Future directions in personality, occupational and medical selection: myths, misunderstandings, measurement, and suggestions

This paper has two objectives: (1) presenting recent advances in the personality field concerning the conceptualization of personality arising from the dynamic interactions of behaviour, biology, context, and states, and (2) discussing the implications of these developments for medical selection. We start by presenting evidence that traits are not longer regarded as deterministic and stable. Instead, they are found to change across generations, the life span, and in response to environmental contingencies. Next, drawing on recent research (behavioural reaction norms and the density distribution model) we posit how the expression of trait relevant behaviour changes depending on the situation, such that personality reflects both stability and plasticity across situations. Thus there is an urgent need to explore how traits change as function of medical education. Third, we demystify that some traits are better than others showing that so-called “good” traits have a dark-side. Fourth, we show how these developments impact on how personality might be assessed, thereby presenting recent evidence on the use of contextualized personality measures, Situational Judgment Tests, other reports, and implicit measures. Throughout the paper, we outline the key implications of these developments for medical selection practices

Steroid receptor coactivator-1 modulates the function of Pomc neurons and energy homeostasis

Hypothalamic neurons expressing the anorectic peptide Pro-opiomelanocortin (Pomc) regulate food intake and body weight. Here, we show that Steroid Receptor Coactivator-1 (SRC-1) interacts with a target of leptin receptor activation, phosphorylated STAT3, to potentiate Pomc transcription. Deletion of SRC-1 in Pomc neurons in mice attenuates their depolarization by leptin, decreases Pomc expression and increases food intake leading to high-fat diet-induced obesity. In humans, fifteen rare heterozygous variants in SRC-1 found in severely obese individuals impair leptin-mediated Pomc reporter activity in cells, whilst four variants found in non-obese controls do not. In a knock-in mouse model of a loss of function human variant (SRC-1L1376P), leptin-induced depolarization of Pomc neurons and Pomc expression are significantly reduced, and food intake and body weight are increased. In summary, we demonstrate that SRC-1 modulates the function of hypothalamic Pomc neurons, and suggest that targeting SRC-1 may represent a useful therapeutic strategy for weight loss.Peer reviewe