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Cardiovascular disease (CVD) was the top cause of premature deaths globally in 2017, contributing to ~17.8 million deaths, including 8.9 million from coronary heart disease (CHD).1 There has been long-standing scientific interest in the cardioprotective effects of fish consumption. A substantial amount of research concerning cardiovascular benefits of fish has focused on long-chain omega-3 polyunsaturated fatty acids (PUFAs, including eicosapentaenoic acid (EPA; 20:5 n-3), docosapentaenoic acid (DPA; 22:5 n-3) and docosahexaenoic acid (DHA; 22:6 n-3)) found in fish, but other nutrients such as protein and vitamin D may also play a role.2 Conversely, fish is also the leading dietary source of mercury.3 Mercury in rivers, lakes and oceans is assimilated into fish by the process of bioaccumulation and its organic form (methylmercury), is found in higher levels among long-living predatory fish. In animal experimental and in vitro studies, mercury demonstrates harmful physiological effects such as causing dyslipidemia, thrombosis and cardiovascular toxicity,3 raising concerns that exposure might increase the risk of CVD. Therefore, understanding the independent cardiovascular effects of putative beneficial and harmful nutrients in fish, such as omega-3 PUFAs and mercury, and their possible interactions, is of crucial public health and clinical importance.
In their Heart paper, Tajik and colleagues examined the cross-sectional associations of serum levels of long-chain omega-3 PUFAs, as well as hair methylmercury levels with exercise-induced myocardial ischaemia.4 The assessment of serum omega-3 PUFAs and hair mercury levels is a notable strength, which are validated biomarkers that reflect their long-term dietary consumption.3 The study was conducted among 2199 men aged 42–60 years participating in the Kuopio Ischaemic Heart Disease Risk Factor Study (KIHD) in eastern Finland, with the exposure and outcomes assessed in 1984–1989. The investigators reported that total long-chain omega-3 PUFAs were significantly inversely associated with risk of exercised-induced ischaemia, with …
Contributors JW conceived the study. XP, MM and JW conducted the study and drafted the manuscript. JW, XP and MM agreed upon the final version of the manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
Patient consent for publication Not required.
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