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Anorexia

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“Working with mice, the researchers discovered that a deficit in the acetylcholine, a neurotransmitter in an area of the brain called the striatum, which is associated with the reward system, can lead to excessive habit formation and precipitate the compulsive self-starvation seen in people who suffer from anorexia nervosa.”

They investigated whether, “donepezil, a medication which is known to increase the presence of acetylcholine in the brain, could have an effect on these compulsive self-destructive behaviours.

““We found that it fully reversed the anorexia-like behaviour in mice, and we believe that it could potentially offer the first mechanism-based treatment of anorexia nervosa. In fact, we are already seeing its effects on some patients with the disease.”

In this review, in addition to reporting the numerous cases described in which autoimmune disorders are associated with anorexia or vice versa, we summarize the many aspects of this relationship between the immune system (IS) and AN. We describe how the microbiota affects the IS, disrupts gut-brain communication, and possibly triggers eating disorders. We also describe the shared immunological pathways of autoimmune and eating disorders and in particular the occurrence of disrupted T cell tolerance and autoantibodies in AN. The described observations represent the starting point for possible, future research directions.

Conclusions: The interactions between EDs and autoimmune diseases support the previously reported associations. The bidirectional risk pattern observed in women suggests either a shared mechanism or a third mediating variable contributing to the association of these illnesses.

In a Danish population-based cohort study of 525 643 adolescent girls, a prior infection in childhood was associated with an increased risk of later anorexia nervosa, bulimia nervosa, and eating disorder not otherwise specified.

The findings suggest that hospital-treated infections and less severe infections treated with anti-infective agents are associated with increased risk of subsequent anorexia nervosa, bulimia nervosa, and eating disorders not otherwise specified and that future studies should investigate whether these associations are causal and identify the exact mechanisms between infections and subsequent inflammatory processes with eating disorders.