20 Ways Trauma Impacts Your Brain: The HPA Axis, Anxiety and Depression

This episode was pre recorded as part of a live continuing education webinar on demand. CEUs are still available for this presentation through all CEUs. Register@Allce.com Counselortoolbox you I'd like to welcome everybody today's presentation on the neurobiological impact of psychological trauma and the HPA axis or our threat response system. Now what we're talking about is not necessarily ptsd. We're talking about the impact of trauma on our HPA axis. And if we have excessive stimulation of that HPA axis, it can contribute to traumatic injury. But not every trauma causes traumatic injury. And we do want to remember that there are things that we go through that or you may have gone through which may have not been caused traumatic injury. It was traumatic, but you had enough resources and resilience and all that kind of stuff that it didn't cause injury or long lasting effects and there are other things or somebody else may have gone through a similar situation and not had those resources and experienced traumatic injury from it. So we do want to recognize that every trauma impacts every person differently at every point in time. What was stressful for you five years ago may not be stressful now, or vice versa. Maybe five years ago you, you were just kind of walking on sunshine and right now you've got a lot of stress and you're already worn down. So we're going to start by defining and explaining the HPA axis, identifying the impact of trauma on the HPA axis and the impact of chronic stress and cumulative stress on the HPA axis. Finally, we'll identify symptoms of HPA axis dysfunction and interventions that are useful for people who are experiencing experiencing HPA axis dysfunction. I'm going to say that a lot. HPA axis stands for hypothalamic pituitary adrenal axis. I call it our threat response system for short. Just because I get tired of saying HPA axis. This presentation is based in part on the article Post Traumatic Stress the Neurobiological Impact of Psychological Trauma that was published in 2011. Neurobiological abnormalities in PTSD or trauma overlap with the features found in traumatic brain injury. Imagine that we actually see physiological changes, shrinkage of the hippocampus and other physiological changes as the result of environmental situational emotional trauma, not just actual traumatic brain injury like from a concussion. The response of an individual to trauma depends not only on the stressor characteristics. You know, let's look at what's what actually happened, but also on factors specific to the person such as their perception of their stressor how close did this occur to the person's safe zone? We have places where we feel safe. You feel safe in your home. Hopefully you feel safe at work. Hopefully. Hopefully if this, whatever this trauma is, occurs somewhere where you thought you were safe, suddenly you don't feel safe anymore, it's going to have a stronger impact than, for example, if you experienced a traumatic incident when you were on vacation 1,000 miles away from your house. Your similarity to the victim, if you are the victim, then obviously you're very similar to the victim. If you are interacting with people and maybe you are the parent of the victim or the great aunt of the victim, or even you are a therapist working with the victim or the survivor, and you feel a great deal of similarities with that person, then it may impact you more. One of the things I see in emergency service personnel is we have some, some first responders that go out to say a child drowning and it impacts them, don't get me wrong, it impacts everybody. But the ones that tend to have a stronger reaction also tend to have or have had similarly aged children at home at some point. So it's very similar. They can almost see their child in that position and the degree of helplessness, how powerless that person felt. Which kind of goes along with what Joseph pointed out. Trauma definitely is affected by, or our ability to handle trauma is affected by our age. Children need to have those social supports. They need to have their parents, their primary attachment figures there to help them feel safe. Children need to have a lot of other resources because they don't have as many experiences. So something that may not seem like a big deal to us may seem like a really big deal to a 10 or a 12 or heaven forbid, a 5 year old. And they don't understand things the same way that we do. They are also very egocentric. A lot of times they feel they think that something they did caused the problem or something they didn't do may have caused the problem. Or in the case of say, a hurricane, they may overgeneralize and start having fears whenever any thunderstorm comes along because they were in that hurricane. So they think that every storm is going to be a hurricane. We do need to make sure that we work with children after stressful incidents to make sure that they understand what happened to the best of their ability. They may not get death, they may not get addiction, and we need to help them depersonalize it so they understand it wasn't something they did or didn't do. We need to present them the information in a way that they will understand and keep reiterating to them that they're safe and help them feel safe. Recognize that a lot of children's behaviors when they are experiencing trauma are often reactions that are designed to elicit control or structure or comfort from those primary caregivers. Regression, acting out those sorts of behaviors. We want to look and say, what is this behavior communicating to us? People who've had prior traumas tend to have a stronger reaction to successive traumas. They found that people who are in a state of hypocortisolism and we're going to talk about that in a little while. But people who've experienced prior traumas and it's impacted their physiology actually are at a greater risk for developing PTSD from future traumatic events. And they're already primed, so to speak, or whatever you want to, however you want to call it. The amount of stress in the preceding months also contributes to our reaction. If you've had a great 6, 8, 12 months leading up to whatever this trauma was, then you're probably stocked up on emotional, cognitive, social resources, your energy's built up. However, if you have had a hell of a year and a lot of times they say that bad things come in threes, usually by the time you get to that third thing, you're done, you're exhausted. But if you've had stressors and challenges, even small ones, they add up and they can wear down your recovery resources, your recovery capital. So you may not be in the place to have the resilience that you, you might have had should you have not had such a hard time in the past few months. Current mental health or addiction issues. Obviously, if you've got something currently going on, then you're starting 20 yards back and we need to take that into consideration. People who are currently symptomatic for some sort of mental health issue are probably going to have more difficulty dealing with the traumatic stress because their neurotransmitters are already out of whack. And the availability of social support, and I'm going to talk about this multiple times, but there are critical windows here. Social support in the first 24 hours is the most critical. If somebody gets social support in the first 24 hours, it helps them process what's going on before they start compartmentalizing it. We can only experience crisis oriented stress for so long before we start having to kind of try to pack it up and do something with it. After about 24 hours, 24 to 48 hours, it's still there, it's still raw. But people have Caught their breath a little bit and they've started to push it back. And social support is still helpful here because it's still easily accessible to process. After about 72 hours, people have had to pack it up and put it that back burner for a little while because it is too overwhelming to continue to feel that level of distress. And it makes it harder sometimes to access it. After about 72 hours, some people may start saying, you know what, I've got it. It's not that big of a deal. And in reality, it probably is. They have just put it away in a box somewhere. That is going to require energy at some point in time. The vast majority of the population has experienced trauma, but their reaction is limited to an acute transient disturbance. It may be a few days, a couple of weeks, something like that. The signs and symptoms of PTSD reflect persistent adaptations of the body systems, the neurobiological systems, to the experience trauma. And you notice I crossed out the word abnormal adaptations. It is a very normal adaptation. The stuff that happens because when we're under stress, that HPA axis kicks off. And I'm fond of it when it's working well because it helps us survive, it tells us fight or flee. Let me give you the energy so you can fight or flee. But. But when it stays active for too long, it starts causing lots of problems, such as destruction of neurons and all that kind of stuff. One of the things that the body does is try to dampen that a little bit so we're not running so hot so often. But that reaction, our body's reaction, to try to balance out that persistent high level of cortisol, glutamate, norepinephrine, results in changes in our neurochemical system, the hypothalamic pituitary, adrenal axis. The HPA axis, or our threat response system, controls reactions to stress and regulates many body processes. Now, I want you to think about why. Why does the HPA axis control these things? Digestion? Well, when we've got a fight or flee, it is not time to be resting and digesting. It's time to get that food out of the system to speed things up and focus the energy on protecting ourselves. The immune system, when people are fighting or fleeing, cortisol actually suppresses the immune system suppresses, initially suppresses inflammation in order to divert all that energy to the current crisis. So people's immune system goes down, Mood and emotions are altered when that HPA axis is activated. Norepinephrine, glutamate, adrenaline, those are coursing through your system. Some dopamine. Those are your. Go get them. Those are your excitatory neurochemicals, which means it is turning down, your body's turning down, if you will, the dial on serotonin, which is more of a calming, and gaba, which is sort of our natural volume and our endogenous opioids, those are going, you know, now is not the time to worry about pleasure. Now is not the time to worry about reproduction. So estrogen, progesterone and testosterone all get altered in their levels and the receptors that are being activated. So our sexuality and our libido goes down. You can see somebody who has a persistently activated HPA axis may have digestive problems, reduced immunity, mood issues, because that serotonin and gaba is not helping to help the person feel calm and happy and relaxed and all those things. Additionally, that low serotonin also reduces pain threshold. So people tend to feel more pain. Energy storage and expenditure is also all over the place. So people with, for example, diabetes have a harder time controlling their blood sugar. Cortisol. One of the things it does is tell your body, dump glucose, dump glucose. We need that fast energy. So if cortisol is constantly surging through your body, then you've constantly got glucose surging through your body. So that glucose, insulin, balance, it ain't there. And it's important for people to remember that, that they may feel hypoglycemic faster, they may get a little bit edgier faster. These are all things that we need to recognize when people are experiencing stress, help them understand why they're having these different systems or symptoms and why it makes sense from a survival point of view. And to a certain extent, that's awesome. I am glad your body is focusing to try to help protect you. The ultimate result of HPA axis activation is to increase levels of cortisol in the blood during times of stress. We call cortisol our stress hormone and it's there to help us get motivated. But when the HPA axis kicks off, cortisol goes really high and it can eventually cause some problems. Cortisol's main role is in releasing glucose into the bloodstream to facilitate the fight or flight response. It also suppresses and modulates the immune system, digestive system, and reproductive system. Cortisol plays a big role. Now, when we think about people who experience chronic stress, what hormone do they have that is generally very high? I'll give you a hint. It's cortisol. We're not necessarily just talking about some trauma. We can Be talking about chronic ongoing stress. They found that there are a lot of lifestyle factors that contribute to HPA axis hyperactivation. The body reduces its HPA axis activation when it appears that further fight or flight may not be beneficial. Remember, think about a bath. You know, you're running a bath, you turn that hot water, you know, wide open. That is your HPA axis. That's your fight or flight. That is the heat, the get up and go. But it starts getting a little too hot and you want to turn on the cold so you don't burn yourself. Well, your body does the same sort of thing. It wants to protect those neurons, wants to protect your body from running too hot, so to speak. But eventually what happens? That hot water, you only have so much. Well, unless you have limitless hot water, but most of us still have a hot water tank. And eventually that hot water runs out and then it starts running cold. If you want to think about it that way. The body's trying to balance against the excessive heat of the HPA axis, but the hot water runs out. The body doesn't cue into the fact that that's happened yet. So it continues to try to protect you from that excessive stimulation, which can lead to feelings of depression. It also can create a situation called hypocortisolism, where the body is actually blocking cortisol from going through because it's saying, okay, we can't have this much cortisol going into the system because it's overdoing it. Kind of like flooding a garden with water, you know, that would be if the farmer put on a nozzle so he wasn't putting so much water out into the garden. Hypocortisolism is seen in stress related disorders such as chronic fatigue syndrome, burnout, and ptsd. And it's actually a protective mechanism designed to conserve energy during threats that are beyond the organism's ability to cope. So this other reason for feelings of flatness and apathy after persistent or ongoing HPA axis dysfunction is the body going, I've only got so much energy left and I'm going to conserve that right now. So when there is a problem, I can spring into action. Oh, but there's a problem with that. When they spring into action, then the HPA axis goes from apathetic and kind of flat and the person is, you know, blah feels blah to emotional dysregulation. There is no middle ground when the HPA axis has gone into this hypocortisol or glucocorticoid resistant state. So we see a Lot more emotional dysregulation until we can get that HPA axis reregulated. And we need to look at all the causes for dysregulation, including sleep disturbances, excess caffeine pain, mood issues, cognitions, lack of social support. You know, there's a whole list of biopsychosocial triggers for stress, and stress activates that HPA axis. Dysfunctional HPA axis activation will result in abnormal immune system responses with generally suppressed immune system for a while. But the interesting thing is, initially, the HPA axis so suppresses inflammation, but after a stress response, the way the system's supposed to work, the cortisol subsides and inflammatory cytokines are released into the body. Why? Because they circulate around and find any places of injury, cause inflammation, cause blood to go to the area for repair and rejuvenation. So it makes sense. But if that HPA axis stays activated and never kind of calms down, then you have this weird situation where you've got cortisol in the system, but you've also got circulating systemic inflammation. What do we know about suppressed immune system and increased inflammation? A lot of times that's related to the development or exacerbation of autoimmune issues. There can be increased inflammation and allergic reactions. Irritable bowel syndrome, such as constipation and diarrhea. Reduced tolerance to physical and mental stresses, including pain. You know, it could be the person that's just edgy and irritable. I say just. And they also may have difficulty tolerating pain, tolerating hunger, tolerating blood sugar alterations. And there are altered levels of sex hormones because the body is still getting this message that it's not safe to procreate. Our little ankle biters aren't going to be safe yet. Fatigue, interestingly enough, when we experience extended HPA axis activation, one of the symptoms is fatigue. And fatigue is actually an emotion generated in the brain which prevents damage to the body. When the brain perceives that first, further exertion could be harmful. So I was at the gym today, and I was doing a lactic acid threshold workout, which, you know, those suck. I will just tell you. And after about 30 minutes of working at 98 to 102% of my max heart rate, I was starting to feel really fatigued. I was like, I don't know if I can finish this segment here. That was my brain going, okay, you done pushed the envelope. It is time to back off, because you are getting to the point where you could start hurting yourself. Fatigue in sports is largely independent of the state of the muscles themselves and is more related to core temperature, glycogen levels. I was fasting before I worked out, so my blood sugar, I had run through it by that point. My blood sugar was really low, My core temperature was high, Oxygen levels in the brain, thirst, sleep deprivation, and level of muscle soreness and fatigue. So thankfully, I only had two of those things working against me, so I was able to complete my workout. But fatigue can be cumulative and we want people to recognize that. And this is true during daily living too, not just in sports. If people's blood sugar levels are not adequate, if their there's not getting enough oxygen to the brain, they're breathing shallowly. If they're dehydrated, sleep deprived, and have muscle fatigue for whatever reason, and sometimes people who are depressed report feeling a lot of heaviness and muscle fatigue, Then you can see that they may be experiencing ongoing fatigue that may be unrelated to sports. It's more related to that HPA axis activation, because the body is still acting as if it is being stimulated by something like running from a lion or sports psychological factors that can be involved in reducing fatigue, including your emotional state, if you are enthusiastic about it, which most of us are not enthusiastic about trauma, but if you're enthusiastic about it, it can reduce fatigue, which is why athletes tend to see that finish line and they start to get enthusiastic and they can push past that fatigue. We want to help people see the finish line. We want to help people feel efficacious. We want to help people see the progress that they've made and see that their destination is not unreachable knowledge of an endpoint. You know, if you're just, you keep going and it's like, eventually maybe you'll feel better. You know, it's hard to keep going. But if you know that, okay, this is 10 weeks of therapy, or, you know, this is a mile run or whatever it is, or, you know that this pain, you know, you had surgery and the doctor says, you know, in three to six weeks you should be feeling significantly less painful. That I know. Shoulder surgery is a huge, hugely painful surgery, but people who go through it, they know, okay, this is really hideous right now, But I know hopefully after this recovery period, I will feel better. Other competitors or motivators can reduce fatigue. So if we have good social support for people who are around us when people are going through trauma, that can be seen as motivators, not competitors, necessarily, when we're talking about trauma. But they are people that are there to motivate us, to cheer us on from the stands, so to speak, if we want to keep with this analogy. And visual feedback can help reduce fatigue. Use baseline charts, use journals, use logs to help people see that they are gradually improving. Fatigue is one sign that the body is getting ready to downregulate the HPA axis to start holding on to those energy reserves. In counseling practice, we need to figure out how we can reduce fatigue and help clients restore HPA axis functioning. And a lot of it comes back to having them have a survivor mentality and a positive emotional state, helping them devise an endpoint so that they can see getting social support and motivation and making sure that they are rested, nourished, and all those other things. Low cortisol has been found to relate to more severe PTSD or hyperarousal symptoms. Sensitized negative feedback loop. In veterans diagnosed with ptsd, I showed that they had greater glucocorticoid responsiveness. So what does that mean? That means that people who've experienced extended HPA axis activation, they go into that period of hypocortisolism and then when there is a threat, there is a greater cortisol response. So when there is a stressor, instead of having, you know, little bit of cortisol dumped into the system, it is wide open. Generally, low cortisol is seen in people who have experienced extended stress as a result of trauma or chronic stress. But when a threat is perceived, there's an exaggerated stress response and I call this flat or furious. So they either feel kind of flat or, or they are super agitated. Evidence points toward a role of trauma experience in sensitizing the HPA axis independent of PTSD development. So HPA axis can dysregulate, we can have problems with it even if the person doesn't develop diagnosable ptsd. Which is why I always say we want to look for traumatic injury. We don't want necessarily want to just hold it out there for only people who meet the criteria of ptsd. As I mentioned earlier, those with prior trauma histories are often more at risk of PTSD from later traumas. So we can help them hopefully prevent the development of PTSD if we notice that they have had a history of trauma or chronic stress. They do have an HPA axis that is dysregulated or dysregulating. We can help them start to take positive holistic steps to re regulate that HPA axis. So if there is another trauma, which in life there's going to be occasional, if there is Another trauma, they are at less risk of developing PTSD because they're not hypocortisol. Ish. Core endocrine features of trauma include abnormal regulation of cortisol and thyroid hormones. Okay. Hypocortisolism in PTSD occurs due to increased negative feedback sensitivity of the HPA axis. We've already talked about that. Studies suggest that low cortisol levels at the time of exposure to trauma often predict the development of ptsd. Glucocorticoids, your cortisol interferes with the retrieval of traumatic memories and an effect that may independently prevent or reduce PTSD symptoms. Cortisol, that fight or flight stress hormone, interestingly says, you know what, you really don't want to remember that. So it prevents some of our traumatic memories from being solidified, if you will. Which is another reason that when people are experiencing stress, when they're experiencing HPA axis dysregulation, they have a harder time with concentration and learning because that cortisol circulating through their system is inhibiting the formation of memories and learning. Core neurochemical fact features of trauma or PTSD include abnormal regulation of catecholamine, serotonin, amino acids, peptides and opioid neurotransmitters, each of which is found in brain circuits that regulate and integrate stress and fear responses. The take home message from that is there are core actual changes in dozens, not just these, but dozens of hormones and chemicals in our body as a result of HPA axis activation and extended HPA axis activation or hypocortisolism. Glucocorticoid resistance results in a whole different set hormone and chemical changes. It's important for us to recognize this. It doesn't mean that it can't be rebalanced. I don't want to say fixed, I want to say rebalanced. We can help people give their HPA axis a break, but eating better, getting good sleep, practicing good cognitions, those things aren't going to fix it overnight. It is kind of like gaining weight. Think about if you gain 100 pounds, you are not going to lose 100 pounds in two, three weeks. What they are carrying is 100 pounds of stress, if you want to look at it that way. And it is going to take time of living right, reducing their stress, practicing some of the tools that they learn in counseling, and dealing with any remaining traumatic memories that they've got in those boxes in order to help them re regulate that HPA axis. The catecholamine family of neurotransmitters includes dopamine, our let's keep doing that again and again. Neurochemical norepinephrine, which is our focus. And let's go get it. Neurochemical. And both of those are derived from the amino acid tyrosine. So we got to eat foods that have tyrosine. It's not hard. Anything with protein in it in order to let our body make those neurotransmitters. When a stressor is perceived, the HPA axis releases cortico crh, which interacts with norepinephrine to increase fear conditioning and encoding of emotional memories, enhancing arousal and vigilance, and in integrating endocrine and autonomic responses to stress. So when that fear response takes over, that fight or flight reaction takes over, the body actually secretes chemicals that make us hypervigilant, that make us more aware of what's going on and alert to threats, which is great from a survival perspective in the short term. In the long term, it really sucks. There's an abundance of evidence that norepinephrine accounts for certain classic aspects of of trauma symptomatology, including hyperarousal, heightened startle responses, and increased encoding of fear memories. So remember that cortisol initially blocks the encoding of those memories, but in an extended exposure, the norepinephrine is going to counterbalance that. Because, remember, in an extended exposure, the body starts turning down or blocking the cortisol from going through. For a lack of a more clinical explanation right now, which means norepinephrine surges and takes over. It can become more powerful and is able to start encoding those fear memories. Poor serotonin transmission in trauma may cause impulsivity, hostility, aggression, depression, and suicidality. Too little serotonin is associated with depression. Too, too much serotonin is associated with anxiety. Too little serotonin is also associated with impulsivity and low pain tolerance. Now, you don't need to memorize these, but I think it's important, and I try to teach this as much as possible. There are multiple types of serotonin receptors, and serotonin is responsible for or integrated in just about every body system and reaction there is out there, from appetite and blood pressure to heart rate, impulsivity, memory, mood, respiration, sexuality, sleep, sociability, and it goes on. Interestingly, certain SSRI selective serotonin reuptake inhibitors, most of them focus on this 5ht1a receptor. But look at all the other receptors that are out there, and they're throughout our body. And some of those can get a little bit wonky. And if you're Taking something that acts on 5ht1a to help with your mood and your cognition and your appetite and your sleep, because you're having those symptoms of depression. But it's actually your 5ht2a receptor that's wonky. Guess what? You're not going to feel much response from that particular ssri. So we do want to educate patients that there are multiple serotonin receptors. There are multiple different medications that target different serotonin receptors, but it's not always about the serotonin. Norepinephrine, dopamine, and some of our other thyroid and gonadal hormones are also involved in the functioning of the receptors for all of our neurotransmitters. And mood depression can be caused by imbalance of any of our neurotransmitters, not just serotonin. GABA has a profound anxiolytic effect, in part by inhibiting the norepinephrine circuits when GABA is released. GABA is created from glutamate, so it reduces glutamate levels, but it also inhibits the norepinephrine. So GABA turns down. It's the cold water, if you want to think of it that way, to the HPA axis hot water. Patients with PTSD have decreased peripheral benzodiazepine binding sites. GABA is one of our natural benzodiazepines. Patients with PTSD don't have as many receptors for GABA as patients who haven't experienced trauma, which is kind of interesting. So it's harder for that GABA system to work. If there are fewer receptors in the body, it may indicate the usefulness of emotion regulation and distress tolerance skills due to potential emotional dysregulation. One of the things we need to do is help reduce excitotoxicity when, which is the fancy word for too much glutamate and norepinephrine in order to reduce distress, improve stress tolerance and enable acquisition of new skills. Harder to learn new skills when that cortisol level is high. We need to help people develop those distress tolerance skills so they can get into their wise mind, which is partly turning down the adrenaline, turning down the norepinephrine, turning down the cortisol so they can focus and think and learn and remember. Our glutamate receptors or NMDA receptors are implicated in synaptic plasticity or our brain synapses ability to function and adapt as well as learning and memory. Glutamate binds to our NMDA receptors and high levels of glutamate are secreted during high levels of stress. So, so when glutamate is going through our body, it's fight or flee. Let's get that energy, let's get to it. Those NMDA receptors are super activated. They are on fire, if you will, which can lead people to feel anxious, hypervigilant, all those other things. One of the things that they found with the ketamine is that it actually blocks the NMDA receptors. One of the interesting side effects and too much to go into right now, except for to hit the highlights. You can read the article by clicking on the hyperlink. But ketamine actually blocks those receptors, so it blocks the glutamate, but it doesn't lead people to feel depressed. It actually leads to more focus and more controlled energy. So it redirects that system instead of turning it off completely, we, what it's doing is helping the body redirect that energy to more task oriented goals. Overexposure of neurons to glutamate. So too much glutamate in our brain is excitotoxic, which means it actually starts causing brain cells to die and results in loss of volume of the hippocampus. In people who've experienced trauma, elevated glucocorticoids or cortisol increases sensitivity of the NMDA recept receptors. So the more cortisol we have, the more sensitive those glutamate receptors are. So when the glutamate comes, comes in, they are super excited, rendering the brain more vulnerable to excitotoxic insults. So instead of being, you know, turning on the heat a little bit, when that glutamate hits those NMDA receptors that have been sensitized, all of a sudden, you know, it's like charcoal that's been primed with lighter fluid. Things we need to remember. It may take clients who've experienced trauma, who have high levels of cortisol more time to master new skills because it's harder for them to focus. That norepinephrine is focused on fight or flee, not learning, memory and concentration. If the brain becomes excitotoxic during stress, it inhibits learning and memory. So exposure therapies for these particular clients may or may not be super helpful. If it's increasing the excitotoxic environment in their brain, too much can be dangerous. Which is why exposure therapies need to be taken very seriously and not just done by somebody who hasn't been well trained. Endogenous opioids, or our natural opioids that we have act on the same nervous system Receptors as morphine and heroin. Opioids, even the endogenous ones are system depressants. They slow things down and exert inhibitory influences on the HPA axis. So the opioids along with GABA and serotonin help turn things down a little bit. Alterations in our endogenous opioids may be involved in certain PTSD symptoms such as numbing, stress induced analgesia and dissociation. Recognizing that again these symptoms are merely outward manifestations of changes in the neurobiology of the patient. Naltrexone, we all know that as the anti overdose drug basically appears to be effective in treating symptoms of dissociation and flashbacks in traumatized persons. The naltrexone basically goes in and blocks those opioid receptors. So the person is not experiencing the emotional numbing and the stress induced analgesia, which they may not be real keen on. Highlight One of the things that this does point out is the risk for opioid abuse for people with ptsd. They may be self medicating because they figured out they may not consciously have put two and two together, but they figured out when they use opioids they get some relief. A hallmark feature of PTSD is reduced hippocampal volume. The hippocampus is a part in the brain that is implicated in the control of stress, memory and contextual aspects of fear conditioning. So the hippocampus tells us let's look around and and identify all the triggers or signs that there is a threat. Prolonged exposure to stress and high levels of cortisol damages the hippocampus. This reduction in hippocampal volume may reflect the accumulated toxic effects of repeated exposure to glutamate and increased glucocorticoids or that whole flat fat, sorry, flat and furious sort of situation which if you're working with somebody, for example, who has borderline personality disorder symptoms, there's a lot of flat to furious and emotional dysregulation in people with those symptoms that we do want to recognize that they may be experiencing trauma on a regular basis, not necessarily what we perceive as traumatic. But for them they are going from flat to furious and that's exhausting. And from a neurochemical standpoint it is reflective of trauma. Decreased hippocampal volumes might also be a pre existing vulnerability factor for developing ptsd. We've already talked about how hypocortisolism or glucocorticoid resistance makes people more prone to develop ptsd. Well they've said, well maybe it's that or Maybe it's only people who've had that for so long that it's reduced the volume of their hippocampus. They're not really sure. But we do know that prior trauma, prior alterations of the HPA axis do prime people for being more at risk for later development of ptsd. The amygdala is a limbic structure involved in emotional processing and is critical for the acquisition of fear responses. It is a very primitive area of our brain, but it is there to protect us. Functional imaging studies have revealed hyper responsiveness in PTSD patients during the presentation of stressful scripts, cues and trauma reminders. Again, looking at the HPA axis goes from flat to furious. There's a dump of cortisol whenever somebody who is experiencing hypocortisolism is exposed to future stressors. PTSD patients further show increased amygdala responses to general emotional stimuli, even the ones that are not trauma associated, such as emotional faces. So they tend to be more emotionally raw, emotionally responsive, sensitive, whatever you want to say. So things that are totally not related to the trauma can trigger a much stronger response in them than in someone who didn't have that pre existing HPA axis dysfunction. Early adverse experiences, including prenatal stress, even you know, when it's the baby's still cooking, and stress throughout childhood has profound and long lasting effects on the development of our neurobiological systems, thereby programming subsequent stress reactivity and vulnerability to develop ptsd. Kids have experienced a bunch of adverse childhood experiences, everything from environmental stress to poor nutrition, to exposure in utero to drugs and alcohol. There's a lot of different insults that the pediatric brain can experience, may set them up without any overt traumatic experience, may set them up to be at risk for emotional dysregulation and potentially even eventually PTSD later in life. It's really important that we get in there with early prevention programs. A variety of changes take place in the brains and nervous systems of people with ptsd. Pre existing issues causing hypocortisolism. The brain has already down regulated, it started blocking the cortisol receptors, so to speak. So there is not as much glutamate and norepinephrine and stuff released. If cortisol can't get through, then it can't trigger the release of all of those excess cytotoxic chemicals like glutamate and norepinephrine. So if the body's already downregulated, the person may experience more ptsd. Remember, if that cortisol can't get through, then when norepinephrine is released, there is more fear encoding. Cortisol is the one that blocks that fear encoding. This points to the importance of prevention and early intervention of adverse childhood experiences. Remember that people with hypocortisolism may or may not have ptsd. I recently wrote an article about lifestyle factors that contribute to HPA axis dysfunction and they found that, or I found in the research that exposure to noise, for example, people who live near wind farms or airports tend to have much higher rates of use of antidepressant medications and symptoms of hypocortisolism and symptoms of hyperactivated HPA axes than people who aren't exposed to that chronic noise. For example, hypercortisolism sets the stage for the Flat and the Furious, leading to toxic levels of glutamate upon exposure to stressors, reduction of hippocampal volume and persistent negative brain changes. Now, once that hippocampal volume has been reduced, a lot of times there's no building it back up. The good thing is most humans only use a very small proportion of our brain, so there is a lot of room for workarounds, if you will. So I don't want people to think that, oh, I've already shrunk my brain, so there's nothing I can do. Totally not it. In most cases. There are a lot of workarounds. Think about people who've experienced massive strokes or massive brain injury. A lot of them regain their abilities to walk, to talk, to write, to do whatever they did before. Sometimes not 100%, but a lot of times the brain is very receptive to functioning. It wants to help people do what they need to do. And it develops its own little workarounds, which I think is really cool. People with PTSD are more reactive to emotional stimuli, even stimuli unrelated to trauma. This is so important for our clients to understand as well as their loved ones and us as clinicians, because it highlights the need for really good self care and really good distress tolerance skills and coping skills, skills and awareness, mindfulness of traumas so they become more aware of, okay, this is going on, it's stressing me out. And they can intervene early before they become super dysregulated. You know, sometimes they can notice that, oh, this is going to be stressful and they can prepare ahead of time. They may be able to mitigate stressors, so they mitigate or at least reduce the impact on that HPA axis because they can start developing a certain level of control over their reactions through biofeedback and the use of a lot of other skills that they can learn. Purposeful action, acceptance and commitment therapy, cognitive processing therapy, dialectical behavior therapy. Those are the big, you know, buzzwords, if you will, for HPA axis resolution or rebalancing. In addition to healthy nutrition, exercise, circadian rhythm balancing, making sure that people are maintaining their circadian rhythms and nutrition, sleep exercise and circadian rhythms. All of those if they are out of whack, if they are poor, then they can contribute to HPA axis activation. That includes the use of caffeine and nicotine. I know I loved my caffeine before I had to give it up. But it's important to help people recognize that there are things that they're doing in their daily life which may be contributing to them continuing to feel flat or have the experience of emotional dysregulation. Feelings of fatigue set in when the brain perceives that continued effort is futile and or the brain says, can't keep running this hot. You know, I'm going to have to turn on some, some cold water because we can't keep, keep sitting in this hot bath. Reducing fatigue can be accomplished in part with psychological factors including motivation and knowledge of competitors. Knowing what is what you're dealing with can help people feel a sense of personal control, feedback about frequent successes, encouragement, helping them know that endpoint. Remember all those fatigue things that we looked at. There are a lot of things that we can take from sports and translate to HPA axis activation because when that HPA axis is activated, it's telling us to fight or flee. So fight or run, if you will. Both of those are sort of sport type things. When that HPA axis is activated, what happens? Our heart rate goes up, our breathing increases. It's as if our body is doing something physical. But sometimes we're still sitting still. So we can take some lessons from that and help people identify ways to feel empowered, hopeful and less fatigued. 46% of people in the US are exposed to adverse childhood experiences, so there is a lot of room for early intervention. We also can provide everyone, not just people with traumatic injury, but everyone, instruction and skills to handle emotional dysregulation, including mindfulness. Being aware of triggers, preventing them when possible, having a plan to mitigate them if you couldn't prevent them. Vulnerability, prevention and awareness. What makes you more likely to respond strongly to something? For me, too much sugar, not enough food, low blood sugar or not enough sleep tends to make me more vulnerable. I tend to get really cranky. Emotion regulation skills, distress tolerance skills and problem solving skills of those exposed to trauma education about and normalization of their heightened emotional reactivity. It's your brain's way of trying to protect you. Totally makes sense. It may really tick you off right now, but if you look at it, have a little bit of a cognitive restructuring and look at it as a survival mechanism, then we can look at ways to help your brain calm down, recognize it's safe, and develop new strategies for dealing with the stress. Okay, so I went through a lot of stuff in 55 minutes, and there's. If you want to download that article that this is based on, which. Oops. Post Traumatic Stress Disorder. The Neurobiological Impact of Psychological Trauma. It is a tough read. I will tell you. It takes. You have to sit down. You can't have the TV going and really focus on it and maybe take it in chunks. It's a longer article, but it has so much wonderful information in it that I strongly recommend. If you work with people who've experienced trauma, even adverse childhood experiences, you take a look at it. Remember that not every trauma causes traumatic injury. So when one of the adverse childhood experiences, for example, is divorce, well, not every person experiences divorce and gets traumatic injury from it, it may actually be an improvement of a situation. So we do want to not necessarily tell people that they're wrong if they don't think they were injured by it, but we want to take into consideration the fact that they may have been injured by it. And every experience we go through impacts our phenomenological reality. So the divorce that your parents went through when you were six, the experiences you had at school, the experiences you had last week, all impact the way you react to every situation henceforth and forevermore. Now you can choose. You can become aware of how the past is impacting you now and choose how it impacts you now. But that is sort of one of those advanced skills after people start being able to get that HPA axis to recalibrate and respond a little bit more mildly to distress. Any other questions? Alrighty, everybody. I am really looking forward to Thursday's presentation on metacognitive approaches to treatment. I'm still in the process of writing it, but I'm really loving the articles that it's based on right now. So I'm excited about Thursday's presentation. Y' all have a great day and I'll see you on Thursday. Between writing notes, filing insurance claims, and scheduling with clients, it can be hard to stay organized. That's why I recommend TherapyNotes. Their easy to use platform lets you manage your practice securely and efficiently. Visit therapynotes.com to get two free months of therapy notes by just using the promo code CEU when you sign up for a free trial at therapynotes.com you. 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. 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