Seasonal Affective Disorder Genetics

A study published in the Journal of Affective Disorders (2009) provides new evidence of the potential link between genetics and SAD, or seasonal affective disorder. Researchers have found that a genetic mutation in the eye may make SAD sufferers less sensitive to light. These preliminary findings may be useful in diagnosing SAD.

While the causes of seasonal affective disorder are complex and not yet fully understood, family history is considered an important factor in assessing a person’s risk of developing symptoms of SAD. Scientists have long suspected a link between genetics and SAD. In fact, researchers at the University of Virginia (2008) report that 29 percent of SAD patients come from families with a history of SAD, which strongly supports a hereditary or genetic component in people who experience symptoms of SAD.

Changes in Body Chemistry

Because genetics play a crucial role in determining our individual chemical makeup, they appear to contribute to the development of SAD. At least two chemicals in the body may be factors in the disorder.

The first is the brain chemical serotonin, a neurotransmitter thought to regulate mood. A drop in a person’s serotonin level can be caused by the reduction in sunlight that occurs in fall and winter. This absence of natural light can lead to depression and symptoms of SAD. Serotonin levels vary from one individual to the next, and genetics is believed to be responsible for these differences.

The second chemical is the natural hormone melatonin, which is associated with sleep patterns. Melatonin is part of a delicate balance of chemicals that control the body’s natural circadian (day/night) rhythm. Your circadian rhythm is essentially an internal clock that tells your body when to sleep and when to wake up. Disrupting this rhythm may be one of the causes of SAD. Irregularities in melatonin production may cause sleep problems, lethargy and mood disorders and, like serotonin, melatonin levels can be affected by the seasonal reduction in sunlight.

Chemistry and DNA

During the winter months of reduced sunlight, the brain produces less serotonin, which may cause depression. At the same time, the body often produces increased amounts of melatonin, which may disrupt the body’s circadian rhythm and lead to lethargy and anxiety. While these changes in brain and body chemistry appear to be scientifically valid, the connection or direct link between genetics and SAD is not clear.

One study published in Medical Hypotheses (1999) linked two specific genes, 5-HTTLPR and 5-HT2A, with serotonin production. The recent study published in the Journal of Affective Disorders (2009) lends support to a genetic component being involved in SAD, albeit through the mutation of a specific gene.

Population Studies on SAD

Researchers have conducted population studies as a means of studying the possible connection between genetics and SAD. These studies have suggested that geographic latitude is an important factor. The further north you go, the great the incidence of SAD.

Some of these studies found that North America has much higher rates of SAD than Europe — twice as many cases, in fact. One possible explanation for this wide disparity may be the greater racial and ethnic diversity found in North America. According to Environmental Illness Resource (2010), Europe’s more genetically homogeneous population may be more genetically resistant to symptoms of SAD.

Further research is needed to understand the specific links between genetics and SAD. The study of genetics may yet yield reliable tools for diagnosing SAD.

Resources

Environmental Illness Resource. (2010). Seasonal affective disorder (S.A.D.). Retrieved July 18, 2010, from http://www.ei-resource.org/illness-information/related-conditions/seasonal-affective-disorder-(s.a.d)/.

Mayo Clinic. (2010). Seasonal affective disorder (SAD). Retrieved July 10, 2010 from http://www.mayoclinic.com/health/seasonal-affective-disorder/DS00195/DSECTION=1.

Roecklein, K. A., Rohan, K. J., Duncan, W. C., Rollag, M. D., Rosenthal, N. E., Lipsky, R. H.