What Effect Does Replacing Saturated Fat in the Diet Have on Heart Health?

Photo by jesse orrico on Unsplash

Part 3 in our ‘All About Saturated Fat’ series

Nutrition doesn’t exist in a vacuum. While we often talk about the ‘benefits’ or ‘risks’ associated with various nutrients (and in particular saturated fat), in the context of the overall diet, any change to longer-term eating patterns that has an effect on health is due to substitutions of foods which results in alterations in macronutrients or sub-types of those macronutrients consumed.

Evidence for benefits of replacing saturated fat with other nutrients is sparse. For example, a 2017 meta-analysis of substitution of saturated fat for unsaturated fats in people with overweight and obesity, found no significant effect on total cholesterol, LDL, or triglycerides, concluding that “Due to null results and a small number of studies included, there is no strong evidence that replacement of saturated with unsaturated fatty acids may benefit lipid profiles in this population.” [1]

In the research presented previously in this series, benefits have been shown for the substitution of polyunsaturated fats for saturated in the diet, but the same effect isn’t seen with substitutions of unsaturated fat in general, nor monounsaturated fat or carbohydrate. This begs the question if saturated fat is independently harmful as is often claimed, why do we not see benefits when saturated fat is replaced by anything other than polyunsaturated fats?

The benefits of substitution of polyunsaturated fat in place of saturated fat could be due to one or more of four possible reasons:

  1. The reduction of saturated fat requires the addition of polyunsaturated fats to be beneficial
  2. Saturated fats are not inherently harmful, whereas essential fatty acids (which are PUFAs) are inherently healthy
  3. The substitution of saturated fat for polyunsaturated allows for a greater intake of essential omega 3 fatty acids
  4. The results are due to the inclusion of inadequately controlled trials as suggested by Hamley. [2]

One other reason suggested for this effect is that polyunsaturated fats reduce ApoB where carbohydrate and monounsaturated fats do not. Notwithstanding that this line-of-thinking also implies that polyunsaturated fats are beneficial and not that saturated fats are detrimental to health, it also ignores that saturated fats are associated with increased HDL-cholesterol and hence ApoA and that this can help to correct for the ApoB-ApoA ratio, a significant predictor of heart disease risk.

It is important to note, as mentioned in a reply to Katan and colleagues, in response to criticism of their meta-analysis, [3] that the desire to reduce saturated fat for cardiovascular disease benefit could have the undesirable effect of increasing intakes of highly-refined carbohydrate and sugar-based foods and that this trend might outweigh any benefits of reducing saturated fat. [4]

The desire to reduce saturated fat for cardiovascular disease benefit could have the undesirable effect of increasing intakes of highly-refined carbohydrate and sugar-based foods

Occam’s razor[1] would suggest that saturated fats are not inherently harmful but instead, that polyunsaturated fats are broadly health-promoting.

Are we simply not getting enough omega-3 essential fats?

It is suggested by the Food and Agriculture Organization of the United Nations and the World Health Organization that omega-6 fatty acids should make up at least 2% of the total energy of the diet and omega-3 >0.5% of the diet (or a minimum of 250–2000mg of combined EPA/DHA) to ensure sufficiency. In studies subject to meta-analysis the ‘control’ or higher-saturated and lower-PUFA groups typically had polyunsaturated fat intakes around 5.5% of total energy while the interventions (which reduced saturated fat and increased polyunsaturated) increase this by 2–4-fold. While the polyunsaturated fat intake of the higher saturated fat groups should have been sufficient to provide linoleic acid in the required amounts, it is less clear whether omega-3 sufficiency was achieved and whether an increase in PUFAs aided sufficiency of omega-3 (and omega-6) fats. This lack of attention to omega-3 fats was a feature of the reply to Mozaffarian et al., by Hooper. [5]

According to data from the 2011–2012 National Health and Nutrition Examination Survey (NHANES) in the United States, the average daily intake of the ‘base’ omega-3 fatty acid (alpha-linolenic acid or ALA) from foods was 1.59 g for females and 2.06 g for males, while only around 90 mg of DHA/EPA was consumed. Conversion rates of ALA to DHA and EPA are very poor for many people and are highly variable. [6] Conversion rates can be as low as 5–10% for EPA and 2–5% for DHA.7 Conversion rates of ALA to DHA and EPA might be even lower in men, and even supplementation with ALA (from flax oil for example) may not always raise DHA effectively. [8–10]

It is highly unlikely that omega-3 sufficiency, let alone optimisation was achieved in those consuming more saturated fat and less polyunsaturated

So, even assuming the highest conversion rates, and adding average DHA/EPA intakes from food, it is highly unlikely that omega-3 sufficiency let alone optimisation was achieved in those consuming more saturated fat and less polyunsaturated. In these cases, reducing saturated fat and increasing polyunsaturated would have the natural consequence of increasing essential (and especially omega 3) fatty acids. This again suggests that polyunsaturated fats are beneficial and that people should prioritise omega-3 rich foods but does not inherently show that saturated fats are ‘bad’. The lack of evidence for benefits of substituting saturated fats for anything other than polyunsaturated fats strongly suggests that we need more PUFAs…not less saturated fatty acids (notwithstanding excess of any nutrient is likely to be harmful at some point).

The lack of evidence for benefits of substituting saturated fats for anything other than polyunsaturated fats strongly suggests that we need more PUFAs…not less saturated fatty acids

Read Part 1: What Do We Know from Observational Evidence?

Read Part 2: What Do We Know from Randomised Controlled Trials?

Read Part 4: Does the Type of Saturated Fat Matter for Heart Health?

References

1. Hannon BA, Thompson SV, An R, Teran-Garcia M. Clinical Outcomes of Dietary Replacement of Saturated Fatty Acids with Unsaturated Fat Sources in Adults with Overweight and Obesity: A Systematic Review and Meta-Analysis of Randomized Control Trials. Annals of Nutrition and Metabolism. 2017;71(1–2):107–17.

2. Hamley S. 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. 2017;16(1):30.

3. Katan MB, Brouwer IA, Clarke R, Geleijnse JM, Mensink RP. Saturated fat and heart disease. The American Journal of Clinical Nutrition. 2010;92(2):459–60.

4. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Reply to MB Katan et al. The American Journal of Clinical Nutrition. 2010;92(2):460–1.

5. Hooper L. Meta-analysis of RCTs finds that increasing consumption of polyunsaturated fat as a replacement for saturated fat reduces the risk of coronary heart disease. Evidence Based Medicine. 2010;15(4):108–9.

6. Mantzioris E, James MJ, Gibson RA, Cleland LG. Dietary substitution with an alpha-linolenic acid-rich vegetable oil increases eicosapentaenoic acid concentrations in tissues. The American Journal of Clinical Nutrition. 1994;59(6):1304–9.

7. Davis BC, Kris-Etherton PM. Achieving optimal essential fatty acid status in vegetarians: current knowledge and practical implications. The American Journal of Clinical Nutrition. 2003;78(3):640S-6S.

8. Burdge GC, Calder PC. Conversion of $\alpha$-linolenic acid to longer-chain polyunsaturated fatty acids in human adults. Reprod Nutr Dev. 2005;45(5):581–97.

9. Brenna JT, Salem Jr N, Sinclair AJ, Cunnane SC. α-Linolenic acid supplementation and conversion to n-3 long-chain polyunsaturated fatty acids in humans. Prostaglandins, Leukotrienes and Essential Fatty Acids. 2009;80(2–3):85–91.

10. Arterburn LM, Hall EB, Oken H. Distribution, interconversion, and dose response of n−3 fatty acids in humans. The American Journal of Clinical Nutrition. 2006;83(6):S1467–76S.

[1] “entities should not be multiplied without necessity” or simply, the simplest explanation is usually the right one

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