Dietary Cholesterol Myth: Saturated Fat is Not An Enemy | Chris Kresser

The Diet-Heart Myth: Cholesterol and Saturated Fat Are Not the Enemy

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To read more about heart disease and cholesterol, check out this eBook on the Diet–Heart Myth.

It’s hard to overstate the impact that cardiovascular disease (CVD) has in the U.S.. Consider the following:

  • Cardiovascular disease affects 65 million Americans.
  • Close to one million Americans have a heart attack each year.
  • In the U.S., one person dies every 39 seconds of cardiovascular disease.
  • 1 of 3 deaths that occurs in the U.S. is caused by cardiovascular disease.
  • 1 in 3 Americans have metabolic syndrome, a cluster of major cardiovascular risk factors related to overweight/obesity and insulin resistance.
  • The total cost of cardiovascular disease in 2008 was estimated at $300 billion.

To put that last statistic in perspective, the World Health Organization has estimated that ending world hunger would cost approximately $195 billion. One might argue that the $300 billion we spend on treating cardiovascular disease in the U.S. is a necessary expenditure; however, a recent study which looked at the relationship between heart disease and lifestyle suggested that 90% of CVD is caused by modifiable diet and lifestyle factors. (1)

Unfortunately, cardiovascular disease is one of the most misdiagnosed and mistreated conditions in medicine. We’ve learned a tremendous amount about what causes heart disease over the past decade, but the medical establishment is still operating on outdated science from 40-50 years ago.

In this 4-part series, I’m going to debunk 3 common myths about heart disease:

  1. Eating cholesterol and saturated fat raises cholesterol levels in the blood.
  2. High cholesterol in the blood is the cause of heart disease.
  3. Statins save lives in healthy people without heart disease.

In the fourth and final article in the series, I’ll discuss strategies for naturally protecting yourself against heart disease and improving your heart health.

Myth #1: Eating Cholesterol and Saturated Fat Raises Cholesterol Levels in the Blood.

Most of us grew up being told that foods like red meat, eggs and bacon raise our cholesterol levels. This idea is so deeply ingrained in our cultural psyche that few people even question it. But is it really true?

The diet-heart hypothesis—which holds that eating cholesterol and saturated fat raises cholesterol in our blood—originated with studies in both animals and humans more than half a century ago. However, more recent (and higher quality) evidence doesn’t support it.

Cholesterol and saturated fat: dietary enemies or innocent victims of bad science?Tweet This

On any given day, we have between 1,100 and 1,700 milligrams of cholesterol in our body. 25% of that comes from our diet, and 75% is produced inside of our bodies by the liver. Much of the cholesterol that’s found in food can’t be absorbed by our bodies, and most of the cholesterol in our gut was first synthesized in body cells and ended up in the gut via the liver and gall bladder. The body tightly regulates the amount of cholesterol in the blood by controlling internal production; when cholesterol intake in the diet goes down, the body makes more. When cholesterol intake in the diet goes up, the body makes less.

This explains why well-designed cholesterol feeding studies (where they feed volunteers 2-4 eggs a day and measure their cholesterol) show that dietary cholesterol has very little impact on blood cholesterol levels in about 75% of the population. The remaining 25% of the population are referred to as “hyper-responders”. In this group, dietary cholesterol does modestly increase both LDL (“bad cholesterol” and HDL (“good cholesterol”), but it does not affect the ratio of LDL to HDL or increase the risk of heart disease. (2)

In other words, eating cholesterol isn’t going to give you a heart attack. You can ditch the egg-white omelettes and start eating yolks again. That’s a good thing, since all of the 13 essential nutrients eggs contain are found in the yolk. Egg yolks are an especially good source of choline, a B-vitamin that plays important roles in everything from neurotransmitter production to detoxification to maintenance of healthy cells. (3) Studies show that up to 90% of Americans don’t get enough choline, which can lead to fatigue, insomnia, poor kidney function, memory problems and nerve-muscle imbalances. (4)

What about saturated fat? It’s true that some studies show that saturated fat intake raises blood cholesterol levels. But these studies are almost always short-term, lasting only a few weeks. (5) Longer-term studies have not shown an association between saturated fat intake and blood cholesterol levels. In fact, of all of the long-term studies examining this issue, only one of them showed a clear association between saturated fat intake and cholesterol levels, and even that association was weak. (6)

Moreover, studies on low-carbohydrate diets (which tend to be high in saturated fat) suggest that they not only don’t raise blood cholesterol, they have several beneficial impacts on cardiovascular disease risk markers. For example, a meta-analysis of 17 low-carb diet trials covering 1,140 obese patients published in the journal Obesity Reviews found that low-carb diets neither increased nor decreased LDL cholesterol. However, they did find that low-carb diets were associated with significant decreases is body weight as well as improvements in several CV risk factors, including decreases in triglycerides, fasting glucose, blood pressure, body mass index, abdominal circumference, plasma insulin and c-reactive protein, as well as an increase in HDL cholesterol. (7)

If you’re wondering whether saturated fat may contribute to heart disease in some way that isn’t related to cholesterol, a large meta-analysis of prospective studies involving close to 350,000 participants found no association between saturated fat and heart disease. (8) A Japanese prospective study that followed 58,000 men for an average of 14 years found no association between saturated fat intake and heart disease, and an inverse association between saturated fat and stroke (i.e. those who ate more saturated fat had a lower risk of stroke). (9)

That said, just as not everyone responds to dietary cholesterol in the same manner, there’s some variation in how individuals respond to dietary saturated fat. If we took ten people, fed them a diet high in saturated fat, and measured their cholesterol levels, we’d see a range of responses that averages out to no net increase or decrease. (If dietary saturated fat does increase your total or LDL cholesterol, the more important question is whether that’s a problem. I’ll address that in the next article in this series.)

Another strike against the diet-heart hypothesis is that many of its original proponents haven’t believed it for at least two decades. In a letter to the New England Journal of Medicine in 1991, Ancel Keys, the founder of the diet-heart hypothesis said (10):

Dietary cholesterol has an important effect on the cholesterol level in the blood of chickens and rabbits, but many controlled experiments have shown that dietary cholesterol has a limited effect in humans. Adding cholesterol to a cholesterol-free diet raises the blood level in humans, but when added to an unrestricted diet, it has a minimal effect.

In a 2004 editorial in the Journal of American College of Cardiology, Sylvan Lee Weinberg, former president of the American College of Cardiology and outspoken proponent of the diet-heart hypothesis, said (11):

The low-fat, high-carbohydrate diet… may well have played an unintended role in the current epidemics of obesity, lipid abnormalities, type 2 diabetes, and metabolic syndromes. This diet can no longer be defended by appeal to the authority of prestigious medical organizations.

We’ve now established that eating cholesterol and saturated fat does not increase cholesterol levels in the blood for most people. In the next article, I’ll debunk the myth that high cholesterol in the blood is the cause of heart disease.

Research Spotlight: Health Coaching and Heart Health

Behavioral Counseling Dose-Dependently Improves Blood Lipid Levels

Oxidized low-density lipoprotein (LDL) cholesterol plays a critical role in the development of cardiovascular disease (CVD). High circulating levels of LDL cholesterol increase the likelihood that LDL may become oxidized, contributing to CVD pathogenesis. Diet and lifestyle changes have been found to reduce LDL cholesterol, but many patients have trouble sustaining nutrition and lifestyle changes over the long term. Behavioral counseling may help patients at risk for CVD maintain a healthy diet and lifestyle behaviors, and thus support improved long-term health outcomes. A 2019 study sought to examine the combined effects of behavioral counseling and healthy lifestyle changes on LDL cholesterol levels in adults with prehypertension and stage 1 hypertension, who are at an elevated risk of CVD.

Study Summary

  • Seven hundred fifty-six adults with prehypertension and stage 1 hypertension were randomized to one of three groups:
    • Advice-Only Group: Participants were given information about nutrition and lifestyle approaches for improving CVD risk factors, including dietary sodium restriction, weight loss, exercise, and a “healthy diet.”
    • Established Lifestyle Intervention Group: Participants were educated about healthy diet and lifestyle changes and provided with behavioral counseling.
    • Established + Dietary Approaches to Stop Hypertension (DASH) Lifestyle Intervention Group: Participants were instructed about healthy diet and lifestyle changes, behavioral counseling, and the DASH diet.
  • Subjects in the “Established Lifestyle Intervention” and “Established + DASH Lifestyle Intervention” groups experienced significant reductions in LDL cholesterol, triglycerides, and total cholesterol after six months compared to the “Advice-Only” group.
  • For every 10 sessions of behavioral counseling, LDL cholesterol decreased by 6.2 mg/dL.
  • The relationship between the number of behavioral counseling sessions attended and reductions in LDL cholesterol and triglycerides was mediated by a decrease in waist circumference, suggesting that the combination of behavioral counseling and lifestyle changes reduces visceral adiposity.

Key Findings

A combination of healthy lifestyle changes and behavioral counseling can reduce LDL cholesterol in individuals with hypertension and may thus reduce their future risk of CVD. Attending more behavioral counseling sessions appears to lead to more significant improvements in CVD risk factors. Frequent health coaching sessions, combined with the administration of nutrition, exercise, sleep, and stress reduction advice, may be a valuable model for improving long-term health in people with CVD risk factors.

Reference: Dose-dependent effects of lifestyle interventions on blood lipid levels: Results from the PREMIER trial.

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546 Comments

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  1. Hi Chris, Great article, waiting for the next installment. Will you be addressing fibrinogen levels in this series? How it gets raised and how best to lower? I think you recommend 200-300 and I have just discovered mine is 5.5 which I presume is 550. I asked for a clotting test as eat/drink lots ginger, herbal teas, take curcumin and had been worried that I may have a clotting problem. Clotting 29 secs but I got a shock when I saw the fibrinogen.

  2. Chris, great insights as usual. I am a big Paleo fan and have increased my egg consumption accordingly. However, a recent article in the Natural Medicine Journal (noted below) reported that dietary intake of choline was linked to a 70% increased risk of prostate cancer death. The article also mentions beef and chicken. Interested in your thoughts regarding the findings. Personally, I have always recommended patients be more concerned about the sources of the foods they eat (i.e. organic, grass fed, open range…). Thank you again for your insights. They are shared regularly with our patients!

    http://www.naturalmedicinejournal.com/article_content.asp?article=411

    • I’ll address this soon, or Chris Masterjohn will. He’s more of an expert in choline metabolism than I am.

  3. Chris, will this post be picked up by the Huffington Post??? This is a subject that truly needs to get out into the mainstream more!

  4. Always a pleasure to read your articles Chris,

    Would you say it is possible or even somewhat likely that a 23 year old male has a TC of 9.74mmol/L, TG 1.18mmol/L, HDL 1.51mmol/L, LDL 7.69mmol/L and ApoB 2.03g/L WITHOUT having Familial Hypercholesterolemia?

    • I personally know several people with cholesterol levels above 7mmol/L (One has a TC of 13mmoml/L). They all have Familial Hypercholesterolemia and are on statins because of it.

  5. Great article. Finally something I can pass something onto my dad – something the layman understands that also goes into the nuances of sub groups (hyper responders) within a population. Thanks

  6. This is the awesome post! I have been telling people that weight loss is about knowing what to eat. Even junk food, people call, could help to lose weight if we know which one to eat. Well, the post like yours can help so many people to lose weight, Thanks for the great post!

  7. While I’m in no way opposed to your message you have not established that eating cholersterol or sat fat does not increase the risk of heart disease – as far as I can see (correct me if I am wrong) – you have established that eating cholesterol or sat fat does not contribute to a ‘worsening’ of biomarkes associated with risk of cardiovascular dieseases

    • The intention of this series is to debunk the diet-heart hypothesis. The diet-heart hypothesis states that saturated fat and cholesterol in the diet raise cholesterol levels in the blood, and that high cholesterol levels in the blood cause heart disease. In this article I showed that saturated fat and cholesterol do not (for most people) raise cholesterol levels in the blood. In the next article, I’ll show that high cholesterol is not the cause of heart disease (though it is associated with heart disease, and can be a proxy marker for LDL particles, which is the driving factor).

      The question of whether saturated fat causes heart disease via some mechanism that doesn’t involve serum cholesterol is not one I’m addressing in this series. That said, there are large, prospective studies with >300,000 participants that show no association between saturated fat and heart disease. Like this: http://www.ncbi.nlm.nih.gov/pubmed/20071648?dopt=AbstractPlus

      • That’s great – and in total concordance with what I wrote. I have a lot of respect for you and your work – and thanks for the link 🙂
        Yet it still stands that your penultimate sentence in the article: “We’ve now established that eating cholesterol and saturated fat does not increase the risk of heart disease for most people.”
        is incorrect – you have shown no such thing (unless I have misread something).
        Don’t take this as more than it is – I just thought that you would want to be called out, when you make somewhat overblown claims – everybody needs to be kept in check – even the best of us 😉

        • There’s never been strong evidence suggesting that eating cholesterol increases the risk of heart disease. Early studies did suggest that eating saturated fat increased the risk, but later, larger, better-designed studies (which I added to this article; see the paragraph beginning with “If you’re wondering…) have not shown an association. Therefore eating cholesterol and saturated fat does not increase the risk of heart disease for most people.

      • It seems strange to me that many (at least 11 out of 24) of the studies included in that meta-analysis adjusted for total cholesterol, and a few even for “blood lipids” or LDL even (see Table 3). Saturated fat consumption causes changes in these things (at least in some people, and driven by this, on average), and these things on their own correlate adversely with heart disease at least in some studies. So “adjusting” for these (depending on how exactly they adjusted) may be inappropriate.

        This is a similar issue to the recently hotly debated issue of whether endurance exercise starts to have negative marginal returns to long-term health after a certain dosage (something like 2-3 hours a week and 8m/mile pace, on avg). Apparently, some of those studies “adjust” for bodyweight, and even blood lipids, both of which are generally positively causatively altered by the treatment variable being studied.

        I don’t know enough about how they are going about these adjustments, but if they are doing it naively (i.e. controlling for them), then this seems statistically invalid.

        Thoughts?

      • “We’ve now established that eating cholesterol and saturated fat does not increase cholesterol levels in the blood for most people.”
        “In this article I showed that saturated fat and cholesterol do not (for most people) raise cholesterol levels in the blood.”
        -This is just inaccurate. You did not show anything other than your interpretation of the data. There is research that shows otherwise: http://www.lipidworld.com/content/10/1/181
        Blood cholesterol certainly increases after eating a high fat/cholesterol meal. The body adjusts to produce less cholesterol and clear it from the blood, but if someone is eating high fat/cholesterol meals on a daily basis, they will have high levels of fat/cholesterol in the blood on a daily basis.
        I support some of the ideas of this article, but it has not shown what it claims to have shown.

        • So right, Jake. Eating lots of fat doesn’t affect people much who already have high cholesterol levels (over 150 mg/dl). Their blood is already milky with fat, in such a state of inflammation already, that the body can hardly respond further to even more fat intake. Since practically everyone on this site has cholesterol over that level, it appears, they are already in the danger of future heart events, according to The Framingham Study, our longest and most reliable heart study. However, if you get your cholesterol below 150 – easy if you are eating lots of vegetables and minimal animal foods (like a great many of the more traditional ‘masses’ over history) – then you can see that fat pushes cholesterol up a lot. The Framingham Study showed that no one who had cholesterol under 150 ever had any sort of heart event. It is our best indicator of risk. I’m not saying it is the CAUSE of heart disease – just a clear indicator.

          • Please check your knowledge on particle size subclasses, and particle numbers versus cholesterol numbers, and also remember that the meal included 15 ml of syrup, which must have increased the triglycerides.

          • “Eating lots of fat doesn’t affect people much who already have high cholesterol levels (over 150 mg/dl)”

            A cholesterol level over 150 mg/dL is not considered high. High cholesterol is considered to be a total cholesterol level of 240 mg/dL or higher; while 200 mg/dL to 239 mg/dL is considered borderline high. Less than 160 mg/dL is considered low, which is most certainly not healthy. Maybe a cholesterol level below 150 mg/dL does minimize heart disease risk; although there is still some risk of heart disease even with a cholesterol level below 150 mg/dL — and the risk of heart disease actually starts to increase slightly once TC falls below 140 mg/dL. However, the all-cause risk of death is lowest at a total cholesterol level of 180 mg/dL to 199 mg/dL and starts to significantly increase once TC falls below 160 mg/dL. To see the overall mortality risks associated with total cholesterol, go to http://thehealthycow.blogspot.com/2013/05/women-cholesterol-and-heart-disease.html and look at the first chart, which is based on the MRFIT study on cholesterol, which compared the mortality in 350,977 men ages 35-57. I don’t know about you, but I’d rather minimize my all-cause risk of dying rather than just my risk of dying of heart disease.

      • I guess I’m not most people then because saturated fat most definitely raises my LDL. I take fish oil (about 3g/day) so as a polyunsaturated I am assuming this has a lowering effect?

      • Isn’t it true that you can’t use a cross sectional design to show correlation between diet and heart disease because of individual variability?? the appropriate design for demonstrating or refuting diet and heart disease is a dietary change experiment, which have been done and all implicate dietary saturated fat. hence the lower saturated fat guidelines from basically every major medical authority.

        Ronald M Krauss: Funded by the national dairy council since 1989 receives research support from the National Cattleman’s Beef Association and the Robert & Veronica Atkins Foundation.

        They didn’t need to falsify data, they knew beforehand the limitations of observational studies

  8. I don’t actually think there’s enough data here to have “established that eating cholesterol and saturated fat does not increase the risk of heart disease.”
    There’s enough to say that it seems unlikely, and that claims that dietary cholesterol and/or saturated fat will increase the risk of heart disease are unjustified.

        • How to decrease your chances of artery plaque: Limit added sugars, processed foods, and anything with the terms “hydrogenated,” “shortening,” “lard,” or “fractionated” anywhere in the ingredients. Also, achieve or maintain a healthy body fat percentage. You can calculate your body fat percentage and category at https://sites.google.com/site/calculateyourbmi/all-calculators/body-fat-percentage-excel_version . If you already know your body fat percentage, enter your age and gender into the calculator, then go to the “Goal Waist Size Calculator” tab and compare your body fat percentage with the ranges in the table at the top.

          To minimize your risk of having a heart attack or stroke from artery rupture, achieve or maintain a blood pressure below 120/80. However, do not go below 90/60, as that could cause other health risks related to low blood pressure.

          • John,

            I agree with three of the four terms, but not lard (and I’m Jewish!). Even if the fatty acids in it were mostly saturated, research finds that it still wouldn’t be bad. However, the plurality of fatty acids are monounsaturated, which are the same type that give olive oil its beneficial qualities. (I still feel that saturated fats are best for you, though).

  9. Thank you so much for putting together this 3-part series Chris. This is exactly the information I’ve been sharing with friends and clients for years. Until now, it has been challenging to find a complete review of these topics that the average person could read and understand rather quickly. I have been sending people over to “The Daily Lipid” (which is a great site and information source) but the average consumer cannot easily understand the articles there without a strong background in nutrition and science. Looking forward to the next 2 posts, thanks again!

    • Thanks, Eric. That’s exactly the point of this series: a concise group of articles in language the layperson can understand. I’ve decided to add a fourth article, which will cover natural prevention of heart disease.

  10. Thanks again for connecting the dots and trying to get the truth out. Came accross the following UK double blind study and all kinds of living anecdotal evidence, including my own in support of your reports this study astounded even me.
    As I understand it as little as 3 servings per week change to grass fed, for 1 month benefited the participants.
    Heart health ( long chain Omega 3’s benefiting blood, body and brain)—Study shows healthy improved blood results after one month of eating grass fattened beef compared to grain fattened–http://journals.cambridge.org/abstract_S0007114510003090

  11. Chris – Some people may not realize that women present very differently with cardiac problems than do men. They have fewer and different symptoms which could be missed even by medical practitioners.
    Sheila

  12. So grateful for anyone who writes about this subject! My blood boils whenever someone talks about being on a “low fat” diet. Much more education is needed. Keep up the great work, Chris!

  13. Hi Chris,

    Great blog. I have several autoimmune diseases including Crohn’s and eczema. I’ve been on the GAPS diet for about 8 months and also using LDN. It took me several months to realize that I was having a severe reaction to organic lard. I am unable to digest any fats; including lard, avocado, coconut oil, etc. I seem to fine with the fat that comes with beef, chicken and duck but only in small amounts. Is this a liver issue?

    Another issue that confuses me is that a few months ago I would be able to enjoy a nice rare steak. Now I am unable to eat any type of red meat unless it extremely well done – meaning absolutely no juices in it. If I don’t I begin to get severely itchy mouth and throat – verging on anaphylaxis. I haven’t been able to find any reference to such a reaction. Do you have any thoughts on it? It doesn’t matter if it is organic or not and also I have tested how fresh the meat is.

    Any help would be appreciated.

    Evram

  14. I can’t wait either. I’ve been Primal/Paleo – ish for the last couple of years – best thing I ever did (thank you Mark Sisson!). Even the healthiest version of the SAD was making me diabetic. Recently learned that while I have typical risk for TIID I have elevated risk markers centered around insulin production (2 diabetic immediate family members, too). But I got my cholesterol numbers for the first time. Total = 210; HDL = 51; Trigs = 45; LDL = 150 (Friedewald formula which won’t work for me – TGs are too low and miscalculates LDL. Iranian: LDL 116. My ratios are good – could even make them better if I was to go 100% strict. I eat hellacious amounts of fat, mostly saturated fat. My carbs are up and down and good and bad. I was completely shocked to learn that LDL isn’t even measured, it’s calculated. Here’s N=1 to eating lots of cholesterol and sat fat will not destroy your numbers. NEXT STEP: VAP test! Meanwhile I’ll be trying to find out why my TSH is 1.000 with everything else smack in the middle of the lab ranges (based on sick people). Thanks to you Chris, I have knowledge that it is probably due to some adrenal issues. I know me and that would make complete sense.

    • And thank you for a comment in an old post about directlabs.com. That is where I’m purchasing my tests.

      • I read that below 1.8 for TSH is out of the “functional” range while still in the lab range. I’m trying to figure out what that means.

        • It’s true that some people consider TSH lower than 1.8 to be abnormal, but I wouldn’t be concerned if your free T4 and free T4 are normal and you don’t have symptoms, unless your TSH is below 1.

    • Hold off on the VAP test. There’s a better test for determining your CVD risk. I’ll be discussing this in next Friday’s article.

    • Heather, You said you eat “hellacious” amounts of fat, mostly saturated. I’d like to do this, also–but I don’t want my wallet to yell at me! How do you do it?

      • Hi Allen,

        The nutrient density in fat is a lot more than in carbs. When you eat a low carb high fat diet, your satiety increases and don’t find yourself going back for more. I personally am still surprised though how I can drink a bulletproof coffee in the morning and go until 1 or 2 before my body tells me it’s hungry, but on days I decide to have even bacon and eggs, I start thinking about lunch by 11 easily.

        I find by focusing on eating real foods, you tend to spend about the same in the end because you aren’t waiting as much food and you are not eating out nearly as often.

  15. Great article, Chris! Great information.

    Busting this myth is important because, in regards to hearth health, it’s not just cholesterol and triglycerides, but inflammation that puts us at risk.

    What’s really killing us is our modern diet of excess sugars, refined carbohydrates, trans fats, vegetable oils, and excess omega 6 from grain-fed beef and fish — it’s killing us as individuals, and consequently the high cost of poor health is killing our competitiveness as a nation.

    One thing that’s often overlooked with saturated fats is the role of palmitic acid. Excessive palmitic acid has been shown to cause inflammation, increase insulin resistance, kill pancreatic beta cells responsible for the production of insulin, and neutralize leptin–the hormone that signals the brain to tell you when you’re full. And the kicker–when you overeat, the excess carbohydrates in your body get converted through lipogenesis into palmitic acid in your blood, which has the same effect as dietary palmitic acid — essentially giving you a double whammy of negative effects; and that’s the main reason why fast food is so bad for you.

    One thing most people aren’t aware of is that the word “napalm” was derived from its two key ingredients: naphthenic acid and palmitic acid.

    • I enjoy the new ideas in this post. I did not realize excess carbs turn to palmitic acid, although I wonder how one would estimate excess.

      • Yip!!!
        I agree. Met a Malaysian Man who said that Palm Oil is killing them!
        Massively produced and massively protected by Politicians and Taxes on healthy oils.

    • Les, what you may be missing about palmitic acid is the following: when you eat it in your diet (fatty t-bone, etc), palmitic acid is always accompanied by oleic acid, which has been shown to be protective of any deleterious effect palmitic acid potentially has in isolation. However, when produced endogenously (via excessive carbohydrate ingestion), the potentially deleterious effects of palmitic acid that are produced remain unopposed (i.e. there is no oleic acid to offer protection). So, all of these untoward effects of palmitic acid could entirely be predicated on carbohydrates ingestion and not saturated fat intake.

  16. Does it matter whether or not you’re ‘fat adapted’? I know folks who do not process fat correctly, myself included. And incidentally I feel horrible on a paleo style high-fat diet.

  17. Looking forward to your next article, as dietary cholesterol and/or saturated fat has indeed raised my total cholesterol levels from about 200 to 350, most of which is LDL – about 260.

      • is it not more about inflammation of the arteries and other serious markers that we should be concerned about? Also on a high fat diet sugars and whole grains/ carbs will start driving your cholestoral through the roof? Is there enough evidence to suggest that Co Q 10 is important enough in the whole conundrum to negate the use of statins??

        • Heres what you do if you want to experiment on yourself. If you suffer from HIgh cholesterol meaning your LDL and Triglycerides are high and your overweight and on the high carb kick like most of the USA.
          Switch off to a solid protein and veg diet. Or you can say way of eating cut out all veges that have high sugar content and also cut out ALL GRAINS!
          You have to have fats for the body to function properly low fat I have found to be bad for us in the areas of losing weight and staying fit. My cholesterol was high LdL and Triglycerides were high. I quit eating carbs and sugars and all grains cut out of my diet. Here are some changes my cholesterol normalized. My weight dropped 90 pounds. No more heartburn and indigestion, grains cause acid reflux more so then the excuse its over active acid in the gut. I was also told by my dr i must have high cholesterol because of my family has a history of it, thing is not true we only started to have a history of it when we started to over consume grains.

            • Excess protein doesn’t damage the kidneys unless you have excess carbs attaching themselves to the overlarge protein molecule and pulling them through the kidneys. Much in the same way of having a high carb 3 to 1 ration of protein shake after a workout, the carbs will pull that protein into the muscle instead of letting it wander around and just being picked up.

            • If you are afraid of saturated fats then eat other fatsmake sure you get lots of monounsaturated.

    • Hi all. I have familial hypercholesterolemia. Both parents and 4 siblings. All are in great shape. All are on lipitor. All have a super reaction to the lipitor of Cholesterol going from above 300 to mid 100 with only 5 or 10mg of lipitor/day.
      All of us want to free ourselves of stain usage, especially since there is quite a bit of dementia and alizimers in our family.
      I have agreed to be the ginny pig. I am one year Paleo. My Cholesterol is 323, Tri 76, HDL 73 and LDL 234. I like my ratio between HDL and Trig but obviously the LDL is scary.
      My primary dr is ok with thought that I have the lg fluffy LDL. My cardiologist (very old school) is pushing hard for the statins again.
      Thoughts?

      • Your cholesterol numbers are just a small bit higher than my mom’s numbers after 6 months after stopping using lipitor. Her cholesterol numbers were all normal before a part of her left thyroid was taken. Thyroid hormonal activity regulates ldl-receptor activity and her free T3 and free T4 levels were just above the lower end of normal ranges, so I think we will increase her levothyroxine dose from 100 mcg to 125 mcg a day for now. Chris Masterjohn is generally the one to follow and I do not know anyone else that can give more info about it.

  18. What about for apo E4? My cholesterol numbers seem to be greatly affected by a higher fat intake. I have also seen this to be true for my dad. He has always had perfect lipid numbers. I got him going on a low-carb, high-fat (a lot of coconut oil for Alzheimer’s) and his LDL shot through the roof.

    • As I mentioned, saturated fat and cholesterol do increase blood cholesterol in some people. The question is: does that matter? I’ll address that in the next article.

      • What is cholesterol? What is it you want it to do? What is it you think it will do?
        What test are you going to do to prove your theory?
        How will you interpret the results?
        Are you getting a result? Optimum health??
        If not was a waste of time. Cholesterol= heart disease is an assumption/ correlation. Not the study of cause and effect. In our company we find that it coincides with healing in detox- mercury/ bacterial infection when you start to balance the chemistry.

      • Chris,

        I believe it does matter because there are enough people on the various blogs who report increased LDL particle number with the higher fat diet. It seems that this IS what increases for some of us switching to Paleo. The rest of the numbers are good – the HDL is high, TG is low, inflammation markers are low, but the LDL particle number skyrockets. It seem to be too common to put it off to FH. I would be very interested in further information on this.

          • Sorry Pauleis, my responses that I intend for you keep going below Josh’s post – not sure what I am doing wrong. Anyway, thanks for the info. I did read your 22 June post and the link article.

        • 25% of the population are apoe3/4 and something like 10% are 4/4
          This will keep LDL in the blood longer. The gene was selected for in sub Saharan African nomads to keep circulating lipoproteins for longer when undergoing periods of fasting.
          On a modern paleo diet replete w nutrients it WILL raise LDL-P, however it matters not unless it becomes oxidized.
          If you are an apoe4 carrier your greatest concern is not LDL it is inflammatory markers/ oxLDL and fatty acid ratios

          • Not sure if this is true. I eat a low-inflammatory diet. My inflammatory markers are fine, not sure about ox LDL, but almost all of my LDLP are large, fluffy which should indicate low oxidation. After working this approach for about 3 years, I recently experienced a cardiac episode – mild heart attack and now I certainly have to reevaluate.

            • if the ldl particle size is safe, and you have a good ldl/hdl ratio, then you have nothing to worry about relating to cholesterol thats why i agree with this article. however that doesnt mean youre not at risk for CV because that can be caused by other things also

        • There are different kinds of LDL. Mainly large bouyant (associated with fat intake) and small dense (associated with fats your body produces from carns, especially fructose). LDL as a whole is a meaningless number.

      • you said that saturated fat intake does increase blood- cholesterol levels in some people. is there a way to know whether it will or won’t? and also, how can one manage high LDL levels with a good diet, to avoid medication?

      • It might not matter much if they are moving from 190 to 230 but it matter if they are moving from 140 to 170.
        Many studies have shown no artery buildup of plaque when the cholesterol is below 150 and the LDL below 100.

        Your studies of people between 185 and 240 prove nothing but that there levels are too high.

        • You’re wrong.

          A total cholesterol level between 185 and 200 is not too high; that is actually about where the ideal is. Yes, a total cholesterol level of 200 or more is too high, with 200 to 239 being borderline high and 240+ being high; however, 160-199 is actually the healthy range, with 180-199 being ideal.

          Also, even people with total cholesterol levels below 150 are not exempt from heart disease. Take the MRFIT study for example, which compared the mortality rates in 350,977 men ages 35 to 57 at various cholesterol levels. As you can see here , there were cardiovascular deaths observed at all cholesterol values. Also, as you can see in the chart, while the lowest risk of heart disease is in the 140-159 range, the lowest all-cause risk of mortality is in the 180-199 range. I don’t know about you, but I would rather minimize all-cause risk of death than just risk of death from one specific cause, such as heart disease.

    • The same happened to me. After one year doing paleo with intermitent fasting, bone broths and a good amount of coconut oil my total cholesterol reached 378 last month (TG: 52, HDL: 84). Now I’m totally confused. I find it’s way too high and maybe I should stop eating saturated fat.

      • Carlos: a total cholesterol this high is often indicative of familial hypercholesterolemia, which is a genetic condition that reduces the clearance of LDL particles from the blood. Please seek out help from a knowledgable health care practitioner, and yes, I think it would be wise for you to eat less saturated fat if you do have this condition.

        • Thanks Chris, although I had never had these levels, it’s true that I have always been in the high range of the “normal” despite having a good diet, I don’t smoke and I’m skinny and active. My father doesn’t smoke either and also has a good diet but he has always been in the high range too. I’ll repeat my tests in 2 months. I’m eating less saturated fat, we will see. On the other side one thing I noticed clearly when I abandoned sugars and cereals is that my HDL went up and my TG went down. You are doing an excelent job.

          • Carlos, your numbers are very similar to mine. I have apo e4. I also have lp(a). I would be interested to hear how your numbers respond to your decrease in fat. I feel that we have a good laboratory here and I am learning from all of it.

        • But surely Chris that is the crux of this whole article and the majority of people with Familial hypercholesterolemia will be the ones attracted to this diet in the first place. So basically what your saying is that the people that were going to have issues with inherited high cholesterol are the ones that should avoid this diet in the first place and the people that didn’t don’t need to worry as its not a significant marker in heart disease anyway.. Think you’ve defeated the whole point of this ( very good) article you’ve constructed?

        • Sorry doc, but NOPE. I and my family have the disease full on and I could NOT find another person with this disease who tried the diet anywhere in the world, so I did! and the more sat fats I eat the lower my cholesterol goes. I am 58. My total cholesterol for first time since birth came down from 13+ to 6.1. ON pill (which we now no longer can tolerate at all) it’s never ever gone lower than 8.8. So for me and mne, it’s goose, duck, butter, double cream, coconut oil, olive oil (the best on the market), lots of eggs lots of greens, the fattiest lamb and beef I can find (NO wheat products) here and there a hand full of berries. It’s easy for me. I eat head to tail but my doctor was ecstatic with my results. When i lower the fat, the numbers go up! THUS the secret is in the fat. I know this for sure. Have the proof! Cheers and thank you

          • Hi Maguerite,
            That sounds a risky step. Even 8.8 is way into the risk zone for heart events. The Framington study found over 30 years that no one with cholesterol under 3.8 (150mg/dL) ever had a heart event. Here’s a really interesting study showing how much coronary arteries clog over a year on a high protein high fat diet, compared with a high carb high vegetable diet from the British Journal of Nutrition just last year: http://www.ncbi.nlm.nih.gov/pubmed/22850317 Keeping your cholesterol high just isn’t safe in the long term. And the only way to bring it into a safe zone is to increase plant foods (at the expense of animal foods). There is no other clinically documented way to do it – other than severe weight loss…such as if you had tuberculosis, or chemotherapy or a cocaine habit. Those things also lower cholesterol heaps – but I don’t think we’d want to recommend them. Rejoicing at having 8.8 or 6.1 cholesterol instead of 13+ is kind of like rejoicing because a person has breast cancer rather than lung cancer. They’re both dangerous. What you have to aim for is 3.8 max! I can tell you from experience – you’ll feel like a new person at that level, bursting with energy and glowing with vitality.

            • But, the overall incidence of stroke goes up with lower saturated fat and cholesterol, especially in women.

              It seems like 200 is the magic number, for women at least.

            • Sorry Mary, but I have to disagree with you on that. A total cholesterol level of 8.8 mmol/L (340 mg/dL) is actually much better than a total cholesterol level of 13+ mmol/L (503+ mg/dL). Also, 6.1 mmol/L (236 mg/dL) is much better than 8.8 mmol/L (340 mg/dL) — it’s the difference between having severely high cholesterol (7.8+ mmol/L [300+ mg/dL]) and having borderline high cholesterol (5.2 mmol/L [200 mg/dL] to less than 6.2 mmol/L [240 mg/dL]). Granted it’s still not healthy, but it’s a huge improvement from 13+ mmol/L (503+ mg/dL), or even 8.8 mmol/L (340 mg/dL).

              Also, it’s not 3.8 mmol/L (149 mg/dL) max that you should aim for; it’s 5.1 mmol/L (199 mg/dL) max and 4.1 mmol/L (160 mg/dL) min that you should aim for. Saying that you have to aim for a cholesterol level of 3.8 mmol/L (149 mg/dL) max is like saying that you have to aim for a blood pressure of 84/54 max, or a BMI of 17.2 max — it’s dangerous advice.

              Also, while there may have been no heart events in over 30 years in the Framington study with total cholesterol levels of less than 3.9 mmol/L (150 mg/dL), the MRFIT study lasted only six years, and almost 0.5% of participants with cholesterol levels of 3.6-4.0 mmol/L (140-159 mg/dL) had cardiovascular disease, and slightly over 0.5% of participants with cholesterol levels below 3.6 mmol/L (140 mg/dL) had cardiovascular disease. The MRFIT study also showed that while the lowest heart disease risk occurs with total cholesterol levels of 3.6-4.0 mmol/L (140-159 mg/dL), the lowest all-cause mortality risk occurs with total cholesterol levels of 4.7-5.1 mmol/L (180-199 mg/dL), followed closely by 4.1-4.6 mmol/L (160-179 mg/dL).

              To see what I’m talking about, you can view the chart here:
              http://1.bp.blogspot.com/-BrNwqzHAwFw/UX6xKNueesI/AAAAAAAAApo/qNHDJ-3xx_c/s1600/mrfit_mortality_in_350,977_men_aged_35-57.png

          • Hi,In my opinion,a low fat diet may induce the liver to to synthesize much more lipids than needed for normal body functions.The ability to store food reserves in the form of body fat has ensured our survival,not so long ago,when we were nomads.

      • Carlos- we can not look at one marker in isolation with a blood chemistry. If heart disease is a concern what is your hsc-RP, ESR, LDH, CK, Albumin, phoshates, glucose, insulin, platelets, free calcium etc.
        Do you have periodontal disease? Do you have heavy metals? What there other things you do on the side of saturated fat? The human diet is complex and we just don’t follow the paleo approach or high fat diet. What is the ketogenic or paleo diet for that matter anyway? Not tailored to the individuals skeleton, also what is it you want it to do to the chemistry?
        Do you smoke? Are you constipated?
        If you do have the gene what are you going to do about it and how will you interpret the markers around the lipoproteins. If the HDL comes up so too the total cholesterol has to move.
        Don’t forget HDLc, HDL 1 in your calculations. Also depends on what range are you using: a statistical average range of the blood pathology results or an optimum rang to strive for?

        • Thanks Bob, I would need more exhaustive tests. On the other side I think I carry a pretty healthy lifestyle. I’ll keep learning and tweaking my diet.

        • Bob, I’m interested in your question about periodontal disease. How does that relate to the discussion on cholesterol levels?

          • Chris, I think periodontal disease has been associated with cardiovascular disease in a few studies, which might explain Bob’s question. I’ve also read that there is a potentially valid mechanism involving translocation of bacteria and endotoxemia that could link periodontal disease with CVD.

      • Get a sonar scan or other means of actually checking out the status of your arteries. If they have a significant amount of plaque buildup I would seriously consider a whole plant-based diet like so many recommend. Look at Esselstyn, Ornish, Fuhrman or the Okinawan Diet.

    • You may want to note what type of LDL particle he has. JAMA reported (in the AtoZ clinical study) that researchers noted LDL particle size changes to type A (large) and actually reduces CVD risk. This is despite raising LDL levels.

      • LDL particle size loses its predictive value after adjustment for LDL particle number. In other words, it’s not the size of the particles that matters, it’s how many you have. This will be the subject of my next article.

        • Chris. People are only spreading this “Large fluffly harmless LDL” misinformation because people like you propogated it. I wonder how many people at high risk of heart disease were chowing down on sticks of butter thinking their jacked up LDL was large, fluffy and protective.

          • I don’t buy into this large, fluffy LDL stuff. I believe it is just grasping at straws for people that want to hold on to their high fat diets. It gives them a false sense of security.

            • Agree with above two comments. Here is a good commentary on LDL size http://www.athero.org/commentaries/comm564.pdf “Contrary to current opinion, both small and large LDL
              were significantly associated with subclinical atherosclerosis independent of each other,
              traditional lipids, and established risk factors, with no association between LDL size and
              atherosclerosis after accounting for the concentrations of the two subclasses”

    • I would suggest taking a VAP (vertical auto-profile) test or NMR test which will give you a comparison of how much of that LDL is small, dense LDL particles (risk factor for heart disease) or large, buoyant LDL particles (essentially “good LDL used by the cells, tissues, hormones, etc.) Low and behold, it appears not all LDL particles are ‘bad’!

    • SUZIE, apoe4 will show a moderate increase, this is helpful in avoiding Alzheimer’s. The trick if you have e4 is to avoid oxidation of LDL by eating an anti-inflammatory diet and limiting stress, which you are doing.
      Imupro offer an extensive lipid panel that shows LDL subtractions and oxLDL. If you have low small dense particles and no oxLDL you are all good.

      • Thanks. I have had extensive testing through HDL Labs, though I don’t think it included oxidized LDL. My LDL particles were very high, even though by far most were large, fluffy. My rise in LDL with a high fat diet is not modest. In fact it almost doubled. I do try to eat a very healthy diet, of the paleo variety. I have recently picked up my exercise because I understand that apo e4 may be more affected by a lack. Hoping this helps.

        • What is it about exercise that helps? For instance, I primarily lift weights. Is the correlation only seen in runners?

          • Susan
            We discuss this all at http://www.apoe4,info. I respond hugely to saturated fat and Ive posted my lipid results in how dramatically I respond to a reduction in saturated fat in as little as a month.

            We do enough n=1 experiments to prove that yes, saturated fat and dietary cholesterol can have significant negative impacts on our lipid profiles. But, substituting the saturated fats with mono fats, can be the key.

    • +1 to APOE 4/4 question!

      It would be really great to see the separate series on the subject! Chris, please, consider researching it thoroughly. You might figure out how to treat/prevent Alzheimer’s while doing so…

    • Your brain needs Cholesterol. Exercise, stay away from processed foods and you’re on the right track. Highly recommend the book “Grain Brain.” Good luck!

    • what kind of oil was used? Organic virgin coconut oil or refined coconut oil? Also what protein was being eaten aswell? Pasture fed beef and poultry or conventional meats? it all makes a big difference. Dairy products should be pastured fed and raw. next best would be organic and pasteurized but not homogenized.

      • Why do you think pasture feed is any different than conventional? Cholesterol is the same! And no humans should not be consuming any dairy! Mammals produce milk for their young and that includes cows! Their milk is designed to grow a calf to hundreds of pounds during the first year of life!

    • overall only changes I have experienced are changes in Triglceride levels. They’ve halved overall however HDL and LDL are still the same as they were wen I was a carb monster. overall my gp wants me on a low fat diet and exercise.

    • The same thing happened with my fiancé. High Fat Low Carb = sky rocketed LDL, doctor keeps pushing Statins HARD, but instead we switched to 100% whole grain + oatmeal/high fiber foods + exercise + daily caloric limit (lost 30lbs). This dropped him back down approximately 75 pts on the LDL…so I’m going with that for now. Interested in what he’s got to say in the next article, however.

      • Try eliminating animal foods and ALL oils such as olive, canola, grapeseed, etc. hopefully this will drop cloresterol. I eat tons of potatoes and brown rice and my blood glucose is perfect. Thought I would pass along info to those in need, or who are concerned. Check out dr Furhman, Esslstyn & others.

        • Your morning fasting blood glucose may be “perfect” but how often do you get blood sugar crashes (irritable, not thinking at 100% etc)?

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