Well other than the reason to relax, women may have another reason to drink their coffee. In the September 26 issue of Archives of Internal Medicine, there’s a report stating that the risk of depression appears to decrease for women with increased consumption of caffeine. Previous studies have hinted to a possible association between coffee consumption and depression risk. Approximately every 1 in 5 women will experience depression during their lifetime. These numbers make depression in women a public health priority.

In a study conducted at the Harvard School of Public Health, women were followed from the study’s start in 1996 through June 2006. Caffeine consumption was measured through questionnaires completed from May 1980 through April 2004. It has been discovered that compared to women who consumed only 1 cup of coffee or less a week, those who consumed two or more cups per day have a 15 percent decrease in risk for depression. Those consuming four or more cups per day had a 20 percent decrease in risk. This was only seen for those consuming caffeinated drinks. No association was found between decaffeinated coffee and depression risk.

Perhaps this study can make some headway into treatments for depression in women.

JAMA and Archives Journals (2011, September 26). Increased caffeinated coffee consumption associated with decreased risk of depression in women, study finds. ScienceDaily. Retrieved September 27, 2011, from http://www.sciencedaily.com/releases/2011/09/110926165904.htm

Spring arrived on March 20^th and it was hard to ignore. It was a hot day in Central Park with fellow New Yorkers rushing out to sit in the sun, play ball, or ride their bikes. In my hometown people rushed to the Bluff just to sit in the sand and stare off into the water of Long Island Sound. There were some die hard jet skiers that took the opportunity to get their jet skies into the water (even though the water was an icy 40 degrees). People are craving to be outside; to shake off the feeling that winter has left behind.

Here on Long Island we had a nasty winter. Every time it snowed it wasn’t  in inches, but in feet. We had record breaking amounts of  snow so when Spring came around the corner, we all rejoiced. For the last few weeks, the temperature has jumped into the 50s and 60s sometimes jumping into the high 80s.

A lot of changes happen once Spring arrives. Migrating birds return. The flowers bloom. The grass begins growing like a weed. But not all the changes are happening in nature. People are changing as well.

Have you ever heard of the winter blues? The winter blues is a set of symptoms closing resembling depression. These symptoms are present in the winter but commonly fade once warmer seasons arrive. Winter blues is another name for Seasonal Affective Disorder, or SAD. SAD is a mood disorder in which people who have normal mental health throughout most of the year experience depression symptoms in the winter months, repeatedly year after year. It has been estimated that 2-9% of adults suffer from SAD.

Those who experience SAD can experience difficulty waking up in the morning, a craving for carbohydrates, a lack of energy, and difficulty concentrating among other symptoms. When the spring comes, it is essentially a role reversal. Those who have been diagnosed with a form of depression in their past have a greater chance of experiencing these winter changes.

There have been some theories on why people suffer from SAD. There is depression, a chronic disorder characterized by depression symptoms all year round. But why have depression only during the winter months and be fine in the spring and summer? The answer may lie in studying other species including our past ancestors.

In many species, activity is diminished during the winter months due to less available food supplies and the difficulties involved in surviving during the cold weather. Several species like bears and box turtles, hibernate during the winter as an extreme way of surviving. A major clue resides in species that don’t hibernate, but still develop changes in their behavior during these less favorable times.

It can be argued that SAD is an evolved adaptation (like our fear of spiders and snakes). This adaptation in humans can be a variant of a hibernation response from an earlier ancestor. Since food was scarce during human prehistory, a low mood would reduce the need for the intake of calories, a good adaptation for the winter months.

If these theories are correct, then Seasonal Affective Disorder would not be a disorder as once assumed. Instead, it would be considered a normal response to colder seasons.

What was so important about Caspi et al.?
The original Caspi paper of 2003 looked at a sample of 847 New Zealanders, and examined whether gene-environment interactions might lead to depression. The research team were particularly interested in genes involved in serotonin transportation and reception - serotonin has long been recognized as an important biochemical in the neurobiology of depression. They identified short and long versions of 5-HTT’s regulatory region. The short allele led to decreased gene expression and therefore fewer serotonin transporters in the the cell. Results of the study found that individuals with the short variant of the serotonin transporter 5-HTT predicted the onset of depression – but only if the individual was exposed to repeated environmental stress. The finding was important because it provided a blueprint for understanding gene-environment interactions: genes came to be viewed not so much as rigid determinants of fate, but part-players in a complex narrative.

What has changed?
A lot. The new paper by Merikangas and colleagues failed to substantiate the gene-environment association for 5-HTT. Normally, this might be viewed as a minor setback, but this study was a meta-analysis of 14 papers covering approximately 12,500 individuals – a huge data-pool by anybody’s standards. The group did confirm an association between stressful circumstances and depression (hardly big news). However, the serotonin transporter, 5-HTT did not enter into the equation. For many researchers in the field this is very disappointing and may force a rethink in our whole understanding of the disorder.

Caspi and co-author Terrie Moffitt are sticking by their guns, however. Science quotes them as saying that the new resarch “ignores the complete body of scientific evidence”, including studies in mice who have an elevated stress response as a result of their 5-HTT genotype. This may be the case, but Caspi and Moffitt are now swimming against the tide. It hard to argue with a sample of 12,500. Moreover, other sources had already begun to question the validity of the 5-HTT association. Recent whole-genome association studies, which have scanned a huge amount of genomes and found several thousand biomarkers did not turn up anything on 5-HTT.
While it is not time yet to close the book entirely on the association, I think it is time for some serious re-evaluation.