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Sociedad Cooperativa Transportes urbanos y microbuses de primera clase de Ensenada

In document INFORME DE DIAGNÓSTICO (página 31-35)

Urbanisation is a challenge for today’s world and its future [48], and this process has had a profound effect in Latin America [23, 49, 63]. The Latin American region has experienced the greatest urbanisation: more than 60% of its population now live in urban areas [48] —mostly in poor conditions [54]. Obesity and rapid changes in lifestyles have already been expressed as a concern in the region of the Americas [64-66].

In relation to migration and CVD, and its risk factors, the literature is quite prominent and has been approached in a systematic way [2]. This section does not intend to be a comprehensive review of the available literature and briefly mention some of the relevant material published on migration and CVD. For clarification purposes and to avoid mixing evidence from different contexts, this section is divided into two: the effects on CVD of international and internal migration.

In terms of migration and CVD, the NiHonSan study constitutes one of the classical studies of international migrant populations. This study looked at men of Japanese ancestry living in Japan, Hawaii and California describing rates of coronary heart disease and stroke for these groups, and is described below [67]. More recently, Kelleher et al. were able to link historical census data from 1850 onwards, involving European subjects that migrated to the United States of America (USA) and native-born individuals, providing further insights into the coronary heart disease epidemic of the USA in the mid-20th century [68].

1.3.1. International migration

International migration is a complex process, usually associated with deep changes in culture. While migrants may move and keep some protective factors for disease prevention, i.e. low levels of smoking and healthy diets, this is not always necessarily maintained in all migrant generations. As an example, a recent publication from the

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Millennium Cohort Study in the UK has shown that after immigration from various countries and settlement in the UK, maternal health behaviours, i.e. smoking during pregnancy and initiation of breast feeding, worsen with length of residency in the UK [69].

When approaching the subject of migration and CVD in the UK it is typical to think about south Asian populations living in this country. Variations in risk factors [70]

and mortality [71], particularly due to ischaemic heart disease and stroke, differs markedly by country of origin, being higher amongst non-UK born population.

Similarly, in the USA, studies of migrants refer somehow to the larger ethnic groups that live in that country, such as “Latinos” or “Hispanic” groups for example [72, 73].

One of the classical studies of migrant populations published more than 30 years ago, the NiHonSan study, looked at men of Japanese ancestry living in Japan, Hawaii and California. It described that rates of coronary heart disease were low in Japan, high in Hawaii, higher in California, and higher still among white Americans, and an opposite gradient was observed for the case of stroke [67].

On the other hand, lower mortality rates from CVD have been reported in migrants from Latin America, China and South Asia that moved to Canada [74]. An

“epidemiological paradox” has also been described amongst Latinos in the USA, who showed lower socio-economic status and also lower all cause mortality [72].

Potential explanations for this phenomenon were attributed to selective migration and the return of those ill to their places of origin, phenomenon also known as

“healthy migrant” effect [72, 75]. Additional explanations could be related to bias in the ascertainment of outcome, particularly in the case of illegal migrants that do not want to declare their health status due to fears of being deported.

Altogether, based on this evidence, it has been suggested that the studies of migrant populations could contribute to the understanding of the aetiology of some diseases, particularly the role played by the environment [1, 76]. In addition to the role of environmental factors, it has been proposed that the study of migrants could

contribute to elucidate the role of the genetic background in the “development” of some specific conditions, such as Type 1 diabetes mellitus [77].

1.3.2. Internal migration

In Kenya, migration from rural to urban areas has been shown to be associated with an increase in blood pressure amongst those who migrated [78, 79]. Similar findings, that migrants had higher systolic and diastolic blood pressure than did the people in the rural areas of origin, has also been described in Iran, with the addition that blood pressure levels of migrants and non-migrants in the city were not much different from each other [80]. In South Africa, on another but closely related disease, the prevalence of diabetes has been described as doubling within two decades in populations that adopted a high-calorie, low-exercise lifestyle as a result of migration to urban areas [81].

In Tanzania, however, after 6 months following migration, migrants appear to have lower levels of blood pressure and triglycerides indicating that the direction of change of risk factors is a much more complex phenomena [82]. These findings supported from research from Cameroon which included data on lifetime exposure to an urban environment [83]. In this West African setting, by Sobngwi et al. suggest that both lifetime exposure to urban environment and recent migration are potential risk factors for obesity and diabetes mellitus [83].

Migrants moving from South Western rural China to the urban area of Xichang City showed an increase in serum total cholesterol lipid levels which could lead to elevated coronary heart disease risk [84]. Similarly, the same group has described an increase in blood pressure levels following rural to urban migration [85, 86]. In Guatemala, migration to a city has been reported to increase sedentary and non-healthy eating habits [87], both recognised risk factors for CVD.

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In document INFORME DE DIAGNÓSTICO (página 31-35)