Dietary Fat and Heart Disease – The Changing Landscape

Fat and Heart Disease - The Changing Landscape

Most of us know that the risk of heart disease can be modified by lifestyle. For more than fifty years, that’s what we’ve been taught by the people we trust, scientists, medical professionals and public health officials.

But the doubters have always been out there, and they ask questions. How do these people know what’s good and bad for us? Well, of course, we’re aware that their evidence is based on scientific data. But, is the data reliable and has it been interpreted correctly?

For decades we’ve been told that saturated fat, the type found in meat, butter, and cheese, raises the risk of heart disease. Health officials have urged the public to avoid saturated fat as much as possible, saying it should be replaced with unsaturated fats like that found in nuts, fish, seeds and vegetable oils. In fact, many consider this to be conventional wisdom, which basically means that it’s undebatable. However, recent research has challenged this view and the debate on the risk associated with consuming saturated fat has grown louder by the years.

One of the main reason saturated fat has historically had a bad reputation is that it increases LDL-cholesterol, the type of cholesterol that is supposed to raise the risk for heart attacks. But the effects of saturated fat on blood cholesterol are probably more complex than that. For example saturated fat also increases HDL-cholesterol, the so-called good cholesterol. However, the effect of polyunsaturated fat (PUFA) on blood cholesterol and traditional lipid profile is generally considered more favorable than the effect of saturated fat.

A few days ago, a scientific study published in the Annals of Internal Medicine caught the headlines of news media around the world. The main reason for the attention is the fact that the study did not find that people who ate more saturated fat had more heart disease than those who ate less. Furthermore, the study did not find less heart disease in those eating higher amounts of omega-6 PUFA or those eating more monounsaturated fat.

The study deserves our attention, not only because it challenges current wisdom and modern dietary guidelines, but because it summarizes a very large amount of data from three different types of studies. However, because it’s not an open access paper, and because it’s a landmark study, I thought it would be proper to summarize the main findings as I see them.

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The Study Design

The study was performed by researchers from the UK, USA, and the Netherlands and was led by a team at the University of Cambridge in the UK. It was a systematic a review and meta-analysis of available scientific data addressing the association between dietary fatty acid intake, fatty acid biomarkers (measured in blood or adipose tissue), or fatty acid supplementation and the risk of coronary heart disease (CHD).

The investigators performed a systematic review of the scientific literature in order to find studies that fitted for their meta-analysis. The studies selected were both observational studies as well as randomized controlled clinical trials. To be eligible, the studies had to fulfill certain criteria. For example, observational studies were eligible if they were prospective in design with at least one-year follow-up and involved participants from a general population (not people with known heart disease). Intervention studies were eligible if they were randomized and recorded CHD outcomes. A total 72 studies of more than 600 thousand individuals were selected for the final meta-analysis.

In order to grasp the results of the paper, it is important to understand that the meta-analysis consisted of three parts. Firstly, the association between the intake of different dietary fats with CHD was studied. Secondly, the association of measurements of fatty acid biomarkers with CHD was addressed. Thirdly the association between fatty acid supplements and CHD was studied.

Saturated fat, Omega-6 and Monounsaturated Fat Don’t Affect Risk

There was no statistically significant association between dietary saturated fatty acid intake and the risk of CHD. Furthermore, intake of omega-6 PUFA was not associated with the risk of CHD. The authors of the paper, therefore, conclude: “Our findings do not clearly support cardiovascular guidelines that promote high consumption of omega-6 polyunsaturated fatty acids and suggest reduced consumption of total saturated fatty acids”.

When studying measurements of biomarkers, it is important to keep in mind that there are many types of saturated fatty acids and many types of PUFA’s. Palmitic and stearic acids are saturated fats that were not significantly associated with the risk of CHD. However, margaric acid was significantly associated with lower risk of CHD. Margaric acid is an odd-chain saturated fatty acid. It’s levels are moderately correlated with milk and dairy consumption. The findings support the possibility that odd-chain saturated fats reflecting milk and dairy consumption, may be less harmful in terms of risk for CHD. Arachidonic acid was the only omega-6 fatty acid that correlated with lower risk of CHD.

Studies of dietary intake and biomarker studies did not find any significant association between monounsaturated fat and the risk of CHD.

Dietary Long-Chain Omega-3 PUFA’s Are Protective

Dietary long-chain omega-3 PUFA was associated with lower risk of CHD. These findings were supported by the blood biomarker studies which showed some evidence that circulating levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid  (DHA) (the two main types of omega-3 PUFA) are associated with lower risk of CHD. Alfa-linolenic acid was neutral in terms of risk.

On the other hand, meta-analysis of omega-3 and omega-6 PUFA supplements suggests that supplementation with these nutrients does not significantly affect the risk of CHD. However, the authors point out that more data is needed because the available data is limited. There is a large ongoing trial on the effects of omega-3 PUFA in primary prevention (VITAL). This study will also address the efficacy of vitamin D.

Trans-Fats Increase the Risk of Heart Disease

Not surprisingly, dietary trans-fats were associated with increased risk of heart disease. However, only five published prospective cohort studies contributed to this analysis.

The Changing Landscape

For the last five years, a number of reports (12345) have concluded that there is a weak association between the consumption of saturated fat or major foods that contain saturated fatty acids (meat and milk) and the risk of CHD. The above study certainly adds strength to these conclusions. It appears that the advice to encourage high consumption of polyunsaturated fatty acids and low consumption of saturated fats is not based on solid scientific evidence, and needs to be reconsidered. In fact, the study suggests that dietary fat composition me play a much smaller role for cardiovascular risk than previously thought.

Finally, a few questions need to be asked. Firstly, is this the final verdict? Well, I guess not. But certainly, these new results have to be taken seriously. Secondly, how did public health authorities manage to get it wrong for fifty years? Was it because the available scientific data was unreliable, or was it because the data was wrongly interpreted? Was it because the pieces of the puzzle had to fit into a preconceived notion? And thirdly, how will we get it right? How will the new landscape on dietary fats and heart disease be introduced to the public, and how will this landscape affect the food industry?

I know for sure that many experts will cover their ass by suggesting that the macro-nutrient approach is outdated, and they’re probably right. Dietary recommendations focusing on how much to eat of different types of fats and how much of our daily energy intake should be carbohydrates, protein or fat, are both misleading and impractical. So maybe we will soon see a paradigm shift in the way medical professionals and public health officials educate people about the effect of diet and nutrition on health and disease.

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93 thoughts on “Dietary Fat and Heart Disease – The Changing Landscape”

  1. I agree with you Axel. I find this meta-analysis compelling. Let’s hope that professional medical organizations like the AHA and its corollaries abroad admit that they’ve been giving dubious advice about diet for decades.

  2. Dr. Chowdhury has admitted to a half dozen errors in his paper that he says do not affect his conclusions. This was partly in response to the comments of Walter Willett, Frank Sacks, and Meir Stampfer, who called his conclusions about MUFAs and PUFAs “seriously misleading.”

    • Good ol’ dependable R O F L.. straight in there with an appeal to the authority of the establishment.. while simultaneously seeking to discredit the study’s authors 😛

      Speaks volumes about how weak your own position must be.

      Where is your source for the “half a dozen errors”..?

      In the Medscape article, I see…

      Regarding assertions of errors in the report, Di Angelantonio [senior author Dr Emanuele Di Angelantonio (University of Cambridge)] said, “We recently spotted some minor mistakes in some of the data that will not in any way affect the main results of the study.” He confirmed that another group contacted him and his coauthors about “some other minor mistake,” adding, “We are making an erratum that will be sent to [Annals of Internal Medicine] in the next 24 hours, so there will be an updated version. But it’s unlikely that the main conclusions will change.”

      Maybe that “other group” should perform their own meta-analysis and elevate the discussion to one of scientific method and review, rather than unsubstantiated opinion?

      Is this yet another example of your reading comprehension issue perhaps?

      Nullius addictus iurare in verba magistri, — quo me cumque rapit tempestas, deferor hospes

  3. I brought up a couple of problems with this meta-analysis in the previous discussion (the low carb thread). Should I copy/paste them here, or could you answer the questions I raised, Axel? I would deem it more fruitful to discuss to quality and nature of the meta-analysis critically than merely repeat the findings as such. Perhaps others are willing to contribute, too.

    BTW, the meta-analysis found that n-3 fatty acids had NO statistically significant effect on coronary effects, not in cohort studies nor in trials. Therefore to state that “omega 3 is protective” is somewhat misleading. In addition, serum TFA had NO statistically significant effect on coronary events (based on cohort studies), either – and at least I would consider serum TFA to be more accurate estimate of the actual intake than estimates of dietary intake, as the human body doesn’t produce TFA.

    • Yes Mie. Why don’t you copy your comments here as well.

      For coronary outcomes in the prospective studies of dietary fatty acid intake, the RR was 0.87 (CI, 0.78-0.97) for total long chain omega-3 PUFA’s which is statistically significant. RR was 1.16 (CI, 01.06-1.27) for trans-fats which is also statistically significant. This is very clearly illustrated in figure one of the paper.

      The authors conclude that “dietary long-chain omega-3 polyunsaturated fatty acids was associated with lower risk of coronary disease“. They also conclude that “total dietary trans fatty acid intake was positively associated with coronary disease risk in our meta-analysis

      • Hmm? According to the table on Medscape

        https://www.medscape.com/viewarticle/822092

        the results for n-3 fatty acids were as I mentioned. Mistake on Medscape.

        With TFA: notice that I mentioned circulating TFA. The results didn’t reach statistical significance there.

        And here’s the copypaste:

        “The authors chose not to consider fat modification/exchange properly and also decided to analyze n-3 and n-6 fatty acid intake separately. If you’ve read the full text, could you explain the rationale behind this? E.g. Ramsden et al 2010 showed that mixed n-3 and n-6 diets had beneficial effects on CHD end points.”

      • Mie.
        You’re right. To me it looks like there is an error in the table published on Medscape. The numbers are different than those published in figure 1 in the original paper. As I said the RR for Total long chain omega 3 PUFA´s is 0.87 (0.78-0.97), thus statistically significant.

      • Ok.

        Now, have you read the whole paper? If so, could you comment on the two issues I brought up above? And any ideas about the lack of statistical significance in the case of circulating TFA & CVD?

  4. Harvard School of Public Health has weighted in:

    “Dr. Willett emphasized that because this meta-analysis contains multiple serious errors and omissions, the study conclusions are misleading and should be disregarded”
    https://www.hsph.harvard.edu/nutritionsource/2014/03/19/dietary-fat-and-heart-disease-study-is-seriously-misleading/

    Jeremiah made an astute observation (2010) the strenght of the association between SFA and CHD becomes stronger in studies utilizing superior methodology, again many people seem to think that every study bears an equal value.

    Good points Mie, well done. At this point, Doc, I tried to warn you not making too much out of this meta-analysis in order to protect your audience from unnecessary confusion, but of course, you wouldn’t listen. That’s a pitty.

    • Well there you have it! If a prestigious edifice like the Harvard School of Public Health has “weighted” (sic) in with an opinion, who are we to try and discuss the science? Heck when a prestigious edifice like the Harvard School of Public Health proclaims an opinion, we should all just shut up and listen! Who even needs the scientific method when we have a prestigious edifice like the Harvard School of Public Health to tell us what to think?

      Walter Willett’s, ( with co-signers Frank Sacks’ and Meir Stampfer’s) OPINION that this meta-analysis is “misleading and should be disregarded” is just that… an OPINION.

      If a prestigious edifice like the Harvard School of Public Health truly does speak with a single voice that, in and of itself, would be a cause of great concern to me, because unbiased science is not based on a consensus. It beggars the question, who is funding the Harvard School of Public Health?

      Obviously not all studies are of equal quality, methodology etc… but that is not to say an higher quality necessarily means the authors are correct in their conclusions. Or that a “weighty” body of evidence cannot be overturned by a single study — a “black swan”

      And the funniest thing is that Dickie-Poo is so cocky about his (repeated and obvious) appeal to authority that he now feels an “I told you so” is in order! R O F L ;-P

      • Frank,

        would you like to comment on the two things I mentioned above: the issue of fat modification/exchange missing and the decision to treat n-3 & n-6 fatty acids separately? “Richard” is obviously not going to provide a critical look into the matter, so it’s up to rest of us.

      • Just to add that my understanding of n-3 and n-6 is that: rather than focusing on absolute amounts of each (within reason), health is a matter of balancing the ratio of the two and that the modern industrial diet tends to lead to an imbalance (in favour of higher n-6). Grass-fed and finished beef (as one example) apparently provides an healthier balance of the two as compared to beef finished in a CAFO. I know some will supplement with fish oils (for example) to redress this balance but my preference is to use real whole food over supplements.

        e.g. https://www.ncbi.nlm.nih.gov/pubmed/15189133

        That said I am puzzled as to why this analysis would treat them separately… without access to the full paper, I’d also be keen to hear what Dr Sigurdsson has to say in this regard.

      • Frank.

        I don’t think it’s wrong to treat n-3 and n-6 PUFA’s separately. The dietary sources of these two types of fats are very different. The study didn’t find a significant association between dietary n-3 consumption and CHD, while dietary long-cahin n-3 (EPA and DHA) was associated with lower risk of CHD.

        In fact this does not contradict the results of the meta-analysis by Ramsden and coworkers who concluded that trials that substituted n-6 PUFA for saturated fat, without simultaneously increasing n-3 PUFA produced an increase in risk of death that approached statistical significance.

        So, I guess replacing SFA with n-6 PUFA’s won´t reduce risk unless you at the same time increase n-3 PUFA’s.

      • Thanks Frank and Axel. Yes, I agree that we do indeed need both, just like Ramsden’s paper suggests.

        Axel, you stated:

        “The dietary sources of these two types of fats are very different.”

        To some extent, yes. But then again, foods such as nuts and seeds and olive oil which are more n-6 heavy are quite solidly connected to better CVD health, just like foods like salmon and other types of fatty fish which have a smaller n-3/n-6 ratio. To me, this hints that n-6 problems originate from elsewhere, e.g. industrial & refined foods.

      • Your right of course Mie. We need both n-6 and n-3. More importantly, we have to look at the food in itself, not only the fat composition. Maybe fat composition plays a much smaller role for cardiovascular risk than we’ve believed so far. The “issue” with industrial and refined foods has to do with many other factors than n-6.

      • It’s kinda hard to make exact comments when the expressions you used are anything but quantatitive. But then again, it IS difficult to quantify the effects exactly in these matters, so I cannot blame you. At least not much. 🙂

        Yes, compared to entire diets, the role of fats in CVD is bound to be minor. But since they are one key factor in e.g. the Mediterranean diet, you really cannot say that the type of fat doesn’t matter, period. That’s a blanket statement, and they’re BS, virtually without exceptions (due to the fact that they ignore the different conditions, contexts and uses for different diets). In addition, that’s inverse reductionism, isn’t it? Plus bear in mind that virtually ALL good options (Med.diet, paleo, certain forms of low carb etc. etc.) do have something in common in the fat department …

        And of course the problem with industrial and refined foods has to do with many other factors besides n-6. But in observational studies you really CAN’T control the role of the sources of a given nutrient that carefully. BTW, here’s Willett et al’s take on the new paper

        https://www.hsph.harvard.edu/nutritionsource/2014/03/19/dietary-fat-and-heart-disease-study-is-seriously-misleading/

        and they point out this same thing (the source of n-6 fatty acids).

        Of course, this works in both ways: the good qualities of e.g. olive oil cannot be reduced to just mufa – what about e.g. polyphenols?

        Where does that leave us?

        Entire diets. Just like you stated:

        “I know for sure that many experts will cover their ass by suggesting that the macro-nutrient approach is outdated, and they’re probably right.”

        Scratch the silly remark about covering one’s ass and the word “probable”, and you’re right on the money.

      • Really nice to notice that there is actually really good discussion going on here :). In my opinion it’s been far too long about “satured/unsatured” battle.

        I believe that quality matters. It matters in case of animal fats(crass fed etc.) as well as it matters for vegetable fats (extra virgin olive oil etc.). One reason for contradictory research results is probably that we have over simplified the matter to satured/unsatured battle, now it’s time go forward.

  5. The meta-analysis by Ramsden and coworkers is often cited to support that replacing saturated with PUFA’s is beneficial. However it is important to keep in mind that the same meta-analysis showed that trials that substituted n-6 PUFA for saturated fat, without simultaneously increasing n-3 PUFA produced an increase in risk of death that approached statistical significance. Ramsden concluded that the advice to specifically increase n-6 PUFA intake, based on mixed n-3/n-6 RCT data, is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death.

    https://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=7930322

    • As far as I know, no one’s recommending an increase in n-6 fatty acids in particular, at least not up to the region of 12-15% of total E (which was the case in the studies Ramsden et al reviewed).

  6. https://ht.ly/uXmB1
    Scientists Fix Errors in Controversial Paper About Saturated Fats

    Chowdhury says the paper’s conclusions are valid, however, even after the corrections. Randomized clinical trials are the “hardest” kind of evidence, he says, and they don’t show a significant effect of saturated or unsaturated fats. But even one of the paper’s authors, Dariush Mozaffarian, of the Harvard School of Public Health, admits that he is not happy with the key conclusion that the evidence does not support a benefit from polyunsaturated fats. “Personally, I think the results suggest that fish and vegetable oils should be encouraged,” he says. But the paper was written by a group of authors, he points out. “And science isn’t a dictatorship.”

    Another study author, Emanuele Di Angelantonio of the University of Cambridge, says the main problem is that the paper was “wrongly interpreted by the media.” “We are not saying the guidelines are wrong and people can eat as much saturated fat as they want. We are saying that there is no strong support for the guidelines and we need more good trials.”

  7. Axel and Mie, your dispute on the outcomes regarding omega-3 fatty acids seem to be due to an error in the first release of the original paper. The error was corrected a couple of days later into the original paper, but Medscape published their text before the correction took place (and never revisited their story?).

    I think it boils down to what are the sources of saturated fats in western diets. Dairy foods do not seem to increase the risk of CHD in meta-analyses but processed meat does. Processed meat also increases CVD mortality in meta-analyses but dairy does not. Dairy is neutral and biggest contributor to total sat fat. Butter usually constitutes only some 20% of total sat fat intake in western populations.

    I have not seen a meta-analysis on the effect of sheer butter on CHD incidence (neither on margarine). There is one on CVD mortality (O’Sullivan et al. 2013).

  8. https://wholehealthsource.blogspot.com/2014/03/corrections-to-new-review-paper-on.html

    “In my view, the most important question is “what foods should I eat”? The answer depends on the individual, but here are my general opinions. Eating synthetic trans fat is probably a bad idea, and it’s generally found in low-quality processed food anyway. Refined seed oils like corn and soybean oil are the nutritional equivalent of white sugar, oxidize during high-heat cooking, and also tend to be found in low-quality processed food, making them a poor choice. I haven’t seen much evidence that makes me concerned about eating the fat naturally contained in meat and dairy, so I view those as acceptable, in moderation. Nuts and wild seafoods seem to be healthy, whether or not that relates to their fatty acid profile, so it makes sense to eat them regularly. Extra-virgin olive oil appears to be one of the healthiest fats, so it’s logical to gravitate toward it as the default added fat.”

    “The primary critiques were 1) that the data were over-adjusted because some of the data had been pre-adjusted for circulating cholesterol levels, and 2) Dr. Ronald Krauss has received funding from the dairy industry. Further analysis by Dr. Krauss’s team confirmed that the result was the same whether one considered studies that had been adjusted for cholesterol, or those that had not. Dr. Krauss was actually not receiving funding from the dairy industry at the time he wrote and published the paper, but in any case this argument is weak unless specific instances of bias can be identified in the paper. “

  9. Thanks Reijo, it seems you’re correct.

    Guyenet’s post (thank you Charles for linking it) brings out many good points. In particular, I would point out that the Hooper et al. which he’s referring to is precisely the case of “devil being in details”. Since it seems that in many RCT’s people simply cannot reach the treatment targets, the results are less than impressive (three little letters: WHI). Now, this doesn’t necessarily mean that the goals itself aren’t worth reaching for. Heck, if that were the case, then lifestyle interventions would be useless – see e.g.

    https://www.ncbi.nlm.nih.gov/pubmed/15824290

    and we’d all be better off on statins. And yet, as trials like Lyon Diet Heart – or to lesser extent, PREDIMED – have shown, the benefits can very, VERY substantial – and not just in the case of CVD. And, of course, medication itself isn’t the “one size fits all” solution: people with a low risk are unlikely to get that much benefit and can be harmed instead.

    I personally take this to mean that more effort is needed and that interventions in fighting CVD need that “extra kick” in addition to what health professionals can provide, for instance, support from the government in the form of legislation and taxation.

    (That was me being optimist. Ask me another day and I might wallow in self-pity. 🙂 )

  10. I agree with Reijo’s points. If anything I think we should give some slack for dairy products. I also think that it’s fair question to ask that is it the satured fat at the end that is the responsible of the negative results for processed read meat. It could be high sodium content, higher heme iron etc. Or maybe all of them together…

  11. Guyenets response is a good example why we ought to be cautious with bloggers from the paleo-sphere. Reijo repeated the exact same flawed arguments in Guyenet’s comment section

    “The primary critiques were 1) that the data were over-adjusted because some of the data had been pre-adjusted for circulating cholesterol levels….Further analysis by Dr. Krauss’s team confirmed that the result was the same whether one considered studies that had been adjusted for cholesterol, or those that had not.

    The meta-analysis by S-T contained 2 kind of studies in regards to cholesterol:

    a) Studies that had over-adjusted for serum lipids
    b) Studies that did non include information about the serum lipids

    S-T simply reported seperately the results for the SFA-CHD link in regards to studies, b. They did have any additional information of the vast body of studies that had over-adjusted for lipids. They did not reconsider these studies.

    Adjustements for cholesterol was only one problem with S-T meta-analysis from the countless of others (Stamler 2010). Perhaps the most compelling argument in my view is the fact that, as Stamler pointed out, the stronger and superior the methodology of the study, the stronger the link between SFA-CHD. In meta-analysis the effects of garbage dilutes the pearls, this is a problem when trying to combine studies that are vastly heterogenous in material.

  12. @ R O F L

    “…the stronger and superior the methodology of the study, the stronger the link between SFA-CHD. In meta-analysis the effects of garbage dilutes the pearls…”

    Which of the studies included in this particular meta-analysis would you (or Stamler) consider to fit in the category of “pearls”… those with a “stronger and superior the methodology”..? Perhaps, instead of trying to discuss innuendos, we should see how well each of these individual studies stands up to scrutiny?

    Meantime I note that you have failed to mention some other potential problems of meta-analyses, that: on occasion, a study — favourable to an agenda — will be re-published multiple times under different titles and altered author lists, or where the findings of a study were not favourable to an agenda, so it is withheld and not published at all… thus “rigging the votes” as it were.

  13. ^I have my favorite pearls, sure.

    Referenced as Oxford Vegetarian. Relative risk: 2.77 for dietary SFA (Mann, 1997).

    “A gradient of risk is apparent with increasing intake of total animal fat, saturated fat, and dietary cholesterol as well as some of the major food sources of these nutrients.”

    To be more precise. Scarborough (2010) pointed out that the meta-analysis by S-T included MOSTLY studies that over-adjusted for serum lipids and that did not have any information on serum lipids. S-T & Co simply reported the SFA-CHD link in regards to the studies that did not have any information on circulating blood cholesterol. They did not go back to raw data of the original studies.

  14. @ R O F L

    Is this the one you mean? I’d prefer to read the source rather than predigested opinion by ideologues like Plant Positive (Pee Pee)…

    https://www.ncbi.nlm.nih.gov/pubmed/10479226

    Was this study included in the meta-analysis we are discussing here? What exactly is your basis for promoting this study as using a “stronger and superior the methodology” than some of the others included… other than its conclusions obviously suiting your own agenda?

    And your “to be precise”…comment… is that an attempt to “move the goalposts” of this discussion..? As there is no clear line of causality between “circulating blood cholesterol” — at least in so far as when you put it so simply — and CHD, then maybe we should stick to studies showing the relationship of SFA to CHD end-points? In other words I’m not prepared to take “circulating blood cholesterol” by itself, as a sign of CHD. There may well be a relationship but it is obviously not as clear cut as you may suit you to suggest

  15. Thanks Charles..

    Yes I had found that PDF but I’m still not sure this study was included in the meta-analysis we are discussing, or why R O F L thinks it is of an higher standard than others… or even if it is the same study as he (or PP) alluded to.. this is dated 1999 not 1997? At first glance I see questionable elements like: the use of diet questionnaires/records, broad groupings like “meat-eaters” vs “non-meat eaters” (even tho’ some 23% of “non” ate meat on occasion) — what else did they eat?, talk of relative risk (as opposed to absolute)….

    Do you see the “A gradient of risk is apparent…” quotation in the PDF.. I haven’t found it so far.. so what is its source? An opinion by Mann or PP perhaps??

    Again I question this “house of cards approach” where SFA has some effect on “lipids”, “everyone knows” that “lipids” inevitably leads to CHD and that CHD inevtitably leads to early death GASP!!! shock
    horror!!!! Except it ain’t anywhere near that simple, nor straightforward.

    Of course I realise that diet-trials with humans are fraught with challenges but I repeat that: I do not see a, established direct line of causality from dietary SFAs->”circulating blood cholesterol”->CHD.. let alone that you can skip over the middle part and jump straight from SFAs to CHD… or stop part way before CHD has been demonstrated. If you want to show that dietary SFA’s leads inevitably to CHD, then demonstrate that.

  16. @ R O F L

    …you make a big deal above about researchers not going back to the raw data and also use the word “garbage” in respect to some of the trials included in this meta-analysis… then you offered one which you claim to be of an higher standard…

    This is how they describe the methodology for collecting the plasma lipid data, used in the Oxford Vegetarian Study (above)…

    “Between April 1984 and January 1986, all surviving subjects under age 70 y were sent a kit … We obtained plasma lipid measurements for 3773 subjects, a response rate of <40%. Total cholesterol concentration was measured directly and LDL- and HDL-cholesterol concentrations were calculated by subtraction as described elsewhere (4). Triacylglycerol concentration was not measured because, for practical reasons, it was not possible to ensure that the blood samples were collected under fasting conditions."

    So less than 40% actually had a (single) blood test, with no concern for fasting or not.

    Sure the researchers then go on to create all kinds of impressive-looking data and statistics from what they have collected but there is another saying related to handling data, “garbage in, garbage out”

  17. For the sake of consistency, since Richard is usually concerned about conflicts he could have pointed out that at least two of the Oxford authors are essentially vegetarian activists.

  18. @FrankG

    Here’s the paper where the quote came from

    https://heart.bmj.com/content/78/5/450.full
    Dietary determinants of ischaemic heart disease in health conscious individuals

    “The findings support the hypothesis that the nature and quantity of dietary fat and cholesterol are key determinants of IHD mortality.2 3 A gradient of risk is apparent with increasing intake of total animal fat, saturated fat, and dietary cholesterol as well as some of the major food sources of these nutrients. Further indirect support for a key role of dietary saturated fat and cholesterol in promoting IHD comes from the difference in serum cholesterol between vegetarians and meat eaters; we and others have reported differences of between 0.4 and 0.6 mmol/l.18-20Law et al estimated that a 0.6 mmol/l difference in total serum cholesterol would cause a 27% difference in IHD mortality and a 10% difference in all cause mortality,21 predictions that are close to those observed in a meta-analysis including our own and four other studies of vegetarians.12 Serum cholesterol differences of this magnitude would be predicted on the basis of the difference in intake of saturated fat and cholesterol between vegetarians and non-vegetarians.13 22”

  19. Thanks again Charles… yes I noticed the other paper was also replete with “predictions” about the health outcomes. I’d rather see the conclusions on observed outcomes, than what they “think” might happen.

    Also worth noting that here we have a prime example of multiple papers, with different titles and different publication dates but both are based on the same study. Great way to skew meta-analyses to an agenda…

  20. Am I the only one who finds it … odd that the blogger chooses to a) include studies which – according to e.g.Stamler (who he cites) – were of “low methological quality” and b) studies that didn’t report CHD deaths accurately?

  21. @ Mie… you mean HealthyLongevity (gotta love these names)..?

    What do you expect… this is just another anonymous veg*n blogger — why do they feel the need to slink around anonymously when they have such conviction about their message… it just makes me think they are not to be trusted —

    As with R O F L, you really can’t expect rational discussion… all bets are off when the only motivation is to reinforce their agenda, by any means

  22. Am I the only one who finds it … odd that the blogger chooses to a) include studies which – according to e.g.Stamler (who he cites) – were of “low methological quality” and b) studies that didn’t report CHD deaths accurately?

    But these were the exact studies that were used in both S-T meta-analysis and in the new meta-analysis published in the Annals of Internal medicine. HealthyL writes:

    In order to ensure that the methods used for the statistical analysis were consistent with those used by Siri-Tarino and colleagues, I performed the meta-analysis in Review Manager (from The Cochrane Collaboration), and pooled the estimates using the random effects model for both within-study and between-study variation. Similarly, risk ratios and 95% confidence intervals were log transformed to derive the corresponding standard error for beta-coefficients by using Greenland’s formula.23 Otherwise, the exact P-value was used where available to derive the corresponding standard error.

    In a meta-analysis including 14 studies, dietary saturated fat intake was associated with a statistically highly significant 24% increased risk of death from coronary heart disease (Fig. 1). Similarly, for the 11 studies included in the Siri-Tarino meta-analysis, saturated fat was associated with a statistically highly significant 26% increased risk of death from coronary heart disease (RR=1.26 [95% CI, 1.14-1.40]). In order to ensure that the methods used for the statistical analysis were consistent with those used by Siri-Tarino and colleagues, I performed the meta-analysis in Review Manager (from The Cochrane Collaboration), and pooled the estimates using the random effects model for both within-study and between-study variation. Similarly, risk ratios and 95% confidence intervals were log transformed to derive the corresponding standard error for beta-coefficients by using Greenland’s formula.23 Otherwise, the exact P-value was used where available to derive the corresponding standard error.

  23. Moreover Mie,

    HealthyL performed a separate sub-analysis excluding the 40% of studies that controlled for either serum or LDL cholesterol. SFA was associated with statistically significant 30% increased risk of death from coronary heart disease, consistent with the findings of Stamler (2010).

  24. Frank: that was more of a rhetorical question. I’ve debated with HL here on Axel’s blog before. I know the type: some good points but also suffering from bias.

    As for anonymity, I don’t consider it an issue – though I may be biased for an obvious reason :-). The information value of a statement doesn’t depend on the person uttering it.

  25. Richard:

    “But these were the exact studies that were used in both S-T meta-analysis and in the new meta-analysis published in the Annals of Internal medicine.”

    I know. I merely pointed out that it’s a bit … strange that one should BOTH embrace Stamler’s points AND yet use the same studies. Plus include studies that didn’t have accurate information on CHD deaths. If that isn’t precisely missing “the devil in the details” – on purpose, as it seems – I don’t know what is.

  26. Mie,

    the problem is not about using poor data per se. The problem was that both S-T and especially Chowdhury made extravagant conclusion and confused the public. These people did not factor the poor methodology of the type of studies they used in their conclusions. And this is a problem, as Willet pointed out. And, S-T did not even look at the link between SFA and CHD mortality in their original paper. HealthyLongevity attempted to clear this confusion. SFA increases the risk of premature death significantly (the strength of this association is most likely diluted due to number of reasons) even when looked at more reductionist, single nutrient fashion.

    David Katz had some excellent remarks of this paper as well; even if this was a sound study (which it wasn’t), it merely illustrated that in the context of Western diet, people eating higher or slightly lower amounts of SFA will have equally much heart disease, roughly speaking; those with SFA intake at the lower end, actually had less CHD (albeit statistically significant finding). However, we just know how to fare much better and butter really does not have a place in these arrangements that fare better (Ornish/McDougall; DASH, Lyon diet, etc).
    https://www.huffingtonpost.com/david-katz-md/bittman-butter_b_5042270.html

  27. @ROFL

    https://www.huffingtonpost.com/david-katz-md/best-diets_b_950672.html

    “What may surprise the staunchest proponents of a vegan diet — such as Dr. T. Colin Campbell and his many followers — is the lack of evidence that veganism is better for our health than well-practiced omnivorousness.”

    “So we are left with evidence of clear health benefits from some mixed diets, without any means to compare them directly to the benefits attached to plant-only diets. The Mediterranean diet — more a class of diets than one per se — stands out. Studies suggest benefits across a spectrum of health outcomes, from weight to cancer, cardiovascular disease to life expectancy. The benefits are not discernibly less, and could even be greater, than those chronicled for vegetarianism.

    A balanced, mixed diet of plant and animal foods was used in the Diabetes Prevention Program, and produced a 58 percent reduction in the incidence of Type 2 diabetes in high-risk adults. In the various DASH diet studies, a diet including low- and non-fat dairy was more effective than a plant-based diet without dairy, at lowering blood pressure.”

    “The theme of healthful eating consistently emphasizes the same foods: vegetables, fruits, beans, legumes, nuts, seeds and whole grains. Some variations include fish and seafood, others do not. Some include low- and non-fat dairy, others do not. Some include lean meats, others do not. All banish highly processed foods delivering concentrated doses of refined starch, sugar, trans fat, certain saturated fats and/or salt to the realm of rare indulgence.

    The contest to determine “the best” diet has simply not been run, possibly can’t be and probably never will be. The theme of healthful eating, however, is very well established. Adopt your preferred variation on that theme, but stick to the theme and let the food you love … love you back.”

  28. @ Mie

    Although I can agree in principle with the statement “The information value of a statement doesn’t depend on the person uttering it.” I hope you can also agree that seeking unbiased advice on race relations would probably be better sourced from the United Nations than from a Neo-Nazi organisation?

    In the same way I prefer not to get nutritional advice from those with an ideology such as veganity… I find it tends to cloud their objectivity.

    I can accept the anonymity of commenters on a blog — especially if they comment frequently enough (even using the same alias each time!) so one gets a sense of their consistency and reliability — i.e. even if we don’t always agree, they at least don’t continually contradict themselves so as to “win points”. Indeed it is to be expected that most commenters (unless they have their own blog or website) are anonymous, so as a mater of course, I read their comments with an appropriately skeptical level of understanding and expectation.

    However I am loathe to accept the trustworthiness of those who set themselves up as “authorities” with their own blog, while consciously choosing to remain anonymous. I suspect that they have something to hide. Someone like PP who has the time (and money??) to devote to endless hours of YouTube presentations droning on and on and on… my immediate suspicions include “what is his agenda” and “who is funding it”?

    There may be gems of wisdom buried in their ramblings but I am assured that such wisdom may be gleaned from other more reputable sources, without having to drag myself through the mire to find them.

    It also is not at all uncommon for bloggers such as PP and HL to spend considerable time and effort bad-mouthing others who ARE publicly accountable as MDs, researchers and/or bloggers with real names, faces and contact details; while PP, HL etc… have no accountability to any of their own readers.

  29. @Charles,

    T Colin Campbell argues that whole-food plant-based diet is the best diet because it’s the only diet that provided extremely low cholesterol levels compared to Western norm. David Katz has never even heard Brown & Goldstein’s research. I personally won’t set up for LDL >70. I am not a vegan, nor does Campbell maintain that people have to be vegans, he says animal foods need to be 70. Very few mammalians in the wild have LDL above 70. I eat milk chocolate weekly and some fish maybe once a month. If my LDL is above 70 I need to quit the chocolate for good.

  30. @ROFL

    1) Why should we assume that Campbell is correct?

    2) You say that David has NEVER heard of Brown & Goldstein’s research on LDL receptors. Can you offer proof for that statement?

    3) Brown & Goldstein said – “The receptor binds LDL optimally when the lipoprotein is present at a cholesterol concentration of 2.5 mg/dl. In view of the 10 to 1 gradient between concentrations of LDL in plasma and interstitial fluid, a level of LDL-cholesterol in plasma of 25 mg/dl would be sufficient to nourish body cells with cholesterol.”

    Based on that isn’t LDL>70 WAY TOO HIGH?

  31. https://www.heartattackproof.com/moderation_kills.htm
    By Caldwell B. Esselstyn, Jr, MD

    They ate no oils, fish, meat or dairy products (except skim milk and non-fat cheese and yogurt). The patients also took cholesterol-lowering medication as necessary to maintain their total serum cholesterol below 150 mg/dL.

    At 5 Years, Heart Disease was Halted

    Eighteen patients adhered to the diet and medications, bringing their mean cholesterol level from 237 mg/dL at baseline to 137 mg/dL at 5 years.

    At 12 Years, the Benefits Continue

    Today, the remaining 17 patients continue to follow the prescribed diet and medication schedules. At 12 years, their mean cholesterol level was 145 mg/dL.

    SO – the patients were on statins for the ENTIRE length of the “experiment”!!

    The question remains – was it the diet, the medications or a combination of both? How is one to know which was more important? If the TC was lowered to <150 by statins alone would that be considered a success?

    Also – skim milk was allowed on the diet! Why that AND non-fat cheese and yogurt (which are heavily processed foods)??

    Inquiring minds want to know

  32. @Charles,

    1) here’s no straightforward evidence to suggest whole-food vegan diet is the best, but there are some strong scientific leads that definitely point to that direction in my view. And the LDL theory is being one, perhaps the most compelling line of evidence. But pay attention to what I wrote, not even Campbell nor McDougall insist one has to be 100% whole-food vegan for health reasons.

    In regards to Esselsntyns study. The patient who showed the most regression of his coronary artery disease measured by angiogram was his colleague who did not take statins. He had his LDL in the range of 38mg/dl.
    https://www.heartattackproof.com/revolution_clip_clip_image002.jpg

    Most of the patient took lovastatin which has never shown to lead to regression of the CHD; its a low potency statin. So statins cannot explain this. Most of the patients of Esselstyn and Ornish did not have the perfect LDL, they were mostly in the range of 80s. Even these people showed dramatic reductions of the their disease after adhering to plant-based diet. Dean Ornish discusses this thoroughly in his book. Accoring to him non-cholesterol plant-food diet results in regression of CHD even though the cholesterol levels would not entirely match up. Although, those who showed the largest drop in LDL, also showed the largest regression in the Ornish study.

    You should read Esselstyns book, as you many unfounded ideas about his regime. He indeed allowed skim-milk and yoghurt initially but banned them in a matter of first weeks during the course of study after reading about T Colin Campbell in New York Times (that was in the1990s).

    2) According to Brown & Goldstein the LDL-receptors get saturated at 60mg/dl (1.5mmol/l) and anything above this is probably harmful. There’s no particular reason I said 70mg/dl, but at least it’s way below 80 and regression of CHD has been shown to occur in when LDL is around the 70s in statin studies. My LDL is currently at 70mg/dl, and I am ok with that. I can pull that lifestyle without having to be too “extreme”. I probably start taking low-potency statins the days when I cheat with chocolate or fish.

    “Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies”.

    B & G; 1985

  33. @ R O F L

    “Most of the patient took lovastatin which has never shown to lead to regression of the CHD; its a low potency statin. So statins cannot explain this.”

    Then why were they prescribed for this study?

  34. @R O F L…

    “He indeed allowed skim-milk and yoghurt initially but banned them in a matter of first weeks during the course of study after reading about T Colin Campbell in New York Times”

    Why is this change in methodology NOT mentioned in the “Method” section of the published article — as seen below from Caldwell B. Esselstyn, Jr., M.D. ‘s own web site https://www.heartattackproof.com/… where incidentally I note you can buy his book!

    Is this common (or even acceptable) practice during a study? Practical changes I can understand but surely these should be highlighted in the text? Or maybe this was not deemed significant.. but then why BAN them?!?

    Notably I do see that the “relaxation and meditation” techniques were abandoned… seemingly due to non-compliance.

    Also notable is a lengthy section titled “Promoting Adherence to the Diet” which also fails to mention any change to the policy on “skim-milk and yoghurt”. Guess you can’t believe everything you read… eh?

    With so much up in the air, one wonders how compliant they were with the rest of the study AND how that might reflect on any conclusions being drawn from it.

    “A Strategy to Arrest and Reverse Coronary Artery Disease: A 5-Year Longitudinal Study of a Single Physician’s Practice

    Methods
    Caldwell B. Esselstyn, Jr, MD; Stephen G. Ellis, MD; Sharon V. Medendorp, MPH; and Timothy D. Crowe

    Therapeutic Interventions

    Participants were asked to adhere to a diet that derived less than 10% of its calories from fat. They were to avoid oils, meat, fish, fowl, and dairy products, except for skim milk and nonfat yogurt. Grains, legumes, lentils, vegeta bles, and fruit comprised the major portion of the diet, which contained adequate amounts of vitamins, minerals, protein, and iron.’6~’7 A list of fat-free recipes taken from cookbooks and other resources that focus on weight loss, nutrition, and lifestyle changes to improve heart health18-26 was provided to each participant. Daily food diaries were kept and reviewed with the physician during biweekly visits. Participants were also encouraged to take a daily multivitamin and were asked, but not required, to moderate their consumption of alcohol and caffeine. There were no prescribed exercise requirements.

    Each participant also received an individualized prescription for a cholesterol-lowering drug. The most frequent regimen included cholestyramine, 4 g twice daily, and lovastarin, 40 mg to 60 mg daily. Time-release niacin was prescribed for a short while but was discontinued when many patients reported nausea, vomiting, and swollen ankles.

    Participants also received several hours of instruction in relaxation and meditation techniques through the Cleveland Clinic’s Department of Psychology. However, all participants discontinued these techniques after only a few weeks of sporadic use, so this part of the intervention was abandoned.”

    https://www.heartattackproof.com/study02_methods.htm

    Once again R O F L, your credibility is stretched beyond the bounds of reason… playing “chase your own tail” with often contradictory ad hoc explanations, for oh so many inconsistencies, must me SUCH hard work 😛

  35. Frank:

    “I hope you can also agree that seeking unbiased advice on race relations would probably be better sourced from the United Nations than from a Neo-Nazi organisation?”

    Yep. However, you do realize that examining a statement in the context of conversation and looking for information PRIMARILY e.g. on a politically motivated website aren’t comparable?

    “However I am loathe to accept the trustworthiness of those who set themselves up as “authorities” with their own blog, while consciously choosing to remain anonymous. I suspect that they have something to hide. Someone like PP who has the time (and money??) to devote to endless hours of YouTube presentations droning on and on and on… my immediate suspicions include “what is his agenda” and “who is funding it”?”

    Feel free to suspect it. Might be a good idea. And of course one should prefer scientific literature over blogs etc. However, certain things are primary concern and others of secondary concern.

    “It also is not at all uncommon for bloggers such as PP and HL to spend considerable time and effort bad-mouthing others who ARE publicly accountable as MDs, researchers and/or bloggers with real names, faces and contact details; while PP, HL etc… have no accountability to any of their own readers.”

    When talking about nutrition, I find it at least as common that MDs, bloggers etc. etc. writing under their own names badmouth scientists, other bloggers etc. etc. Just think of Eades, Colpo, Moore etc. etc.

  36. @ROTF

    “not even Campbell nor McDougall insist one has to be 100% whole-food vegan for health reasons.”

    Wrong!

    https://www.chewfo.com/diets/the-starch-solution-by-john-mcdougall-and-mary-mcdougall-2012-what-to-eat-and-foods-to-avoid-food-list/

    Foods to avoid or limit with The Starch Solution

    Stay away from these foods altogether, all of the time, for the rest of your life.

    Meat
    E.g. beef, pork, lamb
    Poultry
    E.g. chicken, turkey, duck
    Dairy foods
    E.g. milk, cheese, yogurt, sour cream
    Eggs
    Seafood
    Animal fats
    E.g. lard and butter

    https://www.drmcdougall.com/health/education/free-mcdougall-program/introduction/plant-foods-provide-nutritional-building-blocks-to-optimum-health/

    Humans were designed by nature to crave carbohydrates. With their unique combination of sweet flavor, energy and nutrition, carbohydrates regulate our hunger drive. There are no carbohydrates in red meat, poultry, fish, shellfish, or eggs, and most dairy products contain little if any. Cheese, for example, contains only two percent. This is an important reason why people who eat a diet rich in animal foods rarely feel satisfied and become compulsive overeaters. Unless you eat enough carbohydrate foods, you’ll remain hungry and crave more food.

    Unprocessed plant foods like brown rice, potatoes, squash, broccoli, and apples (just to name a few) are loaded with complex carbohydrates – long chains of sugars that must be broken down inside your intestine before they can be used as fuel. The process of digesting these complex carbohydrates is slow and methodical, providing a steady stream of fuel pumped into your bloodstream as long-lasting energy. On the McDougall diet, 70% – 90% percent of your calories are derived from complex carbohydrates, providing you with all the nutrients you need for optimum health, plus a high level of vitality and endurance.

  37. Richard gets honest. Well relatively:

    “There’s no straightforward evidence to suggest whole-food vegan diet is the best”

    Indeed not. As long as diets fulfill certain criteria, there’s really only one key thing: choose a diet which you can adhere to. Be it low-fat vegan, Med. diet, paleo, DASH, etc. etc. – doesn’t really matter.

    But then, the backpedalling starts.

    “In regards to Esselsntyns study …”

    Yes, in regards to this study:

    – no control group –> essentially descriptive in nature –> no ability to determine causal relationship nor suggest that this particular diet is the best

    – medication used alongside diet & no control group –> see above

    Essentially, what Esselstyn is saying (a healthy diet improves the outcomes in patients who are already on medication) is correct. E.g. PREDIMED proved this recently. However, his study simply has no power to answer the questions mentioned by Charles.

    As for Katz never having heard of Nobel prize winners: well, that’s just a case of Richard going boo-hoo since Katz is being HONEST all the way by not claiming that one particular dietary regimen has been proven superior. Now, Richard DID mention the same himself, but Katz’s “crime” was – obviously – that he had too much integrity not to downplay this. Unlike Richard, who thinks of nothing of trying to ignore the methodological shortcomings of EVERY study that supports his interpretations. Much like of blogger “pal”, HL.

    Finally, a question to all who feel like answering:

    In my opinion, when it comes to ignorance, arrogance, cherry-picking and generally bad behaviour on the Internet – when discussing nutrition – you really can’t beat two groups: vegans and low-carbers. Why do you think that is so?

  38. @ROTF

    https://www.heartattackproof.com/reversal01.htm

    “The only goal was to achieve and maintain a total serum cholesterol of <150 mg/dl."

    "Combining a plant-based diet with medication achieves better long-term results than changing diet alone or combining modest diet changes and medication."

    "These significant lipid reductions were undoubtedly because of our unrelenting persistence in dietary compliance combined with a statin agent."

  39. Low-dose statins were prescribed for the Esselstyn patients because his patients were suffering from a severe CHD; chests cut open in the form bypasses, multiple heart events, etc. It would have been unethical to not to prescribe drugs for people with this severe condition. This drugs lower cholesterol. Ornish was several years ahead, and at that time had no similar ethical concerns, as the evidence from statins was not quite yet there. Esselstyn’s own colleague who decided not to take statins was an exception, since he was a doctor himself and knew what he was putting himself into.

    I recommend this article from Esselstyns colleague to Doc. This is a top-snoch cardiologist:

    “During my training at Yale and Harvard with many outstanding physicians and scientists, I learned little about this approach. For years after my training, I applied evidence-based medicine, recommended a “healthier” lifestyle, which typically included a Mediterranean-style diet, and watched as my patients’ diseases often progressed. I became frustrated. There had to be something more
    https://www.forksoverknives.com/the-plant-based-lifestyle-is-the-best-medicine-i-ever-prescribed/

    It is very easy to for us to accept the findings of Esselstyn since they have been replicated years before with rigorously controlled feeding experiments with non-human primates and also in Ornish celebrated study (40% LDL reduction in 12-weeks cannot be explained by Yoga). Esselstyn had a control consisting of 6 people who received the state-of-art treatment. Despite having similar measurable amounts of disease at baseline as the other 18 patients, the 6 non-adherent patients had 13 new cardiac events within the first 12 years of the study despite the fact that they were still receiving standard care. On the other hand, the 18 compliant participants had no further cardiac events while being fully compliant, despite having 49 events during the 8 years prior to the study, of for which most of this time were receiving standard care. To claim otherwise is just an outright lie

    To claim that Paleo trademark diet with 50% of calories consisting of flesh is a sound approach to healthy eating is just blatantly insane. Paleo diet induces significant increase in non-HDL cholesterol on a healthy subjects even in a context of heavy exercise routine. We are not going to see paleo TM as list of healthy diet in website of major Public organizations anytime soon.
    https://kb.osu.edu/dspace/handle/1811/54660

    Esselstyn proved beyond doubt that even 100% regression of CHD (as measured by angiogram) is possible with low-fat diet and lovastatin. But, hey just because he didn’t conduct 100% controlled, double-blinded RCT we can pretend that paleo-diet and whatever fad diet is healthy. Yeah, sure Vegans are just like the low-carbers and Paleo is soon to be promoted by the AHA, WHO, etc. Phew…..you surely bump up to a lot nonsense online.

    American Institute for Cancer Research; the China Study, and Forks Over Knives
    https://www.aicr.org/about/advocacy/the-china-study.html

  40. @ROTF

    https://www.heartattackproof.com/resolving_cade.htm
    “a plant-based diet in conjunction with cholesterol-reducing medication eliminated progression of coronary artery disease over a 12-year period in patients with triple-vessel disease. Most of the 18 patients had experienced an earlier failed intervention of bypass surgery or angioplasty. All patients who maintained the diet achieved the cholesterol goal of less than 150 mg/dL and had no recurrent coronary events during the 12 years”

    Look at figure 2 – Coronary angiograms of the circumflex artery before (left) and showing 20% improvement (right) following approximately 60 months of a plant-based diet with cholesterol-lowering medication

    This is the patient you’re talking about
    “This patient was aware of my ongoing study and was curious for more information. He and his wife consulted me for an in-depth review of the plant-based diet and techniques of this arrest and reversal study. He became the personification of commitment to the plant-based diet. Over the next 32 months, without cholesterol-lowering drugs, he maintained a mean total cholesterol of 89 mg/dL and an LDL of 38 mg/dL. The repeat angiogram 32 months after his infarction showed that the disease was completely reversed.”

    No details about this person’s regimen at all.

  41. @Mie

    “When talking about nutrition, I find it at least as common that MDs, bloggers etc. etc. writing under their own names badmouth scientists, other bloggers etc. …”

    Yes I see the same but my point was more to do with the accountability. For example: if Dr Eades were to make serious medico-legal allegations against another MD or business, he might then face legal or disciplinary action. Similarly if he were to offer individualised medical advice online, or even how, what he writes may be viewed by his peers — affecting his chances of getting on certain medical advisory-boards etc. etc. Anonymous bloggers have no such checks and bounds… blog commenters even less so… just in the last post we had ROFL stating categorically to fellow-commenter VeryLowLDL36 “…you are NOT going to die in CHD”. Can you see Dr Eades making such an unfounded promise?

    This is the internet after all, there are plenty of sources to choose from. I generally start off by giving the benefit of the doubt but once my trust is lost, it is an uphill struggle to convince me otherwise.

    Which brings me to your “…when it comes to ignorance, arrogance, cherry-picking and generally bad behaviour on the Internet – when discussing nutrition – you really can’t beat two groups: vegans and low-carbers.”

    Were you including me in this? Yes my diet is currently based on LCHF principles and by all my health markers I am doing very well on it but what I eat does not define who I am, nor do I consider myself to be part of a group, ideology or belief system akin to veganity. To me the difference is analogous with the way Richard Dawkins talks about fundamental religious individuals… there are some (many?) of these latter who state clearly that no amount of evidence will shake their beliefs, while Dawkins himself is open to accepting the supernatural, if convincing evidence were presented.

    I am currently convinced that the way I eat is healthy for me. I have already changed from low-fat paradigm (and incidentally, also broken away from a strict Catholic upbringing) but I remain open to change even today, IF convincing evidence comes to light. So far, all I see is the same old, same old, repeated ad nausem by people like ROFL.

    If I seem particularly aggressive towards ROFL here, it is because I not only see the potential harm that his dogma has caused and is continuing to cause, but (as you may have gathered) this is not my first encounter with him (she/it.. who knows with proxy servers and multiple aliases). I did start off by attempting reasonable discussion but once I realised the utter contempt he has for others, that seemed to be a fruitless approach.

    As a general rule I do try to follow the guideline of “never write anything on the internet that you would not say to that person’s face” and rest assured that I would speak my mind freely, if face to face to ROFL… in this case the contempt is mutual.

  42. Charles,

    the details are in the book. Its a good book, I recommend it to everyone.

    BTW, there exist some kind of misinformation about statins here. Statins were originally not designed to regress CHD but reduce CHD events (compared to controls). It wasn’t until the high potency statins (rosuvastatin and atorvastatin) hit the market when scientists discovered that these drugs could actually induce regression of CHD at high doses. Lovastatin has never shown to regress CHD, it has only been shown to reduce CHD events compared to those that were not taking the drugs. Moreover, not even high potency statins have been shown to make people immune to future events, even when plaques get regressed and more stable, they can still cause a rupture in people with existing CHD. Esselstyn’s success cannot attributed to lovastatin, far from that.

  43. @R O F L

    so it seems we have gone from your assertions of “stronger and superior methodology” to “the details are in the book”… not even peer reviewed by anyone???

    Where can I get a free online copy of this fantastical book… I’d hate to think that the good doctor might be accused of being motivated by profit from its sales?

    Best I can tell is: we have an anecdotal tale of maybe 11 of Esselstyn’s own patients, in his own words and this is supposed to convince anybody that “Esselstyn proved beyond doubt that even 100% regression of CHD (as measured by angiogram) is possible with low-fat diet and lovastatin”

    …you surely DO bump up to a lot nonsense online… especially from such “top-snoch” sources 😛

  44. @R O F L

    “Moreover, not even high potency statins have been shown to make people immune to future events, even when plaques get regressed and more stable, they can still cause a rupture in people with existing CHD”

    So are you saying that the angiograms used by Esselstyn to show regression of his patients plaque, is similarly no guarantee that it would make them “immune to future events”??? Oh noes!!!

  45. @ROLF

    So -why did Esselstyn use statins for the ENTIRE length of the experiment? Why not take patients off of them?

  46. @ROTF

    “Esselstyn proved beyond doubt that even 100% regression of CHD (as measured by angiogram) is possible with low-fat diet and lovastatin. But, hey just because he didn’t conduct 100% controlled, double-blinded RCT we can pretend that paleo-diet and whatever fad diet is healthy. Yeah, sure Vegans are just like the low-carbers and Paleo is soon to be promoted by the AHA, WHO, etc. Phew…..you surely bump up to a lot nonsense online.”

    My question still remains unanswered – since this wasn’t a 100% controlled, double-blinded RCT how do we know what % of regression due to low TC was caused by the diet and what % was caused by the statin.

    The mantra is to get your TC<150 by ANY MEANS NECESSARY, drugs, diet or a combination of the two – which method is better??

  47. Charles,

    you’ve been answered countless of times already. You are just too confused and busy with your own material. Lovastatins have been shown to reduce cardiadic events next to controls, but it has never shown to result in regression of CHD. You keep treating these two things as synonyms. Lovastatin cannot explain the regression of CHD in Esselstyns patients because lovastatin does not regress CHD. It doesn’t get any more simple than that.

    Anyways, a lot of intense discussion. We have to agree that we disagree, but I am sure we all agree with the message of this great paper written by the prominent paleo authors both having their paleo cookbooks on the market. This is one my “pearls” for you.

    Optimal low-density lipoprotein is 50 to 70 mg/dl – Lower is better and physiologically normal
    https://content.onlinejacc.org/article.aspx?articleid=1135650

  48. https://content.onlinejacc.org/article.aspx?articleid=1135650

    “The normal low-density lipoprotein (LDL) cholesterol range is 50 to 70 mg/dl for native hunter-gatherers, healthy human neonates, free-living primates, and other wild mammals (all of whom do not develop atherosclerosis). “

    While, no doubt, such a statement has been used to boost sales of statins it could equally be taken as motivation to eat more like “native hunter-gatherers”

    “We live in a world very different from that for which we are genetically adapted. Profound changes in our environment began with the introduction of agriculture and animal husbandry 10,000 years ago, too recent on an evolutionary time scale for the human genome to adjust. As a result of this ever-worsening discordance between our ancient genetically determined biology and the nutritional, cultural, and activity patterns in modern populations, many of the so-called diseases of civilization, including atherosclerosis, have emerged. Evidence from hunter-gatherer populations while they were still following their indigenous lifestyles showed no evidence for atherosclerosis, even in individuals living into the seventh and eighth decades of life (15-16). These populations had total cholesterol levels of 100 to 150 mg/dl with estimated LDL cholesterol levels of about 50 to 75 mg/dl.”

    This may suggest, “real whole food” as opposed to processed, packaged etc… but says nothing about “low-fat”, “plant-based” or anything of that kind. Indeed gorillas. although herbivores (with a significantly different digestive tract to humans), have a caecum and colon harbouring huge colonies of bacteria which ferment carbohydrates, particularly fibre, and use it to produce and absorb 60% or more of their diet as short chain fatty acids (SCFA) — principally acetic, proprionic and butyric (as in butter) acids.

  49. Frank:

    “Yes I see the same but my point was more to do with the accountability. For example: if Dr Eades were to make serious medico-legal allegations against another MD or business, he might then face legal or disciplinary action. Similarly if he were to offer individualised medical advice online, or even how, what he writes may be viewed by his peers — affecting his chances of getting on certain medical advisory-boards etc. etc. ”

    Perhaps so. Hopefully so. However, in terms of giving pseudoscientific advice, none of these “gurus” don’t have the same kind of responsibility as e.g. a person’s own physician. Consider, for instance, cholesterol denialism: potentially dangerous notions are being spread with no regard to … well, anything.

    “Were you including me in this?”

    Nope. On the basis of what you’ve written, I see no reason to do so. I wasn’t trying to make a blanket statement, but merely brought out my observation that the further away from e.g. ADA or AHA dietary guidelines people seem to go, the more hostile towards “moderation” or the variety of healthy diets out there they tend to become. Suddenly, it’s “one size fits all” and to hell away with anything that doesn’t fit the formula.

    “If I seem particularly aggressive towards ROFL here, it is because I not only see the potential harm that his dogma has caused and is continuing to cause, but (as you may have gathered) this is not my first encounter with him (she/it.. who knows with proxy servers and multiple aliases). I did start off by attempting reasonable discussion but once I realised the utter contempt he has for others, that seemed to be a fruitless approach.”

    I hear you. And understand.

  50. ^Charles,

    lovastatin induces rather quick reduction on cholesterol levels in pretty much every person, the time factor is crucial for people with severe CHD. However, as Esselstyn’s MD colleague proved, lovastatin is not necessary for a 100% reduction in CHD (measured by angiogram) in humans. This can be achieved by diet alone.

  51. @R O F L

    “the article says nothing about plant-based diets because its written by paleo-authors.”

    There really is no end to your utter contempt for the truth.. in the same breath you will laud a study as a “great paper” because it suits your agenda of low “LDL” at any cost, then turn around and dismiss it as written by “paleo-authors”

    Kind of like how Esselstyn’s write-up of his 11 patients was supposedly using “stronger and superior methodology” than many others, and yet apparently he overlooked mentioning that milk and yoghurt were banned shortly after the treatment started. Given that you claim diet was the main (and only?) thrust of this treatment, I take that as a significant oversight. But then again he himself accepts the role of statins in the treatment while you say otherwise… based on what? As they were used, you cannot dismiss their effect without further trials.

    So far as diet goes with the paper from these “paleo-authors” , I don’t particularly see ANY discussion of it. The comments above were my own… or are you seriously trying to suggest that native hunter-gatherers, or humans neonates achieve these wondrous “LDL” levels by virtue of a low-fat, whole-food, plant-based diet?!? Do I need to link to the nutritional data on human breast milk perhaps? Maybe you can list traditional hunter-gatherers (not religious sects) who are vegan or even vegetarian?

    And I quote “LDL” because: as Paul Jaminet points out, this study does not seem to have any actual basis for the numbers AND because (once again) you are using a 10 year old (at least) paper to simplify the complex subject of “cholesterol”, as if “LDL” is a simple heterogeneous concept, or that it can be considered in isolation from all other health markers.

    You continue to stretch the bounds of credibility, way beyond reason. You are a fraud and not to be trusted. I have to no interest in even attempting reasoned discussion with you, because you show utter contempt for reason… your only interest is in “winning points” by whatever means.. using the flimsiest of ad hoc explanations, contradicting yourself at every turn-about and constant inconsistencies — even when these are pointed out, you simple ignore them and plow on regardless. Nevertheless I shall continue to point them out when I can.

  52. You gotta love Richard’s way of thinking, in a perverse way of course.

    First, Frank presented him an article that argues for THE SAME THING as Richard – LDL levels such as our hunter-gatherer ancestors had. However, this isn’t good enough for Richard because the article doesn’t endorse one specific type of diet. Now, the average reader with a brain & no bias would understand that this is because the article IS NOT A REVIEW CONCERNING DIETS but argues for LDL lowering per se.

    Second, Esselstyn’s descriptive study with several weaknesses (no controls, quite a large initial drop-out rate with 5 out of 22 quitting initially etc. etc.) is supposed to “prove” something. And even more laughable, one patient case (n=1), the MD colleague of his, is supposed to be “further proof”.

  53. ^LOL,

    give me a break. I explicitly highlighted that the article I linked to was written by paleo proponents, and told to you that we can probably all agree with it’s main message: low LDL for the win. If the authors have their paleo cook-books on the market’s we can obviously rely on the fact that no other diets apart from paleo-diet will be espoused. The reason I linked the article was to illustrate that the paleo people have a big elephant in the room. This is indeed an example of twisted logic: to promote low LDL levels and simultaneously promote LDL elevating diet. Brown & Goldstein did not have an elephant in the room:

    “If the LDL receptor hypothesis is correct, the human receptor system is designed to function in the presence of an exceedingly low LDL levels. The kind of diet necessary to maintain such levels would be markedly different from the customary diet in Western industrial countries (and much more stringent than moderate low-cholesterol diets of the kind recommended by the American Heart Association). It would call for total elimination of dairy products as well as eggs, and severely limited intake of meat and saturated fats”.
    https://www.ncbi.nlm.nih.gov/pubmed/6390676

    As said, it’s very easy for us to accept the finding from Esselstyn since low-fat, cholesterol free diet alone has resulted in dramatic reduction in CHD among non-human primates. But if looking single studies in isolation and out of context is your cup of tea, then I guess you can afford to come out as “skeptical”. Not sure such approach is the way scientists work, though. I don’t see why Esselstyn’s drop-our rate should be taken as an argument for the failure of regime to promote immunity from CHD. Obviously at the time of his study, the people did not fully know what to expect. Bill Clinton knew what to expect:
    https://www.examiner.com/article/bill-clinton-improved-heart-health-with-vegan-diet-and-30-pound-weight-loss

    *Real hunter gathers had low LDL most likely due to high fiber intake, seasonal hunger and parasitic burden.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142336/

  54. @ R O F L

    Is this the way YOU think “scientists work” ..?

    “If the LDL receptor hypothesis is correct…” IF and then proceed to build an house of cards on a conditional statement, without proving it to be true. Hmmm…

    And then yet another n=1 anecdote..! From that prestigious scientific journal examiner.com.!!

    “Clinton isn’t a strict vegan because he occasionally has organic salmon and eggs, but his daily diet is largely plant-based. After changing his diet, he also began exercising daily, and now walks two or three miles a day, lifts weights and plays golf.

    The 6-foot-2 Bill said his vegan diet is responsible for his 30-pound weight loss and his boundless energy. He said eliminating animal protein from his diet was surprisingly easy.”

    NOT a strict vegan because he eats fish and eggs..! Is that like not being completely pregnant.. just a BIT pregnant perhaps? I though either you IS or you AIN’T a vegan? And not even strictly a “vegetarian”, as I understand the term… surely eating fish has yet another label?

    But I guess this article does at least show that old politicians (and boy does he look old for his 67 years in that photo) can still be liberal with the truth “…eliminating animal protein from his diet was surprisingly easy”

    Well I guess it all depends on how you define “animal protein” ..eh?!?

    LOL indeed ROFL 😛

    And about this elephant… you assert that “99% paleo-people cannot achieve low LDL, unless statins are prescribed.” What is your source for this wild claim, ‘cos you surely can’t be so deluded as to think anyone would take anything you write, at your word?

  55. Excellent newsletter article of Dr. Ronald Krauss by John McDougall.

    The article covers amazing piece of literature by Krauss from 1986 showing that dietary cholesterol intake is positively correlated with the presencee smalldense LDL particles, and fiber intake is negatively correlated with smalldense LDL: more fiber, less smalldense LDL. This was before Krauss started to work for beef and dairy industry and became a professional merchant of doubt and the most cited author in the low-carb fora.
    https://www.drmcdougall.com/misc/2014nl/mar/krauss2.htm

  56. And to be clear I take no issue with Bill Clinton’s attempt at an healthier lifestyle… I would say, that to me as an outsider just seeing photos, he doesn’t look healthy but what do I know? Losing 30 lbs sounds great but it looks as if some (most?) of that was muscle… maybe not so good.

    No, my issue is with ROFL attempting to use yet another n=1 anecdote as “proof” especially after his sarcastic comments about how to approach science.

    Add to this the fact that Bill Clinton is evidently NOT a vegan (not even strictly speaking a vegetarian) yet the article provide by ROFL is full of misleading statements like…

    Former U.S. president Bill Clinton is winning the war against cardiovascular disease after losing 30 pounds on a vegan diet…

    …said Bill’s daughter, Chelsea Clinton. “He’s probably the world’s most famous vegan. …”

    Clinton, 67, began following a vegan diet in 2011 after undergoing heart surgery in 2010.

    The 6-foot-2 Bill said his vegan diet is responsible for his 30-pound weight loss and his boundless energy.

    Clinton’s veganism has inspired other celebrities to embrace a plant-based diet…

    etc…

    all rounded off with a nice little quote from Dr. Barnard, president of the deceptively named “Physicians Committee for Responsible Medicine”. — Once again I ask why veg*ns feel a need to hide their agenda when they are so confident they have the truth on their side?

    Why (other than utter contempt) are we expected to accept any of this with any degree of credibility?

    This is NOT a valid approach to science ROFL

  57. https://atlanta.cbslocal.com/2014/04/01/study-vegetarians-less-healthy-lower-quality-of-life-than-meat-eaters/
    “A new study from the Medical University of Graz in Austria finds that vegetarians are more physically active, drink less alcohol and smoke less tobacco than those who consume meat in their diets. Vegetarians also have a higher socioeconomic status and a lower body mass index. But the vegetarian diet — characterized by a low consumption of saturated fats and cholesterol that includes increased intake of fruits, vegetables and whole-grain products — carries elevated risks of cancer, allergies and mental health disorders.

    Vegetarians were twice as likely to have allergies, a 50 percent increase in heart attacks and a 50 percent increase in incidences of cancer.

    Overall, vegetarians were found to be in a poorer state of health compared to other dietary groups. Vegetarians reported higher levels of impairment from disorders, chronic diseases, and “suffer significantly more often from anxiety/depression.”

    Subjects who consumed lower amounts of animal fat were also linked to poor health care practices, such as avoidance of vaccinations and a lack of preventive care.

    Chronic problems associated with vegetarians and people eating carnivorous diets rich in fruits and vegetables were linked to more frequent visits to doctors, which the study authors suggest requires public health programs to reduce the health risk due to their nutritional factors.

    The researchers conclude: “Our study has shown that Austrian adults who consume a vegetarian diet are less healthy (in terms of cancer, allergies, and mental health disorders), have a lower quality of life, and also require more medical treatment.”

    https://www.plosone.org/article/fetchObject.action?uri=info:doi/10.1371/journal.pone.0088278&representation=PDF

  58. Yep,

    a crappy paper published in a crappy journal gets people excited. Reverse causation: paradoxical foundlings can have been observed in regards to those who do not consume alcohol at all and those that quit smoking. Those who don’t drink at all are usually former alcoholics and thus automatically at higher risk of death. Those who quit smoking and cut back their intake of saturated fats usually do this because they are at high risk and they’ve bee advised to so by their doctors. These people automatically at higher risk than those who’ve smoked but haven’t had any reason to visit the doctor (yet).

    The results of a recent study from the Netherlands illustrates the critical importance of considering reverse causality in research on plant-based diets. The researchers found that 75% of the vegetarian participants with cancer adopted a vegetarian diet after diagnosis, consistent with previous research which found that cancer survivors are highly motivated to adopt a more plant-based diet with the intention of improving poor health.
    https://www.nutritionj.com/content/12/1/156

    As a n=1 case, I could point out that I have always been impulsive and aggressive (not violent though), I eat a plant-based diet, but that plant-based diet did not cause the impulsiveness. In western culture somewhat marginal people may opt vegetarian diets. This doesn’t mean that vegetarian diet caused anxiety and depression, but it may indicate that people prone to depression and anxiety choose vegetarian diet more often than people who do not face these kind of problems.

  59. @ROFL

    Just got my latest blood work back – taken on 2/24/14

    MNR test results
    LDL-P 401
    LDL-C 47
    HDL-C 44
    Trigs 34
    Small LDL-P 209
    LDL size 21.5
    HDL size 10.3

    AND I eat grass fed beef, full fat raw goat milk, full fat goat milk yogurt/kefir, 1 hard boiled egg/day, raw milk/grass fed cold processed whey protein concentrate in my smoothies, frozen/fresh fruit fruits/veggies, nuts, seeds, raw cacoa powder, etc.

    Also – 10mgs Atorvastatin/day + specific supplements.

  60. @R O F L

    It is really quite entertaining to see you wriggle and squirm to come up with yet another unbelievable ad hoc explanation 😛

    First you dismiss the study out of hand “crappy paper published in a crappy journal” BUT then you go on to rationalise why we should reconsider its findings… so which is it?

    As for many veg*ns being marginal, troubled, anxious, neurotic or sick individuals, I’m sorely tempted to agree in your case but I see little evidence to support that position in general.

    Even if a tendency to mental instability leads a person to veganity in the first place I don’t see that being malnourished can do anything but worsen the outcome.

  61. Psychology Today ~ Low Cholesterol and Suicide
    https://www.psychologytoday.com/blog/evolutionary-psychiatry/201103/low-cholesterol-and-suicide

    Psychology Today ~ Low Cholesterol is Linked to Depression, Suicide, and Violence
    https://www.psychologytoday.com/blog/the-breakthrough-depression-solution/201106/low-cholesterol-and-its-psychological-effects

    Low cholesterol and violent crime
    https://www.ncbi.nlm.nih.gov/pubmed/11104842

    …of course none of these journals come close to the professional heights of examiner.com and their ground-breaking reportage on the 100% “vegan” (cough cough) Bill Clinton.. but hey I guess we’ll just have to make the best of what we can find… 🙂

  62. Yes,

    there are genes that trigger violence and depression in the host (given the right environmental stimuli) these same games can cause low cholesterol levels within the host. And, what should we make about this? Cholesterol lowering with complex carbohydrates has been directly shown to lead better mood scores.

    In regards to low cholesterol and neurological disorders, a mendelian randomization study found that individuals who inherit genetic variants associated with life-long reduced LDL do not have increased depressive symptoms. Also, randomized controlled trials have found that vegetarian diets which are associated with lower cholesterol are also associated with improved moods compared to omnivorous diets. Other randomized controlled trials found that psychological symptoms including depression, hostility and anger improved significantly on a cholesterol lowering, complex-carbohydrate rich diet compared to baseline or carbohydrate restricted diets. Conversely, systematic reviews and meta-analyses of epidemiologic studies have found an association between dairy intake and an increased risk of Parkinson’s disease, and saturated fat and an increased risk of dementia.

    Just few links, I have library of them:
    https://www.ncbi.nlm.nih.gov/pubmed/19444703
    https://www.nutritionj.com/content/11/1/9
    https://archinte.jamanetwork.com/article.aspx?articleid=1108558
    https://www.ncbi.nlm.nih.gov/pubmed/19896503

    The idea that low cholesterol causes horrible conditions such as violent crimes and anxiety is of course very easy to debunk. If low cholesterol was the problem, then we ought to see lot of problems among the native Okinawa people eating their traditional diet. This is not the case. Cholesterol lowering is inherently healthy.

  63. @R O F L

    And still you wriggle and squirm to come up with yet more ad hoc rationalisations 😛

    You surely can’t think that your posts have any credibility.. let alone that you are presenting anything convincing enough to change my mind? You mix unfounded claims with “science” and hope that no one will notice

    “Just few links, I have library of them:”

    WHY? Why do you have a “library” of them? Is that supposed to impress me, or make me think that you are a troll with an (very poorly) hidden agenda?

  64. But one have to remember that in spite of the fact that SFA do not cause heart diseases it has to be avoided while you eat high carb. Carbs form TGs and body fat more strongly while more SFA are in the diet. In other words: the more you mix fuels (carbs and FA) the more fat and ill you will be (eg. modern American diet). While you start avoiding fats or carbs you should expect health improvement. Thus, when people eat HC they should avoid SFA to be healthy. The more SFA they eat the more carbs will be harmless. The other way is to go high fat, but with low carbs. Avoiding fuels mixing is crucial here.

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