Capitalizing on natural experiments in low- to middle-income countries to explore epigenetic contributions to disease risk in migrant populations.

Migration poses a significant and worsening public health problem. As the world becomes increasingly interdependent and the global population continues to expand, rates of bothwithincountry and international migration are rising. Migrants tend to experience differential risks for chronic disease, including cardiovascular and metabolic diseases [1–7]. Differential health outcomes in international migrants are not limited to migrants fromdeveloping todevelopedcountries;migrants fromonedeveloped country to anotherwith regional differences in chronic disease risk may be impacted, as well [8]. Lifestyle factors do not fully explain increased disease risk in some migrant populations. Prior studies have suggested that increases in body mass and blood pressure in migrant populations are related to stress-induced dietary or physical activity changes. These increased risk factors may subsequently influence disease risk [3]. However, individuals that migrated from a subsistence lifestyle on Pacific atoll Tokelau to an urbanized Western lifestyle in New Zealand showed increased blood pressure in men that cannot be fully explained by concomitant dietary changes and weight gain [4]. Migrants often display cardiovascular disease (CVD) risk intermediate to that of non-migrants in their country of origin and to host population natives [5, 9]. These outcomes suggest that setting of origin, together with initial exposures to such settings, plays a role in acquired disease even in the presence of host population lifestyle factors [5, 9]. Although lifetime risks in migrant groups may approach those of the host population over time, there is evidence for differential health outcomes in migrant populations as compared with non-migrants in studies with relatively long follow-up periods. For example, the Finnish Twins Cohort study reported CVD risk intermediate to that of the migrants’ country of origin and of the host population after a 23-year follow-up [5]. Further, in cases in which lifetime risks of migrants do approach the host population over time, the intervening period of differential health is of strong public health interest. Genetic differences do not fully explain differential disease risk, either. Genetic heterogeneity within a country may contribute to differences in health outcomes between migrants and non-migrants if migration is non-random for genetic markers [8]. However, twins that migrated from Finland to Sweden displayed a higher CVD risk than low-risk native Swedes, but a lower risk than their co-twins in highrisk Finland. These data suggest that differential health by the migration status is strongly influenced by environmental factors [5]. In addition, cardiovascular risk factors in * Address for correspondence: J. Jaime Miranda, MD, PhD, CRONICAS Centro de Excelencia en Enfermedades Cronicas, Universidad Peruana Cayetano Heredia, Av. Armendariz 497, Miraflores, Lima 18, Peru. (Email: jaime.miranda@upch.pe)