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Proof that Lifelong Cholesterol Reduction Prevents Heart Disease

“It is well accepted that coronary atherosclerosis is a chronic progressive disease that begins early in life and slowly progresses over several decades” before symptoms arise. However, the average age in cholesterol-lowering drug trials is 63; therefore, people have already been exposed to a lifetime of circulating LDL cholesterol. It’s no wonder pharmaceutical therapies typically reduce cardiovascular disease risk by only 20 to 30 percent.

We know LDL, the so-called bad cholesterol, plays “a central role” in the “initiation, development, and progression” of our number-one killer. In fact, more than 100 prospective studies involving more than a million people have demonstrated that those with higher LDL levels are at higher risk.

“It seems reasonable to assume, therefore, that if lowering LDL-C [cholesterol] levels beginning later in life can slow the progression of advanced atherosclerotic plaques…then keeping LDL-C levels low, beginning much earlier in life” might prevent our arteries from getting clogged in the first place. A reasonable assumption, certainly—but let’s not just assume.

“It would be…unethical to set up a controlled clinical trial in which young adults with elevated serum cholesterol levels were treated or not treated over their lifetime”—just as we couldn’t ethically set up a study in which half the young adults are made to start smoking to see if smoking really does cause lung cancer. That’s where observational studies come in. We can follow people who already smoke and compare their disease rates to those who don’t.

It was around 40 years ago when the president of the American Heart Association tried to argue we should all stop smoking even though there were no randomized controlled trials. You can see a copy of the “Presidential Address” entitled “The Case for Prevention of Coronary Heart Disease” to the AHA’s 47th Scientific Sessions at 1:34 in my video. Those who smoke have a higher risk of heart attack, and the more we smoke the higher the risk. After we stop smoking, our risk drops. The same can be said for high cholesterol.

Young men 18 through 39 years of age were followed for up to 34 years, and their cholesterol levels, even when they were young, predicted long-term risk of heart disease and death. Men in their 20s and 30s who have a total cholesterol just under 200 have a “substantially longer estimated life expectancy”—around 4 to 9 years longer—than those with levels over 240.

“Evidence from observational studies, however, [is] vulnerable to confounding” factors. Eating a diet that is plant-based enough to lower cholesterol below average, for example, may add years to our lives regardless of what our cholesterol actually is. Ideally, we’d have a long-term, randomized, controlled trial.

Nature may have actually set one up for us. Each of us, at conception, gets a random assortment of genes from our mother and our father, and some of those genes may affect our cholesterol levels. Just like there are rare genetic mutations that result in unusually high cholesterol levels, there are rare genetic mutations that lead to unusually low cholesterol levels, “provid[ing] an ideal system in which to assess the consequences of low LDL cholesterol levels independently of other factors that may modify disease progression,” such as confounding diet and lifestyle factors.

Starting at 3:14 in my video, you can see what I mean. About 1 in 40 African Americans have a mutation that drops their LDL cholesterol from around 130 down toward more optimal levels. Now, this group didn’t eat healthy to achieve that drop. It’s just in their genes. More than half had high blood pressure and there were a lot of smokers and diabetics in the group, yet those with genetically low LDL levels still had a significant reduction in the incidence of coronary heart disease even in the presence of all those other risk factors. How significant? How much less heart disease? A remarkable 88 percent of heart disease was simply gone.

The astounding finding was that the risk of heart disease in these individuals was reduced by more than 80 percent, whereas the same 20- to 40-point decrease in LDL from drugs only reduces risk around 30 percent. Makes sense, though, because the folks with the mutation had low levels their entire life. They didn’t simply start taking a pill when they were 60.

“The magnitude of the effect of long-term exposure to lower LDL-C [cholesterol] concentrations observed in each of these studies represents a threefold greater reduction in the risk of CHD,” or coronary heart disease, compared to drug treatment started later in life. (As an aside, for all of my fellow research nerds, check out that p value shown in my video at the 4:30 mark. You’d have to do around a quintillion studies to get that kind of result by chance!)

“Therefore, a primary prevention strategy that promotes keeping LDL [cholesterol] levels as low as possible, beginning as early in life as possible, and sustaining those low levels of LDL [cholesterol] throughout the whole of one’s lifetime has the potential to dramatically reduce the risk of CHD,” coronary heart disease.


If you don’t know your cholesterol level, you should get it checked—maybe even starting in childhood. See my video Should All Children Have Their Cholesterol Checked? to learn more.

What if you do get tested and your doctor tells you not to worry because your cholesterol’s “normal”? Having a “normal” cholesterol level in the society where it’s normal to drop dead of a heart attack (the number-one killer of men and women) is not really such a good thing. See my video When Low-Risk Means High-Risk.

Check out Optimal Cholesterol Level and What’s the Optimal Cholesterol Level? to find out where you should be.

What if your doctor tells you your LDL is large and fluffy? See my video Does Cholesterol Size Matter?.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

Discuss

Michael Greger M.D., FACLM

Michael Greger, M.D. FACLM, is a physician, New York Times bestselling author, and internationally recognized professional speaker on a number of important public health issues. Dr. Greger has lectured at the Conference on World Affairs, the National Institutes of Health, and the International Bird Flu Summit, testified before Congress, appeared on The Dr. Oz Show and The Colbert Report, and was invited as an expert witness in defense of Oprah Winfrey at the infamous "meat defamation" trial.


74 responses to “Proof that Lifelong Cholesterol Reduction Prevents Heart Disease

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  1. Okay, so yesterday I learned that “good” cholesterol – HDL – brings fat to the liver to be broken down and that what makes LDL “bad” is that it is bringing the fats out of the liver into the body where there is already too much fat nowadays and that if we had situations like drought, LDL would be a heroic figure in society, but we have made it a black-hat bad guy.

    What is LCL-C? (third paragraph)

    I never understood what made “good” cholesterol good until yesterday, so when they would debate whether not having enough good cholesterol it was as important as having too much bad cholesterol it was hard to figure out who was right.

    So, who was right?

    I am going to guess that if people are thin and don’t have a lot of extra fat to bring back to the liver, maybe it is less of an issue, but if they are eating fats and fructose and drinking alcohol, being low would be more of an issue?

  2. You brought up smoking and heart disease and what I also learned yesterday is that nicotine increases insulin resistance.

    I learned it because I was trying to double-check Lustig’s concepts of the diets of the people with the most cases of Diabetes, so I went to the first one looking for sugar versus fatty acids and what I found was they were big smokers and the fatty type of seafood. The second most diabetes ate a lot of coconut and processed foods and also fatty seafood.

    Anyway, smoking increases insulin resistance and increases LDL-C and decreases HDL-C, so smoking has cholesterol as one of its mechanisms.

  3. Another thing I learned was that insulin resistance is the “driver” of the bad cholesterol profiles.

    That is how one site described it.

    They said that insulin resistance is what causes people to develop an abnormal cholesterol profile where they get low “good cholesterol” and high “bad cholesterol” and high triglycerides.

    I haven’t figured out the mechanism of it quite yet, but maybe the liver says, “Don’t bring me anymore fat, I am already trying to get rid of it!” and the liver is da boss.

  4. So I guess if it is insulin resistance driving the cholesterol levels, then, we have to back up to what drives insulin resistance and that would be things like NEFA’s, from Saturated fats and Fructose and something about Ceramides.

      1. The article itself is by the usual low carb/keto types trying to sell stuff to the public. I agree that it is worthless in itself.

        It does however refer to legitimate scientific studies on the issue which might be worth checking out.

  5. Totally off this topic, but the site says ask questions in comment section. What would cause water and food to suddenly taste very salty? Water tastes like the ocean. I drink lots of water all day, so not dehydrated.

    1. There are several reasons why water you drink could taste salty, some involving you and some other factors such as changes in your water supply, water softener, etc. It’s good you recognize the possibility of dehydration as the cause and it seems you’ve ruled that out, although if you’re exercising lots and sweating you could have sweat on your lips causing a salty taste. I’m assuming you’ve also already ruled out the possibility of any medication side effects ? Sometimes if you’ve injured your tongue or gums even if no apparent bleeding you might have a sensation of saltiness. If the situation does not resolve you should contact your doctor to review if there are any other medical conditions causing this. In the mean time up your water intake, monitor for other symptoms, and you can read these two articles for additional help in trying to resolve this:
      https://www.health.harvard.edu/diseases-and-conditions/why-do-i-have-a-salty-taste-in-my-mouth

      Why do I have a salty taste in my mouth? – Medical News Today
      http://www.medicalnewstoday.com › articles
      Hope these might lead to some answers for you.

  6. Can you please say something about the need for inflammation in the arteries for cholesterol to stick and cause plaque.

    Here in Holland there are a lot of health professionals who claim that cholesterol is only bad for you if you have inflammations, if you eat lots of fruit en vegetables you would not have inflammations and therefore cholesterol levels are not that important.

      1. Andre

        Yes inflammation happens in veins too, eg deep vein thrombosis Generally speaking though, inflammation of the veins is called phlebitis.

        However, the arteries provide most of the blood supply to the heart and brain.which is why the focus tends to be on the arteries.
        .
        The cholesterol ‘sceptics’ try to come up with all sorts of reasons, bizarre or otherwise, to try to argue that high cholesterol cannot be a problem. They seem to rely on people’s ignorance (and unwillingness to fact-check) to generate superficially plausible arguments to support their claims. This appears to be one of them and has been around for years – despite the fact that the answer to your question and similar ones has been known for even longer. To consider this broad point in more detail, you might eg want to read this below

        http://cholesterolguardian.com/cholesterol-plaques-appear-arteries-not-veins

      2. Your question is a good one and it’s noted in this article that almost all the studies on blood vessels focus on the arteries and very little on the veins:
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6217571/ Mechanical Properties of Diseased Veins

        Veins have larger diameters and larger lumens than arteries so they are not so prone to the inflammation that occurs when plaques develop in arteries. Veins can get inflamed (phlebitis) but this is not so much a clogging of the blood vessel from the vessel itself but from a blood clot which damages vein walls. Hope that clarifies a bit.

    1. Every country has its share of highly vocal cholesterol cranks and quacks who make dangerously stupid statements

      Studies clearly show that high cholesterol itself causes inflammation

      ‘When high levels of cholesterol occur in the bloodstream, excess LDL begins to seep into the inner wall of the artery. This triggers an inflammatory response, which actually speeds up the accumulation of cholesterol in the artery wall. This in turn produces more inflammation—and on and on. Eventually the deposited cholesterol hardens into a plaque, which can rupture and lead to the blood clots that cause heart attacks and strokes—an event that inflammation also appears to help along.’
      https://www.health.com/condition/cholesterol/the-cholesterol-inflammation-connection

      https://nutritionfacts.org/video/cholesterol-crystals-may-tear-though-our-artery-lining/

      1. How does cholesterol seep into a healthy artery wall? Inflammation has to cause injury to the endothelium before cholesterol can get in. You have it backwards.

        1. It’s not me saying this. I am merely quoting.

          In any case, they have published pictures from microscopes showing cholesterol crystals damaging arteries.. All you doing is repeating the assertions of assorted cranks (to put it bluntly).

          Might I suggest you read the consensus statement by the European Atherosclerosis Society pulished just two weeks ago?

          ‘Atherosclerotic cardiovascular disease (ASCVD) starts early, even in childhood.1,2 Non-invasive imaging in the PESA (Progression of Early Subclinical Atherosclerosis) study revealed that 71% and 43% of middle-aged men and women, respectively, have evidence of subclinical atherosclerosis.3 Extensive evidence from epidemiologic, genetic, and clinical intervention studies has indisputably shown that low-density lipoprotein (LDL) is causal in this process…………………….’
          https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehz962/5735221

      2. Mr fumblefingers….I have VERY high cholesterol and NO inflammation markers…so ??? and I also had an angio in 2008 and zero plaque or blockages???

        1. So? There are various inflammation markers. Have you measured all of them?

          High cholesterol is a risk factor but it;s not the only one. There are plenty of people who smoke and have no obvious lung cancer or heart disease. Does that prove smoking is not a risk factor for those conditions?

          Believing the claims of opinionated cranks and people selling sensational books is your choice of course. However, it’s important to look at what medical science has to say about this topic das well as what the self-styled cholesterol sceptics have to say. A good place to start is the latest EAS consensus statement

          https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehz962/5735221

    2. As I learned from Dr. Mercola, wheat is inflammatory in our body, which causes the body to release HDL-C to fight that inflammation, it is just a defense from the body. Of course there are other explanations for it, but being vegan and eating bread will get your HDL-C high.

  7. I have been a vegetarian since I was 25 years old and vegan/plant based for the last 10 years. I am now 72, walk for about 45 minutes most nights and am active. My cholesterol is around 250 even though I eat no foods that raise cholesterol levels.
    My mother was a vegetarian and had the same higher cholesterol levels. She lived to be 96. I realize some of us just make more cholesterol even though our diet is cholesterol free. it is frustrating when you are doing everything right and you see others eating a high cholesterol diet and their levels are normal!

    1. Leslie, yes it’s frustrating, and there are many like you and I that no matter how spartan the diet, high LDL remains. With me it is low estrogen since menopause , plus a genetic factor. My cholesterol was great until menopause on a good but semi vegetarian diet. The male relatives have high cholesterol too.

      The good part is that with eating the Daily Dozen and exercising a lot, my HDL is very good, my triglycerides low.
      All the same, I have been asking for years for Dr Greger to comment on the differences between men and women regarding cholesterol, heart disease, impact of diet on men vs women.

      Also, to address Hans’ comment above, inflammation is a key factor, and Dr Esselstyn has some talks where he says that if you’re diet is ‘ perfect’ but your LDL is stll above desirable levels you should be ok. You are not causing problems with the endothelium.

        1. No Andre, Dr Esselstyn was addressing the people fo.lowing his diet and who had difficulty getting their LDL below 100mg… he said to them (not the general public) that if they followed wfpb with copious amounts of greens etc perfectly then there would be little to initiate the inflammatory response in the endothelium. He said jthis during Q&A after one of his talks. His people also take statins, as do I even with wfpb, no oil

    2. Leslie, the high cholesterol may very well be protective. A British study from around 2013 found that older individuals with high cholesterol lived longer. Also, see my comment below about the Mayo Clinic study.

      1. This is because most people in Western countries have high cholesterol. The major cause of low cholesterol in older people is usually not a healthy diet and exercise but disease states eg

        Why does cholesterol decline in older people? Do they all take up WFPB diets and adopt challenging exercise regimes? Or do older people just tend to be sicker than younger people?

        Sickness and injury cause cholesterol to decline. The sickest people often have the lowest cholesterol. Chronic diseases like cancer and Alzheimers often take decades to develop. Chronic infections like hepatitis can last a lifetime. All these things lower cholesterol often many years before a formal diagnosis eg

        “RESULTS:
        Cholesterol levels in men with dementia and, in particular, those with Alzheimer disease had declined at least 15 years before the diagnosis and remained lower than cholesterol levels in men without dementia throughout that period. The difference in slopes was robust to adjustment for potential confounding factors, including vascular risk factors, weight change, alcohol intake, and use of lipid-lowering agents.
        CONCLUSION:
        A decline in serum total cholesterol levels may be associated with early stages in the development of dementia.”
        http://jamanetwork.com/journals/jamaneurology/fullarticle/793179

        But it’s not just Alzheimer’s, certain cancers can cause cholesterol to fall too – often 15 years or more before a formal diagnosis. Infections, heart attacks and other traumas, various other diseases and even chronic alcoholism can cause cholesterol to declines. These conditions are all more common in older people and explain why simple association studies appear to find high cholesterol ‘protective’ in older people.

        ‘Methods and Results The study was based on 5941 men 45 to 68 years of age without prior history of coronary heart disease, stroke, cancer, or gastrointestinal-liver disease at exam 1 who also participated in exam 3 of the Honolulu Heart Program. The association of TC change with mortality end points was investigated with two different approaches (continuous and categorical TC change) with standard survival analysis techniques. Falling TC level was accompanied by a subsequent increased risk of death caused by some cancers (hemopoietic, esophageal, and prostate), noncardiovascular noncancer causes (particularly liver disease), and all causes. The risk-factor–adjusted rate of all-cause mortality was 30% higher (relative risk, 1.30; 95% CI, 1.06 to 1.59) among persons with a decline from middle (180 to 239 mg/dL) to low (<180 mg/dL) TC than in persons remaining at a stable middle level. By contrast, there was no significant increase in all-cause mortality risk among cohort men with stable low TC levels. Nonillness mortality (deaths caused by trauma and suicide) was not related to either TC change or the average of TC levels in exams 1 and 3.

        Conclusions These results add strength to the reverse-causality proposition that catabolic diseases cause TC to decrease.'
        https://www.ahajournals.org/doi/full/10.1161/01.cir.92.9.2396

        1. I don’t accept the conclusion of the study. How do you know that falling cholesterol didn’t cause the diseases?

          What about comparing elderly people who are healthy? I think that studies have shown that higher levels of cholesterol in such people are protective.

          I don’t accept your premise without proof, that older people have lower levels of cholesterol, especially healthy people. There are healthy people who fall within a wide range of cholesterol measurements.

          1. Because people with stable low cholesterol because of a healthy diet/lifrstyle didn’t have high risk. Only people with high cholesterol that started falling for no obvious reason had the higher risk.

            It is well known (or should be) that infections, trauma, various liver diseases and cancers cause blood cholesterol levels to fall. Even chronic alcoholism does.

            5 out of 6 people who play Russian Roulette don’t blow their brains out. Does that prove that playing Russian Roulette isn’t risky?.

    3. I am in the same boat. I am a vegetarian yet have high LDL cholesterol. Low lipids, very high good HDL cholesterol. I ski, hike, bike etc. I am 70, yet look like I am in my 40s. It is frustrating!

  8. There is often another side that you don’t get with Dr. Greger. Medical professionals are questioning whether high LDL-C increases the risk of heart attacks. Imagine that Dr. Greger was treating a patient who had just had a heart attack. He would try to smash that person’s cholesterol down to very low levels to prevent another heart attack, right? But a recent Mayo Clinic study found that in patients who had been hospitalized with a heart attack, the higher their cholesterol the lower their mortality compared to those with low cholesterol. Those with high cholesterol had a 24% reduction in mortality. Heart failure patients with high cholesterol had a 20% lower mortality. Not only that, but in cases where there were “comorbidities,” that is, in which patients also had cancer or other serious illness, the higher cholesterol levels were found to be protective. I can recall reading about a British study in around 2013 that found that older individuals with higher cholesterol lived longer.

    The article in which I read about this MC study begins by questioning whether the premise by which statins work is correct. And by the way, statins don’t reduce heart attack risk by 30%, it’s more like 3%. 3% is the absolute risk reduction. Cholesterol reduction with statins doesn’t even result in much lowering of risk of heart attack.

    A couple of years ago, Eli Lilly had a promising drug in 3rd stage clinical trials which failed even though it sharply lowered LDL cholesterol and sharply raised HDL cholesterol. It didn’t prevent heart attacks or hospitalizations. Think about that. Here is the article about the Mayo Clinic study.

    “Is the premise behind statins in error?

    That’s a question arising from a surprising Mayo Clinic Health System study published with little notice last month on the relationship between LDL cholesterol and mortality among survivors of cardiac events.

    The matched case control study, published in December in the journal BMJ Open, looked at the risk of death from any cause for 23,000 patients hospitalized at Mayo Clinic between 1996 and 2015 for either myocardial infarction, or sudden worsening of heart failure.

    After matching 14,000 of these patients according to demographic characteristics, the researchers examined the relationship between mortality and hyperlipidemia, which was defined as LDL greater than 100 mg/dL.

    Current practice guidelines hold that the higher your LDL or so-called “bad cholesterol,” the greater your chances for heart failure and early death. This is the argument for statins, the LDL-lowering medications taken by millions of Americans, as well as the next generation of LDL-lowering medications known as PCSK9 inhibitors, drugs including Repatha.

    “Among patients who had heart attack or heart failure, and who had concurrent hyperlipdemia or no hyperlipidemia, there was a clear difference in mortality,” says Dr. Mohammed Yousufuddin, a specialist in internal medicine for Mayo Clinic Health System in Austin and lead author on the paper. “Patients who had hyperlipidemia had lower mortality than patients who had no hyperlipdemia. That’s the primary finding.”

    Yousufuddin said that high LDL cholesterol decreased the risk of mortality by 24 percent after heart attack, and 20 percent after heart failure. The study also found this seemingly protective effect of high LDL effect was dose-dependent. In other words, the higher the LDL, the lower the risk of mortality after a cardiac event, and the lower the LDL, the higher the risk.

    Finally, the authors found that elevated LDL proved protective for patients with a host of comorbid conditions, including cancer, kidney disease, COPD and diabetes. “When these comorbidities occur in association with concomitant hyperlipidemia,” Yousufuddin said, “the mortalities appear to be attenuated. Patients with cancer who have hyperlipidemia have lower mortality than those who have cancer and don’t have hyperlipidemia. So that’s a very interesting finding.”

    Trials of statins have shown the medications lower the risk of mortality when taken as secondary prevention, which is to say, for those who’ve suffered a cardiac event. The authors believe this positive effect of statins may be due to so-called pleitropic effects, or effects unrelated to the drugs’ lowering of LDL. Like aspirin, statins have anti-inflammatory effects.

    For heart attack patients with high LDL, the authors concluded that “clinical care should not focus on lipid targets; rather, evidence-based secondary prevention strategies should be initiated.”

    “This data is mostly for patients in the hospital with a heart attack,” said Yousufuddin. “Most studies of LDL cholesterol assess the association between high cholesterol and subsequent heart attack in relatively healthy patient populations.”

    That, said, the authors concluded as follows: “Further studies are needed to understand the complex relationship between high LDL and mortality … and to define appropriate (LDL) targets to maximize benefits.”

    1. Alan,

      The research publication does not dispute that higher cholesterol levels are associated with increased heart disease; their question was what is the effect of higher LDL-C >= 100 mg/dL (HPL) on survival AFTER surviving a heart attack.

      Intro: “Although cholesterol levels in general population predict new cardiovascular events, it is unclear whether a positive association persists after incident AMI [Acute Myocardial Infarction] or HF [Heart Failure.]” Conclusion: “The current findings, based on large unselected hospital- based patient-populations, provide strong evidence that after incident AMI or ADHF, a diagnosis of HLP [Hyperlipidemia], compared with no HLP, was associated with reduced long-term mortality, a longer median survival and modest attenuation of the magnitude of mortality risk associated with other competing CCs [Comorbid Conditions].” https://bmjopen.bmj.com/content/bmjopen/9/12/e028638.full.pdf

      I haven’t been able to tell whether those patients diagnosed with HLP at admission to the hospital with a heart attack or within 6 mos prior to having one (the definition of HLP) were treated with different drug regimens or even different procedures at the hospital. Though they do state that “[t]he reductions in mortality were independent of benefit attributable to statin therapy.“

      The authors did mention an “epidemiological paradox. According to epidemiologists, these paradoxes may exemplify collider or index event bias where established risk factor for first occurrence of a disease becomes inversely related after the occurrence of an event.” And that the effect of HLP might be concealed in the presence of stronger competing risk factors for mortality.

      However, it does seem clear that avoiding a heart attack in the first place greatly reduces the chances of dying from one.

      1. You are right Dr. J. The study doesn’t dispute the association between cholesterol and heart disease, it is about cholesterol after a heart attack, but the article begins by questioning the premise that statins reduce the risk of heart disease by lowering cholesterol. That questioning is becoming more widespread, especially since the failure of the Eli Lily experimental drug.
        The view that heart disease is caused by cardiovascular inflammation which is itself caused by insulin resistance seems to be emergent. I have read that the CDC has estimated that 1 in 3 adults are insulin resistant, while UCLA has estimated 1 in 2. This means massive numbers of people with pre-diabetes and diabetes of which they are unaware. These are people who cannot process carbs. The problem is sugar and loading up on carbs that are quickly turned into sugar like bread, pasta, potatoes, grains and junk carbs, high glycemic foods. If you are insulin resistant, it’s questionable whether you should be eating grains and fruit like bananas and grapes, etc. Whatever diet insulin resistant people follow, sugar for these people has to be restricted.

    2. So, follow this analogy. After a tornado, your house is destroyed and you want to put it back together as soon as possible, since there is is no other place to live. Should you take away all the trash pieces so you can get clear access to the damage, or use the pieces to fix things while you are buying more supplies? Some of both!
      Cholesterol is used like cement to fix damaged areas until the healthy endothelium can be repaired. The skin under a scab is not immediately available, it takes some time to repair all the surrounding area (connective tissue, blood vesels, nerves etc.) even though what we see is the skin. Inside is the same. It’s not just the endothelium, or just the two layers of the artery that show damage. The whole body is sick, from head to foot.
      So, early in the repair we need the cholesterol, but a steady diet of plant food will bring the faster repair by not only giving the best building blocks, but the best means to carry away the garbage. But excess LDL is always in the way, and clogs every means of repair.
      Picasso (I think it was him) was asked early in his career why he didn’t paint human nudes as that was the ideal form to show his skill. He looked at the older obese woman who was complaining and inquired which nude she thought might be the best example, “perhaps yours?”. The same might be said of a study which purports to show the best method of healing in a diseased state, as an example to those who are not in the same condition.
      The value of these studies is that we have pieces of broken “houses” after the tornado that we can use temporarily as we make changes to improve our current “frame” and eventually come up with something not only better looking, but lasts longer.

      1. A better analogy is your house is on fire. It’s not gone yet, but you have to take immediate action to put out the fire. What will accomplish that? Eliminating the sugar and all of the carbs that are causing the inflammation in your body and the fire in your arteries.
        Eating a lot of vegetables by itself will not put out the fire. You can be a vegan and still have inflammation if you are consuming a lot of sugar, a lot of simple carbs, even grains. And, I believe that lots of vegans do this very thing. A plant based diet in itself is not going to save the house.

    3. Heart attacks cause cholesterol to decline. The more severe the heart attack, the greater the decline.
      It’s little wonder then simplistic associational studies appear to find high cholesterol ‘protective’.

      You see the same thing in intensive care patients generally. The greater their medical problems, the greater the cholesterol decline and the worse the prognosis.

      None of the cholesterol ‘sceptics’ who infest the internet ever mention these issues -, whether because of ignorance or deliberate decision I don’t know,

      1. I guess you didn’t read my comment about the recent Mayo Clinic study that found that heart attack patients with higher cholesterol lived longer than heart attack patients with lower cholesterol. They didn’t both have low cholesterol. They found that the same was true for heart failure patients. And in both cases, the effect was dose dependent, meaning that the higher the cholesterol, the greater the benefit.

        1. Yes I read your comment. People have been saying the same thing for years. It is based on thoroughly confounded observational studies.

          Heart attacks cause cholesterol levels to decline. So does trauma generally. The more severe the attack, the greater the decline. Of course heart attack patients are going to appear to have low cholesterol, and the more severe the attack, the greater the cholesterol decline and the worse their prognosis is.

          .

  9. Something that is worth knowing about statins and cholesterol. It is often claimed that statins reduce the risk of heart attack by 20-30% by lowering cholesterol. Drug companies love to hear this, but it isn’t true and it’s very deceptive. The real reduction is about 3%.
    You have to know the difference between relative risk and absolute risk. If 10 people out of 100 would have a heart attack without using statins and 7 out of 100 would have a heart attack using statins, this is widely touted as a 30% reduction. It’s not. It’s a 3% reduction, 3 out of 100.
    So, all of that cholesterol reduction results in a reduction of heart attacks in statin users of about 3%! This is what studies show.
    Here is an interesting fact. Scientists don’t know how statins work! Previously, it was thought they worked by reducing cholesterol. Now the view is gaining support that statins work by reducing inflammation, because they have properties similar to aspirin. But, as I say, statins are still largely ineffective. The public has been hoodwinked into believing otherwise. As I mentioned in another comment, the Eli Lilly drug that failed in 3rd stage clinical trials, even though it greatly reduced LDL and raised HDL raised a lot of skepticism about the role of cholesterol in causing heart attacks, and heart disease. It may play a role, but probably not a causative role. And the Mayo Clinic study I mentioned in my other comment suggests that we may be harming ourselves by lowering cholesterol and even more so when we are older.

    1. This issue has been studied multiple times around the world by panels of experts. They have all concluded benefits outweigh risks and that in appropriate target groups and circumstances statins are a cost effective option.

      In the UK for example, where the government heavily subsidises approved prescription drugs, they found that statins reduced net adverse events (deaths, heart attacks, strokes) and should continue to be prescribed and subsidised because of the net benefits to population health and total health expenditure.

      https://www.nice.org.uk/guidance/CG181

      As for older people, the American College of Cardiology observes

      ‘There are good reasons to believe that the magnitude of benefit with statins may be substantial in elderly people. As the relative risk reduction with statin therapy is similar for those at low and high risk of ASCVD, the absolute benefit of treatment with statins is highly dependent on absolute ASCVD risk. Even in case of a smaller relative benefit with statin therapy in the elderly, the absolute benefit is likely higher because of the higher risk for CVD events.’
      https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2018/01/02/17/14/primary-prevention-with-statins-in-the-elderly

      1. Are you familiar with the concept of NNT, number-needed-to-treat? I can’t produce all of the evidence here to show how ineffective statins are, but the following quote which was a letter to the editor of the journal or magazine, American Family Physician shows how limited statins are in helping people to avoid heart attacks.

        to the editor: “In this “Tips from Other Journals,” Dr. Crawford-Faucher reviewed the meta-analysis by Brugts and colleagues that concluded that statins are beneficial for primary prevention of cardiac disease.1 I agree with this conclusion, but with some reservations. The review stated that the relative risk reduction for all-cause mortality was 12 percent, which sounds very good; however, I think it is important to look at the absolute risk reduction. All-cause mortality after a mean follow-up of 4.1 years was 5.1percent in the group treated with statins and 5.7 percent in the control group. That translates into an absolute risk reduction of 0.6 percent and a number needed to treat (NNT) of 167. This means that 167 patients would need to be treated with a statin for 4.1 years to prevent one death. Additionally, based on the study data, the NNT to prevent one major coronary event is 77, and the NNT to prevent one major cerebrovascular event is 250.” Grant Phillips MD

        1. Yes. of course I am familiar with NNT. The subject is thoroughly discussed in that UK guidance I linked. Note that the NNT will be different according to whether we are talking about primary or secondary prevention and according to the patient’s assessed level of risk

          CG181 also produces a combined NNT figure (ie death, non-fatal heart attack, non fatal stroke etc). It even provides a patient decisions aid covering this specific issue and accompanying guidance for physicians
          https://www.nice.org.uk/guidance/cg181/resources/patient-decision-aid-user-guide-pdf-243780158
          https://www.nice.org.uk/guidance/cg181/resources/cg181-lipid-modification-update-patient-decision-aid2

          Claims that NNT is an issue that is unknown to or ignored by mainstream medical science, cholesterol guidelines and treating doctors around the world is another misleading claim by these cholesterol ‘sceptics’

  10. I have to respectfully disagree. I think inflammation is the cause of cardiovascular disease, just as it is with many of the chronic illnesses of older people. In January 1996, I had a double by-pass. It was caused by stress, both personal and job related, lack of sleep and a low fat, high carb diet. I retired at 60 in the year 2000. In 2003, I came across some books that change my whole approach to diet. As a result I became a pesca-vegetarian. My dietary guidelines are quite simple: 1. eat the most nutrition consuming the fewest calories; 2. for the plant part of my diet, eat a combination of vegetables that results in a carb-to-fiber ratio no greater than 5:1; and 3. consume foods, including fish high in omega-3, that produce an omega-6 to omega-3 ratio no greater than 4:1. I wish at the time of my operation, I had the hs-CRP test, but I only started taking them in 2013. I have not had one higher than <0.3 mg/L Some have been as low as <0.2 mg/L.

    Since retirement, I have had a stress-free life. I do high intensity interval training 3 days a week and weight training 5 days a week. I mostly do free weights and always max out the total weight for each exercise.

    In recent years there have been studies in a number of countries that appear to indicate that, for people over sixty, those with the highest cholesterol have the lowest all-cause mortality and those with the lowest cholesterol have the highest all-cause mortality. My latest results indicate Total and LDL cholesterol are on the high side ~221 and ~138 mg/dL, respectively. However, my HDL and triglycerides are great at ~72 and ~57 mg/dL, respectively. My Omega-6 to Omega-3 ratio was 2.6:1. At almost 80 years old, my testosterone is thru the roof at 1174 ng/dL with the reference range of 264-916 based upon non obese males between 19 and 39 years old. Insulin is 4.0 uIU/mL with the range 2.6 to 24.9. Body fat between 9 and 11 percent.

    Be HAPPY!

    1. ‘In recent years there have been studies in a number of countries that appear to indicate that, for people over sixty, those with the highest cholesterol have the lowest all-cause mortality and those with the lowest cholesterol have the highest all-cause mortality’

      This is not ‘recent years’, it has in fact been known for many decades.and investigated. The online cholesterol ‘sceptics’ and authors of sensational books don’t like to mention it however. For example see

      ‘A J- or U-shaped relation between blood total cholesterol (TC) level and all-cause mortality has been reported in several1234567891011121314151617181920 but not in other21222324252627282930313233 studies. The reports of inverse relations have caused some alarm and controversy about the implications of low TC in the general population.34353637

      Three interpretations of this association are possible. One view is that a low TC level plays an etiologic role in a variety of nonatherosclerotic diseases (direct causality). Another possibility, however, is that the low TC–mortality relation is attributable to a hypocholesterolemic effect of disease in a preclinical stage (reverse causality). Finally, the association between low TC and mortality may be due to other unmeasured or unknown factors related to both low TC and disease (confounding).38394041 With a few exceptions,48 earlier studies on this topic have not adequately addressed the direct versus reverse causality problem, largely because most statistical analyses were based on a single measurement of TC. Consequently, inferences about temporality could not be made.

      Previous studies in the Honolulu Heart Program (HHP) relating baseline TC with subsequent 9-year,7 13-year,8 and 17-year37 mortality demonstrated inverse relations of TC with hemorrhagic stroke, liver disease, chronic obstructive lung disease, and cancers of the esophagus, colon, liver, and hemopoietic system. The relations for cancer and benign liver disease were stronger in the first 5 years and showed flattening when deaths in the first 5 years of follow-up were deleted.

      …………………………….

      The hypothesis of reverse causality, that low TC is a consequence of disease, would be compatible with a situation in which a declining TC level (resulting from catabolic diseases such as cancer or liver disease), not stable low level, would be related to subsequent mortality. Stated differently, a declining TC level would probably be caused by disease, whereas a stable low TC level would be the result of dietary, lifestyle, or genetic factors.

      …………………………………..

      Conclusions These results add strength to the reverse-causality proposition that catabolic diseases cause TC to decrease.’

      https://www.ahajournals.org/doi/full/10.1161/01.cir.92.9.2396
      https://www.ahajournals.org/doi/full/10.1161/01.cir.92.9.2396

      1. What I have not found are studies that included “inflammation” in a study of all cause mortality in people with high cholesterol versus those with low cholesterol. I would have loved to have known my inflammation level when I had my heart incident, but that was in 1996 when inflammation was not generally recognized as a risk factor. I suspect it was quite high, as I also suspect that my triglycerides were also high, because consuming a low fat diet, as I did, I was consuming foods, many processed, which I now avoid like the plague, that were high in sugar and simple carbs. Today, I have no trouble fasting for 24 hours. Today I eat to live, not live to eat.

        1. There are various markers of inflammation. The best known is probably C reactive protein but there are quite a few others including fasting insulin levels. People don’t necessarily score high on all other markers if they score high on one though.

          However, high cholesterol itself appears to cause arterial inflammation through cholesterol and phttps://www.heart.org/en/health-topics/consumer-healthcare/what-is-cardiovascular-disease/inflammation-and-heart-diseaselaque deposition.

  11. Alan,

    Your comment stated that “Like aspirin, statins have anti-inflammatory effects.” So do plant foods, as noted for example here: https://nutritionfacts.org/video/plants-with-aspirin-aspirations/ Which makes me wonder: how effective are statins in those who eat WFP?

    And the two different risks you mention are relative risk and absolute risk. In your hypothetical example, where statins decrease death rate from 10% to 7%, the absolute risk is decreased by 3%, whereas the relative risk is decreased by 30% (3 out of the 10 patients who would otherwise have had heart attacks did not, due to taking statins). But 7 out of 10 patients taking statins still have heart attacks. A point that seems to be finessed when discussing drug treatments for lifestyle conditions/diseases, instead of discussing lifestyle.

    I’ve forgotten what the risk reduction is in mortality: how many patients do not die from a heart attack, because they are taking statins? Because to me, that is the gold standard: avoiding premature death. As well as disability, or decreased quality of life.

  12. OK, forget all the good/bad, cholesterol damaging vs protective, inflammation… arguments. Dr. G, you’re drawing a false conclusion in your article.

    Just because this group has genetics that naturally results in lower cholesterol levels and they have less of a problem with heart disease doesn’t mean that lower cholesterol (for a longer time) = lower heart disease. It just means that as a group those people have something that is protecting them, it could be genetic like maybe it is the cholesteral (and you’re correct), or maybe it’s that the genes that lower their cholesterol also lower systemic inflammation, but it could be behavioral like they’re never told that they have high cholesterol and eat more eggs and cholesterol-laden foods and they end up protecting them by better supporting the endocrine system (cholesterol is metabolized into the hormones in our bodies need).

  13. I’m surprised that you don’t address the type of cholesterol. Are they hard dense particles or soft fluffy. Also what foods cause the hard dense particles and which ones keep them large soft and fluffy and non artery clogging. The research is 100 percent there! Please do that research if you want to be credible. Hint, look to white sugar, white flour, processed foods loaded with chemicals and colors and artificial food- like substances in them. They are the culprits of hard dense particles. The kinds that kill you! It’s not because we are a societiy deficient in staten drugs. (The drugs that keep our drug companies pockets loaded.) Sorry but I think you have been doing the wrong homework!!! Might start with Mark Hyman. He’s done the right research!

    1. Seems to me Mark Hyman is on the Fumbles “bad” list. He and more than a dozen others for various reasons.

      Am wondering who (other than Dr. G.) is on his good (“reputable”) list.

      1. It’s about what the medical science shows. Hyman espouses views that are simply quackery, for example his claims about cholesterol. He appears not to know that heart attacks cause cholesterol to decline (or chooses not to mention it for whatever reason) eg
        https://journal.chestnet.org/article/S0012-3692(16)35525-8/fulltext

        I have a vague recollection that angina also causes cholesterol to decline but can’t put my hand on a study at the moment.

        Given your belief in astrology,’ medical intuitives’, channelled supernatural entities and Akashic records, I’m not sure that you are a good person to judge the scientific credibility of opinions expressed/promoted by people like Hyman. You do seem to have a fondness for plausible health gurus though.

        1. Hmmm. Fumbles, I think you have me confused with your former wife. You once posted that she believed a lot of this “silly balderdash.” Or words to that effect.

          I don’t recall ever mentioning the Akashic records at this site, but that’s not saying I disbelieve in them.

      1. * Sorry, meant to say Dr Greger has done thousands of videos on hundreds of topics … use the search feature to find videos that interest you. He did a video on the question of cholesterol size, and I posted the link , above.
        Thanks.

  14. That 100 research papers Dr Greger referred to. I wonder if he has any comments to make to Prof Loannidis comments that 90 pct of medical research papers are inaccurate and I wonder how many of that 100 research papers are funded by pharmaceutical companies:

    Loanannidis and Nicholson argue that the peer-review process, in which groups called study sections review and rank research applications submitted by their colleagues, is INHERENTLY FLAWED and ENCOURAGES “CONFORMITY, if not MEDIOCRITY.”

    https://scopeblog.stanford.edu/2012/12/05/nih-funding-mechanism-totally-broken-says-stanford-researcher/

      1. I respectfully disagree with your counter question. That report you mention may also be funded by pharmaceutical companies. I agree with some of the writers here. The difference in mortality between taking statins and not taking statins in a mere 3 pct and these are findings from pharmaceutical companies. 3 pct is within experimental error. Heart diseases are due to inflammation and not cholesterol levels

        1. Why can there only be one cause of heart diseases?

          In reality, there are multiple risk factors. Posing a false dichotomy between high cholesterol and inflammatory is a cynically deceptive tactic. Cholesterol itself is inflammatory.

          Why don’t you read the scientific evidence instead of just believing smooth-talking characters on YouTube and the authors of sensational books?
          https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehz962/5735221
          https://academic.oup.com/eurheartj/article/38/32/2459/3745109

          1. You sounded very much like some strong supporters of pharmaceutical companies in your replies. I have read books by medical professionals as reputable and professional as Dr Greger for example Dr Perlmutter, Dr Thomas Cowan and many others. You must be aware that we all need cholesterol for lots of body functions including our cell integrity, hormones etc..
            Too much carbohydrates can result in cholesterol too by the malvonic route. One need a balance in food intake and not depend on statins which can have bad effects like that Space Doc who created a website to warn the public.. you do sound like a very strong supporter of pharmaceutical companies when Nutrition Facts is supposed to be more towards a plant based diet…

            1. Perlmutter is hardly a credible source of information on anything. He seems willing to willing to write (and sell) any old tosh as long as he can make a buck from it
              https://www.thecut.com/2015/06/problem-with-the-grain-brain-doctor.html

              At least though, he didn’t have his medical licence revoked for “unprofessional conduct” and “gross negligence” in 2017 like Thomas Cowan. Cowan is also apparently a bigwig in the Weston Price Foundation, a vociferous group of appalling cranks. Again, hardly a reputable or credible source of information.

              It’s little wonder such people are so desperate to explain away the scientific evidence that refutes their claim that they they have to resort to ludicrous conspiracy theories.that the entire world’s scientific and medical communities have been deliberately deceived for the last hundred years or so by Big Pharma or the NWO or whatever,

              Instead of spending your hard-earned money on books setting out the claims and assertions of money hungry quacks and alternative health cranks, Why not just read major international reports on the evidence on nutrition and health, and on cholesterol? They are written by panels of world class experts who actually know what they are talking about. They are also free to read and download.

              if there was any truth in the nonsense peddled by these people you’d think that the Iranians, Communist Chinese, North Koreans, Cubans or Venezuelans would have taken these ideas up and run with them them. They haven’t. That’s because those guys might be crazy but they aren’t stupid.

  15. I am curious as to the post-menopause effect on total cholesterol. There is little research on it but there are many who acknowledge it increases as we age. My Total went from under 200 to 260. It goes back and forth each week to 229, 235, or other. My HDL are >100. I would not touch a statin if it was the last med on earth. My doctor is fine with my HDL and ratio.
    I now it goes lower when I exercise every day and hone in my food and increase fiber. I eat clean, organic, veggies, fruits, some grains and wild salmon.

  16. Dear Dr Greger
    A recent study of older people came out with the following findings:
    “The elderly with the lowest quartile of TC (<175 mg/dL), HDL cholesterol (<43 mg/dL) and LDL cholesterol (<100.4 mg/dL) were at higher risk of all-cause mortality."
    https://journals.lww.com/md-journal/Fulltext/2019/12060/Plasma_lipid_concentrations_and_survival_in.25.aspx
    Can you comment on this in the light of your highlighting that lower cholesterol lowers all cause mortality.
    Thanks in advance
    David
    india.david@gmail.com

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