A recent study, published in Frontiers in Nutrition, introduces a neurobiological model suggesting that a therapeutic ketogenic diet (TKD) could serve as an innovative treatment for anorexia nervosa (AN). The model integrates the roles of behavioral traits, brain neural energy metabolism, and neurotransmitter function, providing a comprehensive understanding of how TKD might target the underlying mechanisms of AN.
AN is a severe psychiatric condition marked by extreme emaciation, food avoidance, and body image distortion. It has a high disease burden, with treatment options that are often ineffective and a mortality rate much higher than the general population, especially among young women. Even after weight recovery, individuals with AN often experience persistent fears of body dissatisfaction and weight gain, which can last for years. Despite these challenges, the neural mechanisms behind self-starvation remain poorly understood, making effective treatments harder to develop.
The proposed model suggests that anxiety, stress, and perfectionistic traits disrupt normal brain glucose metabolism in individuals predisposed to AN. This disruption leads to the use of ketone bodies as an alternative energy source, reinforcing the cycle of self-starvation and alleviating anxiety temporarily. The researchers hypothesize that this metabolic shift into ketosis might explain why individuals with AN feel relief from anxiety, which, in turn, perpetuates their eating disorder.
Moreover, the model posits that brain changes, such as alterations in neurotransmitter systems and specific brain circuits, are prevalent in AN. Studies have shown that people with AN often overestimate their body size and face heightened anxiety and stress, exacerbated by environmental factors like social media messages. These triggers condition a fear response and negative emotions, leading to behaviors like food avoidance.
In the proposed neurobiological model, stress-induced disruptions in glucose metabolism create an energy deficit, which is compensated for by the production of ketone bodies. These ketones provide an alternative energy source, contributing to the persistence of AN. The researchers argue that providing ketones to individuals with AN could eliminate self-starvation and help with weight maintenance.
The TKD, which is similar to fasting, increases fat metabolism and produces ketone bodies, such as beta-hydroxybutyrate (BHB), which may improve brain function. By altering brain glucose metabolism and providing an alternative energy source, TKD could help regulate anxiety and improve emotional stability, breaking the self-perpetuating cycle of starvation in AN. Additionally, ketosis increases the production of gamma-aminobutyric acid (GABA), a neurotransmitter that may reduce anxiety and support emotional regulation.
A pilot study involving five adults with weight-restored AN (wrAN) showed promising results. Participants on TKD demonstrated improvements in several measures, including eating disorder behaviors, body image concerns, and social and emotional connections. Notably, some subjects maintained their recovery for at least a year after completing the trial. Although the sample size was small, these initial findings suggest that TKD could be a viable treatment for AN.
In conclusion, this neurobiological model and the initial clinical findings offer a novel approach to treating AN by focusing on metabolic and psychological factors. However, further research with larger and more diverse populations is necessary to confirm the efficacy and safety of TKD as a standard treatment for anorexia nervosa. The integration of metabolic and psychological components in this model emphasizes the complexity of the disorder and the need for multifaceted therapeutic strategies.
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