Here, is described how stress changes eating patterns and wanting. “This association may be mediated by alterations in the hypothalamic-pituitary-adrenal (HPA) axis, glucose metabolism, insulin sensitivity, and other appetite-related hormones and hypothalamic neuropeptides. At a neurocircuitry level, chronic stress may affect the mesolimbic dopaminergic system and other brain regions involved in stress/motivation circuits. Together, these may synergistically potentiate reward sensitivity, food preference, and the wanting and seeking of hyperpalatable foods. Individual differences in susceptibility to obesity and types of stressors may further moderate this process.”
Here, is described “a role for the central ghrelin signalling system in reward from natural rewards such as food.” “It now seems clear that Ghrelin also has a role in motivated reward-driven behaviours via activation of the so-called “cholinergic-dopaminergic reward link”. Stress is a key potentiator of circulating Ghrelin.
Here, regarding the pre-frontal cortex and executive function and stress: “Psychosocial stress selectively impaired attentional control and disrupted functional connectivity within a frontoparietal network that mediates attention shifts. These effects were reversible: after one month of reduced stress, the same subjects showed no significant differences from controls.
Here, we understand how Early Life Stress (ELS) results in deficits in cognitive and affective function.
Here, considering the important connection between internalized weight bias and stress, internalized weight bias was shown to result in greater weight gain, adverse weight related indices, in nearly 14,000 adults engaged in weight management.
Here, Jean-Philippe Chaput describes associations between sleep debt and weight including short sleep and increased food intake, poor sleep and poor diet quality, later bedtimes and increased bodyweight, shorter sleep with increased snacking, larger meal portions and preference for energy rich foods. Also note, Chaput endorses that “excess energy intake associated with insufficient sleep is more driven by hedonic rather than homeostatic factors”.
Here, Karine Spiegel showed that two days of shorter sleep duration than the recommended number of hours induced an 18% drop in leptin. The same study also showed that short sleep duration increased the hunger/wanting hormone, ghrelin, by 28%, and these hormone changes were also associated with reports of increased sensations of hunger and appetite.
Here, “neuronal activity in response to food stimuli are greater after restricted sleep than after habitual sleep”. “A relative increase in brain activity in areas associated with reward,”, was observed. “This study links restricted sleep and susceptibility to food stimuli and are consistent with the notion that reduced sleep may lead to greater propensity to overeat.”
Here, “these results provide evidence that acute sleep loss enhances hedonic stimulus processing in the brain underlying the drive to consume food.”
Here, FMRI studies confirm that sleep deprivation reduces activity in areas that are associated with restraint and inhibition
Here, is a 2010 systematic review and meta-analysis that studied over 58,000 people suggested that obesity increases the risk of depression, and depression was predictive of developing obesity. This suggests that the relationship between depression and weight can be thought of as bi-directional.
Here, Simmons et al. showed using FMRI evidence, that depression-related increases in appetite are associated with overactivity of mesolimbic reward circuit wanting.
Here, Sharma et al. found in mice, that chronic consumption of high-fat food and associated weight gain induced plasticity-related changes in the reward circuit that are associated with depression.
Here, Cserjési et al. studied the relationship between depression and executive function. They found a mediating role of depression between executive self-regulation skills and obesity. This suggests that depression may play a role in diminished executive function in those with both depression and weight gain.
Here, Seymour et al. found that there appears to be significant overlap in the neurological circuits that mediate ADHD and obesity. Specifically, they found overlap within the motivational system and the circuits that mediate response inhibition and regulation.
Physical activity and sedentariness
Here, Shan et al. showed that moderate to vigorous physical activity is associated with decreased brain response to high-calorie food cues in the region of the motivational system, suggesting that physical activity can decrease wanting. They also showed that sedentary behaviour was correlated with greater reactivity and stronger generated WANTING.
Here, Moreau et al, in one of numerous meta-analyses finding the same, found that moderate- and high-intensity exercise has a positive impact on executive function, and restraint is a key executive function.
Going to long without food
Here, we see that ghrelin is produced in the stomach and is at its highest levels before we eat.
Here, Perello and Dickson describe support the notion that ghrelin signalling at the level of the mesolimbic system (wanting) is one of the key molecular substrates that provides a physiological signal connecting gut and reward pathways. All suggesting that when we go too long without food, this motivation system gets temporarily strengthened. Wanting gets stronger. A major supporter of this temporary strengthening is the food intake-promoting hormone ghrelin.