Sunday, May 21, 2017

My Meta-Analysis on Saturated Fat, Polyunsaturated Fat and Coronary Heart Disease

I just published a paper in Nutrition Journal titled ‘The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials’.  Nutrition Journal is an open access journal and the paper shouldn’t be too technical so I encourage you to read it but I’ll also summarise it below:

I begin in the introduction by discussing the effect that saturated fat (SFA), monounsaturated fat (MUFA) and polyunsaturated fat (PUFA) have on cholesterol levels and how this formed the basis of the diet heart hypothesis, which is that replacing SFA with PUFA would be expected to reduce the risk of coronary heart disease (since MUFA didn’t affect total cholesterol it was largely ignored at this time).  Several clinical trials were conducted, mostly in the 1960s and 1970s, to test the diet heart hypothesis.

More recently, several meta-analyses have pulled the results of the diet heart trials and most came to the conclusion that replacing SFA with PUFA would reduce the risk of coronary heart disease.  However, there is a lot of controversy surrounding the diet heart hypothesis, and it is an important topic since the advice to reduce saturated fat is very influential in conventional dietary advice.  So I thought it would be useful to do my own research.

I researched the clinical trials included in the previous meta-analyses and found that the dietary advice or the foods given to the participants in the trials would be expected to result in the high PUFA group having a lower intake of trans fats (to varying degrees) compared to the high SFA group.  I also found other confounding variables such as two trials where the high PUFA group received a multifactorial dietary intervention, one trial where the high SFA group was given a vitamin E deficient diet, and another trial where the high SFA group received more antipsychotic medication that was found to be cardiotoxic.  These issues were rarely discussed or taken into account by the previous meta-analyses.

Therefore I conducted my own meta-analysis by including the trials in previous meta-analyses and then categorising them as ‘adequately controlled’ or ‘inadequately controlled’ based on the degree of confounding variables in each trial.  I considered the adequately controlled trials to be those that most accurately tested the effect of replacing SFA with PUFA, while the inadequately controlled trials to have too much of a difference between the groups to be a valid test of replacing SFA with PUFA.

The main findings are:

  • The results from the adequately controlled trials suggest that replacing SFA with PUFA is unlikely to increase or decrease the risk of coronary heart disease or all-cause mortality
  • This is the case regardless of whether the Sydney Diet Heart Study is included or excluded
  • The suggestion of benefits reported in earlier meta-analyses is due to the inclusion of inadequately controlled trials

In the discussion, I mention that there are issues in drawing conclusions from risk factors (such as cholesterol) and observational studies, and that the issues inherent in these types of studies are likely due to them having discordant results with this meta-analysis.  I also discuss that similarly there are issues in drawing conclusions from nutrients (like SFA) to foods, as foods are made up of many nutrients and other substances that may affect outcomes you’re interested in, such as the risk of coronary heart disease.

So what are the implications of this paper?

  • Saturated fat is unlikely to increase the risk of coronary heart disease
  • Replacing saturated fat with polyunsaturated fat (such as butter with margarine or vegetable oil) is unlikely to increase or decrease the risk of coronary heart disease
  • Results from observational studies and enthusiasm from discovering a new risk factor or discovering a target for an existing risk factor should be tempered with a degree of caution and scepticism until they are tested
  • Dietary guidelines and public health policy should focus on other things that are more likely to be effective at preventing coronary heart disease

If you like talks, the content of the meta-analysis is similar to a talk I have in 2015 at the Ancestral Health Society of New Zealand’s (AHSNZ) international symposium in Queenstown.  You can view the talk here and the other talks here.  There were a lot of great speakers there talking about a diverse range of topics such as nutrition, exercise, behaviour change, sustainability, active transport and mental health.  So it shouldn't be too hard to find something that interests you.

AHSNZ is holding another international symposium in October at Queenstown which you can find out more about the symposium here.  I’ll be speaking again, this time about insulin resistance, which is the focus of my PhD (so this paper is very unlikely to count towards my PhD and has mostly been a weekend project) and will be a focus on the blog over the next several months.


  1. Hi Steven, and thank you for doing this wonderful job, finally compiling the randomized trials about dietary SFA/PUFA substitution in a reasonable, critical way.

    I hope your paper will be widely cited in the nutrition science! :-)

    -Vladimir (from Valtsu's blog)

  2. I am really glad to see this work in print finally - very well done. I notice that in the uncontrolled trials, the reduction in CHD deaths is still not correlating with a reduction in all-cause mortality, as it should if a) CHD deaths were correctly diagnosed and b) the intervention didn't increase deaths from other causes.
    Despite all the good advice in these trials, there still seems to be something wrong.

    1. Thanks George.

      If PUFA was just good for CHD and neutral elsewhere you would expect some dilution, but not equal total mortality like in the LA vets and the Finish Mental Hospital Study (and those two were quite large, so would drive a lot of the inadequately controlled subgroup)

      The LA Vets appears to be double blind and the the primary investigator (Dayton) mentioned some reservations about the diet in the discussion + published the higher cancer and gallstones in the PUFA group (so probably not too biased). Can't say the same for FMHS.

      If the intervention did increase the risk of death from other causes you probably would see it more in LA vets rather than ODHS and STARS much because of the age range, but perhaps also in FMHS because of the study population, which is kind of happened

      However, if PUFA and vegetable oil are good for everything as some modern epidemiology suggests, then you expect what happened in ODHS (modern PUFA epidemiology is like a multifactorial diet trial :p)

    2. What you see is PUFA associated with no benefit in Europe; and SFA with no harm; where maybe people are more skeptical about PUFA oils and spreads and regard traditional foods as healthy, so the PUFA isn't wrapped in a multifactorial fog like it is in the USA....


  3. "there are issues in drawing conclusions from nutrients (like SFA) to foods, as foods are made up of many nutrients and other substances" - this is a valid point. For all I know, neither of the two most atherogenic fats in our diets - to wit, lard and peanut oil - is particularly rich in SFAs. Lard has a saturated fatty acid content of about 38-43% and peanut oil's SFA content is only 17%. Meanwhile, a number of fats with significantly higher SFA concentrations - such as tallow or palm oil - are actually far less atherogenic.

    1. Do you know if lard is actually an atherogenic fat, or is it considered so because it happens to be fat used in animal models of atherosclerosis. I remember seeing a paper regarding peanut oil being atherogenic with the peanut lectin being the likely suspect.

    2. Yes Lectins is one of the main talking points from Dr Steven Gundry MD (cardiologist) - in his view, this is whats driving CVD. He advises to not eat peanuts, cashews and de-hull the almond as these for example contain lectin. As he put it - plants have been on the planet for way more years than humans and have developed defense mechanisms that can make a predator sick - us being one giant one now to them. In his view Wholegrains are bad news and need to b avoided. Tomatoes need to b skinned and de-seeded as any vegetable that has internal seeds contains lectins in the skin for protection . European cultures have always taken skin off and de-seeded but that art has been forgotten in westernised world. Anyway - food for thought as they say

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