The consumption of oily fish as a protective factor against cardiovascular mortality stems from epidemiological observations of Greenland Eskimos (Kromann & Green 1980). Subsequently there have been numerous studies – epidemiological, observational and clinical – that have directly supported the concept that omega-3 plays a role in the prevention of cardiovascular disease (CVD). However recent findings of the Rotterdam Study, a prospective population based cohort study based in the Netherlands, directly suggest that there is no protective effect associated with increased fish intake in relation to the incident of heart failure (Dijkstra et al, 2009).
The study followed approximately 5300 individuals for a period of just over 11 years and, at the time of recruitment in 1990 had no reported cardiovascular issues. Fish intake was estimated using dietary assessment methods such as food frequency questionnaires and from this information the intake of long-chain fatty acids EPA and DHA was calculated using data obtained from the food composition database derived from the TRANSFAIR study (van Poppel 1998).
After adjustment for factors such as age, sex, total fat intake, BMI and smoking etc, the group reported no major protective role in for fish intake other than in diabetic individuals. The subsequent message portrayed by the media was documented as “eating fish does not protect against heart attacks”. Crucially, what the media failed to detail was the significance of the estimated daily intake of omega-3 fatty acids reported by the group. The most recent UK government recommendation for consumption of fish is set at two portions of per week (a portion is approximately 140 g), of which at least one portion should be oil-rich to provide a daily amount of 450 mg EPA and DHA (SACN/COT 2004). In the Rotterdam study, however, the highest average intake of EPA and DHA reported in the study was a mere 313 mg and therefore did not even meet UK government guide lines.
To make such a statement is therefore an unfortunate and grossly inaccurate interpretation of this data. Whilst there have, as yet, been few studies outlining the relationship between fish intake and heart failure the current findings are merely only likely to be through consumption levels being insufficient to offer any substantial health benefits. In order to reach the levels of long chain EPA and DHA to be of significance in protecting against heart failure, the amount of fish consumed must therefore be increased. Given the risk of potential contaminants that fish may contain, such as methylmercury, dioxins, polychlorinated biphenyls (PCB) and organic pollutants from industrial processes the use of purified and concentrated fish oils offer a convenient and safe way of increasing long-chain fatty acid levels.
Dijkstra SC, Brouwer IA & van Rooij FJ (2009) Intake of very long chain n-3 fatty acids from fish and the incidence of heart failure: the Rotterdam Study. European Journal of Heart Failure 11:922-8.
Kromann N & Green A (1980) Epidemiological studies in the Upernavik district, Greenland. Incidence of some chronic diseases 1950–1974. Acta Medica Scandinavica 208: 401–6.
SACN/COT (Scientific Advisory Committee on Nutrition/Committee on Toxicity) (2004) Advice on Fish Consumption: Benefits and Risks. HMSO: London.
Van Poppel G. (1998) Intake of trans fatty acids in western Europe: the TRANSFAIR study. Lancet 351: 1099–1091.