Neurobiology of Obsessive Compulsive Disorder and Co Occurring Mental Health Issues

Foreign. I'd like to welcome everybody to today's presentation on the neurobiology of obsessive compulsive disorder and co occurring mental health issues. This is the second presentation on OCD that we are doing in honor of OCD Awareness Week. I am your host, Dr. Donnelly Snipes. In the next hour, we're going to explore the overlap and concurrence of obsessive compulsive disorder and things like generalized anxiety, eating disorders, addiction, PTSD and body dysmorphic disorder. We will move on to look at how they overlap and why they might occur, you know, concurrently by looking at the neurotransmitters, emotional reactions and cognitive issues involved in each and what that may mean for treatment. I will be kind of throwing out some questions today. They're not rhetorical. If you want to speculate, I encourage you to do so. Like I said, you know, this is an area that I don't work with a whole lot. So I learned a lot. And you know, I can always learn more from people who do spend a lot of time working with people with OCD. To begin, 90% on average, you know, around 90% of people with OCD, obsessive compulsive disorder, have other psychiatric comorbidities. 75% of them also have anxiety disorders like generalized anxiety, panic, agoraphobia. 63% have mood disorders, 40% have major depressive disorder. And we'll talk about why that's kind of interesting when we get down to, to the neurotransmitters. 8 to 12% have eating disorders, body dysmorphic disorder, 9 to 15% with in people with obsessive compulsive disorder compared to 3% in people who don't have OCD. So there's definitely a, an increased risk. 55%, almost 56% have impulse control disorders, and 38.6% also have substance use disorders. So let's just think about this for a second. Obsessive compulsive disorder. Obsessions are anxiety based thoughts that people are having and in compulsions are behaviors that people do in order to find relief from those anxiety based thoughts. So it totally makes sense that there may be concurrent anxiety disorders. It makes sense that there may be concurrent major depressive disorder, bipolar disorder, or even persistent depressive disorder, which used to be called dysthymia. So those things make sense. When somebody is anxious for too long, when they're revved up for too long, it's grossly oversimplified. But think about it as sort of they've Burned through their. Activating their excitatory neurotransmitters. And they are. They start to feel depressed. Ultimately, we'll talk about it with the HPA axis. Their body knows that it cannot run that hot. It cannot be on all the time. So the receptors become desensitized. But you know, for most people, when you're explaining it to clients, when you start talking about receptors and axons and synapses, they're. They kind of go, you know, often to somewhere else, because that's just more than they want to know. But so it makes sense that people with persistent anxiety and OCD may also have concurrent major depressive disorder. We don't want to rule out any of these things. People with OCD often have multiple other psychiatric comorbidities. Eating disorders and body dysmorphic disorder. I'm going to cover those two together because with eating disorders, there is a focus on weight and shape and a fear of fat. And in body dysmorphic disorder, as you know, there is a focus on a perceived foe. Flaw, a perceived attribute that somebody believes is unpleasant or, or grotesque is probably a better word for body dysmorphic disorder. And those issues, those concerns, those things that people have anxieties about, become the source of their obsessive thoughts. And the compulsions generally have to do with trying to eliminate those types of behaviors. In bulimia and purging, anorexia, for example, or even restricting anorexia, the fear of gaining weight is attenuated by either purging, excessive exercise, purging or restricting. In bulimia, obviously, the fear of gaining weight is especially after one eats, is dealt with by purging. So you can see how there's overlap. You can see how the cognitions can make sense. You can see how people with OCD might be more at risk of becoming obsessive about a. Their. Their body weight or a particular. A particular, particular attribute. Impulse control disorders, we're talking about everything from explosive anger to other impulse control disorders. Some of them can fall under, like behavioral impulse control. Some people call them process addictions and substance use disorders. When people feel anxious a lot, it is common to want to feel better. And we're going to learn in a few minutes that there are a lot of overlaps in the neurobiology of ocd, especially as it relates to serotonin and dopamine. And guess what? When people use or abuse substances, it increases dopamine and often serotonin. There may be an element of self medication here due to the differences in neurological and neurochemical profiles of the different disorders. It's important to recognize that treatments need to differ. So for example, somebody with OCD and major depressive disorder may have a different neurochemical profile or disruption than someone with generalized anxiety and ocd. And we'll, we'll look at that in a minute. So it's important to recognize that for some people, you know, what you think might work for OCD may not work for OCDD with major depression or with substance use disorders. The good thing about that is a lot of this stuff is going to be addressed by, by the psychiatrist or the prescribing physician. But it is important that we're aware for ourselves of the neurochemical underpinnings. And we'll also talk about some interventions we can do that are shown and known to be helpful. As we, as I said earlier, obsessions are anxiety based thoughts. And anxiety is a reaction to a perceived threat. Compulsions are designed to reduce the anxiety and protect from that perceived threat. It makes sense. For some reason this person becomes anxious about something and then when they engage in a behavior like they become anxious about germs, when they get engaged in a behavior like washing their hands, they feel better. And you know, then it, then they can start to look around and think where are all these germs coming from? And then they start noticing all these places germs are coming from and suddenly have to feel like they have to start washing their hands, you know, 50, 60 times a day. Part of the treatment for obsessive compulsive disorder is addressing the events and related cognitions that spawn the anxiety provoking thoughts. And you can do this a variety of ways. You can ask them, you know, what happened? Let's think back to, you know, when you started developing symptoms of ocd, what happened that started making you feel anxious about whatever it is, germs, fire, burglars, harm. Coming to others or doing harm to others is generally what the obsessions are are a lot of the obsessions tend to have to deal with. So we want to think back. What was the event or events that may have started you thinking about this? When my son was in the neonatal intensive care unit, you know, we had to scrub down and get gown up and everything before we went in there. And I became much more cognizant of germs at that point in time. And somebody who may already have high levels of anxiety may be predisposed to noticing that and then becoming even more obsessive. When I brought him home from the hospital, you know, I Didn't become obsessive, but some people, because he was coming from a, what you might call a clean environment and coming home, some people might fear that if they don't keep it as clean clean as the neonatal intensive care unit, that something bad might happen to the baby. So they may become very concerned about germs and cleaning everywhere. A lot of times the root of the obsessions dates back to something that happened that caused them stress, anxiety, fear. And it became over generalized. And if we can look back to that, then we can address that underlying issue and we can start using fact based knowledge. Because now when they see germs or when they think about germs, they're using emotion focused thinking. They're thinking, okay, you know, germs are everywhere. I'm anxious, I'm noticing germs everywhere, I have to wash my hands. Instead of fact based thinking such as, okay, yeah, germs are everywhere. However, you know, our skin is there as a barrier to protect us from germs. And if we don't put our hands in our mouth and bite our nails and do that kind of stuff, the germs are going to stay on the outside. And we actually do need some bacteria on our skin to help keep us healthy. So we can help people use cognitive strategies, fact based cognitive strategies, to start addressing some of those underlying thoughts. Now remember, with ocd, exposure and response prevention is the gold standard for treatment. So this will be in addition to erp. But it is helpful for a lot of people to understand where it came from because then it makes sense. And when it makes sense, people have that aha moment and they're like, okay, you know, this is something that now I understand why it's happening, I can do something about it. Another issue that causes some people to have obsessions is come from messages that they got such as, if you do this, you're going to hell. And for example, masturbation, that's a very frequent one. And they received that message growing up when they start to hit puberty and sexual urges start to arise and they start having thoughts about masturbation and they become very scared because they think, oh my gosh, that means I'm going to hell. And then they do everything they can to prevent going to hell and stop those thoughts. So it makes sense. And, and that's always what I come back to. Behavior is, is communication. What is this behavior communicating? Now let's get into the drier. For some more interesting for others, part of the presentation Neurobiology of OCD and other Disorders. And I couldn't obviously cover everything in the dsm, so I just picked some of the ones that are more common in OCD or in people with ocd. Addiction. Obsessive compulsive disorder, PTSD and eating disorders are all associated with, with alterations or perturbations in the frontal cortex area in that higher order executive functioning area. Good to know. We want to evaluate people because of this, make sure they haven't had some sort of traumatic brain injury that may be impacting that. Not that we can reverse it, but that would also help us, you know, put our finger on something. If, for example, you know, maybe there's no particular event they can identify, but they got a concussion or they were in a car accident and got whiplash. When you've got whiplash, your brain hits the front, hits the back, hits the front again. You know, it's kind of bouncing around like a ping pong ball. And it can cause lasting brain damage in some people if it's bad enough. It's interesting to know. And you deal with it obviously differently if it's organic from a TBI than from other things in some ways, but in some ways you're going to deal with it. The same HPA axis dysregulation is associated also with addiction, ocd, ptsd, depression and eating disorders. So we have HPA axis dysregulation and problems in the frontal cortex in all of these disorders. It's interesting to know persistent stressful events, especially from childhood. So if people grew up in a stressful environment and they are regularly under stress, or even if it's stressful now, maybe they're living in poverty, maybe they're living in an unsafe environment and it's, you know, day in and day out, their HPA axis is activated. They are in fight or flight mode. When we're in that mode, what do we notice? We notice the negative things. We notice the anxiety provoking things, which increases that HPA axis activation. When someone is in that state, they want to feel better. They don't want to feel that anxious all the time. They don't want to feel like they're crawling out of their skin. So sometimes there's some superstitious thinking and they can identify something. They can say, okay, I'm feeling really anxious right now. It must be about germs. And then that can direct them to focusing on trying to eliminate the germs. Regardless of what the core beliefs are that are supporting the anxiety. We know that when someone is perpetually stressed, that HPA axis is Turned. Turned up, the body goes into a state called hypocortisolism. The brain knows that it cannot tolerate having that much cortisol and glutamate coursing through it. It becomes what they call excitotoxic. There's so much stimulatory stuff going on that it gets, think about it this way, it kind of gets too hot, if you will. So the brain stops being responsive to the cortisol. So people's, you know, circulating blood cortisol levels become much lower until there's a threat. And unfortunately, the way this happens, I call it flat. Flat or furious. People are kind of flat during this period when they're hypocortisol, when they have hypocortisolism. When your cortisol is low, you're tired. Cortisol is your stress hormone, but it's also responsible for helping you feel awake and motivated and things like that. So when, in the morning, when your HPA axis is activating normally in the morning it peaks and then throughout the day it declines until bedtime when it's at its lowest point, theoretically and melatonin starts kicking in. That is part of your circadian rhythm. When people have hypocortisolism, they, there is not a peak in the morning. They wake up and it's just, it's very often a very flat diurnal pattern. It's no highs, no lows, just kind of flat and low most of the time. But if there's a stressor, the body and the brain says, oh my gosh, emergency. And it results in hyperactivation of that system. So it, they're either 0 or 200. There's no middle ground. This causes alterations in cortisol, glutamate, norepinephrine, serotonin, dopamine, oxytocin, DHEA and gonadal hormones and also thyroid hormones. But I didn't talk much about that in this presentation. HPA axis dysregulation throws the entire system out of whack. So what does that mean? Well, I guess we'll get to what that means in a minute. One of the things that we can help people do while they are working to address their obsessions, compulsions and their, you know, other issues can be to help them learn to regulate their HPA axis a little bit better. Some things that as clinicians we can do, you know, obviously there's some things that only a prescribing physician can do, but cognitively and interactive personally, what can we do? We can address trauma related stimuli to Help them increase safety and empowerment going back to that triggering incident or incidents. Identifying things that are contributing to their obsessions and help them start to identify and address those thoughts and, and feel like they've got some control over those thoughts or at least responses to those thoughts. Help them develop emotion regulation skills to reduce the magnitude of the HPA axis activation. Instead of going from 0 to 200, we want them to start noticing when they feel stressed and be able to use distress tolerance skills or coping skills to prevent overreaction. That may not come until later on. A lot of times, you know, they're in that flat or furious state. And until we can help that HPA axis re regulate a little bit, what we're doing basically is helping them learn skills and tools to deal with that 200, you know, when they're, when they are really dysregulated, helping them develop skills skills so they don't feel completely overpowered by their emotions and overwhelmed and needing to do something, engage in a compulsive behavior to stop that anxiety. We want to start talking with them about those distress tolerance skills. We want to have them improve health behaviors to reduce biological stressors. Biological stressors activate that HPA axis just as much as cognitive stressors. So exhaustion is one of those things. Malnutrition, if the body doesn't have enough building blocks to make what it needs, or if it doesn't have enough, you know, glucose in order to fuel itself, it perceives that as a threat. And inflammation, whether that's caused by injury or whether it's caused by excessive stress. When that HPA axis is activated for too long, people start developing systemic inflammation. Which is why we also see stress is associated with autoimmune issues. But that systemic inflammation can also contribute to HPA axis dysregulation. Pain, difficulty sleeping. A lot of these are very basic interventions. And you want to think of Maslow's hierarchy. Biological needs and safety are right at the bottom of that list. Before people can start focusing on love and self esteem and all that stuff. And we want to address any addictive behaviors which directly or indirectly activate the stress response. Alcohol, for example. When people drink alcohol, it directly activates that HPA axis. For other substances that people may take, it may tamp down the HPA response briefly, but when they start to sober up, go through withdrawal, however you want to phrase it, then the body sees that as a threat and activates the HPA axis. So either when they use or when they're withdrawing or both, the HPA axis is going to get activated because when we ingest substances, especially when we're talking about chemical substances, the amount of whatever we're taking in is perceived to be toxic by the brain most of the time. Okay, so now on to what happens. We said that HPA axis dysregulation causes everything else to, to get out of kilter. We talked about ways that general ways we can help people start learning to re regulate their HPA axis. And a lot of that goes back to Linehan's basic principles in dialectical behavior therapy. Huge fan. So, but what specifically are we talking about? Dopamine is that neurochemical that's responsible for goal directed behaviors. It's not actually a pleasure chemical. When dopamine is released. A lot of times it is the I want to do it again neurochemical. And we want to do it again because it was pleasurable, because it also caused the release of endorphins. So low dopamine is associated with depression and interestingly enough, bulimia. High dopamine is associated with anxiety disorders, obsessive compulsive disorders, PTSD and anorexia. Which means if you're working with someone who is, has depression and ocd, we might want to look at whether there's another neurochemical that's altered that might be contributing to what's going on. Because, you know, based just looking at it on, on the surface, you would provide the person SSRIs, which would increase serotonin and by virtue of that, increased dopamine. But if the person's dopamine is already too high, is that really what we want? So what can we do again, as clinicians, as social workers, address the function and cause of the goal directed behavior. Whatever they're doing, whatever they're feeling pressed to do, address the function of that in addictions, it is to stop the withdrawal symptoms, to, you know, give their body a reprieve if it is washing their hands. You know, we want to identify that that's protecting them from the fear of getting sick and dying. So we want to address those functions and help them figure out how they can mitigate their environment. Part of that will be through exposure and response prevention, which we talked about on Tuesday. But part of it also will be helping them develop environments in the short term that are more conducive to feeling relaxed. Eventually we want to get them to the place where they can be anywhere and feel fine. But we want to set small goals so people have successes. We don't want to set them up for failure. We want to have rapid small successes. So maybe creating, you know, an environment where they may feel safer from whatever it is that is threatening them. And then augmentation of SSRIs with atypical antipsychotics has actually been found to be an helpful. And I read a really interesting article on the new dopamine hypothesis. Not something that we've got time to get into here, but it is interesting to note that since we know that antipsychotics, atypical antipsychotics like seroquel work on dopamine specifically, and we know that SSRIs increase serotonin, which also because when serotonin goes up, dopamine goes up. It's interesting to note that. So atypical antipsychotics in addition to SSRIs in somebody who already has anxiety may not be super helpful, but that's it's dependent on the person. Norepinephrine is another chemical that is mucked up in this process. Low norepinephrine is associated with depression. Norepinephrine is our focus and one of our drive chemicals. It's one of our energy chemicals. High norepinephrine is associated with anxiety, ocd, ptsd, and obviously HPA axis activation. When people are in a stressful situation, cortisol is released, which causes the release of norepinephrine and glutamate. So people who are anxious, people who have a activated HPA axis, are obviously going to. Experience, like likely experience anxiety until it gets to the point where they've reached a state of hypocortisolism in which they may feel flat or depressed. Glutamate and gaba. You may or may not know that glutamate is actually the precursor to gaba. The body breaks down glutamate, which is our main excitatory energy neurochemical. It breaks down glutamate to make gaba. So if there's a disruption in this system, then people are going to have some sort of symptoms, a disruption in the balance between glutamate and GABA neurotransmission within the guess what frontal cortex contributes to symptoms of ocd. Low levels of GABA are seen in people with depression, and high levels of glutamate are associated with HPA axis dysregulation and anxiety disorders. So remember, after the stressor, there's cortisol that causes the release of norepinephrine and glutamate. If that glutamate level stays high in the brain for too long, the brain desensitizes to it as a self protective mechanism. So one of the things that we can do again is to help people with HPA axis regulation so they aren't feeling anxious all of the time. So that HPA axis is not always activated. But it is also interesting to note that with neurotransmitters we talk about not being enough or being too much, high or low levels. But it's important to recognize that that can happen for a variety of reasons. When we eat food, it is broken down, assuming all the proper elements and stuff are there, broken down and converted to neurotransmitters. So if there's improper nutrition or a breakdown in the construction system, not enough may be made and that causes the problem. Sometimes enough is made, but not enough is secreted into the synapse. Okay, sometimes enough is secreted, but not enough is absorbed and carried on to carry on that message. So there can be breakdowns in multiple different places of the system. Simply saying the person doesn't have enough GABA is oversimplifying. So somebody with low levels of GABA may, may not have high levels of glutamate. Maybe they have low levels of glutamate, so it can't be broken down to make gaba. So they have low levels of both. They have high levels of glutamate that may not be getting broken down to make gaba, we don't know. Or they may have very normal levels of GABA and too much glutamate is being made. Excuse me. So it's interesting to ponder what's going on with people. Ultimately we know that GABA is our main calming anti anxiety chemical and glutamate is our main excitatory stress neurochemical, if you want to think about it that way. So if a person is too calm, they're probably not going to be seeing us right now unless they are depressed, but they probably won't have ocd, so symptoms if they've got too much glutamate. We want to help them figure out how to not feel like they constantly have to have the energy to fight or flee. Serotonin is another interesting chemical. And it's important to recognize that as any of these neurochemicals go up, it affects every other one of them. You can't just pluck one out and go, okay, I'm going to alter serotonin and, and expect that norepinephrine and, and dopamine and glutamate aren't also going to be impacted in some way. Which is why psychopharmacology Is so challenging for even for psychiatrists a lot of times to find that right balance. Low serotonin, especially 5ht1a and 5ht2a are associated with bulimia, OCD, addiction, and anxiety and depression. The good news is Most of your SSRIs, your selective serotonin reuptake inhibitors, and your SNRIs Selective norepinephrine reuptake inhibitors act on these receptors. So that's good that multiple different types of medications. Obviously, if an S NRI improves mood, we also recognize that increasing norepinephrine in some people also increases their serotonin. You can't alter one without altering the other. Interestingly enough, 5ht2c. Remember, there are at least 17 different types of serotonin receptors. 5ht2c is a different type of serotonin receptor. It actually suppresses dopamine. 5ht1a and 2a increase dopamine, but 5ht2c suppresses dopamine. Interesting. So what can we do? Well, serotonin is very susceptible or responsive. Whatever you want to say to basic biological alterations, Nutrition is really important. People need to be making sure they're getting enough protein, but they also have to have, you know, all of their vitamins and minerals. They need to talk with their doctor about and have their nutrition assessed, ideally to make sure that they're getting everything they need. The doctor may recommend a multivitamin, especially if they're not eating really well, because in order to break down tryptophan to make 5ht it, the body needs things like folate and iron and magnesium and calcium and, you know, there are a few zinc. I can't list them all right now, but it needs, you know, a lot of different vitamins and minerals. So good nutrition is essential. If people eat things like, you know, enriched cereal, a lot of the, a lot of cereals have vitamins added to them. So they may be getting plenty, which is why it's important to have them consult with their doctor. We don't want to just recommend them start taking something. But nutrition is essential. Sunlight is essential. Sunlight helps our body make vitamin D. Vitamin D is associated with areas in our brain that are have that are rich in serotonin receptors. Vitamin D deficiencies are associated with seasonal affective disorder. And vitamin D alterations are also associated with alterations and circadian rhythms, which is why sunlight light therapy can help modulate the serotonin in our brains. So we feel a little bit happier. We know that, you know, low serotonin is associated with ocd so let's do whatever we can to make sure that the body factory can make and produce and send out serotonin as efficiently as possible. Exercise, not, I'm not talking high intensity exercise. I'm just talking about moving your body. You know, low intensity exercise is associated with increases in serotonin. So that can be helpful if people are willing to do it. And then again, like we keep talking about just general HPA axis regulation, distress tolerance skills can be really helpful. When the HPA axis is activated, serotonin imbalances change and the stimulatory effects of serotonin go up and the calming effects of serotonin are suppressed. So we want to help people feel calmer so they're calming serotonin. Their HT1A and HT2A can be effective. Cortisol is much higher in male and female patients with ocd. One study found that there was a blunted cortisol response that was associated with obsessions in women. So women who have that hypocortisolism actually tend to have more obsessions when they get stressed. They get very, very stressed and they start having those obsessional thoughts. They go from being okay to being, you know, very dysregulated. In men, a more flattened diurnal cortisol slope was associated with compulsive symptoms. In this article, it was specifically ordering. So for men, they don't have, you know, it's, their level is low and flat most of the time. Interventions, circadian rhythm regulation can be helpful. Circadian rhythms regulate our cortisol levels in addition to stress and everything else. But if your circadian rhythms are out of whack, then your body doesn't know when it's supposed to have that peak and then drop off throughout the day. So circadian rhythm regulation can be helpful for cortisol as well as, like we keep talking about HPA axis regulation. I'm going to tie all this up in a nice little bow at the end, I promise, because I know this is really dense material. DHEA is a chemical in the body that's converted into testosterone and estrogen. You may have heard about it as being the anti aging hormone on TV or whatever, but DHEA is an important component that we have and it drops as we age. That's just the way it happens. Estrogen and progesterone have been shown to modulate serotonin, dopamine and glutamate levels, all of which have been shown to be dysregulated in people with ocd. Remember that men have a little bit of estrogen and women have a little bit of testosterone. The impact of estrogen and progesterone obviously is much more pronounced in women. DHEA and cortisol levels have been found to be higher in people with anxiety disorders such as panic disorder, ocd, ptsd, depression and eating disorders due to possibly HPA axis dysregulation that keeps coming up. So what we need to look at is potentially, you know, dhea. It tends to be stimulatory and if somebody has too much DHEA in their system, then they may be overproducing testosterone and estrogen. But, you know, they're really kind of unclear. They just have done the studies and DHEA is one that they can measure in a blood test and they have found that DHEA and cortisol levels were higher. So since DHEA is used to make gonadal hormones, we will now look at gonadal hormones. Alteration in your sex hormones and the hypothalamic pituitary gonadal axis are implicated in anxiety disorders, ptsd, OCD and depression. So we have been talking about the HPA axis, the hypothalamic pituitary adrenal axis, but the hypothalamic pituitary gonadal axis is also implicated. So you know, I kind of look at it as the hypothalamic pituitary adrenal gonadal system, but these are all implicated when our sex hormones are out of whack. It actually does have significant impacts on our mood, on our cognition, and obviously on symptoms of things like ptsd, OCD and mood disorders. Progesterone metabolites, specifically pregnolone and allopregnolone, show anti anxiety properties by increasing gaba. A Now a little quirky thing about this is progesterone itself is known to increase anxiety, but the metabolites are known have been shown to reduce anxiety. So go figure. Low estrogen and progesterone reduce serotonin signaling and are associated with ocd. It's finding a balance with most of these neurochemicals. Too much has gives you certain symptoms, too little gives you certain symptoms. And it's finding this happy balance, this happy blend of neurochemicals for the an individual. Testosterone has been found to be much lower in male patients. In male patients only implicating the HPG axis. Again, people with men with OCD having low testosterone means that they also have low levels of serotonin and potentially lower levels of dopamine. Interventions medical evaluation have them go to their doctor. Anybody in my opinion, anybody who presents in clinic with mood disorders should always be evaluated for any potential physiological reasons for what's going on, including sex hormone levels, DHE level, DHE levels, oxytocin levels and thyroid hormones. Which brings us to oxytocin. And I'm actually going to end up doing an entire class on oxytocin because I learned so much about it and it was fascinating. But oxytocin is our bonding hormone and it's produced in the hypothalamus, helps modulate the HPA axis. It doesn't necessarily increase or decrease it, it kind of keeps it steady, which may be one of the reasons that our social circle, our social supports, are one of our greatest buffers against stress because social supports increase oxytocin. And oxytocin modulates the HPA axis. So interesting thought, but interestingly enough, it is made in the brain, in the hypothalamus, but once it is excreted from the brain, it can't cross back over into the, over the blood brain barrier. They found that intranasal oxytocin somehow bypasses that system and can affect oxytocin levels. So not sure what the takeaway is that from that is except for the fact that there are intranasal drugs that administer oxytocin if somebody's oxytocin levels are happen to be low. So there is hope. Reduced oxytocin can be a result of disrupted attachment in the child or the adult. Which takes us back to attachment theory. You know, when, when the, the person was an infant, if they had insecure attachment, if they had ineffective attachment, they may have altered that, the oxytocin system, if you want to think about it that way, because we found that unless somebody does actively look at it and work at it, if they don't find form effective attachments in infancy and early childhood, they don't ever basically learn how to form successful attachments. They can, you know, if they, if they recognize that it's a problem, they can learn how to form effective attachments. But left unaddressed, these people will often not be able to form effective attachments, which means their oxytocin levels are going to be low in adulthood. You know, we can have disrupted attachments in adulthood. That can reduce oxytocin levels and that can be from a death, from a divorce, from empty nest syndrome. Anything that may alter those oxytocin levels will likely affect the regulation of the HPA axis and can contribute to, to obsessive compul, can contribute to ocd. So interventions. Intranasal oxytocin is an option if the doctor thinks it's warranted. You know, do the blood test, see what the levels are. We can help people improve their attachment relationships. We can help them do things in their life. And oxytocin is one of those easy ones to increase for most people and by improving their attachment relationships so they feel calmer in their relationships, but, but by also engaging in oxytocin stimulating activities. ESAs, emotional support animals are great for this. They found that petting an animal for as little as 10 minutes can increase oxytocin levels. So even if somebody is having difficulty with other people because of trauma issues or, you know, whatever reason, they have difficulty connecting and engaging with others, especially physically connecting with others, maybe they'd be willing to pet a cat or a dog. Treatment with antidepressants. SSRIs modulates oxytocin levels. So. So interestingly, as serotonin goes up, it modulates the oxytocin levels which modulate the stress response and have been shown to improve obsessive compulsive disorder, depression, anxiety and PTSD symptoms. Now, remember, all of the blue links in here, take you to the studies and you know, all the garbledygook that I'm kind of summarizing for you here. So if you really want to do a deep dive here, you've got lots of articles that you can read. There is significant overlap between OCD and other psychiatric disorders. While exposure and response prevention therapy and SSRIs are the gold standard for addressing obsessive compulsive disorder, because remember, as people take SSRIs, it increases their serotonin as well as their dopamine. It's also important to address other underlying issues which may contribute to neurotransmitter disruption. This includes trauma history specifically addressing their feelings of powerlessness and unsafeness and some of those cognitions that they developed in response to the trauma that underscore their powerlessness and unsafeness. Lack of emotional regulation skills. That HPA axis is dysregulated. They need to learn how to rein that in. They need to start feeling empowered to do some self regulation through distress tolerance skills, recognition of vulnerabilities, mindfulness. Those are the three biggies we need to address. Lack of happiness promoting behaviors. We can increase serotonin and dopamine levels naturally by doing things that make us happy, we that make us want to do it again. Lack of secure attachment contributes to oxytocin, so we can help People work on their attachment issues, their relationship skills, poor nutrition, sleep deficiency, iron deficiencies, all are implicated in problems with obsessive compulsive disorder as well as most other mood disorders. Iron deficiency is actually associated with alterations in dopamine levels as well. So like I said, for our body to create and use the neurotransmitters effectively, we need to have a well rounded diet and. And nutritional profile. Hormone imbalances need to be addressed. Obviously, we're not prescribers, we're not doctors, we're not going to be doing it. But it's really important to have them tested because they found such a strong link between gonadal sex hormones and thyroid hormones and obsessive compulsive symptoms that that may need. That may be an issue that needs to be addressed in order to help the person experience some relief. And we also want to look at medication side effects. And I really didn't talk about that a lot, but it's important to recognize in people, people who are taking hormones, whether it is birth control hormones or hormone replacement therapy, or if somebody is transgender and they are taking hormones, Hormones impact mood just flat out, they do. And it may be important to alter the balance of some of those hormones, steroids like prednisone, if you're taking those that can impact mood, as well as thyroid medications, medications for restless leg syndrome, and antipsychotics. So there's a lot of stuff that we can look at and a lot of stuff that we can encourage people to discuss with their physician in order to create a multidisciplinary, comprehensive, integrative, whatever word you want to use, approach to treating the obsessive compulsive disorder. Aaron asks if emotional support animals are unavailable, could items like fuzzy pillows help? I don't know. I don't know the answer to that, whether something like that would help. Now, if you go back to the Bowlby experiments with the monkeys, I would hypothesize that, yes, because the monkeys tended to gravitate toward the stuffed animal as opposed to nothing at all. So I would think yes, but I don't know that for certain. You know, just kind of. Again, I'm. I'm hypothesizing. This is not based on anything that I have read, for certain, but my. We do a lot of animal rescue and we found that when we get kittens, orphaned kittens, they do a lot better if they have a stuffed animal that is kind of like mom, they snuggle up to it, they pad on it, they try to nurse it and, and they tend to be more resilient and healthier than animals who we see that are, you know, orphans that are in a shelter or something where they may not have access to that. So I, I'm hypothesizing that it could be helpful. And you also have people that are, you know, severely allergic to animals and they can't have a, any animals. Remember, allergies are often due to dander, not necessarily fur. So even birds may have too much dander for some people. Some people love birds, lizards. You know, I, I would have them all if I could, but I can't, so I don't. I appreciate you all sticking with me. I. Like I said, I know this was really dense material and you could probably sit there and hypothesize for a while and think about clients that you've had that have had obsessive compulsive traits, if not, you know, diagnosable ocd, and think about, okay, what might be going on with their neurotransmitters. But ultimately, I believe that unless there is a genetic reason or a traumatic brain injury, if the person is able to re regulate and get their HPA axis healthy and their HBG axis healthy, mood symptoms will probably greatly improve. But in order to do that, they need to not feel like they are constantly under threat. If this podcast helps you help your clients or yourself, please support us by purchasing your ceus@allce.com or getting your agency to sponsor an episode. A direct link to the on demand CEUs for this podcast is at allce.com/podcastce. That's allce. Com podcastce. To sponsor an episode of Counselor Toolbox and reach over 50,000 clinicians per week, go to allce. Com sponsor. Thank you.