Gene–environment interactions are central to the expression of obesity.
The condition is strongly heritable (ie, genetic), and most of the
variation in obesity levels between countries and between individuals
can be explained by the effects of obesogenic environments on individual
genetic susceptibilities. The nature of the obesogenic environmental
influences is not clear in detail, but they correlate closely with
measures of affluence. The causes of variation in genetic susceptibility
are also not clearly defined, but their general nature has become
clearer. The failure of genome-wide association studies or large linkage
studies to identify or replicate causative genetic variants, together
with the segregation of obesity-related traits in families, implicates a
heterogenetic mechanism in which rare, dominantly or additively
expressed genetic variants are responsible for most of common obesity.
The search for rare causative variants continues with some successes,
but those identified contribute very little to the overall burden and,
assuming heterogenetics, there are many more to find. The time when
genomic risk factors provide more information than do currently
available markers, such as family history, is a long way off. Genomic
studies to date have contributed little, if anything, to the prevention
and treatment of common obesity and its associated disorders. This
contrasts with the obvious and immediate potential implications of the
well-established overall genetic basis of obesity, which have not yet
been exploited in the clinical or public health arenas. Genomic studies,
which have helped to define the genetic basis of common obesity mainly
by exclusion, will in the future play an increasingly important role in
understanding and managing obesity, but only with parallel studies of
the physiological, behavioral, and economic influences.
No comments:
Post a Comment