According to a recent article in the Boston Globe, the theory of depression as a chemical shortage in the brain is losing ground amongst scientists in favor of a new theory of depression as damage in the brain. It’s not nearly as out there as it initially sounds, and it actually does fit a lot of clinical evidence better. For instance, fluoxetine (the active ingredient in Prozac) raises the level of serotonin in the brain. Yet using other drugs to lower the level of serotonin in the brain does not cause depression, nor does it make depression worse. The release of serotonin caused by fluoxetine is thus probably doing something else to the brain: healing the neurons, not simply restoring a chemical balance.
Now, this only makes sense if depression is actually a mild, reversible neurodegenerative disorder as opposed to a chemical imbalance. The theory goes that people are depressed because their neurons are in bad shape due to a lack of regenerative trophic factors, and the proper treatments (fluoxetine and exercise are both highly effective) increase the production of trophic factors and cause injured neurons to recover/regrow. This explains the observed clinical phenomenon known as “Prozac lag” — serotonin levels go up within hours of starting treatment with the drug, yet it takes weeks for the depression to be alleviated. Well, guess how long it takes to repair/regrow neurons? Weeks, not hours. Fluoxetine is also being investigated as a treatment for lazy eye, which is caused by underdevelopment of the neural cortex. It works in rats, the theory being that the fluoxetine is fostering the growth of new neurons. It’s now starting to be used as a treatment for lazy eye in humans.
Now nobody’s sure if the new way of thinking about depression is completely correct, so don’t go jumping to any conclusions just yet, but it’s now looking more likely than the chemical imbalance theory of yesteryear. The new theory also explains the other factors that are so often coincident with depression — memory problems, smell and taste sensory deficits, and basic bodily process problems with weight control, sex drive, and sleeping. So under this new theory, we don’t think of depression as just sadness, but of an overall lowering in functioning in the brain caused by neural deterioration, of which sadness is simply the most notable symptom.
The new paradigm should make it easier to get people to accept treatment. Instead of telling people that they need chemical happiness (which some people refuse, because they don’t like the idea of a chemical in their brain making them something other than themselves), tell them that they need a chemical to repair minor neural damage. Phrased that way, it’s a lot less off-putting. Who would be opposed to fixing brain damage by taking a simple pill? It has a convenient explanation, too — in the modern world, humans are exercising a lot less often than we used to, and as a result, the trophic factors that promote neural regeneration aren’t being produced in the same quantities. If people aren’t getting enough exercise to replace those lost trophic factors, at least restore their equivalent brain function through the use of a convenient pill.
I wonder what ramifications this theory this will have on the future of neurology. We may soon find out that other psychiatric disorders are caused by some forms of damage to the brain (we already know about the obvious ones, like Alzheimer’s disease). Medical neuroscience may shift away from modifying neural chemical levels towards treating and rejuvenating neurons. It all goes to show how science is consistently digging up new truths and changing our world for the better. Science brought us fluoxetine and now it’s finally explaining how it actually works, creating a bridge of understanding that will hopefully help in the treatment of other disorders.