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Is satiety (lack thereof) the culprit with obesity?

Individuals with mental illness are more likely to be overweight or obese than the general population. When institutionalization was the norm, and individuals spent decades in psychiatric hospitals, the thinking was that high starch diets, restricted environments, and lack of exercise combined to cause the problem. Then psychoactive agents, both traditional and newer versions, were added to the blame package. Now, new research with a focus on individuals with PraderWilli syndrome suggests another causal possibility (Tingley, 2015). Prader-Willi syndrome has a rare chromosomal abnormality, with chief symptoms of low muscle tone and impaired signaling between the brain and stomach. “Because no sensation of satiety tells them to stop eating or alerts their body to throw up, they can accidentally consume enough in a single binge to fatally rupture their stomach” (Tingley, 2015, para. 9). Tingley (2015) reports that researchers (Andrea Prader, Heinrich Willi, and Alexis Labhart) at a Swiss children’s hospital fi rst identifi ed the syndrome in 1956. For 25 years, there seemed to be no clinical interest or further research on the syndrome. Beyond the inability to experience satiety, characteristics include “short stature, disproportionately short arms and legs and small hands and feet; a tendency to pick skin until it bleeds; a high pain tolerance; infertility; excellent spatial memory; and cognitive disabilities” (Tingley, 2015, para. 15). Children affected by this illness all show an early failure to thrive, followed by obesity. The article includes several stories about these children and how their parents have tried to cope with the illness and been blamed for the problem (Tingley, 2015). The relevance for psychiatric nurses is that an understanding of Prader-Willi syndrome and new avenues of research, including pharmaceuticals, would inform their clinical practices. Thinking about obesity in the clients whom they serve needs to shift to considering the error on the chromosome 15 segment, which occurs at conception, and is one of the few known genetic causes of obesity. No other genetic disorder produces the extreme lack of satiety or urge to obtain food. How the dozens of genes within chromosome 15 govern fullness is still unknown. What is known is that PraderWilli syndrome disrupts the functioning of the hypothalamus, but the process is unknown. Individuals with psychiatric illness who are obese and others in the general population may have a chromosome 15 error, but not full-blown PraderWilli syndrome. Leptin and other hormones are known to signal the hypothalamus, affecting sensations of hunger. Leptin is a hormone produced by fat cells and interacts with genetic and environmental factors to infl uence whether overeating occurs. Determining this signaling error could result in a treatment for almost all cases of obesity. Jennifer Miller, an endocrinologist at the University