On the recommendation of Dr. Rod McClymont, of the Center for Eating and Dieting Disorders, Bathurst, Australia, I have been reading a new book, Animal Models of Eating Disorders (Humana Press 2013) edited by Nicole Avena.  The second chapter, by Mary M Boggiano Ph.D., stopped me in my tracks:  “Binge-Prone Versus Binge-Resistant Rats”.

Don’t laugh.  We are mammals; they are mammals.  We study rats to understand the physiology of cancer.  We study rats to understand the physiology of diabetes, of infectious diseases, of immunizations, of metabolic diseases.  And we study rats to understand the physiology of eating disorders.  Why?  Because eating disorders are not lifestyle choices or learned behaviors.  They are brain disorders, and although we differ from rats in important ways, the ways in which we are similar to them and to other mammals are vastly more numerous than not.

To bring you the “cliff notes” of the findings: the authors note that certain rats—those genetically programmed to be binge-prone will override all normal satiety cues and binge on large amounts of highly palatable foods (usually sweet and fat combinations such as Oreo cookies) if they are offered them, despite painful disincentives to doing so. Other rats, born binge-resistant, will self-limit the amount of such foods they consume. And this is not learned behavior either. The binge-prone rats will binge on their very first exposure to highly palatable foods and consistently thereafter, although intermittent introduction of these foods causes more bingeing than if they are exposed to such foods all the time.  I believe Psychology 101 tells us that intermittent reinforcement is the most powerful driver of behavior, and there you have it.

Binge eating in humans is commonly attributed to “cognitive dysregulation, irrational thinking, concern with body weight and image, etc” — otherwise known as gluttony, insecurity and lack of control.  But studies of rats, who presumably do not share these highly human concerns have shown that there is a more basic “reflexive” biology underlying binge eating, the author states — underscoring, in my view, the brain-based nature of eating disordered behavior.

Interestingly, the tendency to become fat was found to be independent of the tendency to binge.  The genetics of the two are quite distinct, although they can overlap in a few individuals.  It is important to note that not all people who are fat or obese — even very obese — binge eat.  And not all people who binge eat are fat. Again, the genetics for the two conditions are distinct.  

Incidentally, a genetic propensity to binge was only seen to emerge after puberty.  

The author made only one statement I would take issue with, and perhaps it was a typo:  she stated that the age of onset for “eating disorders” was after puberty.  I hope she meant that the onset of binge eating disorders (AN B/P; BN; BED) was after puberty, since we clearly see pre-pubertal patients with anorexia nervosa.

Famously, the Kartini meal plan does not include any highly palatable foods (desserts, sweets, etc) for the first year after diagnosis.  Dieting or starvation is known to exacerbate a tendency to binge on highly palatable foods when they are introduced.  This research would tell us that not everyone is equally prone to bingeing, but also that we can’t tell (yet) who carries the genetic predisposition for it.  Likewise, we cannot tell who carries the predisposition to become fat when exposed to a calorically rich environment.  Certainly those who design eating disorder food protocols should understand that even a morsel of highly palatable foods, and sometimes even just the smell can trigger relapse binge eating for some.

I am still digesting how this information will prove useful for those of us who design weight restoration plans for children with anorexia nervosa, and recovery plans for those with bulimia nervosa and other binge eating disorders.  It appears we may need to learn from our fellow mammals.  I’ll take it.  I just want the answer, from whatever corner of science it might arise.