HPA Axis Dysfunction & Mood | Exploring the Mind Body Connection

Dr. Dawn-Elise Snipes explains how chronic stress, trauma, and lifestyle factors like poor sleep and diet keep your HPA axis activated, shrinking brain regions tied to mood and memory. This dysregulation drives depression, anxiety, and immune disease. The webinar covers lifestyle fixes: sleep, exercise, diet, and social support.
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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@allceus.com Counselortoolbox I'd like to welcome everybody to today's presentation on the biopsychosocial aspects of HPA axis dysfunction. I am Dr. Donnelly Snipes. In this course, we're going to review and define and explain the HPA axis. I'm going to go into it in a little bit more detail than I have before just because we've already started covering in previous classes more in depth into the neurotransmitters and hormones and things that are involved in the HPA axis. So we're just kind of building on what we know. But if you haven't been to those classes, never fear, you know, hopefully everything will be make sense to you. Well, identify the impact of trauma and chronic stress on the HPA axis and identify symptoms of HPA axis dysfunction and interventions that are useful for this population. There are a lot of things you will find out that contribute to chronic HPA axis activation, which can exacerbate symptoms of anxiety and depression. And those a lot of those things are what we call lifestyle factors. The good thing is lifestyle factors are extremely modifiable in most cases. So we are going to look at ways that we can help clients basically start helping themselves get better. Kind of like when somebody has cancer or some other disease, you don't want them to just let their nutrition and their sleep and everything else go to, you know, hell in a handbasket. You want them to ensure that their body is as healthy as it can be so it can help deal with, fight off that condition. The same thing is true with depression and anxiety. We want them to be as healthy as they can be so their body can function optimally. Two of the articles that I use that form, the foundation of this are Post Traumatic Stress Disorder, the Neurobiological Impact of Psychological Trauma, and an article I just wrote for the Archives of Neurology and Neuroscience called Lifestyle Factors Contributing to HPA Axis Activation and Chronic Illness in Americans. So let's start out with the HPA axis. We've talked before about the fact that the HPA axis is our fight or flight, our stress response system. HPA is short for hypothalamic pituitary adrenal axis. And if you were in the class last week, there is the hypothalamic pituitary gonadal axis. There are lots of axes. Today we're just going to focus on the HPA axis. The HPA axis controls reactions to stress, regulates digestion, the immune system, mood, emotions, sexuality, and energy storage and expenditure. So it's really integral in everything from helping us have the motivation and energy to get out of bed to getting through our day. The signs and symptoms of HPA axis dysfunction often reflect a persistent and I crossed out the word abnormal because it is not abnormal. It is your body's way of trying to protect itself. It's like, I cannot take this much stress and I need to start putting up walls protecting myself. So it reflects a persistent adaptation of the neurobiological systems to trauma or chronic stress. Think about when things are going kind of haywire in your life and there's lots of chronic stress, and you're like, oh my gosh, I can't take one more thing. It's just constant stress. One of the things that you want to do to protect yourself may be to withdraw. You may separate yourself some. Well, the brain can't withdraw. So what it does is it starts creating situations where the synapses are not as responsive. It says, you know what, guys? Don't worry about responding when you're told to because we can't stay this revved up for this long. In addition to trauma, multiple lifestyle factors have been associated with HPA axis dysregulation, including noise. Now think about wherever you live. I live in the country and I really like it in the country, but occasionally there is noise. It's not persistent, so it doesn't really bother me that much, but there is noise. People who live near wind turbines are exposed to low grade chronic noise. People who live in the city and they hear traffic constantly, that's low ish grade chronic noise. People who live in apartments where the walls are paper thin, and I've lived in those apartments before, and you can Hear your neighbors 24, 7. That's chronic noise. All of those sort of situations, and I'm sure some that I'm not thinking of, contribute to HPA axis activation. Stimulant use, including caffeine, nicotine, or stimulant medications like ADHD medications or anorectic medications, your diet pills are going to activate that HPA axis. Insufficient quality sleep and media exposure are also two other lifestyle factors, and we're going to talk a lot more about those as we go through. More than 50% of Americans suffer from one or more chronic conditions associated with disturbance of the HPA axis. It's estimated that this costs the United States $3.3 trillion a year. Oh my gosh, that is a lot of stinking money. And a lot of these are preventable or at least modifiable if we can help people get their body healthy and get that HPA axis in a state of regulation instead of dysregulation. Conditions associated with the HPA axis dysfunction include major depressive disorder, generalized anxiety disorder, sex hormone imbalances. Think about how many people are on, you know, testosterone supplementation or hormone therapy for something. Diabetes, autoimmune disorders. And this can include lupus and Crohn's disease and fibromyalgia, and the list goes on. I think the number for autoimmune disorders is actually kind of low chronic pain, metabolic syndrome, which we've talked about, cardiovascular disease, hypothyroid, irritable bowel syndrome. Symptoms such as constipation, diarrhea, and just flat reduced tolerance to physical and mental stress, including pain. As our HPA axis begins to become dysregulated, we get to the point where it's like something happens and where we would normally react with a one or a two, it's like, okay, that's an irritant, but what we're at that point that anything kind of sends us into the stratosphere and we react with a six or higher to those stressors. And this can be physical stresses or mental stresses, anything that comes our way. And you see on the numbers that are on the slide that there's a lot of people that experience these different conditions, ranging from cardiovascular disease at 44% of people, that 44% of people, that's almost one in two people, one in two persons, people have some level of cardiovascular disease that is not good, that is not a healthy place to be. And major depressive disorder with 20%. A lot of people have multiple conditions that are going on. And that is expected because as the HPA axis becomes dysregulated, more and more other systems, if you will go offline or become dysregulated. When exposed to a physical, environmental or social stressor, the HPA axis is activated and prompts the fight or flight reaction. Glutamate, your main excitatory neurochemical, and norepinephrine, which is excitatory, but it's also your focus chemical. Those are released. It says, all right, we need to hone in, we need to get the heck out of here. The hypothalamus releases corticotropin releasing factor or crf. And you don't need to know all of these things. But I'm just Going to kind of go through the cascade with you. It releases CRF and arginine vasopressin to stimulate the anterior pituitary gland to produce and secrete adrenocorticotropic hormone which is acth. Acth. Now we're getting to the nitty gritty. ACTH causes the synthesis of cortisol which is a glucocorticoid and that cortisol is released from the cells. Now that's typically stuff that we've skipped over till now but now you kind of see where glutamate, norepinephrine, they're like the front line of this stress response, triggers everything and cortisol's released. Cortisol's primary function, well functions are to increase blood glucose. It says alright, we got a fight or flee, we need energy so let's start dumping that blood glucose. You can imagine what this does to somebody who has diabetes or blood sugar problems. So cortisol increases blood glucose and modifies fat and protein metabolism to fuel the fight or flight reaction. Fat is your long term energy source. If you've taken nutrition classes there are 4 calories per gram of carbohydrates which is where you get your glucose from and there are nine calories per gram of fat, so it's almost double. So fat is a much denser energy source. And the body says all right, let's start releasing those fatty acids into the bloodstream because once the glucose runs out we need to be on it for have energy for the long haul. Cortisol also modulates immune and brain functioning to effectively manage stressors. Now this is, this thing is kind of cool. Initially cortisol causes anti inflammatory responses to allow the organism, which is us, to react to the stressor without experiencing pain or fatigue. If you've hurt yourself before, sometimes you notice, you know when you're doing it, you don't even really notice you're doing it. And then you know an hour later when the cortisol's gone down, all of a sudden you're like oh that hurts. Or you start to see more inflammation. This is self preservatory the body, the cortisol is there and it says all right, the stressor is going on, we need to fight or flee, I've got to keep you from being impaired. The good news is or as cues of the threat wane, the body increases inflammation by releasing the pro inflammatory cytokines to accelerate wound healing. Now the body may not know whether there's wounds or not, but it releases some of these inflammatory Cytokines that they go to the look around to see if there are injury sites. They increase inflammation, which brings blood supply to the area, which increases wound healing. So it's a really interesting system that is designed to help the person get through the fight or flight and then repair and prepare for the next time when all of this is happening. Glucocorticoids or cortisol is going through the brain and it interferes with the retrieval of traumatic memories. One of the things that we find when people go through trauma is that they sometimes they can't remember what happened. Well, that's again, their brain being protective. It says, you know what? You don't really want to remember that. That was really pretty awful. So glucocorticoids can go through your brain. I swear that's what happens during childbirth too. Because most of us, you know, even if you have natural childbirth, few hours later, you're like, that wasn't so bad. Yeah. The stress response is the response of an individual to stress. And it depends not only on the stressor characteristics, but also on factors specific to the individual. Where one person might see a Rottweiler and experience an extreme stress response and terror. I see a Rottweiler and I see a great big cuddly teddy bear with huge paws. The same trigger, the same stimulus, but our response to that stimulus is very different. So we need to consider the perception of the stressor for the person. Is it close to a safe zone? When we're talking about danger, you know, somebody getting shot, or, you know, this dog, you know, is this dog in your house? If this dog is in your house, then you may feel unsafe. If this dog happens to live, you know, three blocks down, you might not think anything about it. The similarity to the victim or situation. If you are not in a situation but you can relate to what's going on, it can increase stress and the degree of helplessness that a person feels to change the situation or protect themselves. Think about situations where, and, you know, we'll go back to that apartment living again where someone is living in an apartment and their neighbors are all kinds of noisy, but there's not much they can do. They can't afford to move out, and they just feel like totally helpless to live comfortably and frustrated that they can't live comfortably in the apartment that they're paying rent for. Prior traumatic experiences also impact people's stress response. If they've got prior traumas, they may be more hyper vigilant. When we're more hypervigilant, we tend to respond With a stronger stress response when we're already kind of sitting there jumping, waiting for something to happen, then when something does happen, we jump higher than the person who was kind of flat footed. If you've ever played tennis, you probably can relate to that analogy. If you're standing flat footed on the baseline, it takes you longer and you're slower to respond to the ball coming at you than if you are not flat footed, if you're bouncing on the balls of your toes. So think about hyper vigilance, like that tennis player that's standing at the baseline waiting for that tennis ball to come over and bouncing on their toes. The amount of stress in the preceding month also impacts people's response to to stressors. If you've had a great preceding six months and it's just been fabulous, something happens. You know, you've got reserves built up, you haven't been bathing your synapses in cortisol and glutamate, so you're good. And it's generally not as overwhelming as if you've had a really bad six months and something else happens, your transmission breaks or whatever and you're just like, I just can't take one more thing. So your stress response tends to be additive, if you will. Current mental health or addiction issues can impact your response to a stressor. If you're already anxious, if you're already depressed, if you've already got ptsd, it's going to, you're going to respond differently than if you were in an asymptomatic or remission period and the availability of social support. Sometimes things can be really freaking stressful. But if you've got social support, if you've got people who can provide practical assistance as well as emotional support, you can get through it. And you don't feel like, oh my gosh, the bottom just fell out and I have no idea what I'm going to do. You feel like, oh my gosh, you know, a bad thing just happened. Let me call my friend Bob and he'll come over and help me and I know we can get through this together. Two different ways of looking at things. Now here's another little interesting tidbit. Compared to positive events, negative events, or stress causes greater awareness and recall of event details, leading to a stronger encoding of negative or stressful events. So when something bad happens, let's say you're in a car accident, heaven forbid, you tend to be more aware of what's going on during that situation. You're aware of the people that were there and you May be aware of what led up to, you know, you were driving along and you were more aware of those things because you're aware of more stimuli in the environment. You're in this hyper vigilant mode and you're in, you know, protect me mode. After something bad happens, then things that happen in the immediate aftermath are going to be encoded and associated with that memory. So when you encounter something in the future that was associated with that traumatic memory, you're going to potentially trigger that memory. Since you tend to encode so many more things when you're in that protect me state, then that means you have that many more opportunities to trigger that memory to come back again. The never model of emotional valence and never stands for negative emotional valence enhances recapitulation, which I thought that was a cool little acronym to come up with. It asserts that the greater the number of stimuli related to the unpleasant event that are remembered, the greater the likelihood the person will encounter reminders of the event and leading to increased recapitulation. And, you know, that's kind of what we just talked about. That's important for us to remember. Additionally, Dr. Aaron Ben Zieve asserts that people tend to perseverate on negative information five times more than positive information. So that's the five to one ratio. Not only are we remembering more things associated more stimuli associated with negative events, but we're thinking about it up to five times more often. To put that in perspective. For every bad thing that happens, you need to remember or focus on five good things that happened to balance it out, to balance that negativity out. Well, most of us don't do that. And that is just one intervention that we can use to, to help people start regaining some balance in addition to encouraging them to look at that, whatever that stressful event was and recognize that that's in the past, that was a stressful event that was there. Some of the stimuli we can decondition or help them decondition, counter condition, so they're not as stressful anymore. I worked with somebody one time who was involved in a really bad situation on the interstate, and one of the triggers for his flashbacks was the smell of exhaust fumes. Well, anytime you're driving on the interstate, you could get caught in some heavy traffic and start smelling exhaust fumes, which could trigger that memory for that person. So that was one of those things we wanted to work to counter condition because there were times he was driving with his family to go to Disney World or something, and it was a positive experience. And Helping him be able to recognize that this is a stimuli, it's triggering this memory. But I am here, I am in the present, and I am safe. So that mindfulness and grounding really comes in helpfully. Recapitulation initially leads to repeated HPA axis activation. So when you remember that trauma, you have this stress response like you're there again. Hyper vigilance, whatever you want to call it, it's not necessarily a flashback, but when you smell that smell, when you feel that feeling, when you know, you see something that reminds you you may momentarily be back there or have an emotional and amygdala based response, and that triggers that HPA axis and your body starts going, okay, are we safe we or are we back there? Over time, the continued stress prolongs the inflammatory response through continued activation of the HPA axis, leading to glucocorticoid resistance. Which means when that ACTH goes into the system, into the system, and the CRH and the cortisol, the receptors become less receptive. They're like, yeah, you know, keep it knocking, but you can't come in. Because a lot of times we talk about receptors like being locks and keys. Well, these locks are sealed with superglue and, you know, the receptors are not going to be reactive to that as a way to protect themselves from excessive stimulation. Low cortisol levels or glucocorticoid resistance at the time of exposure to psychological trauma may predict the development of ptsd. What does this mean? Does this mean, is this true only for people who have prior ptsd? Oh, heck no. This means people who've had chronic HPA axis activation who are in that state of hypocortisolism, glucocorticoid resistance, their brain's just going, I can't take any more stimulation. If something happens, they're going to go from 0 to 260. They're going to have a stronger HPA axis response, which could potentially be related to an increased likelihood of developing ptsd, which means that people with prior trauma, we need to help them figure out, you know, integrate that. And chronic stress exposure as well, may predispose people to ptsd. And yes, this is a perfect example of what we see with people who are survivors of domestic violence. You know, they're constantly, constantly hyper vigilant, waiting. You know, they're looking, making sure the hand towels are right, not knowing what's going to set off the abuser. So their HPA axis is on overdrive all the time and eventually it starts to get worn down and eventually Their body starts saying, you know what? I give up. I can't do this anymore. And then their reactions may become more dramatic. And I don't mean dramatic in a negative sense. I mean more marked when something happens. And the longer that they're in that situation where they are persistently hypervigilant, the greater the chances of them developing ptsd, not only for the psychosocial reasons, but also because their HPA axis just becomes completely dysregulated. And when you think about it, when people are in a state of chronic stress, when that cortisol is coursing through their system, something's going on in their life, whether it's generalized anxiety, social anxiety, obsessive compulsive disorder, mania, or, you know, life factors. You know, life is just handing them lemon after lemon. They're exhausted. So what's going to happen to them socially? They're probably going to withdraw from their social supports, or their social supports are going to be like, you know what? I can't deal with all your drama. You're wearing me out. That's a problem. They may not be able to express how they're feeling. And as people become progressively glucocorticoid resistant, develop hypocortisolism, their reactions look more like what, you know, Linehan review referred to as emotional dysregulation. They go from 0 to 260 at the drop of a hat. And people say, you know what, you're overreacting. You just need to rein it in. And they feel very disempowered because people aren't hearing them. And when you've got glucocorticoid resistance, it also means that time to reregulate. Just like in emotional dysregulation, that time to reregulate takes longer because that HPA axis is kind of staying revved up, going, all right, is it safe? Now, Physiological changes due to hypocortisolism. Again, you're not going to need to know all of these individually, but I think it's important to recognize the widespread impact that stress can have on us physically. Because when we are sick, when we are in pain, when we are exhausted, when we are depressed or anxious, we are going to not have a high quality of life. It is to going. Going to impact our work. It's going to impact our relationships. Sustained HPA axis activation causes persistently high levels of corticotropin, releasing hormone, or crh, which eventually causes a blunting of the ACTH response to the CRH stimulation, which basically means at A certain point, the receptors that are responsible for making acthe CRH comes knocking at the door and those receptors say, you know what? No, we're not releasing any more cortisol right now. We just, we ain't got it in us. So that door stays locked. Disinhibition of corticotropin releasing hormone or CRH and norepinephrine can lead to an exaggerated response to acute stressors and a responding corresponding increase in cortisol, which is what I keep talking about. They go from zero to stratosphere. Exposure to additional stressors produces stronger trauma related symptoms in part due to the exaggerated HPA axis response, causing the stressor to have a stronger emotional valence. Okay, so now you've got a client who has persistent HPA axis activation. They're starting to develop glucocorticoid resistance, you know, low corticoid levels and or low cortisol levels. And then something happens. Their spouse announces that they want a divorce or their dog dies or something. And that stressor, you know, that HPA axis is exaggerated, which means they're going to feel more strongly about it than they normally would, which means they're going to encode more stimuli associated with it. Go back to that never theory, and it's going to give it stronger emotional valence. That means it's going to be more potent in that person's mind and associated with more stimuli. So they're going to probably retrigger that memory more. They're going to have more recapitulation. Exaggerated elevation of cortisol during exposure to acute stressors increases the sensitivity of NMDA receptors, which makes the brain generally more vulnerable to excitotoxic stress. When our cortisol levels are elevated and glutamate is going through our brain, it makes our cortisol plus glutamate makes our brain more susceptible to the toxic effects of stress, which results in hippocampal shrinkage. It actually starts killing neurons. The volume of the hippocampus, which controls not only HPA axis and stress responses, but also declarative memory, is reduced due to the excitotoxic environment. So we start literally, well, pretty literally losing brain cells. Those neurons start becoming defunct amygdala activity. Remember, amygdala is that fear area in our brain that is very primitive and responsible for preservation. Amygdala activity increases and promotes hypervigilance and impairs threat discrimination. So when all this is happening, the amygdala goes, all right, the HPA axis has been on guard for far too long. That means this must be a really stressful, dangerous situation. So I'm going to make sure that you're aware and you stay hyper vigilant and, you know, can protect yourself. But that also means that when that amygdala is active, people are having, will have difficulty using that prefrontal cortex to say, you know, that's not really a threat. That's not really a threat. Everything feels like a threat at that point, or virtually everything. So the amygdala activity increases to protect the person, but at the same time, it starts increasing the emotional valence, the negative emotional valence of lots of other things. And people have difficulty discriminating danger, and they just see danger everywhere. Reduced prefrontal cortex volume impairs executive functioning and impulse control. I talked about the prefrontal cortex just a minute ago. That is where we have our higher order executive functioning and impulse control. When that is reduced, then we have more difficulty controlling our emotions, controlling our impulses. And the prefrontal cortex doesn't actually officially finish developing until we're about the age of 24. When the, when people are under the age of 24, their brain is still developing, which makes it even more susceptible to excitotoxic events or injury. And that's important to remember. We need to really help children and adolescents and young adults learn how to manage their HPA axis and reduce as many lifestyle stressors as possible so that they preserve the maximum amount of their prefrontal cortex and hippocampus as possible. Reduced anterior cingulate volume impairs the extinction of fear responses. So normally we can extinguish, extinguish fear responses. After something bad happens, our prefrontal cortex can kick in and go, you know what, that's not a big deal. The anterior cingulate says, okay, you know, maybe I'll take that one off the high alert list. The anterior cingulate is reduced in size too. So stress, chronic stress, chronic HPA axis activation, and trauma all cause notable reductions in important areas of the brain. It's not just cognitive. There are actual, you know, shrink. There's actual shrinkage that happens. Additionally, thyroid hormones become imbalanced, leading to abnormal T3 and T4 ratios, which increase anxiety. So now our thyroid's involved, and we know that hypothyroid looks like depression, hyperthyroid can look like anxiety, sometimes hypomania. But when we start having thyroid imbalances, that also impacts our, our sex hormones and will also continue to throw off not only HPA axis, but The HPG axis and other axes that are out there, leading to a cascade of effects and increased chronic health conditions. Gaba. We're still talking about the effects of chronic HPA axis activation. GABA activity is decreased and glutamate activity is increased. Now, GABA is our natural volume, so increased HPA axis activation means we can't calm ourselves down as effectively glutamate. Remember, that's the one that is responsible for a lot of excitotoxic damage in our brain. Well, that activity is increased. It's our main excitatory neurotransmitter and it gets us going. GABA has profound anxiolytic effects in part by inhibiting CRH and norepinephrine circuits. Patients with PTSD exhibit decreased peripheral benzodiazepine binding sites. Which. What does that mean? That means patients who have experienced trauma or have HPA axis dysregulation, the benzodiazepine, the GABA sites that normally would be receptive and go, hey, you know, let's, let's link up, they're not there. So that even if the GABA is produced, it doesn't have anywhere to go. And if it doesn't have anywhere to go, it can't assert its effects. This may indicate the usefulness of emotion regulation and distress tolerance skills when working with clients. We need to help them reduce their excitotoxicity in order to reduce distress, improve stress tolerance and enable them to acquire new skills. People don't think and remember and learn new skills too well when they're in crisis. We need to help them get to the place where they can learn and remember and focus. Increased dopamine and norepinephrine levels increase arousal, startle response, fear, memory encoding, and increased HPA axis activation in response to recapitulation. So even just remembering a stressor can increase levels of dopamine and norepinephrine. Now you think dopamine? Well, that's the pleasure chemical. Not exactly. Remember, dopamine is our perseveration chemical. It's the, let's go get it, let's keep after this, let's stick to it. And norepinephrine is our focus and excitatory neurochemical. So we are focused, we are energized to get through it and, you know, succeed and survive. There are changes to the ratios of estrogen, testosterone and progesterone which impact the body's ability to modulate its cortisol levels. Wow. So when you're exposed to chronic stress, not only you know, do you have all this other stuff going on, but your sex hormones start getting out of whack and they're responsible for more than just libido. They are responsible for a lot of other factors. For example, estrogen and testosterone can modulate the availability of serotonin. So if they're out of whack, your serotonin is probably going to be out of whack. Prolonged psychological stress suppresses estrogen, causing amenorrhea, which has profound effects on cardiac, skeletal, psychological and reproductive systems. Well, again, estrogen, that's not something we normally talk about in terms of mood. But when we're stressed, estrogen can be suppressed, which has systemic effects. It's not just our mood, it's not just our libido, it's everything. Serotonin levels are simultaneously decreased in parts of the brain, which disrupts communication between the amygdala, that fear processing area, and the hippocampus, which leads to increased vigilance, startle, impulsivity, memory intrusions, hostility, aggression, depression and suicidality. Serotonin levels are decreased in part because of other things, but also because of changes in the levels of estrogen and testosterone. We know we need serotonin to help us modulate our emotions. And I'm not going to go through all of these serotonin receptors I put on here. It's my little soapbox. Suffice it to say that when we talk about serotonin, we are talking about the five HT receptors. And there are at least seven of them. Each one is responsible for something a little bit different. A lot of them are responsible for anxiety, you can look down here, and addiction and appetite. But then some of them, like 5ht1a, which is the receptor that most of your SSRIs target are also responsible for blood pressure, heart rate, impulsivity, memory, mood, respiration, sexual behavior, sleep, sociability. You can go and look at, you know, 5H2B is also responsible for GI motility as well as anxiety, appetite and sleep. It's just interesting to look at all the different things that serotonin is responsible for and then think about, oh my gosh, when serotonin starts getting out of balance, either too much or too little, or the system itself breaks down, then we could start having wide reaching problems. And it may not start with a problem in the serotonin system. It may start with HPA axis activation. It may start with menopause causing hormone changes. It may start when somebody starts taking hormone replacement therapy or birth control pills. It's important to recognize all the things in our body work in synchrony. And when something gets out of balance in any of those systems, it's likely going to affect every system. So modifiable factors. I've painted a pretty grim picture of what happens when we're under chronic stress. And I repeatedly am saying chronic stress and not just trauma, because there is trauma with a capital T that happens because of an acute event. But then there's secondary trauma, secondary victimization, which can happen to us as clinical clinicians, hearing people's worst events and worst experiences and being exposed to that. But it can also be just persistent activation of that threat response system. When there's too much noise, for example, we can't get quality sleep. When we can't get quality sleep, the primitive parts of our brain say, you know what? If you're not rested, then you're more vulnerable to being the one that gets eaten by the hungry lion when it comes chasing us. I told you it was a primitive part of your brain. So what can we do as clinicians? We can instruct people in skills to handle emotional dysregulation. The faster they're able to reregulate, the quicker their brain cells are not being bathed in glutamate and cortisol and all that other stuff. We can help them identify mindfulness skills to be aware of things in their environment that may be making them stressed out in some sort of way so they can mitigate those or figure out how to deal with them. We can teach vulnerability prevention and awareness. When you're sick, when you're tired, when you're in an environment that is not your preferred environment, it can make you feel edgier, crankier, more irritable. Whatever it is, if you are aware of those things, sometimes you can prevent them. For example, if you live in that apartment and your neighbors stay up till all hours of the night and you know that you need to get sleep, you can look into getting noise canceling headphones or earplugs. That. That may work for you. For some people, that doesn't work because they're like, well, if I do that, then I can't hear my kid when he wakes up and is crying. Okay, well, we need to figure out a different solution there, but we need to start looking at ways to mitigate potential things that could create vulnerabilities. And remember, vulnerabilities are those situations that make us more likely to respond with emotional dysregulation that make us more likely to be irritable. Emotion regulation. We need to teach people, how do you deal with your emotions when they happen? You know, how do you deal when you feel anger, what do you do with it? How do you deal with anger? And there's a variety of skills from the acceptance of commitment therapy, dialectical behavior therapy, cognitive processing therapy. There's a lot of different approaches, but people need to learn how to regulate their emotions. And that doesn't mean just eliminating the unpleasant, because we all have unpleasant. Emotions are part of life. That's our body saying, you know what, something's a little wonky here. But that also means increasing the positive. We need to teach distress tolerance skills, you know, DBT101, so people can learn to, okay, when I'm upset, I can handle this, and I don't need to feel powerless and out of control. And we need to teach problem solving skills which will also help people reregulate if they can feel a sense of control or solution to whatever the situation is. Of those exposed to trauma, education about normalization of the heightened emotional reactivity and susceptibility to PTSD in the future may be helpful. Once people have been exposed to trauma or are in a persistently hyper vigilant state, we want to normalize. Why is it they go from 0 to 360? Well, because their brain thinks they're still a threat and it's trying to protect them. Once that's normalized and they don't feel like they've lost control of their body, they understand why it's doing it. They just don't want to do it anymore. People tend to feel a little bit more empowered to take direction. So what are some other lifestyle factors that can contribute? According to the social signal transduction theory of depression, that's a long theory. Perception of social threat by exposure to social, symbolic or imagined threats and adversity upregulate the HPA axis. What is our main source of exposure to these potential symbolic, imagined or social threats? Modern media. Modern media recasts social, cultural and political events and highlights our current vulnerabilities to terrorism and dystopia. 24 hours a day, you know, you turn on that TV, you are going to hear about somebody getting shot or somebody doing wrong or somebody bad stuff. It's depressing. Chronic HPA axis activation can trigger depressed mood, anhedonia, fatigue, psychomotor retardation and behavioral withdrawal. That is major depressive disorder. And exposure to predominantly negative stories in the news results in increased negative emotional responses. Increasing HPA axis activation. Next time you watch the news, just keep a little Tally mark of how many stories that they presented were uplifting, positive, encouraging, and how many stories were depressing or made you feel unsafe or scared. These messages are of increased concern regarding youth who, depending on their developmental level, may not be able to discern that something is being recast from something still occurring, setting the stage for generalized anxiety. I remember those very vividly during Hurricane Katrina because my son was in kindergarten and we were watching it because, you know, we were in. We were in Florida and we were getting a lot of people from Katrina and my agency was working with a lot of them. So I was interested and, you know, needed to be kept aware. So I had that on a lot. And Sean had difficulty. Well, he couldn't discern the fact that that was over. It was a storm, it came through. It's no longer posing a threat to us. You know, the flooding continued and stuff, and there were things that were continuing, but he was having difficulty. The same thing with 9 11. He was too young to really remember that. But I remember it kept being replayed and replayed. And I remember multiple times turning on the TV going, is that another building coming down? And then realizing, no, that was the Twin Towers. They were just recapitulating. And if you think about, if, you know, you were aware of the Twin Towers coming down during 9 11, you probably going back to that theory, you probably remember a lot more about what was going on that day than maybe the next day that something significant didn't happen. Something, you know, I can remember exactly where I was. My mother used to talk about how she remembered exactly where she was when, when John F. Kennedy was shot. Things like that. We encode more information. HPA axis activation in children is also of great concern because youth and adolescence is a time of rapid brain development, making it more susceptible to injury regarding social media. And we've talked about before about the fact that it's hard to decide whether social media causes problems or problems attract or social media attracts people who already have problems. But in 2016, 98% of young adults used approximately 7.6 different social media sites regularly. And people who spent more than 120 minutes on social media per day or who visited social media sites more than nine times per day has significantly increased odds of depression. Now that sounds like a lot, but have you ever gotten on Facebook and started scrolling on your social media feed or Pinterest or somewhere else Instagram and just kind of lost track of time? Some people do that a lot. Increased time online is associated with decline in communication with, in real life, family Members, reduction in the Internet users in real life, social circle, reduction in sleep and increased feelings of depression and loneliness. And there's a strong positive correlation between the amount of social media usage and perceptions of isolation. So when people are on social media, a lot of times it's activating that HPA axis and you gotta wonder for what benefit. Now, sleep. According to the cdc, one in three adults does not get enough sleep. So that means, you know, one in three of y' all are not getting enough sleep right now. And, you know, I can tell you I'm one of them. I like my sleep. There are many causes of sleep deprivation in American culture. Sleep disruption or deprivation can impair and lead to hyperactivation of the HPA axis and circadian rhythm disruption. So once your sleep's impaired, then it can lead to your circadian rhythms getting off. And circadian rhythms are far bigger than just when you wake up and when you go to sleep. It also controls the release of your hunger and satiation hormones as well as cortisol levels and lots of other stuff. Yeah, cortisol is intertwined in your circadian rhythms. When your sleep is disrupted, there are significant increases in plasma cortisol levels, that stress hormone, which also causes the release of blood glucose, reduction in serotonin and melatonin. So reduction in serotonin, which is involved in mood calming, pain perception and lots of other things, as well as melatonin, because melatonin is made from serotonin and melatonin is that hormone that helps you drift off to sleep and increases in norepinephrine, so your focus chemical may be increased. A recent study of the National Health and Nutrition Examination Survey found inadequate intake of vitamin A, calcium, selenium, carbohydrates, vitamin D and lycopene to be associated with poor sleep. Which again is why it's so important to have people really be mindful of what they're eating. Doesn't mean they have to eat super clean, but being mindful to make sure they're getting all of the nutrients they need. Low levels of zinc and magnesium are implicated in the development of depression through the overactivity of the HPA axis. So zinc and magnesium themselves can cause mood symptoms. A significant negative correlation was found between sleep quality and low quality carbohydrate intake from processed foods. So people who ate more poor quality carbohydrates from highly processed foods had poorer quality sleep. The more junk food they ate, the worse their sleep got. Skipping breakfast and eating irregularly are also strongly associated with hypoglycemia which also causes chronic HPA axis activation and poor sleep quality. When we get hypoglycemia, our body determines there's a threat. We don't have enough energy to go, so it activates that HPA axis releases the cortisol, cortisol causes the release of blood glucose and ah, okay, we're not hypoglycemic anymore until we are again. Lack of access to natural light shift work and overnight work prohibit the body from receiving cues from the environment which would help us regulate a 24 hour circadian rhythm. Our bodies are naturally on more of a 26 hour rhythm, so we rely on cues to keep it in that 24 hour window. When people's circadian rhythms are out of whack, they may have insomnia. At night they're laying in bed trying to get to sleep, they can't. They're tired, but can't sleep. They get frustrated. HPA axis activation, they wake up in the morning, they gotta drag their happy butt to work and they're exhausted all day long. So they start using caffeine and nicotine in order to stay awake, which further activates that HPA axis. Blue light from digital devices and televisions prevents the body from receiving the cue that it's time to make melatonin and go to sleep. 26% of adults have sleep apnea, which is associated with HPA axis activation and sleep apnea. People quit breathing very briefly when they're snoring, which the body deems as a threat. Go figure, you quit breathing, that's kind of a threat. When people started using CPAP machines, however, their cortisol levels went back down, so they can have sleep apnea. But if they use the CPAP machine, it's not going to impact that HPA axis nearly to the same degree. Nighttime noise causes frequent awakening, less deep sleep and increased subjective disturbance and is correlated with an increased risk of HPA axis activation, cardiovascular disease, depression and anxiety. If you've ever had an infant at home, you know what I'm talking about here. You awaken. And people with infants at home a lot of times sleep lighter anyway because they are more hyper vigilant. They're trying to protect that baby. That's a built in, you know, survival of the species kind of response. But that can contribute to difficulty getting quality sleep. 20% of Americans are considered heavy drinkers. Within the USA, it's estimated that the societal cost of alcohol related sleep disorders exceeds $18 billion a year. Alcohol does decrease the time it takes for people to fall Asleep, which, you know, a lot of times is what they want, and it increases the quality of their non rem sleep during the first half of the night, which, you know, score, that's what they want. But the last half of the night is completely disrupted as the sedative effects of the alcohol wear off and the anxiolytic effects kick in. Alcohol stimulates HPA axis and repeated alcohol exposure leads to a blunted HPA axis response. Again, you know, you keep revving that thing up, eventually whatever's causing it to rev up isn't going to cause it to rev up anymore. And this is associated with depressive symptoms, anhedonia, fatigue and behavioral withdrawal as well as widespread inflammation. We know that there's a direct correlation between high levels of systemic inflammation, those inflammatory cytokines that are released by the HPA axis. Depression as well as autoimmune diseases, nicotine, recent nicotine use and lower dependence is associated with increased activation of the HPA axis. So when people aren't very dependent on it, their body's not used to it and they use produces a more potent HPA axis response. But as their body develops a tolerance to it through persistent exposure, the response of the HPA axis decreases, leading to glucocorticoid resistance and tolerance. We do want to recognize that there's a significant reciprocal relationship between smoking and sleep disturbances. As smoking goes up, sleep disturbances tend to increase. Caffeine is found not only in coffee, but also soda, chocolate, over the counter, migraine medications, decongestants, some diet and workout supplements. When caffeine is paired with a mental or physical stressor, mental or physical stressor the cortisol and adrenaline levels exceed when caffeine or stressors were encountered independently. So people who take a caffeine shot before they go to the gym, physical stressor are going to have higher levels of cortisol and adrenaline than if they had just taken the caffeine or just worked out. Again, we want to consider, are the benefits of having these increased cortisol and adrenaline levels worth the costs? A healthy gut microbiome has over a thousand species of bacteria and can decrease depression and anxiety, regulate sleep, appetite and improve cognition. An unhealthy gut microbiome contributes to an exaggerated HPA axis response though due to the vagal nerve. And there's the gut brain axis where the gut communicates with the brain via the vagus nerve. Insufficient levels of tryptophan with the help of iron, magnesium, B6, folic acid, vitamin C and zinc all can contribute to dysfunction. Frequent intake of caffeine or other stimulants can also cause serotonin levels to become depleted. And finally, sedentary ness. Exercise has been shown to moderate both inflammatory cytokines and oxidative stress. We've all heard about oxidative stress and how it makes us age and stuff. And we know that inflammatory cytokines are associated with high cortisol levels as well as depression and autoimmune disorders. Low intensity exercise, and I mean really low intensity with at a 40% of your VO2 max, has been shown to reduce cortisol levels and increase serotonin contributing to the relaxation response. So exercise can help you relax, but what is 40%? And I use the carvonen formula because that takes into account not only your age, but your fitness level. And it's 220 minus your age, minus your resting heart rate, times the heart rate percentage you're trying to get, plus your resting heart rate added back in. So for me, that's 220, minus 50 is 170. 170 minus 50, which is my resting heart rate, is 120. 120 times 4. To get 40% of my VO2 max gives me 48. And then I add back in my resting heart rate, which is 50. My 40% of my VO2 max is 98 beats a minute. You know, that's pretty much walking upstairs for me or, you know, sweeping the house. My point being, exercise at a level that reduces cortisol and increases serotonin does not have to be something super intense. So most of our clients are physically fit enough to raise their heart rate to 40% of their VO2 max without feeling unduly taxed. Obviously, they need to get doctor's clearance, yada, yada, yada. But I want people to get away from this notion that they've got to go to the gym and break this huge sweat. It's just not the case. Gardening, walking the dog, walking around the yard, cleaning any of those things. In summary, some level of activation of the HPA axis is necessary for motivation and energy. We need to get that get up and go. When the HPA axis is activated in response to stress, it impacts the balance of dopamine, serotonin, norepinephrine, gaba, and glutamate, as well as our thyroid hormones. And it modulates the release of our inflammatory cytokines, estrogen and testosterone. It also impacts insulin sensitivity and balance, which is, you know, especially bad news for people who have diabetes. Sustained activation of this bidirectional system, bidirectional meaning when we get stressed it triggers the HPA axis. The effects of the HPA axis can further perpetuate itself. You know when your HPA axis stays activated, you're not going to sleep well. Sleep deprivation activates the HPA axis so you can have this bidirectional system. So sustained activation of this bidirectional system results in brain changes which alter hormones and monoamines or your neurotransmitters which lead to further HPA axis activation. Pre existing issues causing hypocortisolism set the stage for what I call the Flat and the Furious. Toxic levels of glutamate are excreted upon exposure to stressors leading to increased stimuli encoding and enhanced recapitulation. So they go from flat to crisis state. This points to the importance of prevention and early intervention of adverse childhood experiences as well as chronic stress so people don't have that exaggerated HPA axis response. Additional information about the HPA Axis, Gut health and Adrenal Fatigue can be found in our videos on our YouTube channel or the Counselor Toolbox podcast. But basically the take home message is American lifestyles contribute to HPA Axis activation, which contribute to depression, withdrawal, social isolation and development of bad habits like smoking and excessive use of caffeine. So we really want to help people, you know, start unraveling all of the things that are going on so they can identify ways to improve their health and happiness. Between writing notes, filing insurance claims and scheduling with clients, it can be hard to stay organized. That's why I recommend Therapy Notes. Their easy to use platform lets you manage your practice securely and efficiently. Visit therapynotes.com to get two free months of TherapyNotes by just using the promo code CEU when you sign up for a free trial at therapynotes.com. 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@allce.com podcastceus that's allceus.com podcastceus to sponsor an episode of Counselor Toolbox and reach over 50,000 clinicians per week. Go to allce.com Sponsor thank you.










