Sethi Dalai, S., Sinha, A., & Gearhardt, A. N. (2020). Low carbohydrate ketogenic therapy as a metabolic treatment for binge eating and ultraprocessed food addiction. Current opinion in endocrinology, diabetes, and obesity, 27(5), 275—282.https://doi.org/10.1097/MED.00000000000005711
Binge eating and ultraprocessed food addiction symptoms may be a result of changes in neurobiological and metabolic pathways triggered by specific foods, particularly processed foods with high levels of refined carbohydrates combined with fat. New keys to treating these modern-day illnesses of disordered eating may lie in avoiding unnatural levels of sugar in ultraprocessed foods, refined carbohydrates and high glycemic index foods. This
would in turn prevent unnecessary blood glucose spikes and dips, insulin fluctuations and other metabolic hormones that play a large role in the development of binge eating/overeating, exacerbations of hunger and addictive-like neurochemical and
behavioural responses. These conditions are associated with numerous metabolic abnormalities, including inflammation, insulin resistance, obesity and T2DM. The ketogenic diet has been shown to be an effective treatment for obesity, T2DM and paediatric epilepsy. Several advantages of a low carbohydrate ketogenic diet include beneficial effects on
brain metabolism, appetite-satiety signalling, neurotransmission and stabilization of brain networks and blood sugar.
would in turn prevent unnecessary blood glucose spikes and dips, insulin fluctuations and other metabolic hormones that play a large role in the development of binge eating/overeating, exacerbations of hunger and addictive-like neurochemical and
behavioural responses. These conditions are associated with numerous metabolic abnormalities, including inflammation, insulin resistance, obesity and T2DM. The ketogenic diet has been shown to be an effective treatment for obesity, T2DM and paediatric epilepsy. Several advantages of a low carbohydrate ketogenic diet include beneficial effects on
brain metabolism, appetite-satiety signalling, neurotransmission and stabilization of brain networks and blood sugar.