Turning Bad Into Good Fats, AHA Style: How the American Heart Association (Ab-)Uses Scientific Research According to Their (Hidden?) Agenda

As a diligent student of the SuppVersity, you are well aware that the absolute and relative overabundance of n-6 fatty acids (also known as omega-6 or linolic acid) in Western diets literally lies at the heart of heart disease. It is thus dear to my heart to turn your attention to the recent advances of the American Heart Association Nutrition Subcommittee of the Council on Nutrition to reestablish the myth of the heart-healthy omega-6 polyunsaturated fatty acids.

Image 1: You better watch out, other
than the American Heart Association
wants you to believe, one of the
"better fat sisters" (Poly, the one in the
middle) turns out to have a very dark
six-times unsaturated side ;-)

Back in 2009, already, the American Heart Association had published an article (AHA. 2009 Omega-6 Fatty Acids and Risk for Cardiovascular Disease), the putative intention of which was "to summarize the current evidence on the consumption of omega-6 PUFAs, particularly LA, and CHD risk". Cleverly, selecting only those studies that fit their (hidden?) agenda, William S. Harris from the Sanford School of Medicine , who is a speaker for GlaxoSmithKline and a consultant to several other companies, including Monsanto, Acasti Pharma, Unilever and Omthera (Ramsden. 2011), and the other members of the committee put together seemingly conclusive evidence (if you solely rely on the studies the commitee selected, their argumentation is in fact very conclusive) supporting their objectively questionable, if not dangerous advice to the American public to obtain "at least 5%-10% of [their daily energy intakes] from omega-6 PUFAs [in order to] reduces the risk of CHD [chronic heart disease] relative to lower intakes." The board even went so far to conclude that...

[t]he data also suggest that higher intakes appear to be safe and may be even more beneficial (as part of a low–saturated-fat, low-cholesterol diet). [...] To reduce omega-6 PUFA intakes from their current levels would be more likely to increase than to decrease risk for CHD.

As it seems, neither Harris, nor his colleagues Ingeborg A. Brouwer or Dariush Mozaffarian stuck to their own advice, because, now, two years later, they are obviously still healthy enough to defend their sponsors messages against the results of a paper by Ramsden et al. (Ramsden. 2010), who had addressed the very same topic somewhat more objetcive-, or, I should say "scientifically" in December 2010. In a sneaky letter to the editors of the British Journal of Nutrition with the tell-tale title "n-6 Fatty acids and risk for CHD: consider all the evidence" Harris, Brouwer and Mozaffarian indirectly accuse Ramsden, who happens to work for the National Institute of Health in Bethesda, and his colleagues of unscientific practice due to "not considering all the evidence".

In fact, Ramsden et al. had, as Harris and his collaborators point out "stratified studies by whether the vegetable oil intervention included any n-3 PUFA", or not, but other than the guys from the agro-lobby... ahh, pardon me, the American Heart Association would have it, this is the way a meta-analysis of the CHD outcomes of randomised controlled trials (RCT), in which oils were used that contained a natural mix of both n-6 and n-3 PUFAs, must be designed, in order elucidate the individual effects of n-6 and n-3 polyunsaturated fatty acids on heart health. Any other approach, such as the one cited by the authors themselves (Mozaffarian. 2010),  apparently overlooks the "significant different effects on risk of non-fatal myocardial infarction (MI) and CHD death", Ramsden et al.  found in their heterogeneity analysis (Ramsden. 2010) of all the available data. In their aptly titled response "Don't disregard the essential distinction between PUFA species" (Ramsden. 2011) Ramsden, Hibbeln, Majchrzak-Hong and Davis, state:

Harris et al. have not fully appreciated the essential distinction between n-3 and n-6 PUFA species in attributing benefits from our pooled analysis of mixed n-3/n-6 PUFA RCT datasets to ‘vegetable oils rich in n-6 PUFA’ or simply ‘soybean oil’, despite substantial increases in n-3 EPA+DHA in two of the four datasets.

They also point out that the influence of n-3 fatty acids has been (I would say purposefully) underestimated by Harris and elsewhere, and provide the famous Oslo Diet Heart Study as an example:

The experimental dieters in the Oslo Diet Heart Study (ODHS) were actually provided with ‘substantial quantities of Norwegian sardines canned in cod liver oil’ and not simply ‘encouraged’ as Harris et al. state here and elsewhere. Oslo dieters consumed about 5 g EPA+DHA per d (thirty times the average US intake); therefore it is not valid to attribute CHD benefits to LA or soybean oil.

They go on to mention that interventions "specific to n-6 LA", on the other "provide no indication of benefit and a relatively consistent signal toward harm" and draw the yet to be validated conclusion that "lowering dietary n-6 LA [Ramsden et al. suggest to 2% of energy, which would be consistent with evolutionary and historical US diets] is likely to potentiate the benefits of n-3 PUFA and/or have independent CHD benefits".

Guess where I found this advertisement,
right within the official Fats 101 of the
American Heart Association.

The advertisement banner on the left, taken directly from the official Fats 101 of the American Heart Association shall remind you of this blogpost, the next time you read about what the American Heart Association has to tell you about "healthy eating" practices. It may be remotely possible that those are healthy first and foremost for the corn- and soy-driven American economy.