Intended for healthcare professionals

CCBYNC Open access

Rapid response to:

Research

Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies

BMJ 2015; 351 doi: https://doi.org/10.1136/bmj.h3978 (Published 12 August 2015) Cite this as: BMJ 2015;351:h3978

Rapid Response:

Re: Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies

From a public health perspective, the question is, whether it will improve the health of a population when they are given instructions to restrict saturated fat. We should remember that today this applies to all ages - that infants in kindergartens and primary schools do not have access to whole milk because of concerns about saturated fat and heart disease in the adult population. There is an increased incidence of rickets today, which may in part be an unintended consequence of this instruction, as may increased incidences of diabetes and obesity (due to the replacement of natural foods relatively high in saturated fat with grains, refined carbohydrates, and other highly processed foods that may promote over-eating).

If so, this is troubling, because obesity and diabetes are clearly risk factors for cardiovascular disease.

From our point of view, it is easiest for people to control weight and blood sugar if they remove sugar, refined starch, and carbohydrate dense foods in general from their diet. Should they then worry about the saturated fat in the whole foods and minimally refined cooking fats they use?

The chain of causality accepted by another correspondent can be summarised as "1) SFA raises LDL, 2) LDL is associated with CVD, 3) lowering LDL is associated with lower rate of CVD".

However,
1) LDL cholesterol is a calculated figure derived from other measurements and the atherogenicity of the LDL particles depends on factors such as ApoB, ApoC3, small dense LDL particles, etc. which are controlled by the response to dietary carbohydrate than by the response to saturated fats, which tend to increase the proportion of larger and less atherogenic LDL particles. This beneficial response to saturated fat is increased when the carbohydrate content of the diet is lower. [1]

2) Mendelian randomisation shows that 50% of the relationship between LDL cholesterol and CHD risk is due to genetic, rather than diet or lifestyle, factors.[2] For this reason it is not unreasonable to adjust CHD data for cholesterol levels. CHD cases can have higher LDL than age-matched controls even when both groups have been eating the same diet for some time.[3]

3) Replacing saturated fat with carbohydrate lowers LDL cholesterol but is not associated with any reduction in CVD in sub-group meta-analysis of RCTs. On the other hand, cholesterol lowering associated with increased intake of PUFA is associated with a reduction in CVD events, but not fatal events or all-cause mortality.[4]. In prospective cohort studies, replacing carbohydrate from all sources with PUFA is associated with marginally more benefit than replacing saturated fat with PUFA.[5]

We have to get energy from somewhere, and the human capacity to derive energy from extra PUFAs without increased harm is probably limited. Ancel Keys et al in the Seven Countries Study found that the natural human diets they studied supplied between 3-7% energy from linoleate, with minimal contributions from other PUFAs, and did not consider that the minimal cholesterol lowering effect of this small variation in PUFA could accounted for the different heart disease rates between populations. [6] PUFAs are essential nutrients with anti-thrombotic effects and the foods that supply them also supply vitamin E and other tocopherols that might be expected to modify cardiovascular risk through CPK pathways. The essentiality of PUFAs and the presence of other essential nutrients in PUFA foods are confounders when analyzing the effect of replacing other nutrients, such as saturated fats, with PUFA.

Such limits on saturated fats as promulgated in the past have tended to increase the intake of trans fats, and in that part of the population convinced to eat low-fat diets may have even decreased the consumption of polyunsaturated fats.

We have more to gain today by preventing and reversing type 2 diabetes, obesity, and metabolic syndrome, all significant risk factors for CVD mortality, in the context of a nutritionally optimal diet that restricts carbohydrate-dense foods and processed foods, and we can do this most easily if we do not impose artificial limits on the population's intake of saturated fats, an instruction that has probably played a role in increasing the incidence of these conditions.

[1] Siri-Tarino P et al. (2015) Polyunsaturated Fats Versus Carbohydrates for Cardiovascular Disease Prevention and Treatment. Annu. Rev. Nutr. 2015. 35:517–43

[2] Holmes MW et al (2015) Mendelian randomization of blood lipids for coronary heart disease. Eur Heart J. 2015 Mar 1;36(9):539-50. doi: 10.1093/eurheartj/eht571. Epub 2014 Jan 27.

[3] Oliver MF, Boyd GS (1953) The Plasma Lipids in Coronary Artery Disease. Br Heart J. 1953 Oct;15(4):387-92

[4] Hooper L. et al (2015) Reduction in saturated fat intake for cardiovascular disease, The Cochrane Library, June 10 2015. DOI: 10.1002/14651858.CD011737

[5] Farvid MS et al (2014) Dietary linoleic acid and risk of coronary heart disease: a systematic review and meta-analysis of prospective cohort studies. Circulation. 2014 Oct 28;130(18):1568-78. doi: 10.1161/CIRCULATIONAHA.114.010236.

[6] Keys A et al (1980) Seven Countries. A multivariate analysis of death and coronary heart disease. Cambridge, MA; Harvard University Press, ISBN: 0-674-80237-3, 1980. 381 pp.

Competing interests: No competing interests

14 August 2015
George D. Henderson
Researcher
Auckland University of Technology
17 Antares Place Auckland