Part 3: Should I use medications to treat my OCD?
A quick reminder: As an OCD therapist, I can provide information about the research evaluating medication effectiveness and the possible role of medications in OCD treatment. However, I’m not a prescribing professional. This blog post is educational and is not medical advice. Any decisions regarding beginning, stopping, or changing medications should be made in consultation with a qualified prescribing professional, such as a psychiatrist or primary care provider. So, please be sure you consult with your prescribing professional before making any changes to your medication use!
In Part 2 of the “Should I use medications to treat my OCD?” series, we reviewed evidence showing that there aren’t any clinically actionable biomarkers for OCD (you can’t take a blood test or have a brain scan in order to be diagnosed with OCD). At the end of that post, I pointed out something I commonly hear when discussing this subject. I commonly hear something like:
“Well, William, of course OCD is caused by the brain. We aren’t ghosts or disembodied spirits. Human beings are biological organisms and, as a result, of course someone’s OCD will be caused by their brain.”
It’s understandable why so many that I’ve spoken with have this sort of thought. It may seem that the only alternative to the thought that “Of course OCD is caused by the brain” is some sort of view that OCD is purely an affliction of “the soul” or the result of “bad spirits”. And many people (even those who believe in a soul) are skeptical of this way of thinking about OCD. Some might even think that challenging the idea that OCD is caused by the brain means that I’m blaming someone for having OCD (we’ll talk about this blaming idea in an upcoming post in this series).
So, what we’ll be reviewing in this post are a number of thoughts related to the idea of causality and how this relates to OCD and OCD treatment.
To get this review of causality started, let’s begin by exploring a wonderful way of thinking about causality (in relationship to mental disorders) by the late Dr. Scott Lilienfeld (one of the most prestigious clinical psychologists ever).
Scott was on a panel with a number of neuroscientists discussing the role of the brain in addiction. One of the neuroscientists on the panel, frustrated with Scott continually emphasizing the role of the environment and personal agency in the development and maintenance of addiction, eventually stated to Scott:
“Scott. I simply don’t understand why you’re putting up resistance here. Of course the brain is causing addiction. We know that substances like alcohol and cocaine cause numerous changes in the brain. To suggest that addiction isn’t caused by the brain isn’t just at odds with the scientific evidence, it’s at odds with the scientific method. The only alternative to our scientific evidence and scientific method is some kind of dualism, where you see human beings as “floating souls” or “disembodied spirits” and this isn’t something medical science should take seriously.”
Scott’s reply was simple and profound. He responded:
“Let me put it this way. Imagine that you and a friend were discussing a recent airplane crash. You’d both heard that the Federal Aviation Administration (FAA) was sending out a team of expert investigators to gather evidence to determine the causes of the crash. During the conversation, your friend stated something like: “I don’t understand why the FAA is sending people to investigate the cause of the crash. I already know what caused the crash.”
Baffled, you laugh and ask your friend, “Is that a joke? What do you mean?”
And your friend replies, “Of course I know what caused the crash. And I don’t need to go to the crash site or see the flight recorder to know what caused the crash.”
You reply, “What in the world are you talking about? What do you mean you know what caused the crash?”
And your friend gets to the point when he states, “The airplane crash was caused by gravity.”
Oh. In a way, that’s true. The airplane crash was caused by gravity. No gravity, no crash.”
Causality:
This simple story is the beginning of Scott’s point. To say that addiction is caused by the brain can be seen as similar to saying that an airplane crash is caused by gravity. In one sense, it’s true. There would be no airplane crashes without gravity. And there would be no addiction without brains. But the FAA would never complete a report on an airplane crash by writing “This crash was caused by gravity. Case closed.” Likewise, so Scott argued, we should be careful about explaining away addiction, or other mental health conditions, by claiming the brain caused it. Maybe the brain causes addiction, maybe not. But to claim that just because the brain is involved in addiction (which it clearly is) means that the brain causes addiction is not the same thing.
But isn’t it true that we can see the ways in which substances alter the brain or the way in which the brain of those diagnosed with a substance use disorder (“addiction”) are different than the brain of those not diagnosed?
Along the same lines, can’t we see the way that the brains of those diagnosed with OCD are different than the brains of those not diagnosed?
Certainly it’s the case that we can identify, trace, and measure a variety of ways in which substances, or OCD, appear to physically impact the brain. Thus, the next step of Scott’s point is to make the distinction between mental health conditions being mediated by the brain compared to mental health conditions being caused by the brain.
What is the difference between being mediated by or caused by the brain?
One useful way of explaining the difference between mediated by or caused is a method I used in my 2019 article on biogenetic etiologies of OCD, published in the peer-reviewed Journal of Obsessive-Compulsive and Related Disorders. In that article, I used a thought experiment relying on the idea of a computer virus.
The thought experiment goes like this:
Imagine that a team of computer engineers hook up a variety of measurement tools to a computer processor and hard drive. These measurement tools can detect and measure, to a very precise degree, the structure, function, and heat, etc., of the processor and the hard drive. The data gathered by these measurement tools are objective, unambiguous, and easily demonstrated.
Now further imagine that, after these measurement tools are installed on the processor and hard drive, a software engineer installs a powerful computer virus within the operating system of the computer.
Once the computer virus is installed, it causes the operating system to randomly open folders and then duplicate them. The virus causes this opening and duplication of folders to happen frequently and consistently. As you can imagine, it’s really hard for anyone using this computer to get anything done while the virus is constantly opening new folders. What’s worse, if the computer user closes the folders, the virus causes even more new folders to open.
This situation might sound familiar to those of us with OCD, which is characterized by frequent, unwanted, and persistent intrusive thoughts.
Now, after the virus is installed, and the virus is causing folders to open again and again, the computer engineers report on the readings of their measurement tools attached to the processor and the hard drive. They detail that: “The structure of the processor and hard drive is changing. New data structures are being processed and stored. The processor and hard drive are very active. And we can see the temperature of the processor and hard drive heating up.”
The computer engineers might even present to us images showing a “normal” processor and hard drive (without the virus) compared to a “disordered” processor and hard drive (with the virus). These images would clearly (and accurately) show that the normal processor and hard drive are far less active and far less hot than the disordered processor and hard drive. The bright red glowing images would demonstrate their point.
At this point, we’re able to start tying together our ideas.
“Hardware” vs. “Software”
Of course the processor and hard drive of the virus-infected computer are structurally changed, more active, and hotter than they would otherwise be. But does that mean that the structural changes, increased activity, and increased heat of the processor and hard drive are causing the computer virus?
Of course not.
It’s an obvious truth that the computer virus (and the operating system of a computer) relies on the existence of some kind of computer hardware. All operating systems / softwares have some kind of physical underpinning. Computer software, and computer software problems, are mediated by the computer hardware. But the changes in structure, activity, and heat in the processor and hard drive are caused by the computer virus. It’s the software of the computer virus which is causing changes in the computer hardware.
I suspect you’re already starting to see where we’re headed with these ideas. But, to further reinforce this point, consider the difference between software and hardware by observing how two entirely different forms of computer hard drives can have the exact same computer virus and, as a result, cause the exact same dysfunction for computer users.
For those of you who aren’t computer savvy, let’s briefly review a development in computer hardware technology.
For a long time, computer hard drives were platter-based hard drives (HDDs). Within HDDs, the information is stored on magnetic discs called platters. When a computer user wanted to open a particular program or access particular information, the platters would physically spin, like a record, while a reading head (also similar to the head of a record player) would read the data.
Presently, though, hard drives are more and more frequently solid state drives (SSDs). Like HDDs, SSDs store information. But, unlike like HDDs, SSDs don’t have any moving mechanical parts. Unlike HDDs, which spin like a record, SSDs store information in electrical cells which are instantly accessed.
At this point, you might be thinking something like, “William, I’m on your blog trying to learn about OCD. Why in the world are you giving me a lesson on the differences between HDDs and SSDs?”
Here’s why:
You could install the exact same computer virus on a computer with a HDD or a SSD. And, although the HDD and SSD are entirely physically distinct, the functioning of the virus-infected operating system, whether installed on a HDD or a SSD, would be impaired in the exact same way.
How could two entirely different physical entities (the HDD or the SSD) cause the exact same computer-user problem?
Because the problem exists at the level of software, not hardware.
What this discussion is designed to show is that the fact that a computer operating system requires hardware to run does not mean that any malfunction in an operating system is caused by the underlying hardware.
Of course, a computer problem might be caused by the underlying hardware (for instance, if you smashed your hard drive with a hammer). But it could also be caused by software alone (like in the case of a computer virus). And this is why the proper treatment for a computer virus is not to open up your computer hard drive and use a really good pair of tweezers to extract the virus. Instead, the proper treatment is to install antivirus software which identifies and removes the computer virus.
Once the antivirus software is installed and implemented, the computer engineers will report something like, “Oh, we can see that the structure, function, and heat of the processor and hard drive are returning to normal.”
Yes. The structure, function, and heat of the processor and hard drive are returning to normal. They’re returning to normal because of changes in the software.
So, after all this ground work, we’re in a position to more directly link these ideas to OCD and OCD treatment.
Can OCD be measured in the brain in the same way that the computer engineers measured the structure, activity, and heat of the computer processor and hard drive? Well, not as precisely (as we reviewed in part 2), but these changes can be measured at least to some extent.
For instance, Pastre et al., 2024 identified that, on average, there are “serotonin abnormalities” in those diagnosed with OCD.¹ Again, as we reviewed in part 2, these abnormalities are not precise enough to provide an OCD diagnosis. But, on average, they’re present.
But what do Pastre et al. explicitly state in their review? They caution that we ought not take these “serotonin abnormalities” as conclusive evidence of the serotonergic theory of OCD because we don’t know if abnormalities in serotonin function are caused by or the result of OCD. In other words, once again we’re left with an open question of whether OCD is caused by a serotonin abnormality or mediated by a serotonin abnormality.
Now, following the blueprint we laid out in the computer virus example, do we have any evidence that participating in ERP treatment for OCD changes the structure and function of the brain (much like antivirus software changes the structure, functioning, and heat of a virus-infected processor and hard drive)?
Yes. A lot of evidence.
Numerous studies have demonstrated that participating in CBT / ERP causes changes in the structure and functioning of the brain.² These findings are congruent with the well-established concept of “neuroplasticity” – that the brain changes, adapts, and reorganizes in response to new experiences and new learning.³
And, when we combine this evidence with the evidence that ERP treatment of OCD is as effective as ERP + SSRI treatment for OCD (discussed in part 1), we start to have a powerful, integrated way of thinking about OCD as a psychological problem that is mediated by but not caused by the brain.
Of course, human beings are much more complicated than the relatively binary software / hardware distinction we’ve been reviewing.⁴ And, so, it’s an open, empirical question if, sometime in the future, we’ll find a linear, biological cause of OCD. For the time being, though, we have persuasive evidence that we can conceptualize and treat OCD as a problem of our mental software.
In the next post in this series, part 4, we’ll review the other important idea that Jonathan discusses: The idea that medications help treat OCD by reducing depressive symptoms.
References:
Pastre, M., Occéan, B. V., Boudousq, V., Conejero, I., Fabbro‐Peray, P., Collombier, L., ... & Lopez‐Castroman, J. (2024). Serotonergic underpinnings of obsessive‐compulsive disorder: A systematic review and meta‐analysis of neuroimaging findings. Psychiatry and Clinical Neurosciences, 79(2), 48-59.
Bijanki, K. R., Pathak, Y. J., Najera, R. A., Storch, E. A., Goodman, W. K., Simpson, H. B., & Sheth, S. A. (2021). Defining functional brain networks underlying obsessive–compulsive disorder (OCD) using treatment-induced neuroimaging changes: a systematic review of the literature. Journal of Neurology, Neurosurgery & Psychiatry, 92(7), 776-786.
Cao, R., Yang, X., Luo, J., Wang, P., Meng, F., Xia, M., ... & Li, Z. (2021). The effects of cognitive behavioral therapy on the whole brain structural connectome in unmedicated patients with obsessive-compulsive disorder. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 104, 110037.
Moody, T. D., Morfini, F., Cheng, G., Sheen, C., Tadayonnejad, R., Reggente, N., ... & Feusner, J. D. (2017). Mechanisms of cognitive-behavioral therapy for obsessive-compulsive disorder involve robust and extensive increases in brain network connectivity. Translational Psychiatry, 7(9), e1230-e1230.
Poli, A., Pozza, A., Orrù, G., Conversano, C., Ciacchini, R., Pugi, D., ... & Gemignani, A. (2022). Neurobiological outcomes of cognitive behavioral therapy for obsessive-compulsive disorder: A systematic review. Frontiers in Psychiatry, 13, 1063116.
Stephenson, C., Philipp-Muller, A., Moghimi, E., Nashed, J. Y., Cook, D. J., Shirazi, A., ... & Alavi, N. (2024). Effects of cognitive behavioural therapy and exposure–response prevention on brain activation in obsessive–compulsive disorder patients: Systematic review and meta-analysis. European Archives of Psychiatry and Clinical Neuroscience, 1-17.
Zhong, Z., Yang, X., Cao, R., Li, P., Li, Z., Lv, L., & Zhang, D. (2019). Abnormalities of white matter microstructure in unmedicated patients with obsessive–compulsive disorder: changes after cognitive behavioral therapy. Brain and Behavior, 9(2), e01201.Zacharek, S. J., Gabrieli, J. D., & Hofmann, S. G. (2024). Brain Plasticity and Prediction of Response to Psychotherapy. Integrating Psychotherapy and Psychophysiology: Theory, Assessment, and Practice, 101.
Kendler, K. S. (2012). The dappled nature of causes of psychiatric illness: Replacing the organic–functional/hardware–software dichotomy with empirically based pluralism. Molecular psychiatry, 17(4), 377-388.