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Obesogens generate misinformation and drive obesity

Boston University School of Medicine researchers have proposed that obesogens - certain chemical compounds that are hypothesized to disrupt normal development and the balance of lipid metabolism - which have entered the environment in the last 50 years, generate misinformation in our bodies, such as inappropriate insulin secretion or hunger, that lead to obesity.

Dr Barbara E Corkey, professor emeritus of medicine and biochemistry at Boston University Chobanian & Avedisian School of Medicine, who led the research, explained that humans vary in the efficiency with which they burn and store nutrients in response to overeating. Some people waste more energy when they overeat and store less. Those individuals tend not to gain weight easily. Humans also vary in their reaction to food deprivation. Some conserve energy better than others and when they diet, they don't lose weight easily.

"These are normal variations and we are each a bit different, due to genetics, but we respond to the same signals," said Corkey. "The increasing incidence of obesity correlates with heightened consumption of ultra-processed food along with thousands of potential environmental toxins including some derived from fertilizers, insecticides, plastics and air pollutants. Identifying these agents would allow us to remove them or inhibit their ability to generate misinformation."


Obesogens, she believes, can generate changes in redox state (a normal signal of either excess or the need for energy) that are unrelated to energy needs but falsely stimulate hunger or fuel storage when not needed.


Corkey's model, if validated, could impact many if not all obesity-related diseases. Her paper examines readily available ways to test her model. She believes the best outcome from this work would be identification of obesogens and their removal. The second best outcome would be treatments that block their effect on the body's normal regulatory mechanisms for insulin secretions.


The findings, ‘Reactive oxygen species: role in obesity and mitochondrial energy efficiency’, were published in Philosophical Transactions of the Royal Society B: Biological Sciences. To access this paper, please click here

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