Sometimes it seems like depression is everywhere. But for how common it is, it’s still not all that well-understood. Maybe it’s because different people can experience it in vastly different ways, making there no one stereotype that fits everyone. What we do know is that our friends, family members, and maybe even ourselves experience mood symptoms so strong they often have the power to bring our lives to a complete halt. Occasionally, we reach a breaking point and do what we know we’re supposed to: we “seek help.” When we do, we often end up in our doctor’s office, on the couch of a therapist, or across a psychiatrist’s desk. And usually, we end up with a prescription for antidepressants.
Reports from 2013 found that one in six Americans aged twelve and up is on a psychiatric drug, mostly antidepressants, a 65% increase from 1999. 1,2 One survey found that 38% of these people experience side effects while on the drugs, though other studies have found an incidence of sexual side effects as high as 40-93% depending on the drug in question. 3,4 Meanwhile, a war rages among academics over whether antidepressants are more effective than placebo and multiple studies have found that those on antidepressants actually fair worse in the long-run than those with clinical depression who were never treated at all. 5,6
Talk to those who have taken or are currently taking these meds, and you’ll find serious dissatisfaction. Many of those who were quickly offered psych meds by their doctors find themselves on drugs that don’t seem to be working or which have created whole new problems that are often brushed off by their providers. They may start to wonder if they’re destined to go from one medication to another for the rest of their lives, if the least severe side effects are as good as it gets. If and when they try to stop, they may find that even this is not always as easy as they thought, with an under-studied “withdrawal syndrome” which many doctors still dismiss as exaggeration on the part of patients recently beginning to draw media attention.
What About Chemical Imbalances?
People take antidepressants for many reasons, including wanting to feel better and being led to believe by providers that these medications will fix an underlying biological problem which is causing their depression. If this were true, this narrative would be understandable. As it is, our chemical imbalance narrative is more a powerful myth that has captured the public imagination than a supported scientific fact. It’s so burned into our collective psyche that if you asked a room full of people what causes depression, the answers you’re most likely to get are “chemical imbalance” or “serotonin deficiency.” But neither of these is right.
We know that medical research takes an average of seventeen years to reach the practices of our medical providers, so the natural place to look for the science that our healthcare ideally should be based on is research. 7 And when you move from everyday mental healthcare to academia, you find a very different picture. You find less trite comparisons to diabetes with antidepressants likened to insulin. Instead, you find more critiques of the very idea that science ever supported that a chemical imbalance caused depression to begin with. And you find refutations of the hypothesis, born in the sixties, that perhaps low serotonin causes depression. 8
Most people don’t realize that we don’t currently have technology which would allow us to measure levels of neurotransmitters in the brains of living humans. And of all the hundreds of types of neurotransmitters which have been identified, we don’t fully understand all of their roles and continue to discover new types altogether. This means that a simple picture of “dopamine for this, serotonin for that” is sure to be so absurdly simplistic as to be outright inaccurate when compared with the actual workings of neurotransmitters in a human brain. It also means we would have no idea what a “balance” of these chemicals would look like, with some researchers arguing there is actually no such thing as a “normal” brain.
Even if we could measure neurotransmitters more readily, assuming an association of one type of neurotransmitter with one emotional state means that the neurotransmitter caused that emotional state is bad logic and bad science. Frequently taught in college classes as “Correlation does not equal causation,” the maxim reminds us that finding something existing at the same time as something else doesn’t imply that one of those things caused the other. When someone points to brain imaging of depressed individuals (common in pharmaceutical ads), what they’re essentially saying is “Something is going on in the brain chemistry of depressed people!” And of course it is; our brain chemistry is intimately connected with everything we do, feel, and think. If we are living, our brain chemistry is moving alongside (or more accurately, inside) us.
But what we’re learning about the brain is that we can’t break associations down this simply and that it’s at least as likely that experiencing a prolonged emotional state changes the chemistry of the brain as the other way around. With the vast complexity of the brain in mind, it’s fascinating to realize that research has actually found an association of high serotonin with depressed states. 9 Of course, this doesn’t mean that high serotonin causes depression either. It’s just an interesting stepping stone in our constantly evolving understanding of neurology.
Treatment, Or Metaphor?
We know that many people believe that chemical imbalances cause psychiatric disorders and that antidepressants resolve these chemical imbalances. And arguably, many people believe this because they are told this by prescribers or have read it in literature published by mental health advocacy organizations. While you’d be hard-pressed to find a scientist who’d say that a chemical imbalance causes depression, you will find professionals saying something along the following lines: “Sure, it’s not really a chemical imbalance. Nobody thinks that. But it’s a helpful metaphor.”’ 10
The problem is that, if asked, most patients wouldn’t be able to tell you that the chemical imbalance they’re treating with antidepressants is a metaphor. They understandably assume professionals speak to them in scientific terms, not literary ones. If a metaphor of imbalance is helpful in thinking about antidepressants, patients would need to understand that it is a metaphor. Otherwise, it’s just an unethical breach of informed consent, as no one can give “informed” consent to something they are being misled about the mechanism behind.
If antidepressants work, it’s because they have a variety of biological effects (some of which we understand and some of which we don’t) which affect a variety of factors including our moods. Using a drug to take advantage of possibly useful but vaguely understood effects is vastly different than taking a drug to fix an underlying causative mechanism. There is no doubt that therewould still be people who would willingly choose a medication with a handful of effects including a possibility of feeling better. But communicating what we do and don’t know about depression, and what we do and don’t know about antidepressants (and even their effectiveness), allows everyone to make an informed decision about their own healthcare. It creates an ethical and empowering environment of choice, rather than an assumed paternalism of doctors and other mental health professionals over patients.
Dogmatism and ideologies aside, isn’t this what all of us, patients and professionals alike, really want?
1.How Many Adults in the United States Are Taking Psychiatric Drugs? – For The Media – JAMA Network. (2016, December 12). Retrieved from https://media.jamanetwork.com/news-item/how-many-adults-in-the-united-states-are-taking-psychiatric-drugs/
2. National Center for Health Statistics. (2017, August 15). Retrieved from https://www.cdc.gov/nchs/products/databriefs/db283.htm
3. Cascade, E., Kalali, A. H., MD, & Kennedy, S. H., MD. (2009). Real-World Data on SSRI Side Effects. Psychiatry (Edgmont), 6(2). Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719451/.
4. Higgins, A., Nash, M., & Lynch, A. M. (2010). Antidepressant-Associated Sexual Dysfunction: Impact, effects, and treatment. Drug, Healthcare and Patient Safety, 2. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3108697/.
5. Hengartner, M., Angst, J., & Rossler, W. (2018). Antidepressant Use Prospectively Relates to a Poorer Long-Term Outcome of Depression: Results from a Prospective Community Cohort Study over 30 Years. Psychotherapy and Psychosomatics, 87(3). doi:10.1159/000488802
6. El-Mallakh, R. S., Gao, Y., & Roberts, R. (2011). Tardive dysphoria: The role of long term antidepressant use in-inducing chronic depression. Medical Hypotheses, 76(6). Retrieved from http://static1.1.sqspcdn.com/static/f/1072889/14891065/1320009670867/antidep El-Mallakh-tardivedysphoriadarticle1.pdf?token=iSkEnu9nUge/UZbgKyUnFO6B/KE=
7. Brownson, R. C., PhD, Kreuter, M. W., PhD, MPH, Arrington, B. A., PhD, & True, W. R., PhD, MPH. (2006). Translating Scientific Discoveries Into Public Health Action: How Can Schools Of Public Health Move Us Forward? Public Health Reports, 121(1). Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1497798/#B18.
8. Lacasse, J. R., & Leo, J. (2005). Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature. PLOS Medicine, 2(12). Retrieved from https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020392.
9. Andrews, P. W., Bharwani, A., Lee, K. R., Fox, M., & Thomson, J., Jr. (2015). Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant response. Neuroscience and Biobehavioral Reviews, 51. doi:10.1016/j.neubiorev.2015.01.018
10. Lacasse, J. R., & Leo, J. (2015). Antidepressants and the Chemical Imbalance Theory of Depression: A Reflection and Update on the Discourse (with Responses from Ronald Pies and Daniel Carlat). The Behavior Therapist. Retrieved from https://link.springer.com/article/10.1007/s12115-007-9047-3.