Hello, my name is Dr. James Rustad, and I'd like to welcome you to our APA workshop, Caring for Veterans. For introductions, our presenters include myself, Dr. Douglas Nordzy, Dr. Geraldine McWilliams, Dr. Sam Korman, and Dr. Ivan Cheek. We have no conflicts of interest to report. Dr. McWilliams and I are employed by the U.S. Department of Veterans Affairs, but the opinions expressed in this presentation do not reflect those of the VA. With respect to the following presentation, there's been no relevant direct or indirect financial relationship between the parties listed above and or spouse or partner, and for any for-profit company, which can be considered a conflict of interest. Getting started. Providing mental health care to veterans requires empathy and specialized knowledge. This seminar focuses on treatment issues facing clinicians working with veterans. Since September 11th, over 2.5 million U.S. military service members have deployed to Iraq and Afghanistan. This represents the longest continuous period of sustained operations in U.S. history. For learning objectives for this workshop, one is to understand that veterans of these conflicts suffer a wide variety of war-related neuropsychiatric consequences, including post-traumatic stress disorder and traumatic brain injury. We'll be defining the following terms, moral injury, core beliefs, and post-traumatic growth. We'll identify that individuals with PTSD are at increased risk for medical conditions, particularly cardiovascular disease. We will be reviewing evidence-based psychotherapeutic modalities and psychopharmacologic treatments of PTSD and applying screening tools important for the workup of veterans with mental health symptoms, including the Columbia Suicide Severity Rating Scale. And at the conclusion, we will explore the use of physical exercise for managing allostatic load, more on that later, and brain recovery. So I will start with a historical background of war-related neuropsychiatric consequences with a particular focus on post-traumatic stress disorder. I remember seeing this when I was a resident at the University of Miami working at the Miami VA. This sign was posted up, and I thought it was profound and stuck with me that we must remember that not all wounds are visible. In this section, I will introduce the concept of Greek mythology as a metaphor for the difficulties of post-combat readjustment to civilian life. Prior to the Trojan War, Odysseus was reluctant to go to war, not because he was afraid of fighting, but because an oracle warned him that if he fights, his post-war journey will be lengthy. And as you know, after a long absence post-deployment, a soldier can return to a household that's dangerously altered and threatened by outside forces. Odysseus faced many obstacles in his quest to get back home or get back to where he once belonged, which is Beatle's references from the great Paul McCartney. One of these barriers was Circe. She was a powerful enchantress who turned Odysseus' soldiers or sailors into pigs. Odysseus was able to resist her magic with the help of Hermes. They became lovers and had three children, and she ended up releasing his soldiers from her spell. And there you see Circe with the pigs. Circe helpfully warned Odysseus about the sirens, who were enticingly captivating mythical creatures with irresistibly beautiful singing voices, who lured soldiers to their doom. Odysseus craved to hear their music, so he had himself tied to the mast of his ship while his sailors put beeswax provided by Circe in their ears. Circe warned that the sirens were dangerous and wanted to kill the sailors. Their song lyrics were misleading, of course. They sang, the songs we sing will bring you peace. The great sting of the band, the police, once sang, you consider me a young apprentice caught between the scylla and Charybdis. And that's a poetic way of saying stuck between a rock and a hard place. And indeed, Odysseus faced the scylla and Charybdis positioned at the Strait of Messina between Italy's Boot and Sicily, and they were a six-headed beast in a powerful whirlpool. Adjustments in lifestyle often occur after veterans return from combat. The Vet Center offers readjustment counseling for veterans and their family in the transition from military to civilian life. Now moving forward to historical descriptions of post-traumatic stress disorder, I'll describe from the American Civil War, Da Costa syndrome. Now you'll notice that the symptoms included rapid pulse, anxiety, and difficulty with breathing. And this is for soldiers that had experienced combat in the Civil War. And that is quite reminiscent of some of the hyperadrenergic states that are often seen in PTSD. Many of you are likely familiar with this term called shell shock. In World War I, soldiers experienced a reaction to explosion of artillery shells. And soldiers who had not been near explosions, interestingly, also experienced similar symptoms. And another word to describe shell shock was called war neurosis. So as you can see, these are the precursors to what we call PTSD now. Battle fatigue, combat stress reaction. As you can see, American soldiers at Iwo Jima. In World War II, it was seen that benefits of military unit relationships and support became focus of preventing stress and promoting recovery. The VA, including our Burlington Lakeside Clinic, has peer support specialists who coordinate activities like fly fishing and skiing for emotional and physical rehab. Our veterans who are helping veterans are Josh Karisimov and Daphne Zensey. And they're really able to connect with other veterans with these activities. So I think we've learned from some of the lessons from these beneficial relationships which occurred among soldiers in World War II. Researchers studied veterans of the Vietnam War, survivors of the Holocaust, and survivors of sexual assault. And in 1980, the APA added PTSD to the DSM-3. Now going on to deployments, combat deployments affect the physical and mental health of veterans. As you can see, common mental health conditions encountered in veterans include PTSD, TBI, and sleep disturbances. As Dr. Chick will be talking about later, there's elevated suicide risk, especially among combat veterans and veterans with PTSD. And we'll be discussing different ways that we can evaluate and manage these type of symptoms. There are also psychological stressors which occur in combat deployment, including anticipation of combat and separation from home and family. Now we will introduce the concept of moral injury. Service members are frequently challenged with moral and ethical dilemmas during war and may perpetuate or fail to prevent acts that go beyond the bounds of deeply held beliefs. One example of a moral injury would be if a soldier follows orders from a commander that they don't personally agree with, and then they feel like it's violating their moral code. So that would be an example of moral injury. And importantly, this can cause long-lasting impairment. So we're encouraging people to screen combat veterans for suicidality, post-traumatic stress, traumatic brain injury, and furthermore, moral injury. And we're going to talk about how to screen for that. It's defined as damage done to an individual's core morality or moral worldview as a result of a stressful or traumatic life event. And it's actually been shown to significantly impact mental and physical health outcomes. Here is the Moral Injury Events Scale, which is widely available. And as you can see, some of the different examples, being troubled by having witnessed others' immoral acts, acting in ways that violated their own moral code, such as the example that we talked about earlier, feeling betrayed by leaders they once trusted. And there are many soldiers who had ambivalence about the wars that they actually fought in. Moving on to core beliefs. Core beliefs and ruminations may play a key role in psychological outcomes following traumatic experiences. And these are the different examples of core beliefs. And this is really a concept from cognitive behavioral therapy and cognitive processing therapy, which is a CBT modulated to help to treat PTSD. So some of the different mindsets that people can take, and these can either follow the trauma or pursue the trauma, would be a feeling of powerlessness versus being in control, feeling inadequate versus being good enough, feeling vulnerable versus being a self-protector, and feeling in danger versus a feeling of survival. Interestingly, after traumatic experience, some individuals experience positive psychological outcomes. And this is called post-traumatic growth. Now it's found that those who ponder what's happened more thoughtfully and deliberately end up having better outcomes than those who have intrusive rumination. Intrusive rumination itself is positively related to PTSD. So deliberate rumination is intentional cognitive work, while intrusive rumination really represents a symptom of PTSD that can appear. Now I will turn over things to Dr. Korman, who will discuss medical conditions associated with PTSD. Thank you, Dr. Rustad. I'm here now to talk about medical conditions associated with PTSD. PTSD occurs in as many as 20% of military veterans. And although there are changes in diagnostic criteria of the DSM that are occurring, and this might slightly change the prevalence, whatever the prevalence actually is, there will be biological alterations associated with this chronic PTSD. And these PTSD-related psychobiological abnormalities might increase the risk for medical illness among affected individuals. Here we're going to talk about the concept of allostasis. So Schnur and Jankowski proposed that there's a conceptual model of allostasis and allostatic load, which might serve as a mechanism through which stress, and more specifically stress through post-traumatic stress disorder, might precipitate medical illness. Allostasis is the adaptive process of maintaining homeostasis by expanding and directing energy towards challenges, while allostatic load represents the cumulative cost to an organism of enduring repetitive cycles of adaptation. So as you see in the picture here, you know, you have these two elephants or three elephants on a scale, and the idea behind allostasis is that when there's a particular stressor, your body is going to shift a certain amount of energy towards the area of the body that needs it in order to respond to that stressor. And this brings up the human stress system. The human stress system has evolved to maintain allostasis, particularly in response to significant stressors. The stress system is comprised of three major components. The hypothalamic pituitary adrenocortical axis, otherwise known as the HPA axis, the locus coeruleus and norepinephrine sympathetic system, which includes adrenergic mechanisms in both the central nervous system and the peripheral sympathetic nervous system, and the immunological system. So different HPA axis alterations might be associated with different aspects of PTSD, including risk for the development of PTSD. So interestingly, some features of the HPA axis might be altered even before the exposure to a focal trauma. If there are underlying HPA axis predispositions towards the development of PTSD, those predispositions might represent baseline alterations. Now, here's a quote from one of Dr. Rustad's fellowship colleagues, Dr. Ivkovic, who used to say, enough sympathy, how about some parasympathy? Well, we're going to talk about the sympathetic nervous system right now, and under the understanding of allostasis and allostatic load, when there's a particular stressor, our sympathetic nervous system goes into one of two modes, either fight or flight. If you take the example of Netflix's number one documentary, Tiger King, if you have a wild tiger that's going to attack you, if you act like Joe Exotic, you pull out a pistol and you shoot the tiger. That's the fight. If you're overly empathized, you might have a lot of fear and energy and activation and try to run. So sympathetic and parasympathetic activity in those suffering from PTSD, these people may experience increased startle response and disrupted sleep related to increased sympathetic reactivity. In addition, the balance of sympathetic and parasympathetic activity can be disrupted in PTSD. So there will be an autonomic imbalance, too much sympathetic, not enough parasympathetic. This can result in increased basal activity of the sympathetic nervous system and intermittently exaggerated demand on the cardiovascular system, which is your allostatic load, a lot of shifting of energy and stress from stress to the cardiovascular system. Additionally, individuals with PTSD experience higher catecholamine concentrations, which makes sense given the locus coeruleus involvement, and heart rate than do those without PTSD. Pittman and colleagues demonstrated exaggerated physiologic arousal in Vietnam combat veterans during recall of index traumatic events. So here there was a study in which Vietnam vets would read scripts detailing their combat experience. They'd measure heart rate, skin conductance, and frontal EMGs, and they all showed increased physiologic response as compared to controls. Furthermore, high heart rate represents a major risk factor for recurrent cardiac events and mortality in patients with cardiovascular disease, and we know that sympathetic activity in PTSD patients is oftentimes elevated. So the parasympathetic nervous system promotes calm behavioral states and reduces sympathetic reaction to stress, which we know from previous slides is parasympathetic system is not as prominent. In a study here in which there were, excuse me, there's a 2007 study which evaluated heart rate and heart rate variability amongst patients who have already suffered myocardial infarctions. This included 34 male Croatian war veterans already diagnosed with PTSD compared to 34 age-matched control males who had already suffered a myocardial infarction but were non-veterans and did not have diagnoses of PTSD. And they found that war veterans with PTSD showed higher sympathetic activity at baseline. They had higher heart rate, however, there was no statistically significant difference in heart rate variability, which is an index of parasympathetic nervous system withdrawal. And this negative finding was attributed to the relatively small sample size of analyzed patients. Now we're going to talk about diminished vasoreactivity in PTSD patients. So chronic stress as experienced by veterans with PTSD has been showed to diminish vasoreactivity. And one of the theorized methods for this is that there is a decreased amount of biomarkers for synthetic capacity of nitrous oxide production, which helps with vasodilation. So a 2016 study out of the San Francisco VA, including 214 outpatients, were tested for endothelial function and evaluated for PTSD. The endothelial function evaluation was done through endothelial-dependent flow-mediated vasodilation at the brachial artery, which is basically measuring it through a blood pressure cuff. The 67 patients with PTSD were independently associated with having lower levels of flow-mediated vasodilation as compared to controls. So while it's unclear if lower flow-mediated vasodilation is directly associated with cardiac pathology or mortality in PTSD patients, in the general population, we do know that diminished vasoreactivity is associated with cardiac pathology. And one—oh, excuse me. So something further is the idea of increased inflammation. So increased inflammation may represent a mechanism by which PTSD can contribute to atherosclerotic cardiovascular disease. Patients with PTSD showed a low-grade systemic pro-inflammatory state, which correlated with PTSD symptom-level burden. Relevant to this is a 2011 study that investigated the association of PTSD to atherosclerotic coronary artery disease and mortality, and they did this by measuring coronary artery calcium scores. So there were about 637 veterans with known coronary artery disease, and they underwent calcium—coronary artery calcium screening, and then were also evaluated for PTSD. The subjects with PTSD had a higher prevalence of coronary artery calcium, a higher presence of it, and the coronary artery calcium scores were higher than in non-PTSD counterparts. And PTSD was found to be an independent predictor of the presence and extent of atherosclerotic coronary artery disease. And at a mean follow-up of about 42 months, the death rate was higher in PTSD patients, and there was a significant associative link between PTSD and mortality and between coronary artery calcium and mortality. So patients with PTSD and coronary artery calcium scores had a higher relative risk of death than those without PTSD and with a coronary artery calcium score of zero. And those with PTSD and a coronary artery calcium score of zero did not have a different risk from those without PTSD and no coronary artery calcium score. In relation to this and to the endothelial dysfunction, a hypercoagulable state might set the stage for acute thrombotic cardiovascular events in PTSD. PTSD is also associated with poor health behavior such as physical inactivity, medication non-adherence, smoking, all of which are major independent risk factors for initial and recurrent cardiovascular disease events. Metabolic syndrome is an important risk factor for cardiovascular disease and the results from a recent meta-analysis of nine studies show that the prevalence and risk of metabolic syndrome and its components, central obesity, high blood pressure, low concentrations of HDL, elevated concentrations of triglycerides and hyperglycemia are increased among individuals with PTSD. Individuals with PTSD had almost a doubled risk for metabolic syndrome. Taking that even further, type 2 diabetes is another strong independent predictor of cardiovascular disease risk and a recent relative risk meta-analysis comparing controls demonstrated a 50% increased risk for type 2 diabetes for patients with PTSD compared to patients without PTSD. So here's a list of all the stuff we just talked about, potential etiologies of increased cardiovascular risk in patients with PTSD. You have hypothalamic-pituitary-adrenal axis alterations, autonomic imbalance, worse endothelial function, increased inflammation, physical inactivity, metabolic syndrome, and type 2 diabetes. And the consequences for these, these cardiovascular consequences for individuals with PTSD include increased risk for incident coronary artery disease, coronary heart disease, increased risk for incident hypertension, and increased risk for incident heart failure. In conclusion, veterans represent a very vulnerable population to consider given the allostatic burdens of frequent deployments, combat exposure, traumatic brain injury, and military sexual trauma. Psychiatrists must be vigilant in screening for PTSD in veterans as this condition does seem to predispose individuals to the development of medical illnesses such as metabolic syndrome, type 2 diabetes, and cardiovascular disease. Prospective research is still needed to determine whether the treatment of PTSD can decrease the development of medical illnesses. However, there is no evidence that it can decrease the development of medical illnesses. However, targeting PTSD symptoms could potentially reduce the burden of medical morbidity and mortality, thereby improving quality of life and function. And with this, I'm going to hand it off to Dr. McWilliams to talk about evidence-based treatments for PTSD. Thank you, Dr. Corman. Hello, this is Geraldine McWilliams, and I will be talking to you briefly about evidence-based treatments for PTSD. In 2017, the VA and Department of Defense released an update to their clinical practice guidelines for the management of PTSD, an acute stress disorder. They provided guidance based on available evidence with the goal of enhancing assessment and treatment for veterans, optimizing outcomes and quality of life, minimizing complications, and emphasizing patient-centered care. The algorithm includes arriving at the appropriate diagnosis of PTSD and then creating a treatment plan. The first recommended treatment strategy is use of an individual, manualized, trauma-focused psychotherapy with a primary component of exposure and or cognitive restructuring. Examples of exposure therapy would be prolonged exposure therapy or written exposure, and cognitive restructuring would be an approach like cognitive processing therapy. Often, there are barriers to receiving this type of treatment. So if this type of therapy is not readily available or not preferred by the veteran, the next step would be to offer pharmacotherapy or, and or actually, a non-trauma-focused therapy. So as a psychiatrist, this is usually the point at which a veteran may arrive at my office. And to review this slide here, the first-line choice of medication for treatment of the core PTSD symptoms would be sertraline, fluoxetine, paroxetine, or venlafaxine. These medications address PTSD symptoms and are also helpful for the psychiatric disorders that are frequently comorbid with PTSD, such as major depression, panic disorder, and social phobia. I would recommend choosing from this list with attention to the veteran's history. For example, sertraline is a good choice for those with several medical comorbidities and a long medication list, as it has the most favorable drug-interaction profile of these choices. I would also counsel veterans regarding the withdrawal syndrome associated with paroxetine and venlafaxine. These may not be good choices for someone who has difficulty with taking medications on a daily basis and may be more likely to drop out of treatment completely when they experience the discomfort of a withdrawal syndrome. Citalopram, escitalopram, and fluvoxamine have not been studied enough in the treatment of PTSD to be recommended as effective strategies. Mirtazapine, tricyclics, and MAOIs are second-line treatment options. Atypical and antipsychotics are not considered effective monotherapy or augmentation strategies for PTSD. And the evidence does not support use of anticonvulsants as monotherapy or augmentation for PTSD core symptoms. And then finally, to address the use of prazosin in treating PTSD, we have to look at a VA-based study from 2018, which was published in the New England Journal of Medicine. It looked at the efficacy of prazosin in treatment of symptoms of PTSD and nightmares. This multi-site trial showed no difference between effects from prazosin and that from placebo. However, looking more closely at the study, it is notable that many of the veterans included were generally stable, and they may not represent all populations of veterans with PTSD. I think this highlights the possibility that prazosin may still be an effective treatment option, especially for those with more hyperadrenergic symptoms. As a geriatric psychiatrist, I can appreciate the nuances and realities of needing to use benzodiazepines, but I also want you to know and want to emphasize, it is important to just say no to using them when you are treating PTSD. A 2015 systemic... A 2015 systematic review on the effects of benzodiazepines demonstrated major risks and had significant impact and has led to system-wide efforts at the VA to deprescribe and avoid use of this class of drugs. We now know that use of benzodiazepines around the time of a trauma can lead to increased risk of developing PTSD, and then using them as treatment for PTSD causes worse overall severity of symptoms, worse outcomes in psychotherapy, and worsening in symptoms of depression, aggression, and substance use. Just say no. Finally, I would like to emphasize that the treatment of PTSD is an active area of research. Our colleagues here at the National Center for PTSD and White River Junction, Vermont have proposed catering treatments for different PTSD phenotypes. As I previously kind of touched on when considering use of prazosin for those who present with more hyperadrenergic symptoms, Drs. Friedman and Bernardi highlighted phenotypes such as fear-based, dysphoric, dissociative, and externalizing, and allowing for this classification may provide a more individual treatment plan for a veteran. Thank you very much for your attention. I will now turn it over to my colleague, Dr. Cheek. Can you folks hear me? Yeah, yeah, you sound great. Looks good too. Okay, great, thank you. And then same thing, would you mind just going forward and backwards really quick just to make sure that's working for us here? Yeah, awesome, cool. Thank you so much. Okay, thank you. Thank you, Dr. McWilliams. My name is Dr. Ivan Cheek, and I'm a third year psychiatry resident. I'll be going ahead and talking about suicide prevention today. So to start with some statistics, in 2016, 45,000 people in the U.S. population completed suicide. That gives us a total of 1,000 suicides. That gives us a rate of about 14 per 100,000. Between the years 2005 and 2016, in that decade, veteran suicide rate increased about 25%, and that's roughly one and a half times higher than the general population. A number that gets often cited is that roughly 20 veterans die each day by suicide. And if we take a closer look at those numbers, we see that the total counts of suicide happen the most in the older age demographic. As you can see here, in the veteran population age 60 and older, they have a much higher number of suicides. However, if you look at the rate per 100,000, we actually see that the youngest veteran population, those between 18 and 39, actually have the highest rate. So to talk about suicide, we wanna be able to define it, and it's defined as the act or instance of taking one's own life voluntarily and intentionally. So again, this is not, it's not an accident, it's not a car accident. It's purposeful, deliberate, voluntary and intentional. It's the 10th leading cause of death in the US, but the second leading cause among children and young adults. And there's no specific one cause of suicide, which makes it a very difficult disease to treat. You know, if we look at a disease like type 2 diabetes, we have a good understanding that hyperglycemia can affect insulin sensitivity. It could damage our vasculature, leading to kidney disease, affect our eyes, cause heart attacks, strokes. There's this kind of linear progression, and we have a better understanding about that. However, with suicide, it's much more fluid and dynamic, and it's this interaction of risk factors, protective factors, life events, access to support and lethal means, sometimes even in that exact moment in time. So it's much more difficult to study and treat suicide. And this occurs in both veterans and non-veteran population. However, even though it's very difficult to study and treat, there have been attempts to create a model to understand this veteran. A popular model is called the stress diathesis model for suicide. And when I first read about this, the first thing I did was look up the definition of diathesis. And basically, it's a constitutional predisposition toward a particular state or condition, especially one that is abnormal or diseased. So it suggests that patients who have suicide attempts have been exposed to major stressors, but that's actually not enough. At the same time, they had a predisposition towards a response that results in suicide. Many people have traumatic events in life. They have lots of major stressors and never progressed to the point of having suicidal ideation and never progressed to the point of having a suicide attempt. So this model suggests that there's two things in place. There's a major stressor, and then there's a predisposition to respond in such a way that leads to suicide. Some suggestions that have been made to make someone have a predisposed state includes different genes for serotonin metabolism or epigenetic factors as a result from early childhood trauma. Thomas Joiner had another model, and he called his the psychological theory of suicidal behavior. He states that suicide is carried out in individuals that have two things. They have the desire and the ability to die by suicide. And in his model, there are three major components. The first two are perceived burden and the degree of social isolation or low belonging. Those two components comprise the desire to wanna die. Next, we have the ability to cause lethal injury as the second component. And initially, I thought this was only relating to things such as having access to guns and ammunition, stockpile of medications or being close to bridges or something like that. But actually, it's a little bit more. It's the ability to overcome instincts of self-preservation. So evolutionarily, this makes a lot of sense. It's very difficult to overcome that. Not being afraid of dying is huge. And if someone is able to overcome those instincts, that is a critical part in this model to have the ability to die by suicide. Next, we have Klonsky and May's three-step theory of suicide. And in this theory, they use concepts from Joyner's model, but they suggest that suicide actually proceeds in kind of a stepwise manner. And why this is important is that it suggests that these different steps can be researched and intervened separately from different angles so that we can do the most good. So in their model, they suggest that patients go through this mindset, which is one, are they in pain and feeling hopeless? If they are, then they're more likely to have suicidal ideation. If their pain exceeds their connectedness, then those ideations will become much stronger. And finally, if they have that capacity to attempt suicide, then finally, that would more likely lead them to have a suicide attempt. So I'm a resident, and when I get the page at midnight or the page at 2 a.m. to go in and evaluate a patient in the emergency room, I'm not exactly thinking of which step in those models they may be in. I'm really kind of looking at the patient as a whole and trying to get the best picture of them so that I can make my assessment. And more often than not, I think most clinicians will kind of take the same approach in that they look at risk factors and they look at protective factors. When I'm evaluating a patient in the emergency room, I think about things such as, did they have a prior suicide attempt? Do they carry existing mental health diagnoses? Do they have major recent stressors? And do they have access to lethal means, which in our veteran population is particularly important, as I'll talk about later. Then I also think about what are the protective factors? Do they have coping skills? Do they identify reasons for living? Do they have access to care? And do they have that sense of connection with other people? So again, these are the factors that we're constantly thinking about when we're evaluating someone and deciding whether or not we feel it's safer for them to go home or they need to be admitted to the hospital. I do want to take a step back and look again at some veteran specific statistics in that we understand that veterans as a population on the whole have a higher risk of suicide, but a common myth is that deployed veterans have the highest risk of suicide. The highest risk of suicide, but that's actually not the case. If we look at this graph on the left, the black line is the risk in the general US population and among deployed veterans. Among deployed veterans, we see they have a 41% higher risk of suicide in the deployed side, but in the non-deployed veterans, their risk is actually 61% higher. The other point I want to highlight is that the rate of suicide was greatest within three years of leaving the service. So again, when I'm seeing a veteran in the ER and I know they were recently discharged, then that's going to be a risk factor in my mind, as well as maybe whether or not they had a deployment or not. This chart here shows the method of suicide among veteran and non-veteran US adults in 2016. And I want to highlight one thing in particular here. If we look at the percentage of non-veteran adult suicide deaths via firearm, we see it's just under 50%, 48.4. However, if we go to the next column and we look at veteran suicide death, that goes up to almost 70%, so almost three-fourths. So firearm evaluation when doing a safety eval is always important, but it's particularly important when working with veterans because this is definitely a higher risk for that population of using a firearm to complete their suicide. In talking about the history of suicide prevention at the VA, there are two names that I want to highlight. One is Joshua Lee Ombig. He lived from 1983 to 2005. He was in the Army Reserve, served in Iraq. When he returned from his deployment late in 2005, he actually completed suicide in his parents' driveway just before Thanksgiving. It was extremely traumatic, and this led to a lot of advocacy work and ultimately prompted legislation called the Josh Ombig Veterans Suicide Prevention Act. Several years later, there was another veteran named Clay Hunt. He was a Marine, served in Iraq and Afghanistan. And after returning from his multiple deployments, he had difficulties accessing the VA and getting help from them and the benefits. And after his suicide, there was additional legislation passed as well. So the Josh Ombig Veterans Suicide Prevention Act, when it was implemented in 2007, it provided training and education on suicide risk factors and how to work with veterans who may be suicidal. It designated a suicide prevention coordinator, created 24-hour services to be made available in crisis situations, and it established peer support counseling programs. The Clay Hunt Suicide Prevention for American Veterans Act in 2015 required independent contractors to evaluate mental health services, required maintenance of up-to-date information on websites, offered loan repayment for psychiatrists to decrease the shortage, and extended community outreach of the VA. Just another timeline of veteran suicide prevention. In 2001, the first published national strategy for suicide prevention is released. In 2007, we have the Joshua Ombig Veterans Suicide Prevention Act. And again, this mandated the VA develop and implement more programs such as the Suicide Prevention Coordinator, establishment of the crisis line. In 2008, high-risk flagging is implemented. For those that don't work at the VA, high-risk flagging is not a requirement. High-risk flagging is an ability of a provider to notate in a patient's chart that they have elevated risk factors that put them in a higher risk category of completing suicide. So, you know, anybody that's part of that care team, they take extra special attention if let's say an appointment is missed or if they're running low on medications or they need to get plugged into a program or an appointment quicker. 2009, chat becomes available. 2011, text messaging becomes available for crisis situations. 2015, we have the Clay Hunt Suicide Prevention for American Veterans Act. 2016, Crisis Line establishes a call center. In 2018, an executive order signed by President Trump occurs. He's hoping to support more veterans as they support transition to civilian life. So what is the VA doing to address veteran suicide? The veteran population is a large, large population, and we have to understand that not all of them will have a risk for suicide. And among those that do have a risk for suicide, some have an even higher risk for that. So their approach is multilevel. And to start, they want to do a more universal approach. So that includes public awareness campaigns, educational campaigns. From there, they want to do more selective targeting. And among folks and among groups that have a higher risk, such as folks with a history of substance use, recently transitioned to civilian life. Again, discharged from the service three years after that, that's the highest risk. Among those folks, we want to have a higher level of care and services. And finally, for those who have the highest risk, we want to make sure that they're plugged in with all the resources. They understand the role of the crisis line. If they need appointments or walk-in services, they have access to that. As part of a national effort to thoroughly screen for suicide, recent initiatives have been implemented. So there was a recent memo that now VA medical and surgical wards would actually start screening for suicide risk. Previously, suicide screening was essentially done in the PCP office or in specialty clinics, such as pain, mental health, or sleep clinics. From there, if the screen is positive, there are more comprehensive risk assessments done that will gather more data. And the hope is that as more data accumulates, the VA will have a better opportunity to predict who's at higher risk and how to intervene at appropriate times. So there were three distinct phases for rolling out this larger screening tool. And the first happened in 2018. And that was just the number nine question on the PHQ-9, which states, thoughts that you would be better off dead or hurting yourself. So most veterans would get asked this. And if they had screened positive, then they would have what's called the CSSRS completed with them, which is a little bit more specific. And if they screen positives for that, the CSSRS will determine just how high that risk is. And if the CSSRS is concerning, then that proceeds to an even more comprehensive eval called the CSRE. Comprehensive Suicide Risk Assessment Evaluation. So again, this is the three-stage process to screen more veterans and to identify those who are at higher risk. So we have the primary screen with the PHQ-9 question. Then if that's positive, they move on to the CSSRS. And if that highlights concerning signs or history, then they go on to the VA Comprehensive Suicide Risk Evaluation. I want to spend the next moment talking about the Columbia Suicide Screen. And the National Institute of Mental Health in 2007, along with Columbia, University of Pennsylvania, University of Pittsburgh, wanted to create a tool to decrease suicide. This has come to be known as the Columbia Protocol. And it's a tool to aid clinicians in assessing a patient's suicide risk and identifying those at an increased risk. And it looks at the following major components. One, ideation. Two, preparation slash intent. And three, action. So the first section of the CSSRS looks at the presence of ideation. Is the patient even thinking of completing suicide? And from there, it asks about if they're having thoughts, are they going farther and thinking about how to do it? And do they actually want to do it? If the initial questions uncover the presence of suicidal ideation, then it guides us to go on to a suicide behavior report. And in this section, it asks specifically, was any action carried out with the intent of wanting to die? Whether they caused any harm or if it was or was not lethal, but they believed they would die, it's considered an actual attempt. So I've done emergency evaluations where I've had a patient that took emergency evaluations where I've had a patient that took 20, 25 milligrams of melatonin. And I think most clinicians would say the lethality of that is not very high, but I remember one patient specifically, they really thought that by taking that they were going to die. And that concerned me and made my risk assessment much higher of the patient. So again, if they thought they would actually die, regardless of the lethality, then it's considered an actual attempt. Finally, the next section includes an overview of the patient's history of interrupted, aborted, and preparatory actions. And finally, the CSSRS prompts the clinician to review the acute or potential lethality as their attempt as part of the risk assessment. And one thing I want to highlight is the CSSRS is meant to be a tool. It's not, you know, it's not a questionnaire that sums up a score. And if they meet a certain threshold, it says, yes, they absolutely need to be admitted or, you know, no, they're absolutely safe to go home. It's just a tool to help the clinician kind of distill the most important parts of the patient's history to guide the clinical decision-making and to highlight all the different risk factors that we're familiar with. So it's definitely a helpful tool. And to highlight how the CSSRS can change a clinician's decision-making process, I have a couple of vignettes, which I'll go through quickly. So vignette number one, we have Mr. Jones, who is a 70-year-old man with a past psych history of MDD, well-controlled with search-related, and he presents to the ER with suicidal ideation. His wife of 30 years recently passed away a year ago and is coming up on their wedding anniversary. He is living by himself, feels more isolated, lost his appetite, endorses insomnia, anhedonia, and guilt. He says he wants to join his wife, but that he would never actually do it. You would cover the following from his CSSRS screen. Does he wish to be dead? Yes. Thoughts of wanting to end one's life? Yes. Does he have any thoughts or plans? He plans to shoot himself with his gun on his anniversary in two weeks. He endorses intent and denies previous suicide attempts. So how would you sort out his disposition? I think if I were to see a vignette like this, especially with the way the CSSRS is prompting me, I would be very concerned. He has thoughts, he has a very specific plan, he has an acute stressor, and he has new neurovegetative symptoms of depression. So I think using this information from the CSSRS, I would definitely think about hospitalization for this patient. Vignette number two, Mrs. Smith is a 35-year-old woman with a past psychiatric history of PTSD, borderline personality disorder, and weekly therapy who presents to the ER with suicidal ideation. Her fiance recently broke up with her, causing her to move back home with her mom, but reports that she wishes she was not around anymore. You uncover the following from the CSSRS screen. Wishes to be dead? Yes. Thoughts of wanting to end one's life? Denies. Denies thoughts or plans or intent? Denies recent suicide behaviors or history of suicide attempts? So even though this patient endorses thoughts of wanting to die, the CSSRS uncovers that she's not having thoughts, plans, or intent. She's also back home with her mom. So I think that if I had this information, if she can contract for safety and come up with an alternative plan to hospitalization, I would gravitate towards creating a safety discharge home. So what evidence do we have that can help intervene with suicide? So a concrete review in 2016 highlighted that restricting access to lethal means, so that includes firearms, but specifically analgesics, is huge, controlling hotspots such as safety precautions at bridge, as well as confirming the benefits, the anti-suicidal benefits of lithium and clozapine. Interestingly, it had a line that read, insufficient evidence exists to assess the possible benefits for suicide prevention screening in primary care, in general public education, and media guidelines. So I thought that was interesting because that's sort of what the VA is trying to currently implement. And yeah, I think this line just says that there's insufficient evidence at this time. I'm curious after more time is available with what the VA is trying to implement, if we will see any impact on veteran suicide, possibly as a result from these different implementations. New research. So there's a multi-site VA study looking at the effects of lithium in suicide prevention, specifically in the veteran population, the REACH VET program using predictive analysis to identify high risk patients, as well as looking for possible biomarkers for suicide as well. And now I'll hand it over to Dr. Nordzy to talk about physical exercise. So in the next section, we're going to talk about physical exercise and its role in managing allostatic load, as well as supporting veterans in brain health and recovery. Here in this slide, our outline is to start off talking about the neurodegenerative effects of psychiatric disorders, and the neuroplastic and neurogenic effects of physical exercise, which may help to reverse some of the underlying neurobiologic disruption of psychiatric disorders. We'll also talk about the epigenetic effects of exercise, and stimulating neuroplasticity, which supports recovery, but also supports learning in psychotherapies and in functional life improvement. We'll look at evidence on the impact of physical exercise in people with psychiatric disorders and improving symptoms and functioning. And then finally wrap up with some behavioral change strategies for how you can support veterans in making effective change in their physical activity habits. So this older slide is an electron micrographic depiction of a dendritic spine in an individual without a psychotic disorder in the A panel, and then two individuals with schizophrenia in the B and C panels. And what you can see is the dramatic loss of connectivity, the loss of dendritic spines, where one neuron is connecting to another, making synapses. And this is really responsible for the loss of brain volume that's been documented for decades in individuals with psychotic disorders. The good news about this dendritic spine reduction is that it's reversible. This is not neuronal death. Actually, only about 5% of the volume loss in people with psychotic disorders is attributable to neuronal loss. And the vast majority is due to shrinkage, if you will, related to reduction in connectivity. And so that's reversible and is responsible for the loss of reduction in connectivity. And so that's reversible and is responsive to the neurotrophic factors like BDNF, which elevate in response to exercise. And it's the signal telling the brain to increase plasticity and connectivity amongst neurons and circuits in brain regions. And so that's the challenge, is what interventions do we have that can help an individual recover from neurodegenerative volume loss and improve their neuroplasticity? And of course, we see similar findings across many psychiatric disorders in specific brain regions. And in contrast, we know that physical exercise leads to people feeling better, right? We've had the concept of runner's high for many years, that sort of sense of calm, improved mood, improved focus, mental acuity, paired with physical fatigue. When people say they're tired after exercise, they're usually referring to their body, whereas their mind is usually activated. And a sense of fitness, a sense of accomplishment, and of course, improved sleep and brain reward response, similar to what we see when people use substances or have a satisfying social interaction or a meal. Physical exercise also stimulates brain reward. And as I mentioned, we see that a variety of brain functions are enhanced in response to exercise. So our neurotransmitters, including the endorphins and the endocannabinoids, as well as the key monoamines, norepinephrine, serotonin, dopamine, are all elevated in response to exercise, which clearly can be beneficial for mood disorders, for many of the disorders that we treat, post-traumatic stress disorder. And then the neurotrophins, centrally brain-derived neurotrophic factor, or BDNF, as well as a variety of other neurotrophic factors are increased in both release and production in response to exercise, stimulating neuroplasticity and neogenesis. And interestingly, we also see an increase in glycogen storage and astrocytes, parallel to what we see in peripheral muscle, so that the brain has the energy that it needs to respond, particularly in frontal cortex and hippocampus. And then finally, we see that when people exercise regularly, they manage their glucose levels more tightly in response to mitochondrial proliferation in peripheral muscle. And of course, perturbations in blood sugar levels that lead to elevation in blood sugar can be toxic to particular brain regions, especially the insula, and interfere with memory. And so, tighter glucose regulation avoids that damage. So on this slide, then we're reviewing that in response to exercise, blood flow increases. We see increased learning and memory, reduction in cognitive deficits with age, and reduction in neuronal loss with age, self-proliferation and neurogenesis, in addition to plasticity and suppression of the immunoinflammatory response that's been associated with so many psychiatric disorders. So then going into specific psychiatric disorders, we see that physical exercise protects against onset of depression. In this large meta-analysis of a quarter million people, about half male, who were followed for nearly two million person years, that the folks in the highest activity group had about 80% as much likelihood of developing depression as people who were inactive. In other words, 0.8 odds of developing depression. And that was consistent across age groups, across continents, and whether or not depression was defined just as a positive PHQ-9 screen or the full syndrome of major depression. And this is the second of two studies by the Duke group looking at physical exercise directly randomized against an SSRI, in this case, Sertraline. And in this study of 200 patients with major depression who were randomly assigned to treatment for their depressed episode with Sertraline or placebo or exercise, either supervised in a gym or home exercise, all three active conditions, the two exercise groups and the Sertraline group, were equally effective at getting about half of people into remission within four months, about two-thirds by a 16-month follow-up. So no significant differences between the active exercise groups, but at follow-up, people who were exercising and not those taking medication were more likely to stay in remission in the long-term at 16 months, whereas the folks who were taking medication were more likely to relapse, presumably having fade of effect over time. And in this study, they also found that there was an increased improvement in depressive symptoms with the amount of time spent exercising, up to about three hours a week of exercise. Shifting over to cognitive decline then, this study by a group at Washington University in St. Louis found that physical exercise reversed the impact of the APOE gene or APOE allele in leading to amyloid deposition in the brain. So what you see here on the left two bars are individuals who are APOE negative, and even when they exercised, their amyloid deposition was a little lower than folks who were not exercising. But on the right two bars, you see people who are APOE positive and those who were sedentary had significantly higher amyloid deposition on PET scan, whereas the individuals who were regularly exercising essentially eliminated the genetic effect. And so this is really an environment gene interaction where the behavior of exercising corrected the deficit in excess amyloid deposition caused by the APOE4 allele. And so when people with family histories of cognitive, neurocognitive disorders ask you what they can do to avoid developing dementia, there's a very clear answer, which is regular physical exercise, especially if they're APOE4 positive. APOE4 positive. And again, back to schizophrenia, we see that in this study of folks in Holland, 55 healthy controls compared to 63 outpatients with schizophrenia that where folks were randomized to an hour twice a week of either exercise or occupational therapy for the individuals with schizophrenia for a six-month period of time, that the improvement in VO2 max, which is essentially fitness, how much physical fitness the individual increased, was associated with an increase in gray matter volume and reduction in ventricular volume, which as you know, is elevated in people with schizophrenia. And the elevations in cortical thickness were related to expansion in the left frontal, temporal, and cingulate areas in both patients and healthy controls. And Joe first did this meta-analysis looking at cognitive function in people with schizophrenia and found across 10 trials of 385 patients that physical exercise was associated with a moderate effect size at 0.43 of increase in global cognitive function with more exercise associated with greater cognitive gain, working with an exercise trainer who was supervising the exercise being associated with greater efficacy. And specifically the domains of working memory, social cognition and attention vigilance were most significantly enhanced in response to exercise amongst people with schizophrenia. And this is important because we don't have effective treatments to improve cognitive function in people with schizophrenia, which is typically impaired. And we don't have pharmacologic treatments. And so physical exercise represents one of the most promising interventions for helping people with psychotic disorders to enhance cognitive function and therefore improve their psychosocial functioning in the community. This is a study that my colleague Daniel Daly and I did at Dartmouth looking at individuals with psychotic disorders before and after individual exercise sessions where we asked them to rate their momentary experience of a variety of symptoms on a Likert scale. And what we found was that just in the hour that lapsed prior to exercise and then after exercising, people were reporting on a, this was actually on a 10 point VAS scale, about a 10 to 15% improvement in their global wellbeing, cognitive energy, motivation, social interest, clarity of thought and concentration. Again, all of these cognitive and negative symptom domains with suppression and anxiety and depression on about a five to 10% level and minimal effect on psychotic symptoms. Now, other studies have showed some accumulative effect on psychotic symptom improvement over time, which is usually weaker than the impact on mood and cognitive domains and negative symptom domains. But at least in the sort of immediate before and after, and these were a group of people who were regularly exercising, these non-psychotic domains appear to be most cycling in their response and may, that sense of wellbeing that occurs after exercising is an important motivator for people's continued activity. And on this next slide, these are ratings on the subjective exercise experiences scale. And again, you see that after exercise, people were rating an average increase and this is on a seven point Likert scale. So again, about a 10% improvement in the positive wellbeing items, feeling great, positive, terrific, strong, some increase in feeling exhausted, but then you can see suppression of feeling discouraged, crummy and awful in response to exercise sessions. Next shifting over to post-traumatic stress disorder, James Whitworth at the Boston VA did this large national online study of 182 veterans with post-traumatic stress disorder and found that total physical activity time in total leisure physical activity time was associated with direct effects on reducing the avoidance numbing component of the PCLC with indirect effects via reduction in alcohol use on total PTSD symptoms. And when he isolated the strenuous intensity exercise that was associated with direct effects both on the avoidance and numbing and on the hyperarousal domain of PTSD symptoms with indirect effects via improved sleep on total PTSD symptoms, as well as those two symptom clusters. So, and James has been following this up with specific exercise intervention studies that have also demonstrated improvement in post-traumatic stress disorder symptoms in veterans. And this small pilot study looked at the use of exercise as a prime the pump intervention for exposure therapy. And so you can see amongst these nine individuals with post-traumatic stress disorder who were randomized to 30 minutes of exercise or no exercise prior to prolonged exposure therapy sessions that the moderate intensity exercise was associated with greater improvements in post-traumatic stress disorder symptoms as well as elevations in BDNF. And I put this study in here not because the power is really large enough to establish the impact of the intervention on prolonged exposure outcomes in just a group of nine, but the BDNF measure, which you see on this slide is really quite impressive. So again, with just four versus five people in the randomization, the folks who were adding exercise to their prolonged exposure show a dramatic elevation in their BDNF levels about two fold, two and a half fold, whereas the folks who were just doing the prolonged exposure therapy showed no change in their BDNF levels before and after. So a promising study that is one of many looking at this potential for positive interactions between exercise, really using exercise, timing it to occur directly before psychotherapy sessions in a variety of conditions. There's also work in obsessive compulsive disorder and in major depression and psychosis to look at the use of exercise as a way to improve learning and absorption of material in either psychotherapy or cognitive enhancement training. And Matt Friedman, who wrote a chapter in my book on lifestyle psychiatry and reviewed the literature on post-traumatic stress disorder, physical exercise and post-traumatic stress disorder identified a number of routes for improvement, desensitization to autonomic arousal. So helping people to get comfortable with the elevations in heart rate and respiratory rate that accompany exercise and to associate that with a calming, relaxing experience of exercise rather than that sort of trigger for panic that may occur in people with traumatic stress disorders and anxiety disorders. Supporting neuroplasticity and neurogenesis in memory centers, stimulating the endocannabinoids that have some potential for benefit in post-traumatic stress disorder as well as an impact on mastery, trust, and social connection either with a trainer or in a team setting with sports participation. And many of the exercise interventions in veterans involve settings like that where part of the goal is to improve the social trust component. Hyperarousal cluster symptoms seem to be particularly responsive to physical exercise as we saw before, and the need for further research to inform those relationships. As you saw the literature there still in its infancy. There's also then evidence in traumatic brain injury that physical exercise reduces depressive symptoms and the experience of fatigue following traumatic brain injuries. It has anti-apoptotic effects so that less neurons are lost after a traumatic brain injury and enhances neuroplasticity, reduces inflammation in the brain by elevating immunomodulatory factors and improves glial cells, cerebrovascular and blood-brain barrier integrity. And so there's been a real shift away from the approach to traumatic brain injury and concussion of decades ago when we used to isolate people in dark rooms and have them rest until their symptoms were gone. And now really a focus on as soon as possible getting people into physical activity that's low risk for any further brain injury, but a safe form of exercise like getting on a stationary bicycle to help individuals with traumatic brain injury take advantage of exercise and its neuroplastic and neurogenic effects to reduce the impact of their brain injury. And there's some evolving evidence in addiction as well, more animal studies actually than human studies which are very promising. Of course, the animal studies allow more controlled conditions, but human studies starting to emerge as well showing that exercise ameliorates withdrawal symptoms, reduces craving and reduces risk for relapse into substance use. And motivational interviewing and contingency management approaches can be helpful both for initiating and maintaining exercise as well as for the substance use itself. And successful maintenance of exercise has been associated in human studies with improved social support, a greater sense of self-efficacy, making more active choices, health contracts and assurances of safety and positive reinforcement. Shifting over then to suicide risk, there's actually quite dramatic data. This is a large study, a global study of student-based mental health that found that across 125,000 students from 43 countries who were in their teen years, about half female, that 10% had attempted suicide and the prevalence of suicide attempts was associated with increasing sedentary leisure time. So the folks in the most sedentary category of greater than eight hours a day of leisure time spent sedentary had nearly 17% risk of suicide attempts compared to 9% in folks who were the most active with an odds ratio of about 1.5 for a suicide attempt in those who were most sedentary. And so physical exercise may represent one of the important things we can do at a global health level to reduce people's risk for suicide. And of course may also explain the elevating suicide rates as the degree of sedentary activity in society increases in response to our increasingly screen-based, internet-based lifestyles. So finally, let's wrap up with some discussion of how to incorporate physical exercise in psychiatric care. Hopefully I've inspired you to be thinking that physical exercise may be an important component of your care for veterans. And as you see, we reviewed a number of disorders that are quite common in veterans. And so how do we get them off the couch? How do we help people to get active and to view physical activity as a core component of their care? Well, usually we start off with a careful assessment of physical exercise both throughout a person's lifetime and as well as current. And of course, veterans typically share an experience of having been quite physically fit during their service and often pride in that, even if that has faded with age. Some may maintain a lot of physical activity. So we wanna understand, what have they been involved with historically that they enjoyed and what's their current physical activity level? Educate them about the impact of physical exercise on brain activity and brain function. Make clear recommendations for exercise activity as part of their recovery plan. Think about motivation through group activities or joining with a partner or training for an event that may have meaning for the individual. And develop a behavioral monitoring plan, just like we would with any other treatment intervention. If we referred an individual for a psychotherapy or a medication management intervention, we're gonna check on their adherence to that intervention. And similarly, we want to check in with individuals on their success in building an exercise plan and help them to fine tune that and overcome barriers during follow-up. And so generally, obviously starting off with understanding a person's current capacity, our targets are to get to 30 to 60 minutes of physical exercise, three to seven days a week. And as we said in the earlier slide, exercise up to a total of about three hours a week seems to be most effective for psychiatric purposes. The general physical activity guidelines for adults, as you see at the bottom of the slide, are either 150 minutes of moderate or 75 minutes of vigorous aerobic exercise plus two strength training sessions per week. And that's based on World Health Organization guidelines, which really fit in pretty closely with those duration guidelines that we have found in psychiatric studies for optimal brain health. And so we may identify that as where we'd like to get to. And then for an individual who may be already somewhat active, it may be some gradual building of their activity towards those targets. For a person who's currently quite sedentary, we might start with very simple interventions such as walking regularly and then work with a person to observe how they feel after activity and gradually build up in a staged fashion their success at physical activity as they build physical capacity for it. More exercise is better up to a point. As we've said, mixing strength and aerobic exercise appears to be more helpful than aerobic exercise alone, although most studies focus on aerobic exercise because it's easier to study. Those studies that include a strength component do show specific benefit that may be complementary, although further research is needed there. And again, we wanna get people into the moderate to vigorous exercise range. So around 60 to 85% of their maximum heart rate, which can be roughly calculated as 220 minus their age. So for a 20-year-old, that would be about a heart rate of 200 for your maximum heart rate. And then you calculate the percentage of that. So 60% of that would be, or 120 would be the threshold for moderate exercise. And then have the client choose an activity that they're most likely to stick with. So what do they have access to? What are they able to afford? What's familiar to them? What do they enjoy? Are they someone who really wants to be out in nature, doing something different every time, hiking, biking? Or are they somebody who really likes repetition? They wanna have the exact same routine every day. They wanna go to the gym and do their routine or run the very same circuit in their neighborhood every day. Whatever works for that individual to be most successful, helping them to maintain a regular routine. Of course, trying to get to the place where a person meets those physical activity guidelines at the bottom. And then again, we wanna assess the response to exercise as a way to fine tune the plan and help the person to continue to build their success. So how often in the interval since the last visit, have they been successful in adhering to their plan? What changes did they notice in the core symptoms of their traumatic stress disorder or their depression or their psychosis in response to exercise? And what changes did they notice in the sort of more general domains of sleep, appetite, energy, and sense of wellbeing, which commonly respond to exercise? And what changes did they notice in their cognitive function that may not be specific to the disorder, but may drive a person's sense of benefit from exercise, any general health effects? And then refine the plan. If the person's only exercised twice in the interval since the last visit, but both of those times they felt better for 12 hours after exercising, then you might say, terrific, nice job. You learned something from this activity. Let's try to get to four times or increase the amount of time that you exercise in order to help the person to refine their plan and continue to build their success and their goals. So then to summarize, the onset of most psychiatric disorders is associated with brain changes in brain volume, largely driven by loss of neuronal connectivity and loss of circuit communication with manifestations in cognitive rigidity. Physical exercise helps to counter that by stimulating neurotrophic factors that can be reduced in individuals with psychiatric disorders, especially when they're sedentary, increasing blood flow and leading to epigenetic adaptations that actually maintain increased output of neurotrophic factors over time to support brain health and prevent brain deterioration with aging, which then also generates synaptic plasticity and neurogenesis to offset any neurodegenerative effects that may have occurred. This is associated with increased gray matter volume, hippocampal volume, and reduction of symptoms across multiple disorders, including depression, psychosis, and post-traumatic stress disorder with improvement in both cognition and function in people with these disorders. And while we don't yet know how specific the reversal of neurodegeneration is to the disorder in question, certainly increases in gray matter volume are gonna be helpful across psychiatric disorders. And there's potential for neuroprotection and prevention of disease progression, certainly in disorders like traumatic brain injury, but potentially also in disorders like schizophrenia-inspected disorders where early intervention with exercise might help to prevent some of the neurodegenerative loss and progression into more severe cognitive and negative symptoms. Thank you.

Caring for Veterans

Mental health care

PTSD

Treatment modalities

Suicide prevention

Evidence-based treatments

Cardiovascular disease

Exposure therapy

Alternative medication options

Suicide prevention coordinators

Neurobiological effects of exercise

Psychiatric disorders