Fish intake, mercury, and metabolic syndrome: a review of the literature


  • Tamara Soric Psychiatric Hospital Ugljan, Ugljan, Croatia
  • Ivona Dragičević Omnipharma d.o.o., Zagreb, Croatia
  • Miran Čoklo



fish intake, mercury, metabolic syndrome


It is already well established that mercury, as a toxic metal, may induce oxidative stress, inactivate several antioxidant mechanisms, and induce a chronic low-grade inflammation, eventually leading to increased risk for metabolic syndrome development. Even though fish intake is commonly associated with the beneficial effects on health, all fish species contain methylmercury, which may have a toxic effect on the human body. Several studies have reported a higher prevalence of metabolic syndrome among people living in the coastal areas, who usually consume more fish than their inland counterparts. Taking into account the impact of fish intake on mercury concentration, together with that of mercury exposure on metabolic syndrome, the aim of this research was to review the existing scientific data regarding the association of all three factors. To our knowledge, only four studies examined the association between mercury concentration and metabolic syndrome, taking fish intake into account. Three out of four studies indicated that exposure, even to low-dose of mercury is associated with metabolic syndrome or at least some of its components. Two of them determined that total fish intake or the intake of some species containing relatively high levels of methylmercury is a contributing factor for mercury concentration in human body.  For better understanding of this association, it is necessary to obtain larger prospective cohort studies or randomized controlled trails. Further studies should be carried out over a wider geographic area and elucidate all significant contributing exposure sources for mercury levels.


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How to Cite

Soric, T., Dragičević, I., & Čoklo, M. (2017). Fish intake, mercury, and metabolic syndrome: a review of the literature. BioMedicine and Surgery, 1(1), 24–31.