Saturated Fats Cause Heart Disease and the Earth Is Flat

Estimated reading time: 6 minutes

If you think flat Earthism is gone, you’re wrong. Some people still believe the earth is flat. The Flat Earth Society even has it own website. The society’s roots may be traced back to the 1800’s.

However, the members don’t use scientific evidence to support their view. According to an interview with the society’s president in The Guardian three years ago, they believe the earth is flat because it appears flat. The sun and moon are spherical, but much smaller than mainstream science says, and they rotate around a plane of the Earth because they appear to do so.

Most public health authorities still recommend that total fat consumption does not exceed 30 percent of total calories and that saturated fats be no greater than 10 percent.

The British, National Institute of Clinical Excellence (NICE) stated in a document in 2010 that in order to better prevent coronary heart disease (CHD) at a population level, the reduction of dietary saturated fat is crucial. They estimated that halving the average intake of saturated fat (from 14 to 7 percent) might prevent 30.000 deaths annually in the UK.

The public health recommendations are very surprising, considering the large amount of data indicating that reducing total fat consumption or the amount of saturated fats in our diet will not reduce mortality or affect the risk of dying from CHD.

The largest controlled intervention trial on diet and heart disease to date, the Women’s Health Initiative randomly assigned more than 48 thousand women, 50 – 79 years old, to a low-fat intervention or a comparison group. Saturated fat intake was lower in the intervention group as was dietary polyunsaturated fat. However, dietary carbohydrates were higher in the intervention group.

After six years of follow-up there were no differences between the groups in the incidence of coronary heart disease and stroke. So, replacing fat with carbohydrates does not seem beneficial.

The much cited Siri Tarino meta-analysis, published 2010 in The American Journal of Clinical Nutrition included 16 prospective observational cohort studies. There was not a significant association between the intake of saturated fats and coronary artery disease.

Ok, I know what you are thinking: “Now the Doc is going to claim the public authorities suffer from flat Earthism. Their recommendations are not based on current scientific evidence but rather reflect stubbornness and a tendency to stick with outdated, previously held views“. But believe me, these were not my words.

The Influence of the Seven Countries Study

Few weeks ago one of my readers drew my attention to a very interesting paper published in Food and Nutrition Sciences last spring, entitled Food for Thought: Have We Been Giving the Wrong Dietary Advice? The paper is written by Zoë Harcombe, Julian S. Baker and Bruce Davies from the University of the West of Scotland, Hamilton, and University of Glamorgan, Pontypridd, UK. The paper may actually bridge some of the gap between the public recommendations and what I believe is currently available scientific evidence.

The authors went through 20 volumes of Ancel Key’s Seven Countries Study. It is well known the American and European public recommendations on diet and nutrition developed in the 1980’s were largely based on evidence from this study.

The main conclusions from the Seven Countries Study were:

  • The incidence rate of CHD tends to be directly related to the levels of blood cholesterol
  • The average level of blood cholesterol is directly related to the average proportion of calories provided by saturated fats in the diet
  • The CHD incidence rates are as closely related to the dietary saturated fatty acids as to the blood cholesterol levels

This is the foundation for the Diet Heart Hypothesis which is still alive and well according to public health recommendations.

The Macronutrient Confusion

Harcombe and coworkers highlight few classification errors in the Seven Countries Study which are quite scary in light of the huge influence of this study on dietary recommendations for the last forty years.

Firstly, they point out that “the dietary references that were mentioned used unquantifiable descriptions such as “loaded with saturated fatty acids” and “cholesterol from butter cream meats and eggs””.

Secondly, “the study classified cake and ice cream as saturated fats, as opposed to refined carbohydrates. Meat and eggs are described as saturated fat when their fat content is primarily unsaturated. Butter and cream are one third unsaturated fat, which was not noted in their analysis. So, here we have a profoundly influential research project introducing imprecise evaluations of macronutrients which have continued to present day”. 

The authors conclude that “The Seven Countries Study was not a scientifically robust study. The dietary references are vague, sporadic or absent.

There were no comments on causation and no attempt was made to consider association until 25 years post study completion and 10-15 years after UK and USA dietary advice had already been changed based on the recommendations of Key´s work. The study clearly demonstrated that the science surrounding macronutrients and nutrition was not as accurate as it is today. Yet contemporary knowledge is not being applied when considering nutritional advice for the population.”

Finally I want to bring forward some important issues highlighted by the authors which may clear up some of the macronutrient confusion:

  • Biscuits, savoury snacks and processed food should not be defined as saturated fats because they are substantially carbohydrates
  • Red meat is not a saturated fat but a combination of various fatty acids
  • Sirloin steak is approximately 71% water, 21% protein, 3% unsaturated fat and 2% saturated fat
  • Natural food such as meat, fish, eggs and nuts contain saturated, monounsaturated and polyunsaturated fats, only the proportions vary
  • Few people appreciate that it is impossible to eat saturated or polyunsaturated fat alone
  • Dairy products are the only food group with more saturated than unsaturated fat
  • Many of the foods demonized by past research groups, even lard, contain more unsaturated than saturated fat.

 The Bottom Line

There appears to be a large gap between public recommendations on the relative consumption of different macronutrients and currently available scientific evidence.

Although this somewhat strange inertia may be compared to flat Earthism, it’s causes are likely complicated and multifactorial.

However, it appears that a part of the problem may be traced to macronutrient confusion and wrong definitions. In fact, it’s quite scary to learn that the Seven Countries Study classified processed foods, primarily carbohydrates, as saturated fats.

Of course, this may have lead to wrong conclusions, some of  which may have affected public health recommendations on diet and nutrition for the last three or four decades.

78 thoughts on “Saturated Fats Cause Heart Disease and the Earth Is Flat”

  1. Thanks for the article. I have recently read “How to Prevent and Reverse Heart Disease” by Dr Caudwell Esselstyn (https://www.amazon.com/Prevent-Reverse-Heart-Disease-Nutrition-Based/dp/1583333002). As a result, I have moved to a fully vegan diet to try to lose weight and reduce my risk of CHD. This book is amazingly persuasive in its arguments and results (he took 24 patients who had sever CHD and halted or reversed their heart disease by cutting out all oils and animal products from their diet. After reading this post, I am very confused. Are you arguing that we should be eating the very things I have given up?

    Reply
    • Thanks for the post Paul. I don´t have anything against vegan diets and I think they can be effective when it comes to reduce cardiovascular risk, in particular if you are aiming to lower your blood cholesterol, although I believe cholesterol is not the only thing that matters. So, I´m not saying you should be eating the things you have given up. Everybody has to make their own choices. Many people feel well on a vegan diet while others don´t.

      What I am saying is that there is a lot of misunderstanding when it comes to saturated fats and the public recommendations may partly reflect macronutrient confusion and problems with definitions. The fear of saturated fats may have kept us from eating natural foods such as meat, eggs and dairy from grazing animals These foods as well as fish, vegetables, nuts, seeds and fruits are all healthy food choices.

      Reply
      • Axel, you do realize that excessive intake of red meat is linked to increased risks of e.g. cancer and stroke? And that for people with diabetes it may be prudent to limit the intake of eggs, as well? I haven’t seen data that would indicate the same things with e.g. nuts or fish.

        Besides, I kinda … well, feel uneasy whenever someone mentions the word “natural” in relation to food. Not everything that is “natural” is good for you. And not everything that your grandma wouldn’t recognize as food (to paraphrase Pollan’s, in many aspects, silly & oversimplified book) is unhealthy.

      • Mie. I´m not promoting red meat. Remember though that correlation does not prove causation. Furthermore red meat may differ very much. For example there may be a huge difference between grass-fed vs grain-fed beef. The fatty acid composition differs quite a lot between these two. Grazing can make a huge difference. So, putting all red meat together as one is just one more example of an oversimplification which may lead to misunderstanding and wrong conclusions.

      • Axel:

        “Mie. I´m not promoting red meat.”

        What do you call this then?

        “The fear of saturated fats may have kept us from eating natural foods such as meat …”

        It seems promotion to me.

        “Remember though that correlation does not prove causation.”

        Oh, fer Christ’s sake! This is stating the obvious & therefore has very little meaning here. We’ve know a) several mechanisms via which excessive red meat intake may cause the aforementioned problems and b) we’ve got pretty unanimous evidence from large observational studies. To state that “correlation …” doesn’t provide an explanation here.

        If you want to argue that the findings of both the mechanism-exploring studies and cohort studies are flawed, you’ll have to do so IN DETAIL. In the meanwhile, I’d argue that it’s better to be cautious and not promote red meat intake on a population level. Especially since it’s record high in Western countries.

        “Furthermore red meat may differ very much. For example there may be a huge difference between grass-fed vs grain-fed beef. The fatty acid composition differs quite a lot between these two. Grazing can make a huge difference.”

        Care to show anything besides anecdotal evidence (which is what I’ve seen so far)? Surrogate data on differences between grain-fed vs grass-fed and e.g. lipid levels?

        “So, putting all red meat together as one is just one more example of an oversimplification which may lead to misunderstanding and wrong conclusions.”

        I made no such claim (“all red meat is alike”). It has been shown that processed red meat is especially problematic. However, even unprocessed red meat in excess increases the risk.

      • I back up doc on this one. Read meat is too often packed together with processed meat. So often you see “red & processed meat plaaplaaplaa”.

        One of the recent meta-analysis in asia area found inverse correlation between red-meat intake and CVD (https://ajcn.nutrition.org/content/early/2013/07/31/ajcn.113.062638.short). Red meat intakes in Asia, are of course much less than for example U.S, but it is also worth to notice that U.S people eat also more than twice the amount of red meat than finnish people(my home country). We should be discussing what is the proper amount to consume. It is not as simple as “the more the better or the lower the better”. Excessive amount of anything will get unhealthy at some point.

      • “I back up doc on this one. Read meat is too often packed together with processed meat. So often you see “red & processed meat plaaplaaplaa”.”

        You have read this one, haven’t you?

        https://www.pronutritionist.net/onko-liha-epaterveellista/

        (For other readers, sorry about the Finnish link but I know “Someone” to be a Finn, so ….)

        “One of the recent meta-analysis in asia area found inverse correlation between red-meat intake and CVD (https://ajcn.nutrition.org/content/early/2013/07/31/ajcn.113.062638.short).”

        Interesting. Thanks for pointing that out. I can’t access the full text, so it’s impossible to really say anything about it. Healthy user effect? Perhaps, perhaps not – since the association of red meat intake & wealth/education/etc. tends to be much stronger in third world countries than in western countries (where nowadays virtually anyone can afford red meat), I wouldn’t be surprised . The amount of red meat consumed in the lowest vs highest quartile in comparison w/ western countries? Dunno.

        If you’ve read the full text, perhaps you can elaborate?

        “We should be discussing what is the proper amount to consume.”

        Well, yes. Notice that I spoke of “excessive” intake, so inversely that usually tends to mean that moderate intake isn’t harmful as such, right? 🙂

    • Thanks Ted. Exactly, that´s the paper I was referring to. It´s been fixed now. By the way, thanks again for drawing my attention to the Harcombe paper.

      Reply
  2. Thanks for your article. It confirms the sometimes not so well known fact, that there is no concrete truth, neither in religion nor science. We have to follow the road that we find most passable or pleasing…

    Reply
  3. Axel, a few quick comments before dinner:

    1) Old studies such as 7CS are hardly essential in this case, therefore reviewing them is – in my opinion – of little importance. The idea that fatty acids have different effects on cholesterol and therefore can influence CVD risk is WAY beyond 7CS. And I believe that e.g. the problems with processed food and excessive red meat (of which e.g. HSPH often talks about) may be based on e.g. newer epidemiological data.

    Quite frankly, I find the idea that 7CS is somehow an integral part of current views – more or less – BS. On both sides: both those who exaggerate its role and those who consider it to be the “source of corruption” shoudl get a reality check. Seriously.

    2) As you know, the guidelines for e.g. treating dyslipidemia focus on overall effects & roles of different fatty acids and the overall composition of the diet. Therefore the emphasis should be on BALANCED fat intake and BALANCED diet, in general.

    3) It’s likely that SAFA in moderation & in the context of an otherwise decent diet hasn’t that much of an effect on a healthy individual. But the same goes for e.g. sugar. Or – if we’re talking about dietary choices – junk food, candy etc. etc. That doesn’t mean it’s the same in EVERY context. Or that there aren’t BETTER choices. There clearly are. Of course, you don’t need to go overboard with this, but since SAFA doesn’t bring any health benefits whatsoever (according to current understanding), there’s no reason to promote it in your diet or leave it there in case you e.g. need to cut back on your energy intake or reduce your risks for e.g. CVD.

    4) About WHI: since the intervention group dropped the intakes of ALL fats and still didn’t eat e.g. that much vegetables and fruits (judging by the lowish fiber intake), the reductions in risk factors remained small. Thus, small benefits. Besides, trends toward greater reductions in CHD risk were observed in those with lower intakes of saturated fat or trans fat or higher intakes of vegetables/fruits.

    Reply
  4. Axel this is a great article. I was astounded to read the Food and Nutrition Sciences article
    On the Seven Country Study and learn how various foods were misclassified. It felt almost
    as shocking as finding out there’s no Santa Claus! I disagree with the comment that
    SCS is no longer relevant. It still drives many dietary recommendations. I think
    there is ample evidence of the benefits of a PLANT based diet, which does not preclude
    the occasioal intake of meat. Barbara Roberts, MD

    Reply
    • What recommendations and where? Just because it may get mentioned, doesn’t mean it’s integral to our understanding of dietary fats and CHD. Historical background, that’s it.

      After reading the article Axel mentioned, I was astounded how WEAK it was in many ways. Or well, no I wasn’t. I’ve learned a bit about one of the authors. See e.g.

      https://carbsanity.blogspot.fi/2011/08/zoe-harcombe-credentials.html

      https://carbsanity.blogspot.fi/2013/01/zoe-harcombe-credentials-ii.html

      About the paper itself: it is not a systematic review nor a meta-analysis. It has no power to claim anything about current nutritional advice whatsoever.

      And it makes several dubious claims. E.g. what food scientists classify ice cream and cake as “saturated fats”??? This is NOT the same thing as stating that quite a large part of SAFA intake comes from these. And am I the only one who sees section 7, “Swapping …”, as containing ridiculous comparisons, seemingly drawn on purpose to argue that you can’t swap cheese or pork for anything? Why are the authors implying that e.g. replacing pork with equal amounts of mackerel (haven’t they heard that there are other sources of protein?) is the only alternative if you wish to eat fatty fish – or stressing that you double the amount of SAFA when they’ve just claimed that SAFA doesn’t matter?

      Seriously folks. What makes this so interesting?

      Reply
      • Mie. I won´t be drawn into a debate with you. I agree with you that the Harcombe paper is not a scientific study, although it is a peer reviewed paper. It highlights some very important issues relating to our understanding of the macronutrient composition of different foods, and how they are defined when it comes to scientific research and public health recommendations. This is what makes the paper interesting to me.

        In my opinion, providing internet links to blog posts like the ones above in order to negatively affect the reputation of the authors, will discredit you more than them.

      • The main point of my post was that the paper makes silly claims (more of these later). The stab at Harcombe was totally secondary and irrelevant in terms of my main points. Yes, I could’ve left it out, you’re right there. However, I’m not a newcomer when it comes to reading texts from her – or other self-proclaimed “diet gurus” – and quite frankly, I’m disappointed with the lack of standard and open-mindedness they display. It’s not just the “SAFA-kills-not-matter-what” school of thought that embraced polemic & polarized statements at the expense of the big picture.

        And as far as the important issues are concerned … What are they? That increasing unsaturated fat intake (as NICE recommends) is not a good thing? That 50+ year old research is somehow still relevant to our understanding of diet, despite e.g. the recommendations by top nutritionists and epidemiologists which indicate that the big picture matters?

        You and me obviously disagree on what we find interesting. I see no problems there. However, I do see a slight problem with you bringing this paper up as if it could provide a serious challenge to current recommendations. It can’t because it simply isn’t the kind of paper that can accomplish this.

  5. Great article!!
    I adhere to a ketogenic nutritional protocol and enjoy a vibrant and energetic health.
    All my vital stats, blood work and body fat have never been better…achieved effortlessly
    ‘Saturated fats’ have, for the past 40odd years been considered equal, which is far from the truth.
    Keep the papers coming

    Reply
  6. Doc

    What is your opinion on LDL-P? Do you think the number of particles or the particle size is more important?

    Reply
    • I believe particle number (LDL-P) is more important than particle size.

      Patients with familial hypercholesterolemia (FH) usually have large LDL-particles, but their risk of heart disease is very high, and so is their LDL-particle number.

      It is likely that the association between small LDL and heart disease often reflects an increased number of LDL particles in patients with small particles. Therefore, particle size in itself may be less important than particle number..

      Reply
      • Charles. An LDL-P value >2000 may be associated with increased risk of cardiovascular disease. Remember though that it is always difficult to assess risk by only looking at individual lab values. You need to look at the whole picture, including family history, smoking, blood pressure, BMI, other lab values such as Non-HDL cholesterol, LDL-cholesterol, blood glucose or rather glycated hemoglobin. In some cases hs-CRP can help as well.

  7. Again another great article and I thank you for writing it… making it available to the general public.
    Personally I am sick and tired of hearing dieticians pushing the GRAINS and minimising the healthy fats…. except for olive oil (ICK does not suit my taste buds). Dietician’s are trained NOT to want to advise or help patients who go LCHF as I have done. Even when presented with proof that it lowers many risk factors. There are non so blind as them who will not see.

    Reply
  8. Hi Axel,

    You wrote, “The study clearly demonstrated that the science surrounding macronutrients and nutrition was not as accurate as it is today.” But were scientists back then truly oblivious to the fact that foods in nature always contained a variety of fatty acids (both saturated and unsaturated)? I have to say I’m skeptical. For instance, this table shows the fatty acid breakdown of butter (including unsaturates like linoleic acid and linolenic acid) based on a reference from as far back as 1943 – https://antoine.frostburg.edu/chem/senese/101/consumer/faq/butter-composition.shtml

    By classifying certain foods as “saturated fat”, I think Keys et al were trying to say that these foods are major sources of SFA in the diet. They were _not_ trying to claim that the majority of calories in those foods came from saturated fat. Beef tallow may be “only” 50% saturated, but that’s still a higher percentage than most other food sources. Keep in mind that a diet where 16% of total calories come from saturated fat is considered a “high saturated fat” diet. You don’t need to be eating foods containing > 50% SFA in order to reach this threshold.

    You also mentioned the Women’s Health Initiative and the Siri-Tarino meta-analysis. The major confounder in both of these case is refined carbohydrates. Since refined carbohydrates are also bad for the heart, replacing saturated fat with refined carbohydrates could be masking any potential benefit you’d expect to see by reducing SFA. When reducing saturated fat intake, it won’t help if you replace it with something just as harmful. I think Hooper’s Cochrane review of RCTs probably has to contend with this same flaw.

    The Siri-Tarino meta-analysis noted,

    “With respect to dietary carbohydrate, the type of carbohydrate (ie, a high or low glycemic index) that replaces saturated fat is likely important in influencing dietary effects on CVD risk (47). However, there was insufficient information in the component studies of this meta-analysis to permit examination of this issue.”

    So there is perhaps some room open for the possibility that whole grains (or at least certain low-glycemic starches) are still preferable to saturated fat calories.

    Reply
    • will: “You also mentioned the Women’s Health Initiative and the Siri-Tarino meta-analysis. The major confounder in both of these case is refined carbohydrates. Since refined carbohydrates are also bad for the heart, replacing saturated fat with refined carbohydrates could be masking any potential benefit you’d expect to see by reducing SFA.”

      I could never get this replacement argument. I’m sure if a clinical trial is done that replaced whole grains with vegetables or n-3 fats, things would not look too good for whole grains. This does not mean whole grain is “bad”. Same goes for saturated fat. The so call benefits of whole grains are probably overblown based on observational data, not randomized trials – https://www.ncbi.nlm.nih.gov/pubmed/20307353, https://www.ncbi.nlm.nih.gov/pubmed/2571009.

      For saturated fat, the evidence of its so call harmful effect is frankly, pathetic. There is no need to “replace” saturated fat with anything. Since when do foods become mutually exclusive? For example, some days I put butter and on other days olive oil (fats in general improve nutrient absorption) on vegetables and also eat n-3 fats from fish and nuts.

      BTW the Women’s Health Initiative was not the only trial that lowered total and/or saturated fat intake. Dart Trial also reduced fat intake albeit to a small extent and the Research Committee which reduced both total and saturated fat (e.g. reduced whole milk/butter intake) intake considerably. In the latter study reductions in fat were compensated by increases in carbohydrates but it didn’t mention the type of carbohydrates though the intervention group were in fact told to restrict biscuits and cakes. The increased carb intake should not have been that much because the intervention group didn’t compensate completely for the reduction in fat i.e. they were eating about 500 less calories than the fat rich control group. Anyway, all these trials which either reduced saturated fat or replaced it with n-6 oils were all failures and rather than thinking that something was “wrong”, a “flaw” with all these trials the more logical conclusion would be that they are searching for something (harmful effect of safa) that is just not there.

      Reply
      • “The so call benefits of whole grains are probably overblown based on observational data, not randomized trials”

        In the first one

        https://www.foodbase.org.uk//admintools/reportdocuments/547-1-954_N02036_final_report.pdf

        notice the increased calorie intake & short duration. In addition, the intervention group w/ the highest wholegrain intake also dropped out fruits (it isn’t explicitly mentioned to what extent) from their diet. Not very surprising that the results weren’t as expected. In the latter case, notice the words “not significant”. There’s no viable mechanism to explain why increased fiber intake is/can be a detriment. Or at least I’m not aware of any such mechanism (please, no “anti-nutrient” mumbo jumbo).

        “There is no need to “replace” saturated fat with anything.”

        Depending on the context, there may or may not be. Healthy individuals, probably not unless the intake is very high. People with dyslipidemia, on the other hand, are more likely to benefit (you do know what SAFA does to LDL receptors, right?).

        When “crafting” a diet, bear in mind that you need to maintain energy balance or – if you want to lose weight – create a negative energy balance. SAFA offers no known benefits whatsoever in comparison with e.g. unsaturated fat or veggies, fruit etc.. Therefore, I consider your statement oversimplified.

        “Since when do foods become mutually exclusive? For example, some days I put butter and on other days olive oil (fats in general improve nutrient absorption) on vegetables and also eat n-3 fats from fish and nuts.”

        The big picture counts. Foods can become mutually exclusive depending on the context. If you need to reduce energy intake, it’s kinda rational to cut out the ones of which there’s no indication of benefits, isn’t it? Of course, not all foods with high SAFA content are created equal, e.g. there’s data to suggest that whole-fat dairy in the form of cheese & yoghurt in moderation can be beneficial. No such thing for processed red meat or even red meat – at best it’s neutral.

        “BTW the Women’s Health Initiative was not the only trial that lowered total and/or saturated fat intake.”

        I commented on WHI already, did you notice my points? WHI proved – yet again – that dietary interventions offer modest benefits. The case seems to be the same no matter the intervention. That is the primary finding, not that SAFA per se (w/ no regard on the big picture or what is used to replace it with) is good or bad.

      • Someone wrote:

        “One of the recent meta-analysis in asia area found inverse correlation between red-meat intake and CVD (https://ajcn.nutrition.org/content/early/2013/07/31/ajcn.113.062638.short)”.

        First, the study looked at cause specific mortality, which is not a synonym with a cardiadic event. Meat intake is a proxy for wealth in Asia and wealthy Asians have access to statins, diuretics, revascularization (bypass, stents, etc), blood clot dissolving medications, etc. Poor Asians do not have an access to the aforementioned drugs and procedures. Rural Indians f.ex cannot even afford an aspirin after an acute MI and hence stand a poor chance if/when the second cardiadic event takes a place. Looking at mortality alone misses the big picture in a region that is in economic/dietary transition.

        Second; cumulative exposure. Meat intake is still very low overall in Asia compared to the West and nearly all Asians have been raised in very low-meat/flesh diets. This includes those individuals that today show a higher intake of red meat. We don’t expect an individual who just started smoking to be at significantly elevated risk for lung cancer for the next 10 years.

        This paper did not have the methodological strength to show nothing but a goofy correlation. When we have a study that accounts for cumulative exposure with dietary history, sufficient follow-up (+20 years), looking at multiple event-specific end-points, and that is adjusted for socioeconomic factors, then we can speak about “The Asian paradox”, or not.

      • Richard: “Second; cumulative exposure. Meat intake is still very low overall in Asia compared to the West and nearly all Asians have been raised in very low-meat/flesh diets.”

        A low meat intake is not the same as a no meat intake. The former may be far more beneficial than the latter. I know you are here to push your vegan agenda but even if we assume that low meat intake is more beneficial than a high intake, this does not mean that zero intake is better than a low intake.

      • Mie: “notice the increased calorie intake & short duration. In addition, the intervention group w/ the highest wholegrain intake also dropped out fruits (it isn’t explicitly mentioned to what extent) from their diet. Not very surprising that the results weren’t as expected. In the latter case, notice the words “not significant”. ”

        Mie, I never claimed that grains are detrimental. I was referring to the claimed benefits in which case the studies I referenced support my claim.

        Mie: ” People with dyslipidemia, on the other hand, are more likely to benefit (you do know what SAFA does to LDL receptors, right?”

        Yes, but there is no evidence that saturated fat intake is harmful whether it raises cholesterol or not. However, given what is known about hypercholesterolemia, I agree that some people may need to cut down on saturated fat if their cholesterol skyrockets.

        Mie: “When “crafting” a diet, bear in mind that you need to maintain energy balance or – if you want to lose weight – create a negative energy balance. SAFA offers no known benefits whatsoever in comparison with e.g. unsaturated fat or veggies, fruit etc..Therefore, I consider your statement oversimplified”

        A negative energy balance can be achieved or maintained while eating saturated fat or any type of diet. I don’t see what this has to do with saturated fat.

        Mie: “Of course, not all foods with high SAFA content are created equal, e.g. there’s data to suggest that whole-fat dairy in the form of cheese & yoghurt in moderation can be beneficial.”

        I agree!

        Mie: “No such thing for processed red meat or even red meat – at best it’s neutral.”

        Maybe red meat does have benefits, after all it’s a good source of many nutrients. I’m not convinced at all by observational studies prone to many biases in which intake of red meat is usually associated with other unhealthy habits. The only problem may be the iron content but even that depends on the individual and context. Too bad we have no randomized trials on hard endpoints.

        Mie: “I commented on WHI already, did you notice my points? WHI proved – yet again – that dietary interventions offer modest benefits. ”

        It depends on the dietary intervention. Dietary interventions focusing on saturated fat intake even though it lowers cholesterol have been an absolute flop. The key to a successful trial means increasing antioxidant/nutrient intakes through fruit, vegetables and n-3 fat and also avoiding excessive n-6 intake. The WHI failed to accomplish any of this.

        I think you’d agree that a balanced diet is the best recommendation and individuals can adjust from there to suit themselves even if that means low-carb, vegetarian, paleo or whatever.

  9. I really enjoyed. Indeed, my ancestor consumed animal fat (especially tail adipose tissue resulted from fat-tailed sheep) and they never gain weight a lot and were healthy.

    Reply
  10. ZM

    “Mie, I never claimed that grains are detrimental. I was referring to the claimed benefits in which case the studies I referenced support my claim.”

    Fair enough.

    “Yes, but there is no evidence that saturated fat intake is harmful whether it raises cholesterol or not. However, given what is known about hypercholesterolemia, I agree that some people may need to cut down on saturated fat if their cholesterol skyrockets.”

    Well, the lack of evidence you mention has a simple reason, which we already dealt with. This doesn’t mean that there isn’t evidence of SAFA’s problems. There is. What it DOES mean is that efforts focusing on just limiting SAFA intake are of limited value. Which is why e.g. epidemiologists at place like the HSPH recommend a more comprehensive intervention.

    “A negative energy balance can be achieved or maintained while eating saturated fat or any type of diet. I don’t see what this has to do with saturated fat.”

    I already explained: when planning the energy intake, you’d be wiser to emphasize components that are known to have health value. Of course, the big picture counts in the end: a diet with higher SAFA intake can be healthier than one with lower intake if the latter has e.g. less vegetables and fruit, less PUFA etc.

    “Maybe red meat does have benefits, after all it’s a good source of many nutrients. I’m not convinced at all by observational studies prone to many biases in which intake of red meat is usually associated with other unhealthy habits. The only problem may be the iron content but even that depends on the individual and context.”

    Of course observational data has its problems. But since it is pretty “condemning” and since there are several mechanisms to explain the findings … Well. You know. 🙂

    And I don’t think heme iron is the only problem. What about AGE compounds? Nitrates? SAFA intake (see e.g. Krauss’ recent work in low carb context)?

    “It depends on the dietary intervention. Dietary interventions focusing on saturated fat intake even though it lowers cholesterol have been an absolute flop. The key to a successful trial means increasing antioxidant/nutrient intakes through fruit, vegetables and n-3 fat and also avoiding excessive n-6 intake. The WHI failed to accomplish any of this.”

    Yes, I agree with that list, but … I feel compelled to be critical here too even though I strongly favour lifestyle changes as the first option for treatment and prevention. How many successful interventions w/ CVD end point data are there? Lyon Heart? It hasn’t been replicated since. On the whole, meta-analyses of efforts to prevent/treat CVD aren’t exactly flattering to lifestyle interventions. See e.g. this

    https://www.ncbi.nlm.nih.gov/pubmed/15824290?dopt=Abstract

    “I think you’d agree that a balanced diet is the best recommendation and individuals can adjust from there to suit themselves even if that means low-carb, vegetarian, paleo or whatever”

    Agree. Wholeheartedly.

    Reply
    • Mie wrote: “And I don’t think heme iron is the only problem. What about AGE compounds? Nitrates? SAFA intake (see e.g. Krauss’ recent work in low carb context)?”

      I agree that nitrates should be avoided, but again this concerns processed meat. When I pick up sausage from the super market, I make sure it is the one without nitrates.

      AGE compounds is good topic too. One thing too often forgotten is the way you prepare the food as well. It is not same whether you cook your food in low temperatures vs high temperatures.

      About the amounts of meat intake, pronutritionist tweeted table that compared red meat consumption of different countries https://twitter.com/pronutritionist/status/362848719416205312/photo/1 (asian countries, U.S + finland) . I think we get some perspective from there. Read meat consumption isn’t that high in asia as I mentioned, but still the biggest thing from that is that U.S people really consume a lot! :). No wonder, last time I visited texas, I ordered the smallest steak in the restaurant ~ 280grams, while others took the 700g steak 🙂

      Reply
    • Mie: “Well, the lack of evidence you mention has a simple reason, which we already dealt with. This doesn’t mean that there isn’t evidence of SAFA’s problems. There is”

      I don’t agree. I haven’t not seen any convincing evidence that saturated fat is harmful given the lack of evidence from both observational and clinical research. I put far more weight to long term evidence on hard endpoints but even short term studies are inconsistent and seem to depend on context.

      Mie: “And I don’t think heme iron is the only problem. What about AGE compounds? Nitrates? SAFA intake (see e.g. Krauss’ recent work in low carb context)?”

      Yes, I agree context is important and I think iron is the biggest issue. I never said saturated fat or red meat should be recommended for everyone! However this is different from making blanket statements such as “saturated fat or red meat is harmful” made by some people.
      Observational data isn’t going to resolve the issue though.

      Mie: ” How many successful interventions w/ CVD end point data are there? Lyon Heart? It hasn’t been replicated since. On the whole, meta-analyses of efforts to prevent/treat CVD aren’t exactly flattering to lifestyle interventions.”

      There have been a few. I think it is reasonable to say though that many of the trials could have been a lot more successful if appropriate interventions were used. For example, the Oslo Diet Trial without the excessive n-6 intake. Remember also that these trials were for the most part diet trials that didn’t involve other interventions such as exercise, stress reduction, or even iron reduction! The Lyon trial has never been replicated because no one has attempted to replicate it. In the Predimed trial for example the biggest difference between the groups was only the olive oil or nut intake and didn’t come close to achieving the fatty acid ratios that Lyon achieved.

      Reply
      • ZM

        “I put far more weight to long term evidence on hard endpoints but even short term studies are inconsistent and seem to depend on context.”

        Well, since most of them have not achieved the reductions aimed and/or have used refined oils/carbs as replacement etc. etc. it’s no wonder that context matters.

        “I think it is reasonable to say though that many of the trials could have been a lot more successful if appropriate interventions were used.”

        Perhaps. Perhaps not. But then the same applies to the SAFA trials, too, right? 🙂

        “Remember also that these trials were for the most part diet trials that didn’t involve other interventions such as exercise, stress reduction, or even iron reduction!”

        If you’re arguing that the results might have been more impressive with these, it’s quite likely, I agree.

        “The Lyon trial has never been replicated because no one has attempted to replicate it. In the Predimed trial for example the biggest difference between the groups was only the olive oil or nut intake and didn’t come close to achieving the fatty acid ratios that Lyon achieved.”

        … which just goes to show the problem I already mentioned: difficulties of reaching the treatment goals.

      • Mie: “Well, since most of them have not achieved the reductions aimed and/or have used refined oils/carbs as replacement etc. etc. it’s no wonder that context matters.”

        I see it more as targeting the wrong thing. Targeting saturated fat never works while increasing fruit, vegetable and n-3 fatty acids works almost every time. Of course, many of these trials were multi-interventional so many plausible interpretations are possible but this is my interpretation of the evidence I’ve seen.

        Mie: “Perhaps. Perhaps not. But then the same applies to the SAFA trials, too, right?”

        but saturated fat is innocent until proven guilty and we’ve already had many decades of research and nothing substantial has turned up at all. Maybe we should be asking questions such as in what context is saturated fat harmful? In what context is saturated fat harmless or even beneficial? These are much more open minded questions than the dogmatic views that is normally seen. I’m sure you’d agree 🙂

      • ZM

        “Targeting saturated fat never works while increasing fruit, vegetable and n-3 fatty acids works almost every time.”

        Well, the effects are better (even though still somewhat limited). So yes, I’d say that focusing on what you can and should consume instead of what to cut out might be better.

        “Maybe we should be asking questions such as in what context is saturated fat harmful? In what context is saturated fat harmless or even beneficial? These are much more open minded questions than the dogmatic views that is normally seen. I’m sure you’d agree :)”

        As open-minded as I am, I have to say that there’s no research to indicate that SAFA is beneficial, no matter the context, and that there’s no known mechanism to explain why SAFA could be beneficial in any given context. There’s some data to indicate that diet X with the same amount of SAFA as diet Y is more detrimental, e.g. in the context of protein source or other macronutrients (refined carbs).

        So, even though we seem to agree on the composition of a healthy diet (veggies, fruit etc. etc. and mostly unsaturated fatty acids for fat), our angles are different: you consider SAFA innocent, I consider it having gotten away scot-free due to lack of statistical power because of study designs & human nature. The end result? Mostly the same.

      • Mie: “As open-minded as I am, I have to say that there’s no research to indicate that SAFA is beneficial, no matter the context, and that there’s no known mechanism to explain why SAFA could be beneficial in any given context.”

        Mie, there is data on possible benefits. Note the key word here “possible”. No hard data, but at the same time there is no hard data that saturated fat is harmful. Consider for example, a meal of vegetables with butter (which would improve the absorption of nutrients in vegetables and also comes with its own fat-soluble vitamins), in a low iron context. Wouldn’t you consider this meal better with butter than without?
        Remember also that some people don’t have the taste for different oils and I’m sure many would agree that butter is one of the best tasting fats there is.

        Mie: “So, even though we seem to agree on the composition of a healthy diet (veggies, fruit etc. etc. and mostly unsaturated fatty acids for fat), our angles are different: you consider SAFA innocent, I consider it having gotten away scot-free due to lack of statistical power because of study designs & human nature. The end result? Mostly the same.”

        Yes I do consider saturated fat innocent and interpret the data that way because non-causation should be assumed until proven otherwise. Whether it is lack of statistical power or because of study designs, in the end a lack of evidence is a lack of evidence. So we do disagree on that point. Keep in mind though we already agree saturated fat may be harmful in certain contexts.
        I’m not sure I entirely agree with you on n-6 fats and tend to agree more with Ramsden’s position though a randomized trial on hard endpoints is needed to either confirm or refute the hypothesis as agreed upon in this paper – https://www.ncbi.nlm.nih.gov/pubmed/21430375

        Anyway, looks like we agree on the basic concept of a balanced diet without extremes.

      • Z.M.,

        In the meal of vegetables with butter, I wouldn’t count the improved absorption of nutrients as an advantage of saturated fat per se. You could just as easily improve nutrient absorption via olive oil or any other dietary fat.

        I compared grass-fed butter to some alternatives (like olive oil and canola oil) on NutritionData. Butter has more vitamin A per 100g, but olive oil and canola oil have more vitamin E and K. This isn’t a clear victory for butter, either IMO.

      • Will: “I compared grass-fed butter to some alternatives (like olive oil and canola oil) on NutritionData. Butter has more vitamin A per 100g, but olive oil and canola oil have more vitamin E and K. This isn’t a clear victory for butter, either IMO.”

        Will, you can do this for any foods and declare “victory” for one food over another.

        Will: ” You could just as easily improve nutrient absorption via olive oil or any other dietary fat.”

        Yep, and I never said otherwise. I don’t know what your point is.

      • It is also worth noticing that even though olive oil and canola oil comes with decent amount of E-vitamin(antioxidant), we also need more antioxidants if we are consuming those oils since those oils get oxidized more easily than SAFA. Im not trying to say which one is the best, just saying that it’s not that simple comparison.

  11. Agree. Wholeheartedly.

    ummm…Unfortumately, I cannot really join the party. Paleo? LOL!

    Eric Rimm from the Department of Nutrition, Harvard said to Reuters in regards to a major health report produced by the National Academy of Science, which he was an author of that:

    We can’t tell people to stop eating all meat and all dairy produces. Well, we could tell people to become vegetarians… If we were truly basing this on science we would, but it is a bit extreme.

    Interesting findings from Asia, these studies utilized advanced methodology:

    Chinese lacto-vegetarian diet exerts favorable effects on metabolic parameters, intima-media thickness, and cardiovascular risks in healthy men.

    “In healthy Chinese men, the lacto-vegetarian diet seems to exert protective effects on blood pressure, lipid profiles, and metabolic parameters and results in significantly lower carotid IMT. Lower CVD risks found in vegetarians also reflect the beneficial effect of the Chinese lacto-vegetarian diet”

    https://www.ncbi.nlm.nih.gov/pubmed/22412169

    Relationship of carotid intima-media thickness and duration of vegetarian diet in Chinese male vegetarians.

    “A decrease in multiple cardiovascular risk factors such as BMI, blood pressure and lipid profile was associated with vegetarian diet. Moreover, taking a low-calorie, low-protein, or vegetarian diet might have great beneficial effects on IMT through improved lipid profile, and the beneficial effects appeared to be correlated with the duration of vegetarian diet”.

    https://www.ncbi.nlm.nih.gov/pubmed/21929760

    BTW, I am just browsing through an interesting paper from Axel’s homecountry, Iceland. The authors did not find an association of milk with aggressive prostate cancer at later in life, but when accounted for cumulative history (intake during adolescent), a massive RR of 3.2 appeared. This study was a prospective cohort that utilized state of the art technology in regards to dietary recall assessment methods. This is pretty much why dairy is starting to loose its status.
    https://www.svd.se/mat-och-vin/mjolk-mojlig-orsak-till-prostatacancer_6716791.svd#xtor=AD-500-%5Bsvd%5D-%5B%5D-%5BTextlank%5D-%5Baftonbladet%5D-%5B%5D-%5B%5D

    Milk intake in early life and risk of advanced prostate cancer.
    https://www.ncbi.nlm.nih.gov/pubmed/22190107

    The most conservative approach at this stage would be to follow a diet very high in complex carbohydrates, high fiber intake, low in animal foods. The intake of animal products should kept minimium (<10% calories). If animals are to be consumed, egg whites (not yolks) and very low-fat yogurts ought to be preferred in moderation.

    Reply
    • Richard:

      “ummm…Unfortumately, I cannot really join the party. Paleo? LOL!”

      Don’t worry, we all know the limitations of your approach (vegan dogmatism).

      “BTW, I am just browsing through an interesting paper from Axel’s homecountry, Iceland.”

      Seems like a pretty well-designed cohort study, based on a quick read-through. However,

      a) Look at the CI for adolescence & high milk intake (table 4). It’s all over the place.

      b) After a sensitivity analysis no statistical significance:

      “The odds ratio for advanced disease among men with a high milk intake in adolescence was 2.14 (95% CI: 0.62, 7.39).”

      c) No accurate knowledge of actual intake in childhood, of course – the inherent limitation of these studies.

      d) Type of milk: whole, unpasteurized?

      Reply
      • Mie wrote:

        “Don’t worry, we all know the limitations of your approach (vegan dogmatism)”.

        But I just stated that animal foods such as egg whites and very low-fat yogurts can be part of a healthy diet, albeit their consumption should be kept very low as well. Mie, you give up too easily. Its too easy for you to state that I am dogmatic and then just disregard everything I say. At top of everything, you even try to make the fellow reader to just blindly accept that my message is not worth taking into consideration by accusing me of dogmatism. This is very weak from you. It appears that you are not ready for the reality. The truth can hurt. The strength of the evidence is all that matters, dogmatic people (not saying that I am one) are not wrong by default. Even the skeptical must consider the strength and potential of “vegan propaganda”. Vegan males had a impressive RR of 0.74 for overall mortality in the 6-year follow-up of the recently published findings of 7th day Adventist cohort about mortality.

        I think actually that you are the one who is dogmatic. Your views about nutrition are much more “off” from that of the top level researchers than my views are (see the statement by Eric Rimm for example) and most likely your views of nutrition will never change. Its way too convenient for you to just stick with the “everything goes, everything in moderation” -phase.

        I added a well-done journalistic piece where top expert were interviewed about milk. This is not just about one Icelandic cohort. This is about totality of evidence. There are biologically plausible mechanisms which may explain these findings. Researchers at Harvard have already waged a war against milk in the US press. Top level Swedish epidemiologist have spoken against milk in the press as well.

        In this study even skim-milk was associated with increased risk of prostate cancer, and whole milk was associated with the lethal aggressive prostate cancer (1 serving/d vs. rarely consumed).

        Whole Milk Intake Is Associated with Prostate Cancer-Specific Mortality among U.S. Male Physicians
        https://jn.nutrition.org/content/143/2/189.short

        I am very concerned about the findings of the Icelandic cohort, no association of dairy to cancer at later in life, but huge RR when consumption at adolescence was taken into consideration. Very few studies take cumulative exposure into consideration. Milk can be even more hazardous than the most of the new studies would indicate (consumption taken into consideration only at the baseline).

    • There are problems in that blog text, in the case of Ramsden et al and Hooper et al.

      1) Ramsden et al did find out that diets richer in PUFA are beneficial. Ramsden et al state that

      “For non-fatal myocardial infarction (MI)+CHD death, the pooled risk reduction for mixed n-3/n-6 PUFA diets was 22 %”

      2) Hooper et al state that :

      “This updated review suggested that reducing saturated fat by reducing and/or modifying dietary fat reduced the risk of cardiovascular events by 14% (RR 0.86, 95% CI 0.77 to 0.96, 24 comparisons, 65,508 participants of whom 7% had a cardiovascular event, I2 50%).” That was for men, for women the effect didn’t reach statistical significance.

      They also claim that

      “The findings are suggestive of a small but potentially important reduction in cardiovascular risk on modification of dietary fat, but not reduction of total fat, in longer trials. Lifestyle advice to all those at risk of cardiovascular disease and to lower risk population groups, should continue to include permanent reduction of dietary saturated fat and partial replacement by unsaturates.”

      The latter was discussed in more detail in another post on this blog.

      Reply
  12. If anyone has read Good Calories, Bad Calories by Gary Taubes, this has all been covered, and then some. It’s been my main reason other than http://www.marksdailyapple.com for changing my way of thinking about food. We are demonizing the wrong food (meat) when we should be demonizing sugar and it’s related carbs (grains, to a great extent).

    Reply
    • I recommend reading Taubes, too. His work is good for improving your skills in critical reading because it’s full of cherry-picking, out-dated research and plain silliness.

      As far as “demonizing” goes, that is the key problem right there: shaddy interpretations and extrapolations grounded in dogmatic thinking. That’s Taubes, Lustig, Campbell etc. etc. who pay no attention to dose & context or the big picture. There’s no need to “demonize” anything, not meat nor sugar nor grains.

      Reply
  13. Mie,

    American Institute of Cancer Research (AICR) has an important message in regards to Campbell’s work. Overlooking this message may end up in a missed opportunity for healthy longevity.

    AICR, the China Study, and Forks Over Knives

    “Like the China Study, the ongoing results of the AICR/WCRF CUP strongly support a whole-food, plant-based diet for lower risk of cancer and many other diseases”,

    https://www.aicr.org/about/advocacy/the-china-study.html

    Reply
    • Richard and Mie. I have nothing against you two using the discussion forum. However, it wouldn´t be right to let it dominate the forum on every blog post I write, unless it deals with that specific topic. If the two of you are going to engage in an off topic discussion, feel free to do that in relation to some of the older posts, where you have been exchanging words before.

      And by the way Richard. I can´t accept lengthy posts with a lot of copy/pasting, nor comments that include text that you have used many times before when commenting on this website or other blogs.

      Reply
      • You’re absolutely right Axel. I’ll refrain from commenting posts that aren’t related to the topic of your post.

  14. Z.M.

    “Mie, there is data on possible benefits. Note the key word here “possible”. No hard data, but at the same time there is no hard data that saturated fat is harmful. Consider for example, a meal of vegetables with butter (which would improve the absorption of nutrients in vegetables and also comes with its own fat-soluble vitamins), in a low iron context. Wouldn’t you consider this meal better with butter than without?”

    Hmm? That’s a bit far-fetched example, in my opinion. No one’s arguing for a diet lacking in essential fatty acids. And along similar lines, eating e.g. rancid meat could be considered healthy – if the option was to starve. Does that mean it’s healthy when compared to fresh meat? Or butter compared to fatty fish, avocado, e v olive oil etc.? Context yes, but in the context of us westerners with our well-known diet-induced problems, I feel that prudence in certain matters is recommendable. We don’t necessarily have to cut back on our SAFA intake if it isn’t excessive, but rather promote unsaturated fat intake (with emphasis on increasing n-3 intake), just like you pointed out.

    And by hard data, you mean “end points”, right? I don’t think this is the ONLY reasonable criteria, even though it clearly is the best. I already stated that in the case of virtually all templates for a healthy diet where there’s lower SAFA vs higher SAFA comparison, the lower SAFA option produces better surrogate outcomes. And we know why: SAFA is both somewhat pro-inflammatory and detrimental to LDL receptors.

    But since I predict that after having stated this, the discussion will – yet again – drift back to the lack of end point data, I suggest that we’ll just have to agree that we disagree here, to some extent.

    “I’m not sure I entirely agree with you on n-6 fats and tend to agree more with Ramsden’s position…”

    … which is that n-6 fats in excess may be problematic? Sure. However, e.g. their pro-inflammatory effects are often overstated. See this meta-analysis:

    https://www.ncbi.nlm.nih.gov/pubmed/22889633

    And let’s not forget that n-6 fats have beneficial effects, too.

    “Anyway, looks like we agree on the basic concept of a balanced diet without extremes.”

    Yes.

    Reply
    • Mie: “Hmm? That’s a bit far-fetched example, in my opinion.”

      I don’t think so. You said you didn’t think there was any context in which saturated fat was beneficial. I gave you an example of a commonly eaten meal of butter with vegetables, so I don’t understand how that is far-fetched. In fact, I think it’s far-fetched to be comparing rancid meat to fresh meat.

      Mie: ” Or butter compared to fatty fish, avocado, e v olive oil etc.?”

      The replacement/comparison argument is usually made by people who want to demonize certain foods. Comparing butter to other foods does absolutely nothing to cast guilt on saturated fat. I mean, you can make comparisons with all sorts of foods and find that many foods are better than others.

      Mie: ” I already stated that in the case of virtually all templates for a healthy diet where there’s lower SAFA vs higher SAFA comparison, the lower SAFA option produces better surrogate outcomes. And we know why: SAFA is both somewhat pro-inflammatory and detrimental to LDL receptors.”

      Well sorry Mie, I’m not convinced by short term studies on surrogate markers the effects of which have yet to show up in any long term trial on hard endpoints to date for whatever reason or opinions of others. So yes, I strongly disagree on you here.

      Mie: “And let’s not forget that n-6 fats have beneficial effects, too. ”

      We will talk when these benefits show up, again, in long term trials compared to saturated fat.

      Reply
      • Z.M.

        “I gave you an example of a commonly eaten meal of butter with vegetables, so I don’t understand how that is far-fetched. In fact, I think it’s far-fetched to be comparing rancid meat to fresh meat.”

        Notice what I stated? “No one’s arguing for a diet lacking in essential fatty acids.” And no diet in this context (Western world) is going to be lacking in fats so as to hinder the absorption of fat-soluble vitamins.

        In addition, your argument has a tendency to render the concept “healthy” meaningless, in general sense. E.g. added sugar: clearly not a good idea. However, if you’re starving, then yes, it could be considered healthy. Sensible?

        Not to mention that your point is not based on actual studies. SAFA is, depending on the context (realistic one), neutral at best.

        “The replacement/comparison argument is usually made by people who want to demonize certain foods. Comparing butter to other foods does absolutely nothing to cast guilt on saturated fat. I mean, you can make comparisons with all sorts of foods and find that many foods are better than others.”

        Well, since you already agreed that e.g. in the context of people with dyslipidemias, replacing SAFA is a good idea, I don’t quite follow you now.

        Of course foods must be compared to others, yes. In that sense there are always better options. If taken to absurdity, this would mean that virtually nothing can be eaten. However, just because you have to draw the line somewhere doesn’t mean that drawing the line is not sensible. When there’s clearly an improvement in replacing something for something, why not? I’m not arguing for a 0% SAFA intake, you know.

        “Well sorry Mie, I’m not convinced by short term studies on surrogate markers the effects of which have yet to show up in any long term trial on hard endpoints to date for whatever reason or opinions of others. So yes, I strongly disagree on you here.”

        You do realize that data on such diets isn’t based on just surrogate data (e.g. Mediterranean diet)?

        In addition, you’re making a very simple error here: just because the hard evidence is lacking, doesn’t mean you shouldn’t pay attention to other types of evidence. E.g. low carb diets: do you consider them meaningless just because there’s no end point data on CHD mortality? Paleo?

        Plus somebody already mentioned Ramsden et al and Hooper et al, both of which indicate benefits for PUFA and when replacing SAFA with PUFA.

        “We will talk when these benefits show up, again, in long term trials compared to saturated fat.”

        A case of the same problems as above.

        However, you might want to read this too:

        https://www.ncbi.nlm.nih.gov/pubmed/19171857

      • Mie: “E.g. added sugar: clearly not a good idea. However, if you’re starving, then yes, it could be considered healthy. Sensible?”

        Mie, you are one who claimed that saturated fat has no benefits so maybe you should explain what you mean by “having no benefits” or else this argument is going nowhere fast.

        Mie: “Well, since you already agreed that e.g. in the context of people with dyslipidemias, replacing SAFA is a good idea, I don’t quite follow you now. ”

        Well, obviously I’m not talking about people with dyslipidemias.

        Mie: “When there’s clearly an improvement in replacing something for something, why not? .”

        because there is no need to replace. Why can’t I enjoy the benefits or possible benefits of all types of fats?

        Mie: “I’m not arguing for a 0% SAFA intake, you know”

        and I’m not arguing for excess intakes.

        Mie: “You do realize that data on such diets isn’t based on just surrogate data (e.g. Mediterranean diet)?”

        What do you mean by “such diets”? Low SAFA?

        Mie: “In addition, you’re making a very simple error here: just because the hard evidence is lacking, doesn’t mean you shouldn’t pay attention to other types of evidence.”

        Just because I came to a different conclusion to you doesn’t mean I haven’t took other types of evidence into consideration.

        Mie: “Plus somebody already mentioned Ramsden et al and Hooper et al, both of which indicate benefits for PUFA and when replacing SAFA with PUFA.”

        The only fat that has actually showed benefits in clinical trials are n-3 fats in both food and supplemental form and probably Olive Oil based on Predimed. Same cannot be said of both n-6 fats or saturated fat. This does not mean however, that n-6 fats or saturated fat are “bad” or are not beneficial.

        Mie: “A case of the same problems as above.
        However, you might want to read this too:
        https://www.ncbi.nlm.nih.gov/pubmed/19171857

        I’ve already told you I side with Ramsden on this issue – https://www.ncbi.nlm.nih.gov/pubmed/19627662

      • ZM,

        The amount and type of dietary fat to a large extent determines the number of circulating LDL particles and blood levels of total cholesterol. Moreover, SFA with 12–16 carbon atoms are the most potent LDL- or total-cholesterol-raising fatty acids (Pedersen et al 2011).

        In the 7CS, the amount of SFA in the diet explained 89% of variability in serum cholesterol levels across the 16 different cohorts, exactly as would be expected based on the findings from metabolic ward.

        We know that the strength of the (independent) association between blood cholesterol and CHD and strokes is diluted in most studies (regression dilution bias).
        https://aje.oxfordjournals.org/content/150/4/341.full.pdf

        Now are you suggesting that saturated fats elevate LDL cholesterol in some kind of safe way, so that it would no promote CHD? Are the assumed dangers of elevated LDL now dependent on the mechanism used?

        It is well documented that SFA impair LDL receptor activity thus forcing liver to produce more cholesterol. Is it OK if the LDL receptor activity is degraded as long as the degration of the receptor activity is mediated via SFA feeding?

        Brown & Goldstein demonstrated that the human LDL receptor is designed by evolution to properly function under exceedingly low levels of LDL cholesterol, the saturation point after which the receptors start to work less efficiently is around 1.5mmol/l (LDL-C). What are the chances for humans to achieve biologically normal cholesterol levels (that nearly all other free-ranging mammalians have) if SFA is present in the diet in “moderation” (let alone in excess). Doesn’t this piece of evidence mean anything to you?

        You know, you are allowed to used logic and sound scientific reasoning. .

        Bonus: a nice cohort study from Denmark

        High dietary intake of saturated fat is associated with reduced semen quality among 701 young Danish men from the general population
        https://ajcn.nutrition.org/content/97/2/411.short

      • Richard, we’ve been through this many times before so I’m not going to respond except to point out your double standard of citing observational research when it suits your ideas but any that contradicts it are flawed.

  15. Axel,

    point understood. But I haven’t addressed my points in a neat way that summarizes it all. Hence, I try again. I hope you reconsider adding this.

    When Siri-Tarino et al. considered 7 of the 11 studies included in their original meta-analysis paper that addressed the association between saturated fat and fatal coronary heart disease they found an 18% excess risk that almost reached statistical significance (0.99-1.42).When Stamler considered all 11 studies he found a 32% excess risk despite over-adjustments for serum lipids and a number of other problems addressed in his editorial that would expected to have significantly weakened this finding (regression dilution bias). The SFA – fatal CHD RR of 1.32 (Stamler 2010) is actually slightly stronger than that of meta-analyses of the association between passive (second hand) smoking and lung cancer which have produced an RR of around 1.27.

    Here is a list of estimates from some of the cohort studies that found a stronger positive association between saturated fat and fatal coronary heart disease. Note that in these studies saturated fat is primarily compared to all other sources of calories which is predominantly refined carbohydrates and refined oils.

    Strong Heart Study 5.17 (ages 47-59, high vs low intake)
    Mann et al. 2.77 (high vs low intake)
    Health Professionals Follow-Up Study 1.72 (high vs low intake)
    Health and Lifestyle Survey 1.40 (women, per 100 g higher intake)

    The closet to definitive types of studies supporting diet-heart are not observational, they comes from 4 independent lineages of research

    1) Thousands of animal studies showing that saturated fat establishing that cholesterol accelerates atherosclerosis across virtually every type of vertebrate, and that they are the sine qua nons for the dietary modification of experimental atherosclerosis. This includes mammalian, avian and fish species- herbivores, omnivores and carnivores, and over one dozen different species of nonhuman primates. Again this cannot be attributed to the way that the animal was raised as when taking into consideration the amount of antioxidants and carotenoids as well as the lack of cholesterol, tropical plant fats high in lauric, myristic and palmitic acids will also accelerate atherosclerosis in animals to a similar degree as saturated animal fats.

    2) Hundreds of rigorously controlled metabolic ward studies establishing that dietary cholesterol and saturated fat elevate LDL and total cholesterol. The cholesterol raising effects of saturated fat is not the result of how the animal was raised as tropical plant fats high in lauric, myristic and palmitic acids will also raise total and LDL cholesterol.

    3) Meta-analysis of 108 randomized controlled trials with 300,000 subjects and with a mean follow-up of only three years establishing that lowering LDL significantly reduces both coronary heart disease and all-cause mortality independent of changes to HDL cholesterol and triglycerides, and non-lipid effects of specific interventions.

    4) A meta-analysis of mendelian randomization studies with over 312,000 individuals demonstrated that inheriting any of nine studied genetic variants that modify lifelong LDL cholesterol concentrations, but not any other known risk factors predicted a 55% lower risk of coronary heart disease for each mmol/l (38.7 mg/dl) lower LDL cholesterol. This represents a three-fold greater reduction in coronary heart disease per lower unit of LDL cholesterol than the statins trials which lasted only 5 years and the average participant age was 63. The p-value for this finding was 0.000000000000000000843. This is also expected to also translate into a 3 fold lower risk of all-cause mortality.

    Reply
    • Ok Richard
      I´ll finally accept this comment.

      Firstly, I don´t think we should confuse the diet heart hypothesis with the lipid hypothesis. Much of your argumentation above surrounds the role of LDL-cholesterol in atherosclerotic heart disease. A correlation between LDL-cholesterol and the risk of heart disease does not prove that saturated fats are bad. So we shouldn´t really be discussing the lipid hypothesis.

      I know there is some data indicating that high consumption of saturated fats raise LDL – cholesterol. However, if you read my article you can see that I referred to the Hooper meta-analysis which didn´t show any effects of reducing saturated fats on mortality or cardiovascular mortality. Replacing them with carbohydrates was certainly not beneficial.

      Reply
      • Thanks Axel,

        you are the legitimate cardiologist here, and I respect that. Everyone can make their own conclusions about SFA and dietary cholesterol based on the four lines of evidence I presented (1-4).

        The evidence from RCTs is not supportive to the idea that smoking cessation is beneficial to prevent lung cancer, neither is it supportive that physical inactivity is harmful. Outside the pharmacological context, we shouldn’t make too much of RCTs. That’s what I think.

        BTW, I am just reading an article about the Bedouins living on wheat-based diets by a diet-heart legend, J.J Groen. An average Bedouin once consumed 25 slices of whole-grain wheat bread per day, some wheat-porridge, some vegetables and milk, and not much else. The intake of carbohydrates accounted for 78% of calories, fat intake topped at 11%. Only 53mg of dietary cholesterol was consumed per day. The mean serum cholesterol for Bedouins was 151mg/dl: no CHD nor strokes, no diabetes, no obesity. Physical activity level was quite low especially for women who spent most of the time of the day inside the tent year around. This was the kind of well documented ecologic evidence that was used by Pedersen et al (2011) to indicate that complex carbohydrates prevent CHD and strokes.

        Nutrition of the Bedouin in Negev desert
        https://ajcn.nutrition.org/content/14/1/37.full.pdf#page=1&view=FitH

        Effect of bread in the diet on serum cholesterol
        https://ajcn.nutrition.org/content/20/2/191.full.pdf#page=1&view=FitH

  16. Someone:

    “It is also worth noticing that even though olive oil and canola oil comes with decent amount of E-vitamin(antioxidant), we also need more antioxidants if we are consuming those oils since those oils get oxidized more easily than SAFA. Im not trying to say which one is the best, just saying that it’s not that simple comparison.”

    But in the context of current intake nothing suggests that oxidation is a major issue, nor in the context of increased intake for that matter in the case of olive oil (Med.diet trials). Remember Ramsden et al: intake of n-6 fatty acids had to be several times higher than according to e.g. NHANES for detrimental effects to appear. And even then there was no statistical significance in the findings.

    Reply
    • Yeah, it’s possible that it’s not a problem. Chris MasterJohn brought up interesting points about E-vitamin and vegetable oils in this article: https://www.westonaprice.org/blogs/cmasterjohn/2012/05/17/ajcn-publishes-a-new-pufa-study-that-should-make-us-long-for-the-old-days/ (I think someone has pasted this link earlier too if I recall correctly).

      He points out that E-vitamin levels in plasma are usually first raising while using PUFA-oils but then trend starts to get worse by the time. Unfortunately studies made are not long enough that we could make any conclusions of the matter. Studies following the effects of increased PUFA usage for over then years would be interesting. Too bad that most of the studies are rather short term.

      Reply
      • I’m well aware of Masterjohn’s position. And I’m not convinced. Naturally, there will never be a decade-long trial on dietary fats. What we do know, however, is that in the case of “normal” intake, there are benefits for PUFA-rich diets – and even in the case of excessive intakes, the data on possible problems is pretty much non-existent (see Reijo’s comments).

        As for the vitamin E claim, his claims are based on one rat study and a couple of older studies SUGGESTING that there MIGHT be something there. However, as he himself points out, later trial evidence disputes the claim. Then he turns to “not long enough” claim and speculating about this and that. Asking questions is fine, but that really isn’t enough if you a) downplay the lack of evidence to support your views (or ignore the fact that vitamin E supplementation has been a near total failure in terms of preventing CHD and cancer) and if b) your own answers are … well, just another set of questions.

      • Yeah. I did not claim anything,i just said that he raised interesting questions. Also i was not trying to give any answers. Some people have desperate need to know All the answers and that may drive them to make rapid conclusions. You love disagreeing with others even one is not take any side in the argument.

      • “I did not claim anything,i just said that he raised interesting questions.”

        And I didn’t claim that YOU claimed anything, now did I? Instead, I discussed the reasons why I find Masterjohn’s position weak.

        “You love disagreeing with others even one is not take any side in the argument”

        Pardon me, but I thought that we’re here to DISCUSS issues we consider interesting. Sometimes I agree on something, sometimes I don’t. Should I refrain from commenting if I don’t? And anyway, since you yourself just stated that you didn’t make any claims – implying that you don’t agree with Masterjohn – I really don’t understand what is your problem here.

        Or did you think that I was referring to you in the sentence “Asking questions is fine, but that really isn’t enough if you …”? Rest assured, I wasn’t.

  17. Someone wrote:

    “Richard, we’ve been through this many times before so I’m not going to respond except to point out your double standard of citing observational research when it suits your ideas but any that contradicts it are flawed”.

    The way public health measures are shaped is nicely described in the book “merchants of doubt” which ducuments the journey of climate change and tobacco denialism.

    When we have a substance that is known to promote disease in laboratory and metabolic ward (Tobacco & SFA), we are more senstive to correlations in observational studies even though they may not be always statistically significant (see second-hand smoking f.ex). Those correlations that are highly biologically plausible must be taken with more caution as opposed to findings that are not biologically plausible. The scientist are always bound to the rules of logic in the end. Scientists are not bound to being impartial in regards to correlations while safeguarding the public interest. Some correlatioons are more important that others. For cholesterol denialists this may feel like an act of great injustice. Similarly, the asbestos industry feels like its been treated unfairly since there are no randomized, controlled trials demonstrating that exposure to asbestos is harmful.

    Reply
    • Richard your entire post just confirms how pitiful the evidence is against saturated fat. The fact that you would even bring up the faulty analogy with tobacco confirms that you have already admitted that the evidence against saturated fat cannot stand on its own.

      Reply
  18. The LCHF (low carb high fat) diet is very popular particularly in Scandinavian countries. I’ve read many comments about the effects of the LCHF diet such as losing weight without exercise, improving blood sugar, reversing type 2 diabetes, optimal blood pressure and lipid panel, more energy, better sleep, no longer suffering hunger pains, IBS, fibromyalgia, joint pain, ADHD, fungus, bleeding gums, depression…

    I eat plenty of cholesterol and saturated fat in my diet and have for decades. My cholesterol, HDL, LDL, and triglycerides are excellent. Fungus? Never suffered with it. IBS? IB..what? LOL

    Reply
  19. Z.M.

    “Mie, you are one who claimed that saturated fat has no benefits so maybe you should explain what you mean by “having no benefits” or else this argument is going nowhere fast.”

    No benefits in reducing CHD mortality in general population or in high risk population or in CHD patiens. I though this was obvious?

    “Why can’t I enjoy the benefits or possible benefits of all types of fats?”

    Of course you can enjoy different types of fats, if you choose to do so. I, however, fail to see why you’d have to try & justify your own way of enjoying life with narrative of “vegetables meeting butter” instead of data. An analogue: there’s nothing to indicate that a sweet roll every now and then is detrimental. However, this doesn’t mean that it provides any health benefits.

    “and I’m not arguing for excess intakes.”

    But … You’ve stated that fat modification / replacing SAFA isn’t necessary, period. How is that NOT arguing for intakes from low to excessive?

    “What do you mean by “such diets”? Low SAFA?”

    Yes.

    “Just because I came to a different conclusion to you doesn’t mean I haven’t took other types of evidence into consideration.”

    Well, unless you care to elaborate why you choose to virtually ignore e.g. the quality of studies included in Hooper et al. and therefore its limits – or the well-known mechanisms related to both LDL receptor functionality and inflammation – this will lead us nowhere. So please, do so.

    “The only fat that has actually showed benefits in clinical trials are n-3 fats in both food and supplemental form and probably Olive Oil based on Predimed.”

    Err, you do realize that the studies Ramsden et al. discussed were clinical trials that showed benefits for mixed n-6 & n-3 diets? That is, BOTH. And as for the evidence on supplemental n-3 on CHD, see this

    https://www.ncbi.nlm.nih.gov/pubmed/21626218

    for secondary prevention. Patients following treatment guidelines received no benefits, those who didn’t get proper medication did. But this was based mostly on Lyon Heart Study, which was a multifactorial study. Primary prevention? No data apart from JELIS in which the findings were statistically non-significant.

    “Same cannot be said of both n-6 fats or saturated fat. This does not mean however, that n-6 fats or saturated fat are “bad” or are not beneficial.”

    But didn’t you just state – several times for that matter – that only what is shown counts? If there are no benefits shown for SAFA, how is it not beneficial?

    “I’ve already told you I side with Ramsden on this issue –”

    Despite the fact that his meta-analysis of clinical trials with hard data on end points showed no statistically significant detrimental effect with sky-high intake levels (from refined oils), whereas the study I cited showed point to a plethora of evidence on the benefits at recommended intake levels? Of course you’re entitled to your opinion, but since your position obviously isn’t very solid, I’m kinda curious to know why?

    Reply
    • Mie: “but since your position obviously isn’t very solid”

      Love the arrogance.

      I had originally written a response to your points but then thought it was pointless because it is clear we are never going to agree and you misunderstand many of my points which makes this discussion tedious. So I’ll end it here.

      Reply
      • Your choice, of course. However, we did agree on quite a few things and the conversation remained civil. At least I considered this civil. Maybe not that much in real life, but for me it was a nice change to partake in an Internet discussion where I didn’t get called names or accused of being on the payroll of Big Pharma / Egg Council / you-name-it. 🙂

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