Sentences to ponder

alone by Lst1984
alone by Lst1984

Marc Schuckit discussing findings from a 30-year study of nearly 400 men:

“If you’re an alcoholic, you’re going to have a lot of mood problems,” Schuckit said. “And you may be tempted to say, ‘Well, I drink a lot because I’m depressed.’ You may be right, but it’s even more likely that you’re depressed because you drink heavily.”

Racial disparities in antidepressant prescriptions

Fluoxetine (Prozac), an SSRI
Fluoxetine (Prozac), an SSRI (Photo credit: Wikipedia)

A study on racial disparities in antidepressant prescribing:

A research group at the University of Michigan and Indiana University concluded that physicians were 1.52 times more likely to prescribe antidepressants to Caucasians than to Hispanics for the same major depressive disorders.

The researchers also found that whites were more likely to be prescribed newer, more expensive antidepressants, which also happen to be considered the “first line” prescription for the disorders.

It would be interesting to look at differences in the course of their depression.

Emotional pain without context

MRI coronal view of the hippocampus
MRI coronal view of the hippocampus (Photo credit: Wikipedia)

Siddhartha Mukherjee provides a brief history of the serotonin hypothesis of depression, its demise and why dismissing serotonin may be an “overcorrection.”

Part of this story is an emerging theory of depression:

A remarkable and novel theory for depression emerges from these studies. Perhaps some forms of depression occur when a stimulus — genetics, environment or stress — causes the death of nerve cells in the hippocampus. In the nondepressed brain, circuits of nerve cells in the hippocampus may send signals to the subcallosal cingulate to regulate mood. The cingulate then integrates these signals and relays them to the more conscious parts of the brain, thereby allowing us to register our own moods or act on them. In the depressed brain, nerve death in the hippocampus disrupts these signals — with some turned off and others turned on — and they are ultimately registered consciously as grief and anxiety. “Depression is emotional pain without context,” Mayberg said. In a nondepressed brain, she said, “you need the hippocampus to help put a situation with an emotional component into context” — to tell our conscious brain, for instance, that the loss of love should be experienced as sorrow or the loss of a job as anxiety. But when the hippocampus malfunctions, perhaps emotional pain can be generated and amplified out of context — like Wurtzel’s computer program of negativity that keeps running without provocation. The “flaw in love” then becomes autonomous and self-fulfilling.

He proposes an alternative understanding of the role serotonin may play:

An antidepressant like Paxil or Prozac, these new studies suggest, is most likely not acting as a passive signal-strengthener. It does not, as previously suspected, simply increase serotonin or send more current down a brain’s mood-maintaining wire. Rather, it appears to change the wiring itself. Neurochemicals like serotonin still remain central to this new theory of depression, but they function differently: as dynamic factors that make nerves grow, perhaps forming new circuits.

This still doesn’t explain the variation in responses to psychotropics. He acknowledges as much and alludes to the need for new typologies of depression. (Remember the dark ages when we talked about endogenous vs. exogenous depressions?)

The layers of speculation can obscure or illuminate just how crude our understandings of depression and the brain are. This, along with the history of psychiatric fads and abuses, makes one wonder if we should proceed a little more cautiously and work a little harder to capitalize on non-pharmacological tools like exercise and social support.

Treating depression and substance use: no significant difference from control

On the Threshold of Eternity
Image via Wikipedia

Another study finds treatment as usual to be just as effective as specialized CBT:

Few integrated substance use and depression treatments have been developed for delivery in outpatient substance abuse treatment settings. To meet the call for more “transportable” interventions, we conducted a pilot study to test a group cognitive–behavioral therapy (CBT) for depression and substance use that was designed for delivery by outpatient substance abuse treatment counselors. Seventy-three outpatient clients were randomized to usual care enhanced with group CBT or usual care alone and assessed at three time points (baseline and 3 and 6 months postbaseline). Our results demonstrated that the treatment was acceptable and feasible for delivery by substance abuse treatment staff despite challenges with recruiting clients. Both depressive symptoms and substance use were reduced by the intervention but were not significantly different from the control group. These results suggest that further research is warranted to enhance the effectiveness of treatment for co-occurring disorders in these settings.