Although one expects a paper about “endocrine psychiatry” to offer information on the relationships among hormones, the brain and behavior, one does not expect such a paper to provide much in the way of entertainment.  But Ned Shorter’s piece is as enjoyable as it is erudite.  His wit makes complex ideas and data far more digestible than they would be otherwise; he’s the only person I know who makes this topic amusing. And I always learn something from Ned. Like Andrew Winokur, I thought I knew of the main players in this field but Ned introduced me to Lavastine and his seminal work.

My only quibble with Ned is the term “endocrine psychiatry” itself. That term seems to imply that the relationship between hormones and psychiatry is a separate branch or division of psychiatry. There are bidirectional influences between psychiatric symptoms and other systems as well, the immune system and the cardiovascular system to name just two. But I think it’s problematic to treat these various influences as separate categories or disciplines of psychiatry.  I can imagine a plethora of psychiatric subspecialties -endocrine psychiatry, immunopsychiatry, cardiovascular psychiatry and so on-with uncertain and artificial boundaries . And the term “endocrine psychiatry” is not entirely accurate.  However one looks at the relationship between hormones and psychiatry, much more than hormones and psychiatric symptoms come into play; neurotransmitters, brain circuits and somatic symptoms are drawn in.  

Ned depicts several of endocrine psychiatry’s lost opportunities. Probably foremost among them is the unfortunate tale of the DST. Clinical and basic researchers stopped looking at the pituitary adrenal axis in depressive illness after the DST failed to satisfy hopes-understandable but unrealistic – that the DST would be psychiatry’s first laboratory diagnostic test. As Ned points out, although the DST and other measures of pituitary adrenal function are not useful as screening or diagnostic tests they have the potential to provide information about the pathophysiology of depression.  They could provide a rational way to subtype this extraordinarily heterogeneous illness.  A second look is clearly in order.  

Another lost opportunity, or perhaps more accurately an unexploited opportunity, provided to psychiatry by the endocrine system is the potential of the psychological symptoms induced by both endocrinopathies and the administration of hormones to point to the pathophysiology of these symptoms. The well known influence of testosterone on libido, cognition and other psychological events comes to mind. Many of the brain processes and intermediate steps that mediate the relationship between testosterone and behavior have been elucidated. And a good bit is now known about how premenstrual shifts in gonadal steroids bring on the irritability of severe PMS.  Over the past two decades studies using an array of research designs and techniques have identified brain serotonin and its enhanced sensitivity to  gonadal steroids as a a key element of PMS pathophysiology.

But other potentially informative endocrine effects have not been explored. The ability of corticosteroids to induce hypomanic and manic states is a case in point. The hypomania and mania induced by corticosteroids and ACTH mimic in every detail the hypomania and mania characteristic of bipolar disorder, including their prevention by lithium. Elucidation of the brain changes that mediate the effects of corticosteroids on the mood and behavior characteristic of mania might uniquely inform our understanding of the pathophysiology of bipolar disorder. The technology is available to take a look at this matter but it remains to be fully explored.

Walter Brown
December 26, 2013