Camron Bryant: Triangulating the genes leading to binge eating

The following post is the first in a series of question and answer exchanges with biomedical researchers about recent high-impact neuroscience discoveries from their labs. Animal research will be central to many of these posts, with the goal being to explain the importance and implications of this research. We welcome suggestions for future posts, which can be emailed to jdavidjentsch@gmail.com

A recent article in the journal Biological Psychiatry reveals new information about the possible genetic factors that may lead to excessive overeating and its health consequences. The team was led by Dr. Camron Bryant, Assistant Professor of Pharmacology at the Boston University School of Medicine who has agreed to answer some questions about the group’s research and the significance of their exciting new findings.

Help us to understand what binge eating is and why it is important to study this behavior?

Binge eating is defined as the uncontrolled consumption of a large amount of food (typically high energy foods) over a very short time period. Key features include the lack of control over eating, i.e., the compulsion to start eating and difficulties with stopping. Also central to this behavior, in humans, is the feeling of guilt or remorse following a binge episode. Binge eating is a symptom that can be observed in patients with any one of the three main eating disorders, including Binge Eating Disorder, Bulimia Nervosa and (in some cases) Anorexia Nervosa. Binge eating is both a cause and consequence of disordered eating patterns and can be a component of a larger pattern of repeated cycles of bingeing followed by food restriction. It can lead to severe health complications, including weight gain, malnutrition (e.g., with cycles of food restriction), anxiety, and depression. A better understanding of the neurobiological basis of this key behavioral symptom could lead to treatments that normalize eating patterns and thus, improve outcomes for eating disorders, which are currently among the most lethal of all neuropsychiatric disorders.

Take us through your research. What did you do, and what did you discover?

We know that binge eating has a genetic component, based on decades of human research. However, the specific genes that influence it remain completely unknown. We utilized a large group of mice that exhibited differences in their eating behavior; using an unbiased approach, we mapped and validated a relationship between binge eating and the gene, Cyfip2 (cytoplasmic FMR1-interacting protein 2). We hope that this finding will facilitate the search for binge eating related genes in human, an effort that is currently limited in its power to detect statistically reliable results. We also found that the increased susceptibility to binge eating as a consequence of a mutation in Cyfip2 was associated with a binge-induced decrease in the expression of myelination genes in the white matter of the brain. This was an unexpected finding and suggests that promoting remyelination in the brain could represent a novel strategy to lessen binge-eating behavior.

Mouse
When intermittently offered flavorful foods rich in sugars and fats, some mice binge eat in a manner very similar to humans

Why did you choose to study binge eating in mice? In what ways is the mouse genetically similar, or dissimilar, from humans who overeat?

Mice remain the premier mammalian model organism for genetic studies. Greater than 90% of human genes have a mouse homolog, and mice and humans share many of the same basic features of the dopaminergic reward circuitry in the brain that is thought to be critical for binge eating behavior. Mice, like humans, will readily binge on high sugar/fat foods when it is intermittently available in limited amounts. This is not unlike humans who typically binge after periods of either normal or restricted eating.

In humans, binge eating is not always associated with obesity and can be distinguished from more constant patterns of overeating that are frequently associated with excess body weights. This is similar to our model; the mice bingeing on palatable food do not gain any additional weight relative to normally eating mice. In fact, recent data from our lab indicate that some mice may actually lose a little bit of weight after demonstrating robust binge eating behavior., These observations suggest that the bingeing mice actually reject the standard food they receive in their home cages in anticipation of the more rewarding palatable food they are occasionally offered.

What is the social significance of your findings?

There is a growing appreciation that maladaptive eating behaviors associated with eating disorders, including binge eating, share some of the same psychological features as drug or alcohol addictions, including loss of control, compulsive behavior, an inability to refrain from the behavior in spite of known detrimental health consequences, anxiety, depression, and relapse.

Furthermore, research is beginning to show that the same genes can lead to multiple neuropsychiatric disorders. Of direct relevance to our study, the binge-eating related gene that we found had been earlier reported to affect sensitivity to cocaine-induced behaviors. Thus, the concept of food “addiction”, while not identical to “substance use disorders”, is very real and has implications for understanding the biology and how we might develop effective treatments for maladaptive feeding behaviors such as binge eating.

What are the next steps for your research?

We are currently applying our mouse model of binge eating to other genetic crosses and populations to identify additional genes and adaptations in the brain that underlie binge eating. We know that many genes likely contribute to binge-eating, and a more comprehensive set of discoveries are needed. We hope to continue to provide new insight that will inform human genetic studies and potential pharmacotherapeutic treatments for binge-eating which, at the moment, are limited to amphetamine-like compounds that themselves have the potential for addiction liability.

Thank you for your research, Dr. Bryant, and for participating in this interview. In closing, I wonder if you could share with us what inspired you to become a scientist and what fuels your passion to continue this kind of research?

My scientific interest began in high school when I started to learn more about psychiatric disorders. I thought I wanted to become a psychologist or psychiatrist so I chose to major in psychology when I began my undergraduate career at the University of Illinois. I took a class called The Brain and the Mind and was blown away by what I was learning, including a series of psychopharmacology lectures by Jeff Mogil who would eventually become my undergraduate mentor. Jeff is an incredibly inspirational and enthusiastic scientist and got me excited not only about drugs but the scientific process in general. I worked in his lab for two years and was exposed for the first time to behavioral neuroscience and behavioral pharmacology and I immediately began to appreciate the power of how observing animal behavior can actually provide insight into what happens in the human brain. At that point I decided that this is how I want to make a living.

Dr. Camron Bryant can be found on twitter @CamronBryantPhD

Join the conversation

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s