The AJCN has a nice short “consensus” paper from many of the top researchers examining the supposed link between saturated fat and cardiovascular disease, which is open access here.
Arne Astrup and Walter Willett organized an invitation-only symposium last year with big names in nutrition research; among the other participants were Frank B Hu, Ronald M Krauss, Jørn Dyerberg, Peter Elwood, Kjeld Hermansen, Marianne Uhre Jakobsen, Frans J Kok, Jean Michel Lecerf, Philippe LeGrand, Paul Nestel, Ulf Rise’rus, Tom Sanders, Andrew Sinclair, Steen Stender, and Tine Tholstrup. These 17 names were among 21 attendees in total, and of 30 who were invited. As it is important to get a sense of how they were selected, in the Supplementary material it is stated that Astrup and Willett “drew up a short list of 30 scientists recognized as authorities within the field” who “have made major scientific contributions in peer-reviewed journals in the field of “dietary fat and cardiovascular disease and type 2 diabetes” of either mechanistic, observational and interventional studies, with emphasis on recent major pooled analysis, meta-analysis, randomized controlled trials, or a long standing carrier within the area.” The scientists represented at least 5 different countries. They discussed 19 papers and 10 presentations and eventually drew conclusions to be published. It should be noted that 3 of the participants declined to co-author the paper because of the conclusions (doesn’t state which).
Just keeping one eye on what is being published lately, it was pretty easy to guess what their general conclusions were (in my words):
- Coronary Heart Disease (CHD) risk is slightly reduced when saturated fatty acids (SFA) are replaced with polyunsaturated fatty acids (PUFAs).
- It isn’t clear that replacing SFA with carbohydrates reduces CHD risk, but possibly if the carbs are unrefined.
- There is not enough evidence for replacing SFA with monounsaturated fats (MUFAs).
- The amount of SFA intake relative to refined carbohydrate intake on the risk of insulin resistance and diabetes is not apparent.
- Single biomarkers are insufficient to determine CHD risk, they suggest using multiple biomarkers and endpoints.
- You cannot predict a foods’ effect on CHD only by SFA content.
- More research is needed to compare the effects of specific forms of carbohydrates relative to SFAs on CHD risk.
- Foods should be studied themselves.
I highly recommend reading the full thing to get the big picture, but some specific things worth mentioning:
- 1 prospective study suggests carbohydrates may have more negative effects on lipids and CHD risk in overweight and inactive subjects with insulin resistance, suggesting health context must be always considered.
- They note that prior to 1990, declining CHD rates in the U.S. and Poland correlated with SFAs being replaced with PUFAs.
- Type of cardiovascular disease must be considered.
- For assessing CHD risk, they suggest a “comprehensive risk score made up of multiple biomarkers of CHD risk, including total and HDL cholesterol, blood pressure, body fatness, glucose tolerance, and inflammatory markers.”
- Individual SFAs may have varying effects on CHD; they note that stearic acid has some supportive epidemiological evidence there, though it is not feasible to make separate recommendations on individual SFAs given that they obviously come in combinations from food.
- Short- and medium- chain saturated fatty acids have less evidence on CHD risk.
- They note that the Mediterranean diet has sufficient evidence (for them) on CVD risk factors and endpoints to suggest benefit.
- Toward the end they state indirect evidence hints that SFAs could be replaced with MUFAS or unrefined carbs.
They bring up the dietary recommendation of <10% of energy from SFAs, but seem to struggle through suggesting what is ideal- if you do that then carbohydrate and likely refined carbohydrate increases, and there isn’t enough research to put MUFAs in place of SFAs. This next paragraph is perhaps the most important of all (emphasis mine):
Food-based recommendations are more practical for the general public than is nutrient-based dietary advice. However, the evidence linking individual foods or food patterns to CVD risk is more limited. The epidemiologic data provide strong evidence that a high intake of processed meat products, a major source of SFAs, is associated with an increased risk of CHD (32). There is no consistent evidence that a higher intake of dairy products is associated with CHD risk in epidemiologic studies* (34), but data do support the beneficial effects of dairy products on type 2 diabetes risk (34, 35). However, intervention studies on the effect of dairy fat on the risk of CHD and diabetes are lacking; thus, the role of SFAs in dairy fat still needs to be investigated. There is increasing evidence to support that the total matrix of a food is more important than just its fatty acid content when predicting the effect of a food on CHD risk, eg, the effect of SFAs from cheese on blood lipids and CHD may be counterbalanced by the content of protein, calcium, or other components in cheese. In addition, the special fatty acid profile (rumenic acid, trans vaccenic acid, and short-chain fatty acids) may modify the effect on CHD risk. Another example is dark chocolate, which has a high content of stearic acid, oleic acid, and polyphenols, and observational studies, mechanistic studies, and RCTs show that dark chocolate reduces risk factors of CVD (36).
*Willett, Hu, and others published a paper earlier this year suggesting milk consumption may have an inverse effect on CVD.
A valuable way to communicate the message is to describe the broad dietary pattern that decreases CVD risk. Note that only a minority of different populations adhere to a healthy dietary pattern. A healthy dietary pattern is primarily plant-based and low in SFAs, but can include lean meats and low-fat dairy products in small-to-modest amounts.
They state that because CVD is the the biggest disease in most countries and since saturated fat currently isn’t linked with other diseases, it should have more weight in dietary recommendations to influence the majority. Unfortunately, they don’t mention what amount they would set. It doesn’t seem that there is strong evidence directly linking fatty meat consumption with CVD (especially considering the review/meta-analysis published last year but after this symposium met by Micha et. al suggesting no link between red meat and CHD but one exists for processed meat) if we go by the arbitrary standards based on this paper, and of course meats vary considerably in the relative amounts of the different fatty acids.
It should also be noted that there are other excellent researchers who would disagree with these concenses. For example, last year Ramsden, Hibbeln, Majchrzak, and Davis published a meta-analysis that concluded increasing omega 6 PUFAs may increase risk of CHD, as they carefully considered the effect from omega 3 PUFA intakes in the trials as well- a limitation in previous analyses. None of these authors were present at the symposium, or were and elected not to be included in this paper. So there are certainly valid counter arguments that could weaken the concenses. I am sure I left out other important studies (this isn’t an area I usually read about, just trying to get the gist of where we are).
Obviously randomized controlled trials with disease and mortality as outcomes aren’t viable for many dietary conundrums, macronutrients included. “The definition of sufficient evidence is not always clear.” Further reading on that here.
I wonder how many people really understand the lack of certainty for many of these issues? It is refreshing to continue to see the emphasis to focus on whole foods in the literature at least.
Arne Astrup, Jørn Dyerberg, Peter Elwood, Kjeld Hermansen, Frank B Hu, Marianne Uhre Jakobsen, Frans J Kok, Ronald M Krauss, Jean Michel Lecerf, Philippe LeGrand, Paul Nestel, Ulf Risérus, Tom Sanders, Andrew Sinclair, Steen Stender, Tine Tholstrup, & Walter C Willett (2011). The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? The American Journal of Clinical Nutrition : 10.3945/ajcn.110.004622