EATING DISORDERS – STILL A MYSTERY

Eating Disorders – Still a Mystery

Let’s begin this article with an important “disclaimer” – namely no one has a definitive answer as to what causes an eating disorder and, more importantly, one definitive approach to treatment that offers a cure or is “superior” to another. Although I tend to subscribe to the belief a blend of genetic, emotional, and biological elements account for an eating disorder, I suggest we acknowledge the need to approach treatment with each of these factors in mind. Although there is limited ability to change the genes we inherit, there is however an ability to address the remaining psychological and biological components associated with them. Doing so affords an opportunity to better understand, and measure, the various treatments and programs available at this time.

Genetics:

At times controversial, there is a contingent of researchers and clinicians suggesting genes play a major role in causing eating disorders. Briefly stated, our genes play a significant role contributing to personality traits common to people who later develop anorexia and bulimia. These include a tendency to suffer with anxiety and depression, as well as. harboring traits such as perfectionism, people-pleasing behaviors, obsessiveness, and later a drive for thinness. There is also speculation genetics play a role with predisposition to those eating disorders associated with over consumption [BED, Bulimia, and related disorders]. Last, but not least, there is a growing body of evidence demonstrating an association with alcohol and substance use disorders with some forms of disordered eating. (1)

Biological:

As mentioned, there is significant evidence to suggest most eating disorders have similar neurobiological mechanisms as other addictions or substance use disorders. As the research begins to focus on these mechanisms specific to anorexia, bulimia, and binge eating it becomes apparent the net effect at the time of onset is one of altered brain chemistry and cognitive functioning when compared to non ED affected individuals. This also holds true “post recovery” per the more recent research. (2) The alteration of reward receptors and the exaggerated response to food cues and consuming palatable* foods has been clearly observed with both PET [Positive Proton Emission] and FMRI [functional magnetic imaging] studies. Of particular importance with these studies is a tendency for anorexics [restricting type] to experience palatable foods as anxiety provoking and prompting avoidance behaviors [starvation, hiding food, weight loss]. In contrast to subjects with overeating components and / or purging aspects to their ED, there exists the opposite experience-namely an increased “reward” experience. With both disorders there eventually begins a “tolerance” phenomenon whereby eating palatable foods [or most foods for that matter] becomes increasingly more “painful” for restrictors and less pleasurable for overeaters. The regulation of appetite and eating behaviors remain complex with the interplay of hormones, neurotransmitters, and altered brain anatomy part of the mix. However, the differences with reward processing in the midbrain and the impairment of motivation, learning, and judgment centered in the forebrain [prefrontal cortex] represent the most prominent feature accounting for differences between someone with an eating disorder and individuals who do not have an eating disorder. As mentioned, substance abusers appear to demonstrate a similar portrait of reward processing and judgment impairment as those with an eating disorder and different from their non chemically dependent contemporaries.

Cognitive:

Some may argue personality traits among people with an eating disorder appear to be acquired and a result rather than a cause of disordered eating. Others point to a blend of inherited personality traits lending themselves to being vulnerable to an eating disorder. As such, there is little consensus as to the “chicken or egg” dilemma. Its worth noting, however, most EDs suffer with a mood disorder, some predating the ED or for others, after the fact. These usually are diagnosed as recurrent depressive or anxiety disorders. In addition, anorexia includes a distortion of perception related to body size and distorted beliefs rooted in fears of losing control with respect to weight gain or maintaining “thinness.” Distorted thinking is also prominent in relation to food and the effects on the body. Other EDs appear to have learning histories leading them to use and abuse food as a form of self-medication for a variety of negative emotional states. In effect, the need to minimize emotional discomfort takes the form of either avoidance of food for some and abusing food for others. What does appear interesting is the benefit of approaching the cognitive and behavioral elements of disordered eating by utilizing a combination of cognitive behavioral therapies. Some of these include harm reduction principles and skills training borrowed from Marsha Linehan’s DBT therapeutic principles. In addition, some aspects from the treatment of substance use populations have proven useful. These include encouraging attendance and participation with relevant community based support groups, addressing lifestyle changes, and abstaining from habitual patterns of self harmful behaviors.  Last, but not least, recognizing insight oriented therapies [analyzing the history of events leading to the onset of an eating disorder] have limited value is important for both patients and providers to acknowledge. Teaching practical living skills, challenging distorted thinking, and providing an alternate means of regulating emotions appears key to enhancing the probability of positive outcomes.

Marty Lerner, PhD.

CEO, Milestones Eating Disorder Program

800-347-2364