Hypothalamic digoxin, hemispheric chemical dominance, and eating behavior

Area of Science:

• Neuroscience
• Biochemistry
• Endocrinology

Background:

• The isoprenoid pathway generates digoxin, an endogenous inhibitor of membrane Na+-K+ ATPase, crucial for regulating neurotransmitter and amino acid transport.
• Altered neurotransmitter patterns and digoxin synthesis are implicated in eating disorders, with potential links to hemispheric dominance.

Purpose of the Study:

• To investigate digoxin synthesis and neurotransmitter patterns in eating disorders.
• To compare these patterns between individuals with right and left hemispheric dominance.

Main Methods:

• Measurements included serum HMG CoA reductase activity, RBC membrane Na+-K+ ATPase activity, serum digoxin, magnesium, tryptophan catabolites, and tyrosine catabolites.
• Analysis was conducted on individuals with anorexia nervosa, bulimia nervosa, and varying degrees of hemispheric chemical dominance.

Main Results:

• Anorexia nervosa and right hemispheric dominance showed increased digoxin synthesis, upregulated tryptophan catabolism, and downregulated tyrosine catabolism.
• Bulimia nervosa and left hemispheric dominance exhibited reduced digoxin synthesis, downregulated tryptophan catabolism, and upregulated tyrosine catabolism.
• Decreased membrane Na+-K+ ATPase activity and serum magnesium were observed in anorexia nervosa/right dominance, while increased levels were found in bulimia nervosa/left dominance.

Conclusions:

• Hypothalamic digoxin and hemispheric chemical dominance are central to regulating eating behavior.
• Anorexia nervosa aligns with a right-hemispheric dominant/hyperdigoxinemic state.
• Bulimia nervosa corresponds to a left-hemispheric dominant/hypodigoxinemic state.