PMC:4157149 / 6190-7141 JSONTXT

{"project":"2_test","denotations":[{"id":"25152454-15995696-2052641","span":{"begin":303,"end":305},"obj":"15995696"},{"id":"25152454-20331573-2052642","span":{"begin":347,"end":349},"obj":"20331573"},{"id":"25152454-20935630-2052643","span":{"begin":513,"end":515},"obj":"20935630"},{"id":"25152454-24097068-2052644","span":{"begin":687,"end":689},"obj":"24097068"},{"id":"25152454-21785715-2052645","span":{"begin":795,"end":797},"obj":"21785715"}],"text":"Gene-environment dependence could arise in a number of ways. There is likely to be a genetic component to many of the established risk factors for which interactions are sought. In addition to the examples above, variants in genes involved in alcohol metabolism have been associated with alcohol intake,23 which is a risk factor for many diseases.24 GWASs have identified numerous variants associated with obesity, an established risk factor for many complex disorders including type 2 diabetes and breast cancer.25 Similarly, multiple variants that influence low-density lipoprotein cholesterol levels, one of the strongest risk factors for cardiovascular disease, have been identified.26 Even the more exogenous exposures, such as urban environment, might conceivably have a genetic component.27 However, on a per-gene basis, knowledge of biological function could be invoked to argue that a given gene is unlikely to affect an exposure of interest."}