Neurocircuitry in bulimics

New research in an article on the brain differences in bulimics appears in the January issue of the Archives of General Psychiatry. The study consisted of 40 participants (20 with bulimia who had a median duration of illness of nine years and 20 healthy controls). While undergoing functional magnetic resonance imaging, participants were shown pictures with arrows pointing left and right and were asked to identify which direction the arrows were pointing, regardless of where the arrows were on the screen. This is also known as the Simon Spatial Incompatibility Task.

The results showed the bulimics were faster but less accurate on more difficult trials which indicated impulsivity and less self-regulatory control. During correct trials, those with bulimia had less activity in their frontostriatal region than healthy controls. In incorrect responses, bulimics activated the dorsal anterior cingulate cortex more often. This contrasted from the healthy controls who activated the anterior cingulate cortex while responding correctly more and the striatum during incorrect responses.

The importance of researching the frontostriatal region of the brain is because it regulates both serotonin and dopamine. Research has often implicated serotonin and bulimia, but dopamine hasn't been studied as frequently.

The other interesting question this brings up is what Daniel le Grange, author of the new book Help Your Teen Beat an Eating Disorder asks, "Does the abnormality occur because someone has bulimia nervosa, or does it contribute to developing it?"

This reminds me of the chicken and egg syndrome which invariably can be different for everyone. Depression and eating disorders is often used as an example. Some will say it was the depression that set off their eating disorder, while others say it was vice versa. I don't know if there is one right answer. But what I do think is that the perceptibility to an eating disorder already exists, whether through genetics or neurocircuitry, and perhaps through engaging in more disorderedness, the brain further changes. I could be completely wrong though too and maybe it's just rewiring from the beginning. More research is already underway looking at adolescent brains whose onset of illness is of less duration than those in this particular study.

Seasonal mood disorders and the brain

Summer is almost over and fall will soon make its debut. Honestly, I can't wait, because I am sick of 90+ degree temperatures! Fall is my favorite season, but at the same time, I do have a tendency to get a bit sadder, missing the sunlight.

Seasonal mood disorders, also known as Seasonal Affective Disorder (SAD) affect many people worldwide. SAD is a type of depression that occurs cyclically with the change of seasons. The majority of people experience SAD during the fall and winter months, but it can also occur with the spring and summer months. Though symptoms do not necessarily qualify for major depression, SAD does impair the quality of life for certain individuals. Symptoms include depression, fatigue, changes in appetite, oversleeping, social withdrawal, anxiety, irritability, insomnia, agitation, increased sex drive. Some people also experience reverse SAD, with symptoms higher energy levels, increased sociability, and elevated moods.

The causes of SAD are unknown but clinicians feel circadian rhythms, melatonin, and serotonin can all have an impact. Other factors for SAD are a family history and living in northern locations. Treatment for SAD is similar to major depression with medications and psychotherapy. Light therapy can also be used for SAD during the fall/winter months.

Recent research for SAD has looked at the variable serotonin levels in the brain. In this article from the Archives of General Psychiatry, titled seasonal variation in human brain serotonin transporter binding, scientists studied the brain through Positron Emission Tomography (PET) scans. The serotonin transporter is significant in regulating the intensity and spread of serotonin signals across the brain.

In this study, 88 individuals underwent a PET scan to assess serotonin transporter binding potential value, an index of serotonin density. Each scan was grouped into fall and winter or spring and summer.

The results showed that individuals in the fall and winter group had significantly higher serotonin transporter binding potential value which means less serotonin was circulating throughout their brain than the spring and summer group.This may explain the hyposerotonergic symptoms like lack of energy, fatigue, oversleeping, and overeating that often occur during this time in those individuals who experience SAD. Thus, this provides more physiological evidence of the role of serotonin and variability of seasons throughout the brain.

New Brain imaging and Anorexia

In recent years, researchers have been looking at brain images and activity of a variety of illnesses, including eating disorders. Dr. Walter Kaye from University of Pittsburgh and University of California at San Diego has been one of the forerunners in researching the genetics and brain functions of those with eating disorders. In a 2005 study, it was found there was an overactivity of dopamine in the brain in those who had recovered from anorexia. Another study published earlier this fall showed how there were links between starvation and ectasy. This latest one on brain imaging and recovered anorectics using fMRIs is the hot article of the week. What is interesting about this study is that researchers are able to see how anorexia works in the brain in "real time" with the use of fMRI.

Personally, I think this is really helpful in terms of how the brain works with those with eating disorders. Now, this is of course can't be a blank statement until more studies are done are a larger representation sample. Hopefully, more funding will be available for studies like this.