The very first book I ever read on eating disorders was The Golden Cage by Hilde Bruch. She wrote that book in 1978 at the age of 74 after a long and rich clinical career. Bruch fled to England in 1933 to escape persecution and immigrated to the United States in 1934 where she studied pediatrics and psychiatry and was trained in psychoanalysis by many of the masters. I had the opportunity to re-read The Golden Cage recently as I was preparing for a lecture in Tübingen, Germany, which I called From Families to Twins to Genomes: The Evolution of Eating Disorders Genetics. The occasion of this lecture was to receive this year’s Hilde Bruch Award awarded by the Kompetenznetz für Essstörungen Tübingen and the Schattauer Verlag. My host was Professor Stephan Zipfel and if your German is up to speed, you can read more about the lecture and the award ceremony here. The prize came with by far the most beautiful bouquet flowers I have ever received.

There are aspects of Bruch’s work that would meet with criticism today. Some might say that she placed too much emphasis on familial factors when discussing the etiology of eating disorders. But in rereading, I did her the honor of digging deeper into her clinical insights and ultimately chose to intersperse some very perspicacious observations from her work throughout my talk on genetics. As I have said before, at times it feels as if much of our research is just verifying what the great clinicians have seen and written about for decades before us.

During the lecture, I discussed how my immunologist and rheumatologist colleagues are intrigued by the fact that individuals in the acute phase of anorexia nervosa do not exhibit typical sickness behaviors such as lethargy, fatigue, and pain. I discussed our theory that something about the starvation state may reduce the inflammation that we typically see in somatic and in psychiatric illness. Bruch of course had captured this phenomenon in her work, quoting a patient who said, “I enjoy having this disease and I want it. I cannot convince myself that I am sick and that there is anything from which I have to recover.” That sentiment, and indeed the physical sensation that accompanies it, is one of the major hurdles to bringing treatment to people with anorexia nervosa who are desperately in need of it.

Later, I questioned the factors underlying the “tipping point” that indexes when an individual makes the switch from simple negative energy balance (associated with dieting, illness, or over exercise, for example) to developing anorexia nervosa. I have been thinking and writing about this quite a bit lately and it reminds me of so many patients and parents who describe the descent into anorexia as a “switch.” One day he was this way and the next day he was another way. Identifying the genetic and brain mechanisms that contribute to that switch is a major current push of our research. Needless to say, this same question intrigued Bruch who wrote in 1978, “Relatively little is known how this changeover takes place from what looks like ordinary dieting to this inflexible self-destructive but hotly defended fixation on weight and food.”

Prof. Dr. Stephan Zipfel, Dr. Wulf Bertram, Dr. Gaby Resmark, Prof. Dr. Patrick Sullivan, Prof. Cynthia Bulik, Prof. Dr. Tobias Renner, Prof. Andreas Fallgatter (c)Weiche, Schattauer Verlag

My lecture moved into some of the new work emerging on genetic correlations, which revealed a negative genetic correlation between anorexia nervosa and obesity and a positive genetic correlation between anorexia nervosa and schizophrenia. The negative genetic correlation with obesity suggests that some of the same genes are operative in anorexia and obesity but with effects in opposite directions. The same genes may contribute to dysregulation of weight on both ends of the spectrum. This finding underscores the importance of us studying the metabolic components of anorexia, not just the psychiatric ones. Professor Bruch was already on the topic describing what she perceived as an “inaccuracy in the way hunger is experienced” as well as a clear observation of family history of overweight in relatives of those with anorexia. She observed, “It is not uncommon that there is an overweight sister or cousin in the family.” Bruch was not ascribing this familial pattern to shared genetic factors, but rather she ascribed more of a psychological mechanism to the process, namely that the individual with anorexia observed how much “pain is provoked by being fat,” prompting the caloric restriction. She is pardoned for missing the genetics because she was spot on in identifying the negative impact of weight stigma long before the concept ever existed.

In terms of the positive genetic correlation between anorexia nervosa and schizophrenia, this is not the most common comorbid condition that we see in family members at all—that position is typically occupied by other eating disorders, anxiety disorders, and depression. Yet, schizophrenia does occur in relatives and many clinicians and researchers have wondered whether the nature of some of the perceptions of individuals with anorexia do fall into the quadrant of delusional thinking or hallucinations (i.e., their perceptions and very fixed beliefs represent a definite break from the consensus reality). This has not been a terribly popular or well-researched area, and typically we think about anorectic cognitions as being more similar to the overvalued ideas that we see in individuals with obsessive-compulsive disorder. This positive genetic correlation does encourage us to dig deeper into this area to clarify what the nature of anorectic cognition is. But, alas, once again Professor Bruch was one step ahead writing, “The whole behavior may be so severely disturbed that it borders on psychotic disorganization.”

As I re-read her book and these astonishingly accurate perceptions just continued to leap from the pages, I briefly considered feeling demoralized about the fact that she had said everything that I have been thinking about thirty-seven years earlier! But, being the good cognitive-behavioral therapist that I am, I restructured that thought and realized that it really meant that our research is on the right track. Granted we should be farther ahead than we are, but we are asking the right questions and we are applying modern tools and techniques to answer fundamental questions that have been being asked by the most brilliant clinicians that ever to put their mind to understanding eating disorders.

In addition to deep gratitude for being honored with this award, I am also grateful that it afforded me the opportunity to engage in this exploration of where we are and where we have come through the lens of a very gifted clinician.