Depression is not a chemical imbalance–that’s what the best data on the subject suggests.
Now please don’t misunderstand me. I believe that major depressive disorder is inherently biological. I just remain unconvinced that brain chemistry alone tells us much about depression. At it’s best, the “chemical imbalance hypothesis of depression” is an outdated theory. More cynical observers might say that it’s an oversold marketing message.
The belief that depression is a chemical imbalance comes from a misunderstanding of the monoamine theory of depression. According to this theory, depression is caused by dysfunction in one of the monoamine neurotransmitter systems. These neurotransmitters–serotonin, norepinephrine, and dopamine–are certainly related to mood, but changing the absolute levels of these chemicals in the brain has not been consistently shown to affect mood. Correlation (as I’m sure you’ve heard) isn’t causation.
The most convincing argument against the chemical imbalance hypothesis comes from clinical research into antidepressants. The most commonly prescribed antidepressants are the selective serotonin reuptake inhibitors, also known as the SSRIs. Within hours of taking these drugs, the effective level of serotonin is increased at every serotonin-containing synapse in the brain. But unfortunately, patients who take SSRIs feel no better than patients taking placebo for at least 2 weeks (and realistically, it takes most people 4-6 weeks to really start feeling any effect at all). If depression was caused by a simple chemical imbalance, we’d expect a much more rapid response. And this long time to effect happens with all FDA approved antidepressants, regardless of their action on the serotonin, norepinephrine, or dopamine systems. (I’ve heard some well-meaning doctors tell their patients that the drugs take 4-6 weeks to reach a significant dose in the bloodstream. However, the vastly different half-lives of these drugs and the remarkable consistency in their time to effect argues strongly against this explanation.)
So what causes depression? Depression seems to be related to dysfunctional brain circuitry. A depressed person may very well have problems with one of the monoamine neurotransmitter systems, but it is the system that is impaired, not necessarily the chemical concentration. For recovery to occur, neurons in the brain must find a way to appropriately reconnect with each other.
Thankfully, the brain is remarkably resilient. While as many as 20-40% of the population will experience at least one episode of major depressive disorder, a surprising number recover without any treatment. This isn’t to say that treatment doesn’t work (it does) or that the risk of untreated depression is trivial (it isn’t). It’s just to point out that the brain has mechanisms in place to rebuild dysfunctional synapses. And if you really want to kickstart recover, every known treatment for depression has been shown to increase the levels of neuronal growth factors. The most well known of these factors is brain-derived neurotrophic factor (BDNF), and it is increased by antidepressants, talk therapies, electroconvulsive therapy, and even experimental treatments like ketamine. However, the diverse targets of these therapies may trigger growth in different regions in the brain, which could explain why certain people respond better to one treatment than another. In most cases, the best initial treatment is a combination of antidepressants and cognitive-behavioral therapy.
Why does it matter that we stop talking about depression as a chemical imbalance? For one, an accurate understanding of science matters. When you realize that depression is caused by impaired brain circuitry, it makes sense that depression arises from a combination of genetic, environmental, and psychological factors. On a more human level, calling depression a chemical imbalance trivializes the disorder. A chemical imbalance sounds like something that can be rapidly reversed. It makes us think that there is a magic pill that can quickly fix things. It’s the biological equivalent of the words “why can’t you just snap out of it.” Overcoming depression–especially severe depression–takes time and appropriate treatment. Finally, thinking of depression as a problem with circuitry helps us conceptualize depression as a complex set of disorders with unique causes, manifestations, and treatments. It gives us a reason to approach all sufferers as individuals that cannot be treated with a one-size-fits-all approach.
This model of depression isn’t perfect, and my explanation is, of course, a gross oversimplification. But when we recognize that depression is a circuit problem, it enables us to take some responsibility for rebuilding and maintaining the circuitry that brings us happiness. This is what cognitive-behavioral therapists have been telling us all along. By learning how to combat the thought and behavior patterns that worsen depression, you can help yourself rebuild the faulty circuits within your own head. Conquering depression often takes the help of competent professionals, but recovery without learning to help yourself is almost impossible.