Behavioural Susceptibility Theory: Professor Jane Wardle and the Role of Appetite in Genetic Risk of Obesity.

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obesity 836 Wardle. This review summarises the evidence for the role of appetite as a mediator of genetic risk of obesity .Recent FindingsVariation in appetitive traits is observable from infancy, drives early weight gain and
obesity 1567 than 1 in 10 by 1990, and currently it is 1 in 4 (Health Survey for England). Combining overweight and obesity together, almost three in four UK adults carry too much body fat (Health Survey for England) and one
obesity 2981 to the ‘obesogenic’ environment, and the basis of this variation has been of great interest to obesity researchers. One hypothesis put forward is that differential susceptibility to obesity has a genetic
obesity 3068 interest to obesity researchers. One hypothesis put forward is that differential susceptibility to obesity has a genetic basis, and excess weight gain arises from a combination of genetic risk and environmental
obesity 3527 as the mediating mechanism [[]].BST has important implications for the prevention and management of obesity and public health policy. Genes set our potential for becoming obese, but the environment determines
obesity 8788 studies to identify common genetic variants contributing to variation. A variant in the fat mass and obesity -associated gene (FTO) was the first to be discovered and has the largest effect size of all known variants
obesity 9713 is observed with twin studies, the environment also modifies the impact of measured genetic risk of obesity . In a large European sample of children (n = 4406), low parental socioeconomic position accentuated
obesity 9942 on adiposity [[]], and in an adult sample, the higher risk variant of FTO was only associated with obesity risk in participants with no university education [[]]. Age-related increases in the magnitude of the
obesity 10097 education [[]]. Age-related increases in the magnitude of the association between measured genetic risk of obesity (indexed using FTO and composite genetic risk scores) and BMI have also been observed [[]–[]], in
obesity 10374 evidence yet has come from a recent study showing that the association between measured genetic risk of obesity (using a composite score) and BMI was significantly larger for more recent birth cohorts, i.e. those
obesity 10639 ‘obesogenic’ environment [[]].Together, these studies provide convincing evidence that genetic risk of obesity depends on exposure to an ‘obesogenic’ environment. The question is how ‘obesogenic’ environments
obesity 11444 variation in appetite causes differences in body weight. The idea that appetite plays a causal role in obesity is not new; it was first proposed by Stanley Schachter in 1968 [[]]. In a series of innovative experiments,
obesity 12492 make the link between these appetitive characteristics identified by Schachter and genetic risk of obesity . She developed the BST in which she hypothesised that genes influence weight at least partly via biological
obesity 13279 opportunities to eat.Fig. 1How appetite mediates the interaction between genetic susceptibility to obesity and environmental exposure. Individuals who inherit a set of genes that bestow greater responsiveness
obesity 14562 considerable advantages to undertaking research with infants and children. Adults with longstanding obesity may have abnormalities in appetite as a result of physiological changes caused by the excess weight
obesity 14828 children are unlikely to be dieting and are too young to have experienced long-term effects of chronic obesity . Studying infants prospectively into childhood provides the opportunity to study the cause-effect relationship
obesity 19901 population-based samples, the genetic basis of appetite and the role of appetite in mediating genetic risk of obesity . The majority of research has focused on the scales that characterise the appetitive traits relating
obesity 26840 trigged by external food cues) and ‘emotional eating’ were also associated with genetic risk of obesity , and these appetitive traits mediated part of the association between the genetic risk score and adiposity
obesity 27269 key sites of central appetite regulation [[]••].The magnitudes of the associations between known obesity -related genetic variants and appetitive traits (and body weight itself) are often disappointingly small,
obesity 27545 endeavour. Establishing causal pathways can guide researchers towards targeted interventions to reduce obesity risk. The evidence for genetic risk of obesity operating (at least partly) via appetitive mechanisms
obesity 27592 researchers towards targeted interventions to reduce obesity risk. The evidence for genetic risk of obesity operating (at least partly) via appetitive mechanisms suggests that behavioural processes may serve
obesity 30964 eating too much each time (weakened satiety sensitivity).BST points very strongly to the likelihood that obesity rates would diminish should the wider food environment change dramatically. The reality is that large-scale
obesity 31830 appetite is observable and measurable from early postnatal life, this might provide a useful marker of obesity risk for public health obesity prevention initiatives. Wardle’s work on the BST has also provided
obesity 31861 measurable from early postnatal life, this might provide a useful marker of obesity risk for public health obesity prevention initiatives. Wardle’s work on the BST has also provided a firm conceptual framework for

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