Thursday, March 19, 2009

Cortisol and eating disorders

I was excited to see that my recent survey about sleep/wake habits here on the blog supported my hypothesis: that those with restrictive patterns tend to rise earlier, and those with more binge/purge patterns rise later. Of course, in order to really look at the data, I'd need to compare the early bird and night owl percentages of each category with those of a non-ED sample.

Although many things affect circadian rhythm--most of which are under genetic control--one of the key hormones is cortisol. Released from the adrenal cortex, cortisol levels generally peak upon waking and reach a low point shortly after you go to sleep. What's more, cortisol is released during times of stress or anxiety, increasing both blood pressure and blood sugar. A PubMed search of eating disorders and circadian rhythm produced mainly results on night eating syndrome. However, one study found a negative correlation between awakening cortisol response and "high anxiety, disinhibition and hunger scores, as well as poor body esteem and a high weight preoccupation" in women, but not men. That means that women with a low awakening cortisol response have high levels of anxiety, poor body esteem, etc. Of course, we don't know if this is cause or effect- just that it exists.

A study in men found a significant relationship between cortisol and perfectionism, which makes sense. Perfectionism is stressful (and don't I know that!), and higher stress means higher cortisol. As well, abnormalities in cortisol have been found in other psychiatric disorders, such as depression.

In otherwise healthy women who did not have regular menstrual periods, cortisol levels were increased compared to normal women, indicating stress on the body (the authors hypothesized that the reason for this amenorrhea was insufficient fat intake, despite sufficient calories and without excessive physical activity).

And indeed, women with anorexia were found not only to have higher cortisol levels but a significant proportion lacked a circadian cortisol rhythm. These abnormal cortisol levels are directly related to the starvation state- after weight restoration, cortisol levels return to normal. I'm not sure how the lack of cortisol rhythm is important. In general, starvation disturbs the sleep cycle, and refeeding is typically associated with improvements in sleep. The general school of thought is that the body is urging the starving person to go get food, and this may be true. But the high levels of cortisol brought out by the stress of malnutrition and starvation may also play a role. High cortisol levels in people with AN have been positively associated with both osteoporosis andhyperactivity.

Although one study found that overall daily cortisol rhythms in normal weight bulimic women were pretty much the same as in healthy women, another found evidence of greatly increased cortisol levels. It appears that, in bulimia, cortisol levels might be much higher than usual, although they still have a daily rhythm, unlike in anorexia. Even recovered bulimic patients continued to show a hyperreactivity to corticotropin-releasing hormone, which stimulates the release of cortisol, indicating an underlying neuroendocrine dysfunction.

Yet when cortisol levels were examined in relation to impulsivity, researchers found an inverse relationship between cortisol levels and impulsivity:

Patients with bulimic symptoms had significantly higher rates of cortisol suppression than controls and than restrictive anorectic patients. Percent cortisol suppression showed a strong and significant correlation with the patient's score on the Barratt Impulsiveness Scale. A hypersensitive cortisol response to dexamethasone, which might reflect hypothalamic-pituitary-adrenal axis dysfunctions might be specifically associated with impulsive subtypes of eating disorders.

Clearly, cortisol is just one player on a much larger field. Nor is it clear whether abnormalities in cortisol levels are cause or effect, and perhaps it's a little bit of either. Certainly the eating disorder exaggerates any underlying abnormalities. Whether the ED behaviors themselves cause the specific differences observed in cortisol levels in anorexia and bulimia, or whether these differences are part of the underlying risk factors for these illnesses also remains unclear.

(originally posted at ED Bites)

1 comment:

Anonymous said...

I suspect that you will find interesting the article below, which discusses the function of cortisol in the body as a hormone that inversely mobilizes the body against potassium wasting intestinal diseases, and in with the references and links. If you see anything that can be improved please let me know. You may see a journal article that discusses this briefly in the 1998 vol. 51 issue of Medical Hypotheses, p 289-2
It is proposed that the primary purpose of the glucocorticoids, including cortisol (hydrocortisone), is to mobilize the body to resist infection. They do so by normally altering processes which increase pathogens' growth or their adverse effects and then declining when under attack. Cortisol is for intestinal disease (diarrhea) and corticosterone serum disease. Glucocorticoid mobilization for fight or flight is an adjunct, made possible because most processes which resist infection impair fight or flight. A different hormone controls those which do not.
Potassium loss is the most serious aspect of intestinal diseases, so the electrolyte capabilities of cortisol, but not corticosterone, are oriented toward conserving potassium. Low cell potassium reduces adrenal synthesis of cortisol, but not corticosterone. Sodium, water, glucose, amino acids, chloride, hydrogen ion, copper , and numerous others are controlled by cortisol in such a way as to survive during intestinal disease.
Some gram negative bacteria have an endotoxin which subverts this strategy by forcing the secretion of huge amounts of ACTH, which is the chief mediator of cortisol. A glucocorticoid response modifying factor (GRMF) and interleukin-1, raises the effective set point of cortisol. The immune cells thus take over their own regulation, using interleukin-1 to mediate production of cortisol via ACTH.
Scroll down to INTRODUCTION below.
If you wish to see the whole article, please let me know, no charge.