#481: Why Saturated Fat Really Does Impact Heart Disease Risk

In Podcasts by Danny Lennon2 Comments


While it has long been acknowledged that high intakes of saturated fat can increase risk of atherosclerotic cardiovascular disease due to their impact on blood lipids, there are some who question the association between saturated fat and heart disease.

Specifically, they may state that the evidence for this association is weak or non-existent, typically by pointing to some commonly cited studies that show null associations between saturated fat and CVD outcomes.

On this basis, they may conclude that there is no basis to aim to limit saturated fat intake to current recommended levels or that reducing saturated fat intake will not actually improve health outcomes.

In this episode, Alan and Danny look at the four most commonly cited publications showing a null association, highlighting some key issues. Beyond that, they look at a number of other lines of evidence on saturated fat that allows one to come to a confident answer on this question.

So does reducing saturated fat intake to recommended levels actually reduce heart disease risk? Let’s discuss…

Co-hosts for this Episode

Dr. Alan Flanagan has a PhD in nutrition from the University of Surrey, where his doctoral research focused on circadian rhythms, feeding, and chrononutrition.

This work was based on human intervention trials. He also has a Masters in Nutritional Medicine from the same institution.

Dr. Flanagan is a regular co-host of Sigma Nutrition Radio. He also produces written content for Sigma Nutrition, as part of his role as Research Communication Officer.

Danny Lennon has a master’s degree (MSc.) in Nutritional Sciences from University College Cork, and he is the founder of Sigma Nutrition.

Danny is currently a member of the Advisory Board of the Sports Nutrition Association, the global regulatory body responsible for the standardisation of best practice in the sports nutrition profession.


  • The Claim: “Saturated Fat Doesn’t Lead to Heart Disease”
  • Cited Studies:
    • Siri-Tarino et al., 2010 Meta-analysis
    • Chowdhury et al., 2014 Meta-analysis
    • De Souza et al., 2017 Meta-analysis
    • PURE – Dehghan et al., 2017
  • Understanding Over-adjustment
  • High Saturated Fat and CVD/CHD
    • Seven Countries Study
    • Metabolic Ward Studies
    • Substitution Effects
    • Core Trials on Replacing Saturated With Polyunsaturated Fat
    • Hooper et al. – Saturated Fat Cut-offs

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  1. I am not a statistician and have some doubt about the over-adjustment critique discussed in this podcast. It was mentioned that the main causal impact of saturated fat is modulated through LDL or Apo-b. I also learned from the podcast that there is a huge variation in how individuals levels of LDL are impacted by the intake of saturated fat. Hence, what is the problem for adjusting for LDL when examining the negative impact of ingesting saturated fat. Let me clarify with a hypothetical. Suppose an individual has very little increase in LDL as they increase their saturated fat intake. By adjusting for LDL one can control for the response variability, and the analysis will capture that this person perhaps has little increase in CVD risk. If we ignore LDL adjustment then the segment of the population that has low response on LDL from saturated fat will be assessed the same risk as the segment that has a high response. Can someone clarify?

    1. Author

      Hi Raj,

      The increased risk from high SFA diets is via increasing LDL-C/apoB. So the risk at an individual level is based on their blood lipid response.

      So let’s consider two people who have normal LDL and start eating a diet of 18% of calories from saturated fat. Say one of them sees a large increase in LDL-C, and the other doesn’t see any change at all. Then, yes, the person with no change is not increasing their risk of atherosclerosis as their LDL is still low.

      So it’s primarily the impact on blood lipids that leads to the risk increase. Thus why adjusting for LDL levels is considered over-adjustment.

      Our point is not that saturated fat is just inherently harmful. Rather, that on average, high SFA intakes tend to lead to elevated LDL/apoB, and this is a causal risk factor for atherosclerosis. So saying “saturated fat is not a problem” is misleading.

      As a note, above I’m just talking about atherosclerosis and therefore focused on blood lipids. However, high SFA diets also can have other detrimental effects; e.g. liver fat accumulation, particularly in context of hypercaloric diets.

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