Depression and obesity: evidence of shared biological mechanisms

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Abstract

Depression and obesity are common conditions with major public health implications that tend to co-occur within individuals. The relationship between these conditions is bidirectional: the presence of one increases the risk for developing the other. It has thus become crucial to gain a better understanding of the mechanisms responsible for the intertwined downward physiological spirals associated with both conditions. The present review focuses specifically on shared biological pathways that may mechanistically explain the depression-obesity link, including genetics, alterations in systems involved in homeostatic adjustments (HPA axis, immuno-inflammatory activation, neuroendocrine regulators of energy metabolism including leptin and insulin, and microbiome) and brain circuitries integrating homeostatic and mood regulatory responses. Furthermore, the review addresses interventional opportunities and questions to be answered by future research that will enable a comprehensive characterization and targeting of the biological links between depression and obesity.

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Interoceptive predictions in the brain.

Lisa Feldman Barrett, W Simmons (2015)

Intuition suggests that perception follows sensation and therefore bodily feelings originate in the body. However, recent evidence goes against this logic: interoceptive experience may largely reflect limbic predictions about the expected state of the body that are constrained by ascending visceral sensations. In this Opinion article, we introduce the Embodied Predictive Interoception Coding model, which integrates an anatomical model of corticocortical connections with Bayesian active inference principles, to propose that agranular visceromotor cortices contribute to interoception by issuing interoceptive predictions. We then discuss how disruptions in interoceptive predictions could function as a common vulnerability for mental and physical illness.

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Benno Roozendaal, Bruce McEwen, Sumantra Chattarji (2009)

Emotionally significant experiences tend to be well remembered, and the amygdala has a pivotal role in this process. But the efficient encoding of emotional memories can become maladaptive - severe stress often turns them into a source of chronic anxiety. Here, we review studies that have identified neural correlates of stress-induced modulation of amygdala structure and function - from cellular mechanisms to their behavioural consequences. The unique features of stress-induced plasticity in the amygdala, in association with changes in other brain regions, could have long-term consequences for cognitive performance and pathological anxiety exhibited in people with affective disorders.

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Martin Paulus, Murray Stein (2006)

We propose a general hypothesis that integrates affective and cognitive processing with neuroanatomy to explain anxiety pronenes. The premise is that individuals who are prone to anxiety show an altered interoceptive prediction signal, i.e., manifest augmented detection of the difference between the observed and expected body state. As a consequence, the increased prediction signal of a prospective aversive body state triggers an increase in anxious affect, worrisome thoughts and other avoidance behaviors. The anterior insula is proposed to play a key role in this process. Further testing of this model--which should include investigation of genetic and environmental influences--may lead to the development of novel treatments that attenuate this altered interoceptive prediction signal in patients with anxiety disorders.