Bulimia and brain inflammation

Bulimia nervosa is another example of a behavioral condition that for thorough assessment, treatment and optimal outcomes should be examined for its neuroinflammatory component. Consider this paper published in the journal Clinical Endocrinology that identifies the brain as the source of the inflammatory cytokine TNF-α (tumor necrosis factor alpha) in individuals suffering with bulimia.

"Tumor necrosis factor-α (TNF-α) is a cytokine with numerous immunological and metabolic activities. In addition, TNF-α can stimulate a variety of physiological, neuroendocrine and behavioural responses of the central nervous system. In experimental animals, TNF-α induces changes in physiological and behavioural parameters which have also been observed in eating disorders."

They measured plasma concentrations of TNF-α and its receptors, TNF-RI and TNF-RII (which are shed in increased amounts when TNF-α is released) in bulimic individuals compared to normal controls. What did the data show?

"Plasma TNF-α concentrations in BN [bulimia nervosa] were significantly higher than those in N [the normal group]...plasma sTNF-RII concentrations in BN were significantly higher than those in N."

Hence their conclusion:

"Our present findings suggest that the adipose tissue may not be the immediate source of TNF-α in bulimic patients but the increase in plasma TNF-α in these patients may be derived from the central nervous system sources."

That means increased brain microglial inflammatory activity. The practical message is that bulimia nervosa should be evaluated with the appropriate objective tests to resolve the brain inflammation component, the foundation of the biological component of treatment for this disorder.