Professor Bruce Griffin, from the University of Surrey, was one of the guest speakers at a satellite symposium at FENS (October 20, Berlin). He provided an overview of the current evidence examining saturated fat (SFA) intake and CHD risk. Particularly timely as recently there’s been much debate around SFA, with claims suggesting dietary recommendations to reduce SFA intake have been over exaggerated.
As way of background, he presented data, both from prospective cohort studies and statin trials, which clearly support the relationship between blood cholesterol and CHD mortality. In terms of dietary factors, studies going as far back as the 1950s have confirmed the association between SFA and blood cholesterol. But how does this association impact CHD risk? It’s now becoming increasingly apparent this is dependent on what is used to replace SFA in the diet. One meta-analysis found replacing SFA with PUFA reduced the risk of CHD deaths by 26%, yet there was no effect when carbohydrates replaced SFA, and in some cases an adverse effect[i]. A more recent study, published in 2015, found when SFA was substituted with an equivalent number of calories from either monounsaturated fat, PUFA or wholegrain carbohydrates there was a reduced risk of CHD – PUFAs having the greatest effect[ii]. Conversely trans fats and carbohydrates from refined starches/ added sugars increased the risk.
Despite this, the latest controversy has arisen following a number of recent analyses failing to find an association between SFA and CHD risk. Examining these in closer detail, Professor Griffin highlighted a number of limitations with these studies.
Firstly, a 2013 study re-evaluated data from the Sydney Heart Study and found dietary linoleic acid was associated with an increased risk of death from CVD[iii]. However this study had design faults including the large amount of linoleic acid consumed in the intervention group (15.4% of energy – far higher than recommended) and not taking into account trans fat.
Secondly, a 2010 meta-analysis of prospective cohort studies found no significant evidence that SFA was associated with CV risk[iv]. In 2014 the Cambridge Epidemiology Group came to similar conclusions following their analysis of recent studies[v]. However in the latter analysis the researchers included the problematic Sydney Heart Study. A re-analysis of the data without this study came to quite different results – a reduction in SFA was associated with a 20% reduced risk of coronary disease. Other limitations of these types of meta-analyses include the use of cohort studies (which show associations but not cause and effect), not taking into account what is used to replace SFA, not considering the differing effects individual SFA have on LDL-C or considering the effects of SFA from different foods – the food matrix and nutrients may interact with SFA resulting in different outcomes.
As well as their effect on LDL-C, the influence of SFA on other important elements of CV health must not be overlooked. SFA has been associated with increasing arterial stiffness, visceral and liver fat, whereas the opposite is true for PUFA.
Based on the totality of evidence, Professor Griffin believes the dietary recommendations to reduce SFA to 10% of total energy are still valid and if PUFA is used to replace 1% of dietary energy from SFA, CHD incidence could reduce by around 2 to 3%. One way to achieve this healthy balance of fats is to eat a more plant-based diet.
[i] Jakobson M et al. (2009) Am. J. Clin. Nutr.89,1425-32
[ii] Yanping L et al (2015) J Am Coll Cardiol 66, 1538-47
[iii] Ramsden CE et al (2013) BMJ 346, e8707
[iv] Siri-Tarino PW et al (2010) Am. J.Clin.Nutr. 91;535-46
[v] Chowdhury R, et al (2014) Ann. Int. Med. 160(6);398-406