Saturated Fats Linked To Heart Disease Once Again

–But critics say that observational studies can’t establish causal relationship.

A prominent group of nutrition researchers have once again linked saturated fats to increased coronary heart disease.

The new paper, published in BMJ, is the third paper in the past year to decry saturated fats. Along with the previous two papers, published in JACC and JAMA Internal Medicine, the BMJ paper uses data from two large observational studies to support the widely held view that high intake of saturated fat should be replaced with unsaturated fats, complex carbohydrates, or plant-based proteins. The senior author of all three papers is Frank Hu, the Harvard University nutrition researcher who has been a leading figure in the prosecution of saturated fats.

But some critics, including a BMJ editorialist, continue to raise concerns that observational data like this is not capable of demonstrating the negative effect of saturated fats. The new paper also raises additional concerns about the role of co-authors who work in the food industry.

The BMJ paper is based on 24-28 years of followup of 73,147 women in the Nurses’ Health Study and 42,635 men in the Health Professionals Follow-up Study. In this report the investigators focused on the role of individual saturated fatty acids (SFAs) and found a strong correlation with all the main SFAs and coronary heart disease. They calculated that replacing 1% daily energy intake of SFAs, —including lauric acid, myristic acid, palmitic acid, and stearic acid— with an equivalent number of calories from polyunsaturated fats, whole grain carbohydrates, or plant proteins would lead to a 6-8% reduction in the risk of coronary heart disease.

“Owing to similar associations and high correlations among individual SFAs, dietary recommendations for the prevention of coronary heart disease should continue to focus on replacing total saturated fat with more healthy sources of energy,” they concluded.

But, in an accompanying editorial, Russell de Souza and Sonia Anand (McMaster University) warn that “the results of cohort studies must always be approached with caution.” In an email interview, de Souza elaborated: “Epidemiologic studies are observational studies. This means that people who tend to eat High (or Low) saturated fats tend to also do other things that may reduce or increase risk of heart disease. For example, in this study, those who ate more saturated fat also ate more protein from animals, ‘refined’ carbohydrate, and trans fats. They also ate less fiber, fruits and vegetables, and whole grain carbohydrates. They were more likely to smoke. Though the authors carefully controlled for many of these confounders in their analyses, the risk of what we call residual confounding is always present.”

Regarding “the breakdown of risks by each particular fatty acids” de Souza said it is “a challenge to translate” these into food guidelines, since it’s “not common knowledge as to which foods contain which fatty acid; and many fatty acids are found in many foods.”

In their editorial de Souza and Anand warn against a close focus on individual nutrients. “Dietary advice about single nutrients that fails to consider dietary context is problematic…. A narrow focus on SFAs might result in diet that meets one target (for example, low in saturated fat) but fails to meet another (owing to a high intake of refined carbohydrates).”

Another potential source of concern regarding the BMJ paper is that three of the co-authors work for Uniliver, the food company that is the largest producer of margarine and other food spreads. I asked Fiona Godlee, editor-in-chief of the BMJ, for a comment about this:

“The BMJ stopped publishing research funded by the tobacco industry a few years ago because of strong evidence that it couldn’t be relied on. We have no such restrictions on research funded by the pharmaceutical or food and drinks industries, but the evidence of systematic bias in industry funded research is something we in the scientific community must keep under review. This study was funded by the NIH and has been subjected to rigorous peer review. The fact that four of its eight authors receive funding or are employed by Unilever, which is a major manufacturer of vegetable oils, is one of the many uncomfortable realities of 21st century medical research.”

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Comments

  1. How many of the «peers» reviewing has the same view on saturated fat as Frank Hu. Is there anybody outside the echo chamber that had reviewed this study ?

  2. When the intake of saturated fat is based on a complete burger meal with everything, they eat horrendously amounts of sugars and white flour that completely rapes our coronary system. To blaim this damage on saturated fats is just plain stupidity.

  3. John Halgren says:

    Robert Asklund hits the nail on the head. Bravo.

  4. How did they know what their subjects had eaten, and in what amounts? The answer is ‘questionnaires’ so I snort in derision and recommend that when all else fails one should always try science.

    In other words, I question whether it is even “observational data”.

  5. Curiously, the baseline energy intake in the NHS cohort (the female majority of the study participants) has increased dramatically since Wang et al, the JAMA paper earlier this year.
    In that study it averaged an implausible ~1500 kcal a day, now it is a more reasonable (but still unlikely, given the BMIs and likely workloads) ~1800 kcal.
    So either this is not the same data sets, or it has been adjusted to cover “missing data”, or there is some other difference that I am frankly not interested enough in this matter any more to discover.
    Of the earlier paper, at any rate, one could say “how can they predict the effect of a 5% or 1% energy exchange when 20% of their energy intake is missing in action”?

    This is an example of pathological science; weak and inconsistent associations are worried over and over again by people who present this matter, and by association themselves and their institutions, as real and important. But if it was real, of, if real, important enough to be worth studying in this detail and at this expense for 60 years the research would have produced strong associations and effective interventions. This lack of result does not yet stop the faithful, but one notices that fewer and fewer are flocking to their banners.[1]

    It is likely that, malnutrition and contamination aside, the major influence of food on disease is via insulin resistance and hyperinsulinaemia. The serum markers for these conditions – 2 hour insulin and its cheap proxies, HDL, the fasting TG/HDL ratio, and HbA1c – correlate with CVD and most cancers strongly and consistently and certainly to an extent not seen with any macronutrient, even sugar.
    Experimentally, saturated fat does play a role in elevated insulin in humans, but only in the context of diets rich in refined, or rather degraded, carbohydrates. As these carbohydrates (sugar, flour, processed potato, and fruit juice) are present in the diet in much larger quantities than saturated fat (50-55%E vs 10-15%E) and as they are overall associated with less nutritious foods (bread and soda vs meat and cheese), and as, if 5% of energy from any bloody thing should be replaced with whole grains or lentils it is surely refined grains, and as eating more of any kind of fat available will increase the intake of PUFA and MUFA regardless of its SFA content anyway, worrying about saturated fat in anything but biscuits and cakes is pointless.
    In fact, as Nina Teicholz has pointed out, the high-risk subgroup analysis from the PREDIMED trial found that SFA was strongly associated with CVD mortality, but in this case there was no association with the SFA in meat, processed meat, or dairy, the only significant association was with the SFAs from pastries and other processed foods (cookies, donuts, bakery, sauces, pizza, other).[2]

    As for the business of the Unilever employees, this is odd as their role in the paper was minor and unnecessary, restricted to help with interpretation, revision, and approval, which are editorial rather than scientific functions. NIH funded the paper so Unilever money wasn’t needed, which is not to say they haven’t made donations to Harvard Chan for allowing their employees to share in the publication of a paper that will be widely cited and can be used by Unilever to promote their products. Unilever is the largest user of certified palm oil, and their approval of this paper indicates that they plan to either move away from palm oil or modify it to contain more C:18 and less C:16.

    We only ate palm oil in the first place because we were harassed and terrorised with health scares to stop us eating animal fat. Animal fat is an inevitable byproduct of our animal protein production. Its avoidance constitutes food waste, as does the focus on lean meat at the expense of organ meats and other cuts. To compound this waste we are then supposed to clear land to replace animal fat with vegetable oil, as it happens dooming the orangutan in the process, and build factories to extract these oils using chemical processes harmful to exposed workers and the surrounding environments, as opposed to gently heating the suet from a carcass or mechanically churning butter from cream separated by milk by a little standing. We are also required to build vitamin supplement factories to replace the nutrition our foremothers fed us from organ meats.

    “Mechanistic understanding of the initiation of the fatty streak and atherosclerosis calls into question the avoidance of ruminant or porcine fat. Due to high levels of oleic acid, a low n-6 : n-3 fatty acid ratio in some groups, and the presence of specific micronutrients including vitamins and essential fatty acids, animal fats are of benefit in human nutrition. Animal fats can be obtained in minimally processed form making them a convenient source of energy and micronutrients.”[3]

    [1] https://en.wikipedia.org/wiki/Pathological_science

    [2] Guasch-Ferré M, Babio N, Martínez-González MA, Corella D et al. Dietary fat intake and risk of cardiovascular disease and all-cause mortality in a population at high risk of cardiovascular disease. Am J Clin Nutr. 2015 Dec;102(6):1563-73. doi: 10.3945/ajcn.115.116046.
    http://ajcn.nutrition.org/content/early/2015/11/11/ajcn.115.116046.full.pdf

    [3] Barendse, W. Should animal fats be back on the table? A critical review of the human health effects of animal fat. Animal Production Science, 54 7: 831-855. doi:10.1071/AN13536
    http://www.publish.csiro.au/AN/pdf/AN13536

    • Pudd, I searched in vain in the grocery store (including Whole Food) for a substitute butter without some type of palm oil and came up empty handed. Not one! Good luck orangatangs. There is an solution though, with little chance of success, and that’s to eat a vegan diet and avoid all oils and butters as espoused by vegan drs. John McDougal, Caldwell Esselstyn, Michael Greger, Colin Campbell et al. Not much chance of that wide scale
      but I made the switch and my life has dramatically changed for the better. Score one for the orangatangs, but just one..

  6. “Of the earlier paper, at any rate, one could say “how can they predict the effect of a 5% or 1% energy exchange when 20% of their energy intake is missing in action”?” One could ask the same of the global warming crowd: about 20% of their carbon dioxide flows are unaccounted for (or were when last I looked into this aspect of it.)

  7. Stefhan Gordon says:

    when you go to the “Conflicts portion, you find the following: “… GZ [Geng Zong the lead author] is supported by a postdoctoral fellowship funded by Unilever R&D, Vlaardingen, Netherlands; AJW [Anne J Wanders], MA [Marjan Alssema], and PLZ [Peter L Zock] are employees of Unilever R&D (Unilever is a producer of food consumer products); FBH has received research support from California Walnut Commission and Metagenics…”
    —————————————–
    So low and behold what does Unilever make? Well here are some of Unilever Brands (not inclusive): Country Crock (a popular brand of margarine), I Can’t Believe It’s Not Butter, Hera (a vegetable oil based spread sold in Eastern Europe), Mazola (vegetable cooking oil including rape seed and safflower oil), Rama (margarine and cooking fats made from vegetable oils), Doriana (spreads and cooking oils made from seed oils), Perla (margarine sold in Eastern Europe), Planta (margarine). Stork (margarine sold in the UK, Ireland and South Africa), Thea (margarine sold in Austria), Astra (vegetable oil spreads sold in Sri Lanka).

  8. When you eat saturated fat your digestive system breaks those triglycerides down into free saturated fatty acids because the triglyceride molecule is to big to be absorbed into the arteries. Similarly, the triglycerides stored in your own fat/adipose cells/tissue are too big to get out and into the arteries so the fat cells break the triglycerides into free fatty acids. It’s the same fatty acids entering the arteries to be metabolized whether it’s coming from the gut or the adipose tissue. It’s just entering via different pathway.

    So why then would eating saturated fat cause heart disease but dieting off your own saturated fat does not?

    If you lost 100lbs of body fat over 400 days you’d be losing fat at a rate of 1/4lb per day. That is the equivalent volume as eating a stick of lard/butter ever day for 400 days. A cardiologist might tell you that eating a stick of butter/lard every day was going to give you hear disease. Yet, he/she wouldn’t thing twice about telling someone to lose weight at rate equal to eating that same volume

    • puddleg58 says:

      This is true.
      However, the depot fat you will be burning will be around 30% long chain SFAs (mainly C:16 and C:18), 60% MUFA (almost all C:18.cis1) and a smattering of PUFA and shorter chain SFAs.
      This is equivalent to eating a 50:50 mix of butter and olive oil, with a small addition of coconut oil.

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