max heart rate at 14K feet while sprinting to the summit. No issues whatsoever.

Making the available data even more tenuous, I am a cyclist and I wonder if runners could have different risks due to much higher impact and stress versus cycling. In cycling, the body when properly fitted and positioned acts as a shock absorbing spring, sparing the chest from stress. In a runner the stresses may be quite high if descending, but even on flat ground there is joint-killing pounding going on continually.

Another cardiologist weighs in:

Based on your numbers, I wouldn't put you on a statin. You're healthy, your HDL is excellent, and you have no family history of CAD. Trust me, I've saved way more lives putting people on statins than putting in stents. They are good and safe drugs. That being said, I wouldn't put on a statin. Sure, you've got some coronary calcium - it's not too uncommon - but I'd probably hold off for now. If you wanted the lowest cardiovascular risk, then you could take a statin, but with your family history and high HDL, I don't think you're entirely likely to benefit from it.

As an aside, getting down to that low of a body fat percentage is sketchy. the TdF riders that can do that only get that low briefly. The risk for illness and increased inflammation may be higher. I don't know, but be careful.

WIND: I have felt very healthy at 8% body fat, but I looked like a skinny teenager, and lower than that is probably risky.


Up to 1527MB/s sustained performance

2017 Mercedes Sprinter: Is it Going to KILL ME by Failing to Move at a Crucial Time?

Prior post:

Mercedes Sprinter Issues and Breakdowns: Sprinter Will Not Go, RPMs Drop Very Low (Normal idle, put into D or R, RPMs drop, Engine Lugs

I had quite a scare about a week ago.

Returning from a daylong hike with temperatures in the 40's, I started up the Sprinter, let it warm up for a minute or so.

Checking in both directions for traffic (none seen), I put it into D (drive) and being pointed downhill, it rolled away easily. Cranking the wheel to turn uphill, I was now straddling both lanes on a blind corner at night. The accelerator pedal had NO EFFECT, just as described.

I immediately floored the accelerator pedal and held it there. The Sprinter would not move. The engine did not die, but it would not go anywhere either. I do not recall if the RPMs dropped in this case, being more shocked and afraid of being hit by an oncoming vehicle, but at the least there was no increase in RPMs.

Slowly, reluctantly, about 30 seconds later, the Sprinter started going and I drove away. Once warmed up, it behaved normally as is always the case.

Lately, even on relatively warm nights (not much below freezing), I cannot get the Sprinter to move (R or D) until warmed up several minutes. With colder temperatures, it 8 to 10 minutes to go anywhere, dropping to 500 rpm and lugging badly and going nowhere. Put into N or P, the engine RPMS are as high as 1400 when cold, and the engine revs freely when pressing the accelerator pedal.

Diagnostic code

The following diagnostic code is found:

ECM-EngineControl ($7E0) P0506 PowerTrain Confirmed Idle Air Control System RPM Lower Than Expected


Up to 1527MB/s sustained performance

Biodiesel is the Kiss of Death for Mercedes Sprinter

I keep meeting Mercedes Sprinter owners who fail to break-in their Sprinter properly (the fault of Mercedes using inappropriate oil* for break-in), who change the oil far to infrequently (naively following the service interval).

And... some who have fueled up with biodiesel B20 or worse, covered in detail in:

Mercedes Sprinter Maintenance: Biodiesel is the Kiss of Death for Your Sprinter

Biodiesel should not be confused with renewable diesel, which is a far higher quality product, arguably better than petroleum diesel, albeit with dubious lubrication properties due to its ultra ultra low sulfur content (~5 ppm vs 15 ppm for ULSD), which in theory could result in fuel pump failur due to inadequate lubrication from the low sulfur content.

* Using 5W 30 oil will not break in a diesel engine properly because the piston rings will not seat properly into the cylinders, the oil being too “thin” (low viscosity). So you get 1% or 2% better fuel mileage for a few thousand miles when new, but the engine now has leaky piston rings forever. Thus it leaks fuel into crankcase oil (“fuel accretion”), particularly during a DPF burnoff cycle, which dilutes the crankcase oil and damages its lubrication properties. Over time, the engine suffers increasingly premature wear, which results in shortened lifespan along with reduced fuel economy over its usable lifetime. Mercedes won’t tell you any of this, which is awful, but regulatory bodies hold all the cards and call the shots, so Mercedes isn’t going to fess up on any of it.


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