Hello, and welcome to Against Utopia, a newsletter that lifts the veil of authoritarian utopianism in science, technology, politics, culture, and medicine, and explores anti-authoritarian alternatives. This is Issue One, published March 10th, 2018.
Depression has been in the news lately, specifically in the mainstream scientific backlash against Johann Hari’s book, Lost Connections.
In Lost Connections (which I haven’t read yet), Hari purports to have found the real causes of depression and real solutions, and furthermore, they have nothing to do with the “chemical imbalance” theories you may have heard of (e.g. serotonin, “the happy molecule”). Before I even read the book I want to get this out of the way – I believe him.
“How can you so hastily agree with something you haven’t read!?” you might think. It’s easy, allow me to explain.
The key part of my blind agreement rests in unpacking the terms “chemical imbalance”. What do these terms mean? Presumably, a number of things, but currently, in 2018, when someone says the words “chemical imbalance” when referring to depression, they’re usually referring to an “imbalance” of serotonin. The dogma of serotonin’s involvement in the manifestation of depression is of course popularly accepted, but why? This requires further investigation.
What do we mean when we say “chemical imbalance”? Presumably, our scientists and doctors have done the leg work to define what an acceptable level of serotonin is in the brain of normatively well-functioning people who are not depressed or anxious. When we invoke the term, we’re referring to serotonin being either too low or too high, and we’re also referring to the resulting lived experience of the person who now has low or high serotonin. Except that’s not really true at all. We’ve never really measured the levels of serotonin in the brain and mapped them to specific depressive phenotypes, and we certainly haven’t mapped them to the much more fluid, and consequently harder to define, lived subjective experience of depression.
The problem is that this attempt at mapping specific levels of serotonin in the brain to subjective lived experience falls prey to utopian simplification. This view neglects the immense complexity of serotonin in the brain, gut, lungs, and circulatory system. If 95% of the body’s serotonin is not in the brain, if platelets carry it throughout the body, if serotonin is intimately involved in blood clotting, how can it be so implicated as the just the primary culprit in depression? Is there more complexity here than meets the eye, that we might be ignoring?
If we’re ignoring said complexity, the commonly accepted dogma is then in actuality a heroic simplification of what is going on in the depressed brain, and is at best a utopian view of brain chemistry that does little to illuminate our understanding of depression. And the numbers would back that up.
What does utopia have to do with this? The term utopia was coined in the early 1500s by Sir Thomas More, to describe a fictional, perfectly organized, and rational society off of the coast of South America. The book was published about 150 years before the Enlightenment, but its values were deeply embedded in what was to come. The Enlightenment is known for the proliferation of liberal values such as liberty, tolerance, fraternity, and reason as the primary source of authority as separate from God and the Church.
In addition to these, the most important thing to realize about the Enlightenment is that it gave us reflexive rationalist social engineering (organizational hierarchy justified by reason and not God) and scientism (the application of the scientific method to social problems with which it’s knowledge extraction and justification methods are ill-equipped to deal). These two phenomenon working in concert made concrete the ability to understand and perfect Man™ – with enough categorical reductionism, skeptical empiricism, and time, we could figure anything out with science!
Except that real world maps for complex phenomenon are exactly that – just maps. Some territories are more mappable than others (DNA!), and some we are only just discovering how to map (metabolism, proteomics, etc). In the realm of mental health, with a methodology for the perfectibility of Man™ within sight, and the actual delivered progress of the scientific method, at the beginning of the 20th century we must have thought that mental health would surely be cracked.
The complex interplay between genetics, metabolism, psychology, physiology, doesn’t care about our mental models, our attempts to reduce depression to a single locus that can then be perfected with empiricism. This complexity will rear it’s head whether we abstract it away or not. The efficacy of the drugs for depression speak to our understanding of depression well enough – and that is precisely why I believe Johann Hari without having read his book.
The way that we know the science of depression, otherwise known as the epistemology of depression, is through this rationalist heroic simplification of mental health, and in order to form a more complete picture within which we might take action, we need to understand where these ideas came from, and how they came to be.
What is a serotonin “receptor”?
How did the normative definitions of sound mental health come to be, and why are they based on scant clinical trials of small sample size from the 50s?
How did two alkaloids, reserpine and tianeptine, make us think down is up, and right is left? What is the resultant jumble of word salad (atypical antidepressants anyone?) we’ve invented to make sense of it all them and depression?
What do crickets, bears, and squirrels have to do with this?
In next week’s issue, we’ll begin to examine the history of these concepts, who and what put them in place, how they culminate in our modern shared understanding of what depression is, and what we can do with this information as a result.