I sit here typing this from a desk in a Manhattan hotel room. After months of burnout and an all-around lack of inspiration, I suddenly feel compelled to write a new article. Conveniently, my own experience of burnout and, more specifically, disillusionment with philosophy, can readily be framed as a philosophical topic to be discussed and explored. The relevant philosopher is Descartes, and the topic in question is Cartesian skepticism.
There are actually many parallels one can draw between Descartes and early-Medieval philosopher and theologian St. Augustine. Augustine emphasized the philosophical basis of religion as “belief seeking understanding”. That is, to address the question of how one can have “knowledge” of God, or how religion and philosophy need not be mutually exclusive, Augustine thought the progression of things, in this case, was that one first needed to believe in order, then, to know. This is something of a messy characterization, but sufficient for our purposes here. Descartes, in a “contrasting parallel” thought he first needed to doubt everything, in order to know anything. This is basically what he termed ‘methodological skepticism’.
I’m not sure if this is a common misconception, but in case it is, I’ll address it here: Descartes was not a skeptic through-and-through. I haven’t taken a modern philosophy course in some time, but my understanding is that his skepticism had a clear telos, or aim, and that aim was, put simply, not skepticism. Descartes’ aim was always at something beyond skepticism. He sought to overcome it, but only by submerging himself in it. He sought to demolish everything, only so as to be able to identify what could not be destroyed, and then what could be reconstructed from the ruins.
Of personal relevance is this idea of ‘skepticism-for-a-cause’, that is ‘methodological skepticism’, as opposed to something like pure metaphysical or epistemological skepticism.
So, methodological skepticism here means employing skepticism as a sort of thought experiment, in order to see where it leads one, usually with the goal of arriving at a justified belief, or a piece of knowledge. For instance, say I’m an interrogator and don’t know whether someone is guilty or innocent of a crime. I will question everything, assuming I know nothing: where they were at the scene of the crime, what they were doing, etc. My end goal is clearly to determine innocence or guilt; it isn’t to toss my hands in the air and say “well, we just can’t know whether a person is innocent or guilty”. The idea here is that through enough deconstruction, something “true” will remain and thus be revealed to us, and from there we can build a foundation of knowledge.
Epistemological skepticism would be more like questioning the very basis of inquiry—i.e., how we can know things or be justified in what we know or believe. The epistemological skeptic might say we are just in no position to gain knowledge, or in no position even to know how we might set about gaining knowledge! The metaphysical skeptic might say that knowledge itself may not exist, or that certain things are by nature unknowable or indeterminate. The lines between these distinctions are blurry at best, but I hope it’s at least somehow clear that these latter two are not entirely what Descartes was going for. Rather, he was employing these latter two “types” of skepticism for a specific end.
In the early stages of my philosophical disillusionment, I had a number of thoughts. On reflecting back on my previous three years at Cornell, I came to the startling realization, once again, that I really didn’t feel like I knew much of anything, despite all I had “learned”. It’s quite natural for a philosophy major to end their undergraduate degree with more questions than answers, but this was more startling…a sense that all I had learned was for naught, that I’d been focused on the wrong questions all along, that I had wasted time chasing shadows in a sense. I thought, perhaps I would have been better off studying biology, or computer science, or sociology—something “clearly useful” in the world, something with a neatly laid-out career-path, something seeking solid answers and practical action instead of more questions and more debate.
For the first time, I questioned my choice of major. Indeed, I knew I wanted to study philosophy by the time I was in middle school. There was no doubt in my mind all throughout high school and my first three years of college that I’d made the right choice. To me, there really was no choice. Philosophy was all there was, for me. Senior year of undergrad, though, I think, has a way of messing with your head.
Though it wasn’t clear at the time, I eventually came to realize that my problem was not with philosophy itself, but that, much like Descartes, I had ventured away from my primary frame of reference (the philosophical approach and worldview) only in order to re-enter it with newfound confidence and invigoration. I had been philosophically stagnant for a long time, remaining locked in certain views and presumptions. And so getting “burned out” was actually a blessing in disguise, a call for action, as it forced me to take on and search for other points of view. And perhaps like the parable of the prodigal son, I eventually found my way home, though not as exactly the same as I was before.
Most relevantly, I delved into some very scientific topics, like psychopharmacology, with real interest and vigor, only to end with questions and critiques that only philosophy could, in my mind, satisfactorily address.
I’d consider a recent conversation with a friend (a fellow philosophy major who graduated a few years ago) as what officially re-ignited my passion for philosophy and belief in its importance. One point of our discussion was, coincidentally, that breakthroughs are seldom the result of linear thought or action, but rather, often occur spontaneously or when least expected, as the result of some chaotic or mysterious process.
The Philosophy of Psychopharmacology
And so, in order to get away from philosophy, I entered the world of psychiatry and psychopharmacology. I’ve always been interested in the mind and consciousness, so I thought to approach it this time around from a physicalist perspective. To be, for a while, primarily a scientist instead of a philosopher.
I could, and would like to, devote much more time and space to explaining how certain scientific lines of inquiry inspired in me a philosophical line of questioning. It also is completely true that scientists themselves ask similar questions, but I think the difference is just (in part) which set of questions one focuses on, or takes to be primary (i.e., “how do SSRIs work in the brain, how do autoreceptors and the processes of up- and down-regulation factor into pharmacotherapy?” vs. “what is the nature of a treatment, or the phenomenology of a disease, and how do determine the legitimacy of such categories?”)
In exploring pharmacology, particularly pharmacodynamics (what drugs do to the body—in this case the brain), I had a number of ideas and questions of a philosophical nature arise. I’ll address them and conclude my article with this series of inquiries which, in a way, demonstrates by itself how I regained my love of philosophy.
It is a common mischaracterization, I think, to say scientists studying treatments for depression, anxiety, and other disorders think they are all a just a simple “neurochemical imbalance”. In short, I think this is more something the media has latched onto and the “neurochemical imbalance theory” has become an overly reductionist term for what scientists are actually studying and positing. However, it is true that much of the focus on anxiety treatment, for instance, is devoted to certain neurochemicals (like norepinephrine and serotonin) and how to create drugs which specifically affect these neurotransmitters. But all most scientists are saying is that anxiety and depression, for instance, seem to have something to do with levels of neurotransmitters in the brain, since increasing certain types of serotonin (e.g., 5HT-1A) in certain parts of the brain, concurrently seems to alleviate some symptoms of anxiety and depression.
However, an interesting question to me is how something so physical (a pill, a chemical substance) can produce such wide and varying phenomenological changes. Even if we eliminate dualism and mind-body interactionism as viable options, within a physicalist framework this is still fascinating because at least qualitatively, the mind and body are experienced as vastly different things. Holding a pill and knowing its exact chemical mechanisms of action is one thing, while taking a pharmacological treatment and experiencing its effects is to directly enter into a phenomenological experience of something we only somewhat understand intellectually.
One might consider neutral monism, and hold that reality is neither primarily mental nor primarily physical. Though, as a friend pointed out, this seems to invoke dualism once more, though not postulating it explicitly. Why? Because the question still re-emerges of how two things of such a seemingly different nature (material and experiential) are the same thing, or even how two very different-seeming things impact one another (i.e., drugs alleviate symptoms of anxiety, but so do certain forms of non-drug therapy). We might argue that what both drugs and therapy have in common is that they affect neurotransmitters in the brain, but even if that is the case, the mechanism of causality seems different (to clarify, even if there is a direct physical effect, that does not necessarily presuppose an ontologically physical cause or origin). That is to say, perhaps certain mental states (feeling anxious, for instance) are coincident with certain brain states (decreased prefrontal cortex activity or increased monoamine oxidase activity, for instance) but the question of which is more fundamental or primary remains to be answered, or may even be an ill-formulated question. This is by no means a new idea, and by no means an authoritative explanation of it. The relevant analogy here is simply that mental states and biological correlates are, perhaps, two sides of the same coin. But then, what exactly is the coin? Who knows!
Similarly, in treating psychiatric disorders, we aren’t actually making steadfast claims about their etiology nor their ontology. Just like a headache can be treated with aspirin but is not an aspirin deficiency per se, we often treat anxiety or depression with SSRIs, but this doesn’t necessarily mean that anxiety or depression are a serotonin deficiency. There may be a third variable at play, we may want to ask what is driving such a deficiency, or we may want to look at what else serotonin does in the brain (for instance, increasing serotonin can decrease dopamine, and certain antipsychotic medications actually work on serotonin in order to affect dopamine levels…I won’t delve more into this because it gets fairly complicated and isn’t relevant to the article). These are questions both philosophers and scientists would be interested in. But once we start asking, fundamentally, what is a disorder, and what is a treatment, we enter the realm of philosophy.
How ought we to conceptualize a disorder? Categorically? Statistically (i.e. if you’re in the 90th percentile on a certain trait like ‘scrupulosity’, we’ll probably consider you “disordered”, though there’s not an exact cut-off), or perhaps culturally, or in some other way.
There is also quite a discrepancy between clinical practice and “what the research says”, at least in psychiatry. For instance, ask a clinician whether SSRIs are effective, and they’ll undoubtedly say they are very effective, very useful, and definitely helpful. However, many studies (Kirsch’s, for instance) show that antidepressants may not be much more effective than placebo, having only a modest effect at best. I’ll leave that discussion off here, because a lot of statistical explanation and interpretation is wanting, but requires more time and length than is prudent. Suffice it to say that what research shows doesn’t really match up with what clinical experience says, and it’s interesting to think about why this could be. My final comment on this matter is that taking patient experience into account seems like something the field could really improve on. I think both side-effects and positive effects of drugs are likely vastly underreported, and lack of knowledge in this area may inhibit both sides (clinical and research) from asking the right questions, pursuing fruitful avenues of inquiry, and so on.
Back to the concept of a disease, we might reconsider whether such a distinct thing as ‘anxiety’ actually exists. No doubt some unpleasant experience exists, but when so many people experience anxiety in so many different ways, and anxiety encompasses a myriad of symptoms (for instance, spanning from dry mouth to racing thoughts) we may reconsider the label itself. Or, instead, try to find some physiological mechanism that ties these seemingly disparate symptoms together neatly—something I obviously take scientists as aiming to do. However, in naming something (presupposing there is something to be named), we certainly face the problem of drawing lines around disparate symptoms that don’t really comprise a distinct disease, syndrome, or condition. We also run the risk of missing out on other connections…for instance, in 2021 we’re on the cutting edge, yet we are still in an epistemologically disenfranchised position since, one might imagine, 100 years from now we may very well have entirely different diagnostic categories, diagnoses, treatments, and so on. But, at the present, it is impossible to know what these are. Many people indeed may be suffering from some yet unnamed condition. Therefore, to name something is a kind of double-edged sword; it can both help and hurt. But in the meantime, this raises questions for clinical practice: should we aim at treating the person? Treating the disease? Treating the symptoms? And what does this all mean?
Furthermore, in order to know what it means to be cured or treated, I think we also need a comprehensive understanding of what it means to be diseased or unwell. If we treat symptoms, are we necessarily treating the condition, or are we simply masking the disease? Is there, in effect, a disease underlying the symptoms, or are the symptoms all there is? It seems clear in the case of a common cold that we can mask the symptoms (runny nose, fatigue, headache) but still consider a person to be sick. But what about the case of depression? Is someone on SSRIs who is feeling subjectively great still depressed deep down? And can someone with OCD ever be “cured” if the nature of their disorder is comprised of both disordered thinking and disordered neurobiological structures? For instance, OCD can be effectively treated using cognitive-behavior therapy with exposure and response prevention. But the person with OCD will still have certain biological markers of the disorder, such as structural abnormalities: increased cortical thickness in some frontal, temporal, and parietal brain regions.
A more straightforwardly physical example is that many people have something called a herniated disc, in their spine. However, many of these cases are totally asymptomatic. However, in some cases, someone has pain, an MRI reveals a herniated disc, a doctor says “this is the cause of your pain” and treats the disc issue. It may very well be the root cause of the pain, or it may not be. What allows some people to experience these structural abnormalities asymptomatically, while other people experience great pain (even controlling for the exact severity of the disc herniation) is an interesting question.
Similarly, there is a fairly rare neurodevelopmental anatomic abnormality called incomplete hippocampal inversion (IHI). This is a sort of malrotation of the hippocampus, which can be detected by a brain MRI. IHI is correlated with temporal lobe epilepsy and, debatably, schizophrenia, among other disorders—yet most people with IHI don’t have temporal lobe epilepsy or schizophrenia. Interestingly enough, I have neither epilepsy nor schizophrenia, but I do have incomplete hippocampal inversion. Are we to consider IHI at the far end of the normal spectrum of brain anatomy, something sometimes pathological but not necessarily so? It is, at least, a curious case. Of course, we could posit that there is a third factor at play, that IHI reflects an underlying predisposition to certain disorders, but needs that third factor in order to cause the pathological state. But this remains to be investigated by philosophers and scientists alike.
Ashley Gasdow