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Which Came First, an Eating Disorder or Concussion?

Updated: Aug 12, 2023

As a Primary Care Sports Medicine Physician and Certified Eating Disorder Specialist I have become very interested in the parallels between eating disorders and concussions. From my clinical observations one's relationship to food can change dramatically after a head injury.

The acute metabolic changes following a concussion causes autonomic hyperarousal resulting in catabolism and subsequent weight loss. Patients possibly have an increase in hunger since they need more energy for healing? I have seen patients with diabetes requiring a higher dose of insulin for weeks following a concussion. The mild hyponatremia associated with head trauma commonly leads to a decrease in appetite initially. A high percent of my eating disorder patients report a history of a head injury. The number of patients I diagnose with an eating disorder from my concussion clinic really has me scratching my head.

I believe there is a relationship to taste and the inability to intuitively eat following a concussion. Taste sensation involves communication from the thalamus to the nucleus tractus solitarius to the insular cortex. Taste receptors combine information in the hunger dependent region called the orbitofrontal cortex that assimilates cognitive, visual and olfactory influences. All of this can spearhead an insatiable appetite.

In general, most patients with eating disorders have a predominance of right frontal and temporal lobe pathology on neuroimaging. Similar findings have been reported in patients following a concussion. Studies among patients with eating disorders, specifically bulimia nervosa show vascular thalamic injuries. Neuroimaging in patients with bulimia nervosa and binge eating disorder have demonstrated reduced cortical volumes and diminished activity in the front striatal circuits of frontal lobes which is associated with self-regulation. The hypothalamus is the center for satiety and homeostasis and this is dependent on incentive-correlated inputs that initiate eating behavior.

I would also consider the relationship between neurotransmitters, TBI and hunger. Brain injury leads to excessive accumulation of neurotransmitters in the brain. GABA, an inhibitory neurotransmitter, increases to high levels following axonal damage. When in excess this can alter the level of excitatory neurotransmitter and subsequent function (dopamine, NE, E, glut). How quickly this alteration can take place is still up for debate. A head injury can damage areas in the hippocampus, striatum, and frontal cortex which would affect dopamine levels too. Direct mechanical damage of neurons and/or the promotion of cell death can cause dopamine to be deficient which would affect motivation and emotion. I would assume if an excitatory neurotransmitter such as dopamine could be altered following a head injury, serotonin could as well. Eating disorder studies have shown patients with bulimia nervosa to have serotonin circuit malfunctioning. When compared to anorexia nervosa, patients with bulimia nervosa had a larger drop in serotonin levels when going without food for long periods of time, this led to increased irritability and binge eating.

A recent study found an increase in serum cortisol immediately after head trauma which has a linear relationship with the severity of injury. Since cortisol stimulates the metabolism of fat and carbohydrates, insulin would be released to maintain blood sugar levels. This would result in an increase in appetite and probably cravings of high-fat, sweet, and salty foods.

I don’t think we have a direct relationship between head injuries and disordered eating patterns but only because the science is not available yet. Hopefully with head injuries the cell death will resolve and the patient will return to intuitive eating patterns. Treatment options to consider would be direct serotonin support like 5HTP or l-dopa to enhance dopamine (supplement mucuna/velvet bean) but I have no studies to back me up. SSRIs only work if serotonin is present, in severely malnourished individuals (anorexia nervosa). I dose SSRIs very high while monitoring every few weeks since they are not able to make sufficient amounts of serotonin well on their own being underweight. Again, there is no evidence that this is the case or even beneficial following a TBI. One could also argue that the patient recovers prior to the 4-6 weeks that it takes for SSRIs to be beneficial. Zinc supplementation has been helpful in eating disorders to regulate taste sensation. More so in anorexia nervosa to enhance taste but maybe it would balance out a patient with an insatiable appetite if you think that the increase in food isrelated to an altered taste perception. Consider testing cortisol levels and using a product called cortisol manager from ITI to decrease levels if needed (I don’t have any disclosures to report with them).

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