This was a paper I wrote for a philosophy class a year or so ago.
Introduction
Obsessive-Compulsive Disorder, also known as OCD is a disabling and distressing disorder that can be characterized as having intrusive and recurring thoughts that can result in compulsive behavior (DSM V). These thoughts are unwanted and can be obsessive in nature. A typical example might go as follows: Erica is driving to work when she has the thought “Did I turn off the stove?” She might quell the thought and continue on her way to work. But the thought comes back. And it will not go away. “I can’t remember, I must have left the stove on!” She begins to run through every scenario in her head where her house is on fire, all of her photos of her kids are gone, her cat burned in the fire, and it is all her fault because she left the stove on! She turns around and speeds home to check, and the stove is turned off. This might happen multiple times in one day. Or it might happen on a daily basis, resulting in her lateness to work and subsequent firing for her inability to be on time. OCD isn’t some kitschy need for sameness or repetition, rather, it is a debilitating condition for the individual.
A similarly debilitating condition is depression or Major Depressive Disorder (MDD). Those with depression experience a consistent sense of hopelessness, sadness, and loss of interest in things which normally are pleasurable. For example, Peter has MDD. He consistently feels an utter sense of hopelessness and disregard for life. He used to go out biking, visit friends, and generally enjoy his job as an ophthalmologist. Nothing extraordinary happened, but these days he has no drive to work or enjoy life. He claims that it is pointless and that things will never be good again. Common among people with MDD are claims of hopelessness, pointlessness, and irreversibleness of life.
What is the utility of discussing both OCD and MDD? Both are disorders of attention. Both are cases of genuine epistemic akrasia. And, both are cases of malfunctioning doubt. Here, I will parallel the case for OCD as a case of genuine epistemic akrasia argued by Samuel Kampa with the case for depression as genuine epistemic akrasia as well. Then I will add to Neil Levy’s argument for OCD being a disorder of attention by showing what MDD can clarify in cases such as this as well as what the role of memory is in cases such as these. I then introduce how psychedelics have an effect on healing these sorts of disorders and how the changes psychedelics produce in patients with OCD and MDD help us understand the epistemic component of these disorders.
Epistemic Akrasia
Epistemic akrasia is “the phenomenon of voluntarily believing what you think your epistemic reasons do not support.”[1] So, a person is epistemically akratic “just in case she holds a doxastic attitude she thinks she (epistemically) should not hold or fails to hold a doxastic attitude she thinks she (epistemically) should hold, and she has control over her attitude.” This involves a type of level-splitting, meaning one level is either a person can hold a doxastic attitude they think they should not hold and the other level is a person can hold a doxastic attitude that they think they should not hold. In either case, a person is epistemically akratic.[2] The problem is, according to Kampa, that people with OCD, despite having significant insight into their condition, they fail to resolve their level splitting. So, Kampa argues for an account of doxastic (belief) attitude formation using attention and evidential salience as a way to explain how people with OCD might be able to voluntarily control their obsessions.[3]
Evidential salience is contrasted with phenomenal salience. In phenomenal salience, an object becomes salient when a person is inclined to pay attention to it. A famous example of this is the gorilla experiment.[4] People are asked to count the number of passes that are made between players on the white and black basketball teams. In the middle of the video, a gorilla walks out and beats its chest and walks back off. The majority of people do not report seeing the gorilla. This is because their attention is focused in on the passing of the basketball. Evidential salience is the amount of attention given to a piece of evidence. Just as in phenomenal attention, different evidences attract different amounts of attention. Kampa claims that this model helps explain epistemic akrasia, “when someone is epistemically akratic, she believes that objectively nonsalient evidence is subjectively salient to her.”[5]
So, the case of Erica, when she has the thought that she left the stove on, some thoughts or evidences become much more salient than others. Importantly, one must be able to control or modulate one’s attention for it to truly be a case of genuine epistemic akrasia. Say then, for example, that Erica had gone to therapy in an attempt to overcome this problem and can control her attention but lacks the power to resolve the problem. Erica can hold that she should not epistemically hold her doxastic attitude that she left her stove on yet still hold that the stove is on. In which case she is genuinely epistemically akratic.
Consider the case of the depressed person, Peter. Peter holds the doxastic attitude that he is completely worthless. He believes that things are hopeless. They will never get better. As a person with MDD he also shows the signs of level splitting. Yet, Peter also knows that he shouldn’t hold this belief. He has a wife that loves him, a stable job, friends, etc., yet he still holds that he is worthless and things will never get better. Consider further, that he has series of depressive episodes. Peter might know he is not epistemically justified in believing that things will never get better because he knows he has had episodes like this in the past and they always pass. Despite that, he cannot shake the problematic doxastic attitude. And so it seems that there can be genuine epistemic akrasia in cases of depression as well. Too much attention is focused on the subjectively salient aspects which are objectively nonsalient. Just as Kampa claims that CT is useful for treating patients with OCD,[6] CT would also be useful in treating cases of depression as well.
Disorder of Attention or Memory?
Neil Levy argues that OCD is caused by a dysfuntionally heightened and focused attention.[7] He argues that heightened attention to thoughts and actions produce various over precise pushmipullyu representations. These representations are at once both descriptive and directive representations, ones that “simultaneously depicting a state of affairs and generating a set of motor representations aimed at bringing that state about.”[8] This causes a cycle of increased anxiety which heightens attention further which then causes actions to be taken to change the input or precisfy the signals.[9] Levy posits that OCD starts with heightened attention to certain thoughts (likely too the objectively nonsalient thoughts). Attention is “upregulated either by surprisal or by increasing the stakes such that errors are costlier.”[10] But, increasing the stakes can make OCD worse. In OCD, the subjectively salient but objectively nonsalient thoughts have high stakes. In Erica’s case, potentially burning the house down puts quite a lot at stake and thus focuses her attention on it. In her case though, she doesn’t know that she turned the stove off. In Peter’s MDD case, the opposite occurs. The stakes are astronomical: “Is there a point to living life? Am I a worthwhile person?” And yet, in his case, certainty increases. Both depression and anxiety have a common denominator here: memory.
Levy’s account follows in the footsteps of the usage of predictive coding for understanding cognition. Key here, is the usage of the predictive machinery to “understand the actions of self and others and to generate motor commands.”[11] He argues that the same models that have the function of inferring the likely causes from certain inputs are used for the inverse function of inferring the motor commands that are required to realize the desired goals. These models are made via predictions. Predictions are based on memory. People with OCD have memory impairment, specifically with respect to complex visual stimuli and the individual’s own actions. They also report to have less confidence in their recognition memory.[12] In OCD there seems to be a selection bias against memories of an individual performing a certain action.
Given an impairment in memory, then it would make sense for one to feel it necessary to increase the precision of prior beliefs. If the foundation upon which the knowledge of whether one turned the stove off or not, the memory, is missing then all that remains is the objectively nonsalient aspects—the worries. In an effort to abate this impairment of memory, more precise pushmepullyu representations seem to be required—representations that describe the state of affairs and direct action—action to form precise memories that give the basis for the predictive coding. A compulsion is an attempt to form a memory of performing an action in order to abate the potentially negative consequences of not doing said action—or of lacking memory of doing something important.
Similarly, memory is also impaired in the depressed person.[13] Similarly to OCD, there is a lack in autobiographical memory. One aspect of memory retrieval in depression is characterized by a lack of specificity. Only general memories remain. It is further characterized by a lack of associated positive memories. Matthew Ratcliffe notes that, “Many remarks suggest that depression can involve forgetting how things were before one was depressed. For example: You can’t. . . even remember what it’s like to go and do something and feel pleasure from it. You look at the world, the array of things that you could do, and they’re completely meaningless to you.”[14]
So, it seems that in depression, the opposite of what is occurring in OCD happens. In OCD, the individual has compulsions that are an attempt to overcome the skepticism of not knowing whether they turned the stove off or not. In depression, the lack of memories associated with the opposite viewpoint (that Peter is worthwhile) leads to a belief of certainty or knowledge that one is not worthwhile. Or, perhaps, the same thing is occurring and depression leads the person a step further than simply worrying “what if the house burned down?” or “what if there is no hope?” Depression says, “The house burned down. I’m certain of it!” and “There is no hope. You are worthless.” In place of uncertainty, there is certainty. In either case, there is a focus of attention on the objectively nonsalient aspects of the experience. The fault lies in what is being viewed as subjectively salient. Things that should not be informing the beliefs much are carrying the majority of the weight in knowledge production.
Empirical support for the similarities between OCD and MDD comes from both disorders’ reliance on the malfunctioning serotonin 5-HT2A receptors in addition to the default mode network in the brain.[15] Further, the 5-HT2A receptors play an integral role in memory, attention, and cognition.[16] These receptors are also where psychedelic substances have the most effect. And, psychedelics reportedly have shown to have strong therapeutic effects for both MDD and OCD.[17] One way of describing what they do is an analogy given by Robin Carhart-Harris. The brain is like a ski resort, he says. Over time, ski paths get dug into the snow and any subsequent skier follows in those paths, carving them out even more than before. However, psychedelics are like a fresh new snow storm. All of the carved paths get covered and the mountain is fresh; a skier can carve out new paths. This idea is a part of his theory called the entropic brain.[18] In it, a low entropy state of the brain is described as one with low disorder and very rigid states. This includes things like depression, OCD, PTSD, addiction, etc. The general state of consciousness in humans is closer to this state than to a high entropic one. Disordered states are on the extreme low end of entropic states. They are exceptionally rigid and stuck in the patterns of thought production.
The high entropic state is characterized by high disorder and flexible states. This includes things like the psychedelic state, REM sleep and dreaming, magical thinking, divergent/creative thinking, and the like. This is the state where new information is able to be processed effectively and accurately. New insights, ways of thinking, and knowledge are produced in this sort of state. What psychedelics do is take the low entropic state of the brain and throw a wrench in it, increasing disorder and clearing out traditional and/or problematic heuristics so that it is possible for a new way of thinking to take hold. They disrupt ordinary consciousness enough to allow the user to take off the lenses through which they traditionally view the world.
In other words, psychedelics take the problematic, focused attention of the individual with MDD or OCD and refocuses it on the objectively salient aspects of experience. How exactly psychedelics do this is not understood. Researchers have started to grasp the biological mechanisms, but from an experiential standpoint little has been done. Some suggest it works a bit like cognitive therapy. Kampa focuses on CT for OCD, and his ideas might provide insight into why psychedelics work the way that they do. He argues that CT targets the obsessions indirectly, through the metacognitive negative appraisals.[19]
The negative appraisals are what are problematic in OCD and cause extensive suffering for the individuals with OCD. The negative appraisals, he says, can cause someone to believe that thinking about the obsession makes them a bad person, so they need to suppress the obsession because if they think about it then the person is likely to act on it.[20] In other words, the person with OCD gets stuck in a narrow train of thought. And despite them believing that this thinking tracks onto reality, it does not work that way. Psychedelics might act on these metacognitive negative appraisals by refocusing the metacognitive systems towards actual reality.
Psychedelics
What psychedelics in conjunction with disorders like OCD and depression might tell us is about the relation between contents of consciousness and levels of consciousness. Levels of consciousness are associated with wakefulness. A low level of consciousness would be something like a coma with sleep somewhere in the middle and conscious wakefulness as a higher level of consciousness. The contents of consciousness are the things that we are aware of ranging from perceptual experiences, imagery, bodily sensations, etc.[21] What seems to be occurring in the individual with OCD is a heightened level of consciousness, meaning, their state of awareness is heightened as it in fight or flight mode. This state, in conjunction with the problematic ability to remember, colors the contents of their conscious experience guiding the metacognitive negative appraisals. And, in part causing them to assume they don’t know that they turned the stove off. The depressed individual is in a lower state of consciousness, there is less arousal, which also colors the contents of their experience. Perhaps, because of the lower arousal, they are less inclined to be skeptical, and thus claim to know that they are worthless. In either case, they are failing to track reality. This, in part, might be caused by the default mode network (DMN).
The DMN is a group of brain regions whose activity is closely connected with certain other brain regions and this grouping can function either as a distinct network within the brain or as a connection between areas of the brain. The major regional hubs of the DMN include the posterior cingulate cortex (PCC), the medial prefrontal cortex (mPFC), precuneus, and angular gyrus.[22] The default mode network is characterized by much higher activity levels or metabolic activity during the resting state, when an individual might be focused internally rather than externally, or when participating in attention-demanding tasks. These specific parts of the brain individually are associated with things like memory and perception, future goals and events, and the connecting of perception, attention, spatial cognition, and action. As a whole, the default mode network has been associated with controlling autobiographical memory, introspection, prospection, and moral reasoning. The mPFC is centrally involved in attributing personal relevance to actual or simulated autobiographical episodes in which activity increases during the attribution and then quickly decreases again.
Spreng et al., have shown that autobiographical memory, introspection, and prospection all have a common pattern of brain activity which focused in the midline structures of the frontal and parietal lobes.[23] The same common pattern of brain activation has been observed in the right medial temporal lobe, left-lateralized activation in inferior frontal gyrus, temporal pole, lateral temporal lobe, and inferior parietal lobule—all regions contained within the default mode network.[24] These tasks all activated default mode network regions much higher than spontaneous default activity.[25] The one difference was that autobiographical memory and introspection required greater frontal and parietal midline activity. This is in part due to the focus of attention on internal representations rather than external stimuli.[26]
Additionally, the DMN plays a major role in the disorders of OCD and MDD.[27] It is also important to note that psychedelics (and meditation) decrease the DMN activity significantly. Higher than normal activity occurs when those with OCD and MDD are asked to recall specific memories and the meaning of said memories. After a session of psychedelics (in which the DMN decreases to near zero activity), the patients with OCD and MDD’s DMN is normalized. Given this information, and the role of the DMN in memory and introspection, this might explain the malfunctioning attributions of knowledge in those with OCD and MDD.
One option of what could be occurring might look something like the following. Erica is minding her own business when her brain inserts the thought that she might not have turned the stove off. She then tries to recall whether or not she turned the stove off, increasing activity in the mPFC. Instead of normal function, in which another person would recall the memory and activity would then decrease, there’s a sort of misfire. The memory didn’t code in correctly and so she doesn’t have access to it. This leads to Erica racking her brain trying to remember whether or not she turned the stove off. Which causes further increase in the mPFC and DMN activity causing an overstimulation which results in a heightened level of conscious states. And, remember, higher activity in the DMN regions is associated with decreased attention to external events and increased attention to internal events. This might cause attention to be focused on the subjectively salient/objectively nonsalient evidences that are internal and decrease the attention focused on the objectively salient evidences. In an effort to avoid this, ritual compulsions might take place, in an effort to be able to code a memory that might function properly so as to avoid the worst case scenario event. Given its continual failure to do so, it exacerbates the cycle which Levy characterizes as “a vicious cycle of increasing anxiety, heightening attention still further, and the performance of actions (overt and mental) to change the inputs or precisify the signals.”[28]
Perhaps, what causes Erica to identify with and “know” that the worst case scenario took place or will take place is that, given the faulty autobiographical memory, the panic latches on to a memory of seeing a news story or the like about a house burning down. Once Erica’s brain has associated forgetting whether or not she did something with the worst case scenario, this pattern becomes reinforced each time the cycle occurs.
The same sort of process seems to occur in someone with MDD like Peter. Except, in his case, instead of a forgetting of the specific memory like Erica, there is a selection bias towards negative memories. Peter’s brain then latches onto the only remaining memories and builds his foundation of knowledge from that causing him to “know” that he is worthless and that things will never get better. The heightened state of brain activity (despite the generally lower level of consciousness) in depression can be attributed to the same sort of anxiety that occurs in OCD. Depression and anxiety are nearly always comorbid, leading to a fluctuation of higher and lower states of arousal and oscillating between having the feeling of knowledge and lacking it. The faulty memories and attention loci at work are what seem to give justification for the beliefs of both Peter and Erica.
Psychedelics and Changing Beliefs
Each case could explain why a psychedelic resetting of the default mode network or a “blanket of fresh snow over a ski track” as Carhart-Harris characterizes it is so effective in alleviating the symptoms of OCD and depression. It reboots the system, leading to a more correct attribution of knowledge. Psychedelics healing in these cases fits in the predictive coding framework as well. Carhart-Harris and Karl Friston propose that the principle action of psychedelics is a relaxing of the precision weighting (or felt confidence) of prior beliefs.[29] What this does is create a state where the typical beliefs that have a constraining influence on the rest of the systems of beliefs are relaxed allowing for other beliefs to arise. Carhart-Harris and Friston propose that psychopathologies such as OCD and MDD develop gradually. This comes through an “entrenchment of pathologic thoughts and behaviors, plus aberrant beliefs held at a high level” and that these problematic beliefs are given excessive precision, weight, and influence.[30]
What is occurring in the case of depression and OCD is a slow development of a particular type of thinking that takes a top-down approach. This thinking begins to constrain all others. Psychedelics reduce the weighting that the DMN-based thinking patterns have in the brain.[31] By decreasing the weighting or emphasis the problematic beliefs that the DMN controls, individuals become more sensitive to context and their beliefs and thought patterns are more easily subjected to revision. This allows for different information to be weighted allowing for shifts in perspective (which are felt as insight or knowledge) to occur. Carhart-Harris and Friston propose that transformations that occur under or after psychedelic experiences are principally epistemic in nature.[32]
One strength of their argument is that it is able to account for cases of OCD and MDD having the quality of being genuine epistemic akrasia. They report patients as saying things like they were being reminded of things they already knew but couldn’t act on, they were able to reconcile what they knew to be the case and what their disorder was compelling them to think, etc.[33] The patient’s ability to modulate their attention was in line with what they believed they had epistemic reasons to believe. The initial split on their account is caused by the differing levels of the brain. The holding or non-holding of a doxastic attitude that one should or should not hold is grounded in the split between the top, problematic level of the brain requiring that one should or should not hold the belief with the lower, suppressed states saying otherwise. Thus, when psychedelics enter the picture, the beliefs become reconciled and the individual is able to both hold and have epistemic reasons for holding a certain doxastic attitude.
This account gives credence to Neil Levy’s critique of Moore’s claim that OCD involves giving the predicted narratives of disaster excess weight arising from the security motivational system.[34] This would suggest that Levy is correct in saying the increased weight of catastrophe predictions are modulated by the dysfunctional attention. But, what Levy doesn’t say, and what Carhart-Harris and Friston’s account clarifies is the role the differing systems within the brain play.
This isn’t to say that Carhart-Harris and Friston are arguing for simply a 2-systems approach to the brain. They envision it as more of a hierarchical structure with certain processes having more of an effect than others. By going through repeated thought patterns and compulsions those with MDD and OCD strengthen the neuronal connections supporting that frame of mind, then, when something comes in and disrupts the system (which is what the psychedelics do), the system is wiped clean and correct neuronal connections can be made supporting healthier lines of thinking which track reality better. In this way, the brain is able to enter the higher entropic states where creativity and insight can occur. In this state, new information is able to be processed effectively so that beliefs can be updated correctly using correct information. Instead of the person with obsessive-compulsive disorder or major depressive disorder not having the ability to update beliefs based on new information, they are able to accurately weigh the relevance of new sensory input.
What we don’t have much data on yet, is how psychedelics impact the memory of individuals. As has been shown, psychedelics seem to alleviate the symptoms of OCD and depression. They seem to work on modulating the attention so that it functions correctly. But, what hasn’t been studied is whether or not psychedelics repair the memory problems in those with OCD and depression. It might repair the pathways in the patient with OCD so that memories code properly and the individual can access them correctly again allowing the proper focus of attention to occur. Or psychedelics might just bypass the memory issues somehow. In depression, what psychedelics might do is give the individual back his ability to select for positive memories again which changes the focus of attention on positive from the negative experiences, causing a shift in their claim to “know” things are hopeless. Perhaps what this shows is that memory has less of an impact on immediate claims to knowledge than we might expect. The present moment is what is most relevant for claims of knowledge. Though, this doesn’t seem quite right because it still is the case in the individual with OCD they don’t know if they turned the stove off or not, which is based on a past action. More work will have to be done on this.
Affective Feeling
Juliette Vazard has argued that the problem in OCD is a failure of hyperactive feelings of uncertainty.[35] She argues that the persistent doubting of people with OCD is because of an inability to generate the feelings of certainty that should normally be available after performing a task. She also argues that epistemic anxiety plays a role in OCD because it signals that a proposition might imply a possible threat.[36] This plays a role in signaling what the practical costs of an action or doubt might be. She argues that in cases of OCD, like Erica’s case, the practical cost of forgetting to turn off the stove because the house might burn down is made salient by the feelings of anxiety that arise. The anxiety fuels the problematic attention because the feeling of certainty never occurred. Vazard claims that there is an adaptive system of doubt which can be accounted for in the underlying mechanisms that malfunction in the cases of people with OCD. The only kinds of doubt we should take seriously are ones that present a certain proposition as demanding our immediate attention.[37] This malfunctions in OCD, presenting propositions that should not demand their attention as demanding their immediate attention at great practical costs. What is interesting is that while on the one hand, individuals suffering from OCD view it as practical to doubt the smallest of cases because the feeling of uncertainty won’t go away, the opposite is true in the depressed person. The feeling of certainty won’t ever go away. Despite it being completely practical to try to figure out whether or not Peter is actually worthless, in his case he is certain that he is. There is no feeling of uncertainty. No epistemic anxiety. There is no signal of possible threat towards the proposition of being worthless. In the case of depression, there might also be malfunction reward centers as well.
Vazard argues that scenarios that offer possibilities are considered as either potentially rewarding or potentially threatening through the affect.[38] We vary the amount of resources invested in beliefs based on the expected rewards for accuracy or the expected costs of inaccuracy.[39] This is why the feeling of uncertainty and epistemic anxiety plays a role on her account. The amount of resources invested into a belief for those with OCD is significantly higher for beliefs that the neurotypical wouldn’t invest in. This is because the expected cost of inaccuracy, the practical cost, is significantly higher for Erica. The stakes are raised. This could be because of a malfunctioning rewards system within the OCD individual’s brain.[40] All that is left to activate is the threat system. This provides motivation to seek further precision as Neil Levy argued.
On the other side, those with MDD, like Peter, also have a malfunctioning rewards system. It fails to activate when it should. And, instead of having a functioning threat system, the depressed individual takes whatever the affect, the feeling of certainty, might be and accepts it.[41] Even though it might seem practical to figure out if one is actually worthless or not, the individual with MDD does not do so.
What this seems to show is that the rewards system has little to no impact on beliefs or knowledge but that the threat system does. Both the individuals with OCD and MDD lack a sort of rewards system, yet one seeks to clarify doubts while the other doesn’t. The difference between the two is a functioning threat system. The threat system seems to provide the affect of uncertainty which leads to doubting and a higher standard of precision for knowledge. What also seems to be apparent is that there is a role attention plays in it, but that role is not the sole reason for OCD. Depression also has faulty attention mechanisms. And, in both cases, epistemic akrasia can occur even with help training their attention in therapy. The attention seems to be controlled by the threat or rewards system making it so that, in the case of OCD, attention is signaled out as the problem. What psychedelics might potentially do, is not just fix the attention malfunctions, but actually fix the underlying threat or reward mechanisms that are malfunctioning in cases of people with depression or OCD. They might reset these mechanisms allowing for the malfunctioning attention to function correctly again. What this seems to show is that the rewards and threat system plays a larger role in knowledge than is attributed to it in epistemology.
[1] Samuel Kampa. “Obsessive-Compulsive Akrasia.” Mind and Language (2019): 1-18.
[2] Ibid., 2-3.
[3] Ibid., 8.
[4] Christopher Chabris and Daniel Simons. The Invisible Gorilla: How our Intuitions Deceive us. Harmony Reprint Edition, 2011.
[5] Kampa, 9.
[6] Kampa, 7-9.
[7] Neil Levy, “Obsessive-compulsive disorder as a disorder of attention.” Mind and Language 33 (2018): 3-16.
[8] Ibid., 4.
[9] Ibid., 14.
[10] Ibid., 11.
[11] Ibid., 9.
[12] Jeffrey Muller and John Roberts “Memory and attention in obsessive-compulsive disorder: a review” Journal of Anxiety Disorders 19:1 (2005): p. 1-28.
[13] Cedric Lemogne, et al. “Episodic autobiographical memory in depression: Specificity, autonoetic consciousness, and self-perspective.” Consciousness and Cognition 15:2 (June 2006): 258-268.
[14] Matthew Ratcliffe, Experiences of Depression: A Study in Phenomenology. Oxford University Press: 2015, p. 116.
[15] Michael Choi, et al., “Association between Major Depressive Disorder and the –1438A/G Polymorphism of the Serotonin 2A Receptor Gene.” Neurobiological Psychiatry 49 (2004): p. 38-51.; Karen Adams, et al., “Patients with obsessive–compulsive disorder have increased 5-HT2A receptor binding in the caudate nuclei.” International Journal of Neuropsychopharmacology 8 (2005): p. 391-401.; Katrina Wahl, et al., “Differences and similarities between obsessive and ruminative thoughts in obsessive-compulsive and depressed patients: A comparative study.” Journal of Behavior Therapy and Experimental Psychiatry 42:4 (December 2011): 454-461.
[16] Gongliang Zhang and Robert W. Stackman. “The role of serotonin 5-HT2A receptors in memory and cognition.” Frontiers in Pharmacology 6:6 (October 2015): p. 225-245.
[17] Francisco Moreno, et al. “Safety, Tolerability, and Efficacy of Psilocybin in Patients with Obsessive-Compulsive Disorder.” Journal of Clinical Psychiatry 67:11 (November 2006): p. 1735-1741.; Carolyn Rodriguez, et al., “Randomized Controlled Crossover Trial of Ketamine in Obsessive-Compulsive Disorder: Proof-of-Concept.” Neuropsychopharmacology 38:12 (November 2013): p. 2475-2483.; Robin Carhart-Harris and Guy Goodwin, “The therapeutic potential of psychedelic drugs: past, present, and future.” Neuropsychopharmacology 42 (2017): p. 2105-2113.; Robin Carhart-Harris, et al., “Psilocybin with psychological support for treatment-resistant depression: six-month follow-up.” Psychopharmacology 235 (2018): p. 399-408.
[18] Robin Carhart-Harris, “The entropic brain—revisited.” Neuropharmacology 142 (2018): p. 167-178.
[19] Kampa, 6.
[20] Kampa, 6-7.
[21] Morten Overgaard and Rikke Overgaard. “Neural Correlates of Contents and Levels of Consciousness.” Frontiers in Psychology (October 2010): 164-170.
[22] J. Andrews-Hanna et al., “The default system overlaps activation during theory of mind and episodic memory retrieval tasks.” Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, Program No. 421.17, (2007).; J. Paul Hamilton et al., “Depressive Rumination, the Default-Mode Network, and the Dark Matter of Clinical Neuroscience.” Biological psychiatry 78:4 (2015): 224-30.; Arnaud d’Argembeau, et al., “Modulation of medial prefrontal and inferior parietal cortices when thinking about past, present, and future selves.” Social Neuroscience, 5:2, (2010): 187–200.
[23] R. Nathan Spreng et al., “Intrinsic architecture underlying the relations among the default, dorsal attention, and frontoparietal control networks of the human brain.” Journal of Cognitive Neuroscience 25:1 (January 2013): 74-86.
[24] Ibid., 76-78.
[25] Ibid., 77.
[26] Ibid., 82.
[27] Koch et al., “Increased Default Mode Network Connectivity in Obsessive–Compulsive Disorder During Reward Processing.” Frontiers in Psychiatry 9 (June 2018): 254-261.
[28] Levy, 14.
[29] Robin Carhart-Harris and Karl Friston. “REBUS and the Anarchic Brain: Toward a Unified Model of the Brain Action of Psychedelics.” Pharmacological Reviews 71:3 (July 2019): 316-344.
[30] Ibid., 325.
[31] Ibid., 326.
[32] Ibid., 334.
[33] Ibid., 333.
[34] Levy, 7-8.
[35] Juliette Vazard, “(Un)reasonable doubt as affective experience: obsessive-compulsive disorder, epistemic anxiety and the feeling of uncertainty.” Synthese (December 2019): 1-18.
[36] Ibid., 15.
[37] Ibid., 3.
[38] Ibid., 10.
[39] Ibid., 4.
[40] Martijn Figee, et al., “Dysfunctional reward circuitry in obsessive-compulsive disorder.” Biological Psychiatry 69:9 (May 2011): 867-874.
[41] Anna Hoflich, et al., “Circuit Mechanisms of Reward, Anhedonia, and Depression.” International Journal of Neuropsychopharmacology 22:2 (February 2019): 105-118.; Roee Admon and Diego Pizzagalli, “Dysfunctional Reward Processing in Depression.” Current Opinions in Psychology 4 (August 2016): 114-118.