Welcome to Addiction as a Brain Disease, Knowledge for Justice Settings, a presentation put on by the Opioid Response Network. The Opioid Response Network is SAMHSA-funded and assists states, tribes, organizations and individuals by providing resources and technical assistance to locally address the opioid crisis and stimulant use. Technical assistance is available to support the evidence-based prevention, treatment, recovery and harm reduction of opioid use disorders and stimulant use disorders. ORN provides local experienced consultants to accept requests for education and training. Each state and territory has a designated team, led by a regional technology transfer specialist who is an expert in implementing these evidence-based practices. If you have any questions or would like to submit your own TA request, please visit the website below or reach out to the email listed. The objectives for today's training are listed here. Looking to identify opportunities to recognize and manage stigma in different settings, to improve interactions and increase support for persons with substance use disorder, utilize scientific explanations of how substance use impacts the brain to enhance understanding of addiction as a chronic medical condition, recognize basic signs of opioid use disorder and identify symptoms of opioid withdrawal, describe why long-term medication therapies are effective for managing addiction as part of a medical model and whole-person approach to treatment, and review the overlapping landscape of justice involvement and substance use. Addiction is a brain disease. The National Institute on Drug Abuse, the American Society of Addiction Medicine, and the American Medical Association, amongst others, are all in agreeance that addiction is a chronic relapsing disease that affects the brain and causes compulsive drug seeking and use despite harmful consequences. We know that substance use changes the brain structure and function, and even if the initial decision to use may be voluntary, the impact of repeated use affects a person's self-control and ability to make decisions. And keeping in mind that the introduction of substances for many people happens at a young age, well before the brain is developed enough to fully understand how to make informed and logical decisions that weigh the pros and cons and costs and benefits of such choices. The addiction is also chronic and relapsing, similar to other diseases, but also like other chronic diseases, can be managed successfully. What's really important here is understanding that the medical model is imperative when understanding and treating substance use disorders and is best paired with a whole-person approach to treatment and care. Let's discuss some neuroanatomy, so what is going on in the brain. We know that addiction affects multiple brain circuits, including those involved in reward and motivation, learning, memory, and inhibitory control over behavior. So we have receptors throughout our brain and our body, and receptors are just a chemical structure on the membrane of a brain cell or a neuron, and when another chemical that the receptor is sensitive to is present, those chemicals stick together. I like to think of receptors as like little buckets throughout our brain and our body, and certain chemicals are more attracted or have a stronger effect or a greater affinity to those buckets, thinking of like that child's toy where the square block goes in the square hole and the circle block goes in the circle hole. Certain chemicals are going to be a better fit for certain receptors, and therefore they have a stronger bond to those receptors. And when they have a stronger bond, they're said to have a greater affinity, meaning that things that are shaped and ready to fit those receptors are going to have a stronger impact than other chemicals that may be present that aren't a good shape for those receptor buckets. Opioids are a class of drugs that include pain relievers that are available legally by a prescription, as well as illicit substances like heroin and synthetic opioids such as fentanyl. When opioids are present in the brain and the body, they bind to and activate opioid receptors that are on cells located in the brain, as well as the spinal cord, our digestive tract and other regions in the body. When opioids attach to these receptors, they have a variety of functions, one of the main being that they block pain signals sent from the brain to the body, and alongside that, they also release large amounts of dopamine, and we'll talk a little more about dopamine here in a minute. Opioids often can make people feel relaxed or have a strong sense of euphoria or a high, but they also can cause drowsiness, confusion, nausea, constipation, and slow breathing. How do drugs work in the brain to produce pleasure? So generally speaking, the pharmacological mechanisms for each class of drug are different, but the activation of the reward system is very similar across all substances. Nearly all addictive substances, directly or indirectly, target the brain's reward system by flooding the circuit with dopamine. Now dopamine is a neurotransmitter that is present in regions of the brain that regulate movement, emotion, cognition, motivation, and also reinforce rewarding behaviors. And so when activated at normal levels, this system rewards our natural behaviors. An example of that being, if I'm very hungry and maybe I'm feeling a little tired or lethargic, or I have a headache, and I go and I make myself a sandwich and I eat that sandwich. When I eat that sandwich and I bite into that first bite, I actually get a reward and a boost of dopamine that floods my brain and my body. And part of that release of dopamine is that dopamine is one of those feel-good chemicals, but it's also part of that reinforcement of behaviors. And so my brain is feeling that this was a very good choice. If I'm feeling all of these symptoms and signs of being hungry, when I eat a sandwich, I get rewarded by that. And part of that reinforcement then is that my brain remembers that this is rewarding. And so the next time I find myself feeling hungry and tired and have a headache and need something to eat, I am going to remember that, hey, when I eat a sandwich, that actually feels good, and I'm going to kind of rinse and repeat that behavior over time. Same thing goes with if I'm thirsty, right? If I'm, you know, haven't drinking any water or maybe I've been outside or I've done a very intense, you know, exercise routine. When I drink that first sip of water, I get a rush of dopamine and that's my body telling me that water is good for you. You need water to stay hydrated. This feels good. And I want you to remember the next time you're thirsty to do it again. So we have a lot of things that are kind of just hardwired into us when we do these things that are good for our survival. Our brain rewards us with that and it remembers and reminds us to do those things in the future. And part of this is, you know, mostly happening behind the scenes. Maybe we're not super plugged in or paying attention to that, but these types of behaviors are very important for our survival. So our brain and our body is kind of ensuring that we're going to keep doing these things over and over to ensure our successful survival moving forward. The problem being that the system will grate for kind of our normal, natural behaviors of things that are, you know, good for our survival can also be kind of overstimulated with substances. And when that happens, it produces effects which strongly reinforce the behavior of drug use, teaching the person to repeat it. And so this is kind of that hijacking of a system that is good for us and good for our survival, but because it's been taken over by substance use and manipulated by the substances that have been introduced into the system, this is where we see that structure and function of the brain start to change and adapt to the response of something from the outside being introduced in. These are some examples of behaviors that have an impact on releasing dopamine. And these are a list of chemicals that also have an impact on releasing dopamine. So when we talk about dopamine release, it's also important to consider the hedonic threshold or the pleasure threshold. And essentially what this means is the dopamine is a naturally occurring neurotransmitter that can, you know, be released in response to behaviors or activities or any other stimulus from our environments. But with that, there's a certain level or threshold or ceiling of how much dopamine can be released in response to any of these given stimuli. And so there's only so much dopamine that our body is going to produce and reward and reinforce behaviors with, just because that's kind of the limits of what we're able to do kind of without any manipulations to the system. And so with that, you know, over the course of a day, a week, a lifetime, we're not having a static amount of dopamine that is going to ebb and flow over time. There's going to be kind of peaks and dips depending on what's happening and what's going on and which behaviors are pleasurable and rewarding and which behaviors maybe are not that are going to have an impact on how much dopamine is present at any given time. And some of the behaviors we discussed earlier, like eating that sandwich or drinking that bottle of water, we're seeing that it's paired with a modest amount of dopamine release, you know, definitely not the peak of how much, but enough that it's measurable, significant to be kind of registered and remembered by the brain that, hey, when I'm hungry, I eat that sandwich. When I'm thirsty, I drink that water. It's good for my survival. I need to remember to do that again. Similarly, procreation is good for our survival, you know, as a species and that's kind of hardwired into us. So we see that we have a release of dopamine, you know, that's a little higher on that scale, but also again, it's significant, it's measurable, it's, you know, telling the brain that this is behavior that is good. We need to make sure that we remember that this is important and we do it again. So these are examples of kind of naturally occurring things, and they're going to, you know, hit kind of at variable levels. But for the most part, you know, we're not able to supersede this threshold of what's built in. So any of the behaviors and activities and things that we're engaging in are all going to fall kind of under this threshold. Now the difference being is when we start to introduce substances that aren't naturally occurring in the brain and the body to begin with, we have the ability to see how this is going to have an impact on the amount of dopamine that gets released behind the scenes. So when you start introducing alcohol, nicotine, cocaine, opioids, methamphetamines, we're now obviously very much superseding the threshold that is kind of hardwired and built in, and we're creating these kind of false, you know, releases of dopamine at a much higher rate. And while we may understand kind of objectively that like, oh, we're getting this type of response because we're putting something in the system that's not naturally occurring, the problem being that the brain and the body don't understand that. All it's going to do is read how much dopamine is being released, and now we've kind of basically dysregulated the system because it's been operating on the assumption that that threshold is exactly, you know, where the peak is, and that behaviors will be up and down kind of in this range, and the introduction of other substances has really created some chaos behind the scenes. And we'll break that down a little bit more in future slides. So behind the scenes, generally speaking, the body seeks equilibrium. So we've got that little scale there, right? Before we start disrupting the naturally occurring system, prior to any of this neurotransmitter disruption, our natural metabolic system is balanced. And that just means that receptors, those buckets that we talked about that are in our brain and all over our bodies, and endorphins, which is just a category of those feel-good chemicals that are also naturally occurring in our bodies, are kept in a general balance. And so when we get boosts of, you know, endorphins and feel-goods, our body responds with an appropriate amount of receptors to make sure that every chemical and receptor kind of matches up to each other. It doesn't want too much or too little of either of those. It likes that perfect balance. So when we flood the brain with exogenous or outside substances, the problem being is that these substances, they mimic those natural endorphins, those natural chemicals that already exist behind the scenes. But by kind of putting something in there and flooding the system, it confuses the system. And so the brain and the body kind of read and respond to that and understands that, oh, okay, we must be making way too many endorphins, so we're going to shut that process down. So the natural occurring process of endorphin making and chemical making behind the scenes gets shut down and turned off because the brain is just reading that response of the dopamine flood and thinks it's doing something wrong because it shouldn't have that much going on. So with that, the brain now is out of balance, right? There's too much chemicals and there's not enough receptors. So the brain actually produces more receptors to help increase the uptake to balance that out, right? I've got all this extra chemical, I need more buckets to match so that everything can kind of fill and attach. And again, we'll be able to seek that balance and equilibrium back again. And so now over time, right, I've created all these extra buckets to meet all of this extra chemical, but as that chemical wears off, right, I'm going to be out of balance again. So I'm going to have all these empty buckets and that's not equilibrium, that's not balance. Our brain and body doesn't like it. And so now we're going to have to crave and seek and want to fill those buckets with something. And keeping in mind that we've already shut the process down of naturally occurring endorphins and chemicals, meaning our body isn't going to produce anything right away. And so now it knows that the easiest way to fill these buckets and produce that same effect is going to be to add more of that exogenous substance into the system again to fill all those buckets and kind of balance it back out. With that though, we're also finding that the receptors will start to become desensitized over time. So when we flood the system with an outside substance, the first time it filled, you know, all of the buckets and everything was fine. But the next time you introduce a substance, it's not going to fill all the buckets all the way. You're going to get kind of a decreased impact over time. And part of what's going on there is keeping in mind that the brain in the reward system is also wrapped very closely to memory. And so the first time we introduce something into the system, it's new, it's novel, it's never been experienced before. You're actually going to get a much larger dopamine release for something that's new and novel and exciting and has never been experienced before. But each subsequent introduction of that same stimuli, that same substance, that same, you know, activity is not going to get the same response over time. So you're going to have that first response be much more enjoyable and much more pleasurable according to how much dopamine is going to be released. But every time after that is going to be just a little bit less. And the result being that the entire system just ends up being dysregulated. So for my visual learners out there, this is another example of what's going on with dopamine and substance use. And so you're seeing that first introduction of substance use kind of being off the charts, right? You've got that kind of normal baseline threshold there in the middle of where our dopamine levels are, generally speaking. And once we've introduced a substance in there, we go kind of high up and off the charts, right? You have that really, really high peak. But now as that substance starts to wear off, you don't actually just go back down to baseline. You actually start to go into a deficit. And that's because keeping in mind, right, that the brain and the body has recognized all of this flood and release of dopamine. So it stopped doing the things that it would naturally do to produce these feel-good chemicals on its own. And so instead of going back to kind of that normal baseline, you actually go to a very low dip. And you have that really kind of dysregulated level and really uncomfortable space. Because again, now the body is out of balance, right? We have too much of something and not enough of something else. And so what does the brain want us to do? It wants us to rebalance that back out. And it knows that the quickest way to do that is to say, hey, when you introduced the substance before, we got a big boost, let's do that again. And so this is where drug seeking and drug craving comes into play. And now you're going to take that second use of a substance, right? But you're not going to get that same high peak anymore. Because the novelty of something has kind of worn off. And so it's not new, it's not as exciting. It's not something that it's never experienced before. And so the brain is able to kind of respond at a much duller dopamine release. And with that, the brain also now remembers that not using takes us back down to that deficit, that low. And so in anticipation of that, it tries to tell the brain and the body to make choices to do something else to keep all of these receptors full, so that we don't go back to that low. And then you kind of see this rinse and repeat pattern over time, right? So now I don't want to feel miserable and be in a deficit and, you know, start feeling in withdrawal. And so I'm going to use again. But each time, right, that peak of using, because the system has come desensitized, is now going to be a little bit less of dopamine release than it was the time before. And then at some point, you're using just to try and sort of feel 75% of that old baseline. And then you're just trying to use to feel 50%. I mean, and this is really kind of that journey of substance use over time, right, where it started out as this big high, this big, you know, euphoric, exciting, fun thing. And now you're kind of in the space of you're trying to chase and regulate something. And at some point, though, the toll is very clear on the brain and the body and the consequences of this over time. And so even though it's no longer enjoyable, even though you're not even able to feel what that old normal behavior was, that normal baseline that was there before, you're stuck in this pattern because the system and the structure and the function of the brain have been changed and are now adapting to this new pattern of behavior. So what happens next? We are very clear now that the system has become reliant upon outside substances. it stops doing the things it normally does, it becomes reliant on these substances as this kind of quick fix to keep that system in equilibrium and balanced out, but we're also having that tolerance effect, right, where the body's needing more to try and get that same effect because the system becomes desensitized and it's not as rewarding every time, you know, that comes after that first time. And so now you're in this place where the balancing act is to just try and avoid withdrawal and to keep things moving and to do the best that you can with what you have, even though now the system is really just starting to kind of fall apart and is very inefficient and is no longer doing the things that it's supposed to be doing. The system becomes unstable and then of course when the substance is removed, or in this case maybe the substance is no longer introduced anymore, right, the whole body starts to go into withdrawal, and with that you're gonna see runny nose, fever, sweating, stomach problems, mood changes, nausea, and keeping in mind here that withdrawal isn't just withdrawal of the brain. Those receptors that we talked about are all over the rest of your body, right, they're in the brain but they're also in the spinal cord, they're in your digestive tract, they're in your peripheral neurons, and so all of these issues are because the brain isn't the only thing that's in withdrawal. Your whole body is actually in withdrawal at this point and you're feeling and seeing the symptoms kind of collectively throughout the brain and the body. So let's revisit the dopamine threshold that we talked about a few slides back. So generally speaking, before we've done anything to mess with kind of our naturally occurring system, we have this kind of threshold, this line, this limit of the things that we can experience when it comes to how much dopamine is released from the behaviors and activities that we're engaging in on a day-to-day basis. The other thing that's important to keep in mind, right, is that the things that, you know, are enjoyable objectively, right, like a family vacation or a job promotion or winning the lottery or your fantasy football team, right, these types of things need to produce enough dopamine that registers as being enjoyable by the brain and the body. And a system that has not been dysregulated yet or has not been altered in any way, we're going to feel these things as being enjoyable, we're going to get enough dopamine that is recognized as being enjoyable, and these are kind of the things that make us happy, healthy, and successful in our survival moving forward. The problem being that when we introduce outside substances into this system, right, from that other slide we've shown how much more dopamine we kind of falsely introduce into this naturally occurring system, and what our brain does is it looks at that and says, oh, I thought this was our threshold, I thought this was how much dopamine we needed to feel to be able to register something as enjoyable and to reinforce the behaviors, but actually the introduction of substances has now taught the brain that says, never mind, this is the new dopamine threshold, this is how much dopamine can actually be released, and this is how much needs to be registered in order to kind of qualify as an enjoyable or a pleasurable event. So unfortunately though what we've done is we've created a gap now, so the old threshold and the old day-to-day enjoyable things that used to meet that threshold and feel good, part of that pleasure-seeking ability there, now we've created a gap where there's an actual inability to feel pleasure and hedonia, so that family vacation, that job promotion, that winning the lottery is now nowhere near what this new threshold has been created because of the substances that have been introduced into the system, and so that inability to feel pleasure from anything but substances is very real behind the scenes because we have moved and adjusted based on the information that's been introduced and substances have changed the structure and function of the brain. The good news is is if we take out these substances and we let our systems kind of heal and regulate and be able to kind of adapt and move forward, the good news is is that eventually the brain and the body will readjust and say okay I guess we don't have a dopamine threshold that's this high, nothing we're doing is meeting this threshold, and it starts to kind of re-regulate and readjust back closer to where that old dopamine pleasure threshold was in the first place, and now we find ourselves eventually back into a place where family vacation, job promotion, winning the lottery are now enjoyable again and able to be registered as pleasurable based on the amount of dopamine that gets released from those activities. The good news is that dopamine receptors will regenerate or upregulate and so we can reset this hedonic pleasure threshold, but it's going to take some time. Even just abstinence you're looking at a year, more accurately and realistically it's probably a couple of years because even though acute withdrawal is that kind of physical withdrawal that is you know 7, 10, 14 days for your body to physically withdraw from something post acute withdrawal syndrome or pause is up to a couple of years, 18 to 24 months on average for the brain and the body to heal and adjust and adapt, and so when we start really understanding that it's not just getting the substance out of the system and getting through acute withdrawal, that it is a very long arduous process for the brain and the body to heal and adapt and create a new normal behind the scenes, and so it's very understandable that early recovery, especially in those first couple of years, we do often see an uptick in recurrence of symptoms because it can be very hard to kind of get over this you know this hurdle of no longer being in active use but also not being in your new normal yet, not enjoying anything and having a very hard time just kind of navigating the day-to-day, and so this is also where evidence-based treatment like medication-based therapies can help during this period of time and can be very useful. Substance use disorders are chronic medical conditions. It's important to remember that a return to use is not an indication of failure. Substance use therefore is a symptom of substance use disorder. Relapse is a recurrence of symptoms and symptoms have reappeared. This usually indicates that treatment needs to be adjusted. It's also important to remember that recurrence rates of substance use are similar to the recurrence rates of other chronic conditions. There's no cure, but patients who comply with treatment regimens have more favorable outcomes. Looking at a comparison of recurrence rate for chronic conditions, we see that substance use is right on par with rates for other types of chronic illnesses. It also means that substance use should be treated and evaluated just like any other chronic condition. Along those same lines, it means that the treatment plan may be very variable for somebody with substance use disorder, just like treatment plans are going to be variable for people with other types of chronic conditions. For some, lifestyle changes may be enough to produce an outcome that's sustainable and manageable over time. For others, there may be lifestyle changes paired with medication temporarily that can, you know, achieve the change that is needed and then maintained over time. And for some, despite all of the lifestyle changes and best efforts, may still find that medication is necessary to manage and fill in some of the space that the the body is not able to do on its own. And that's what it means to be managing a chronic illness over time. You're not cured, it doesn't go away, but maintenance and treatment will look different for everyone, and not everyone is going to fit into the same box or the same length of time for their treatment plan. Having a substance use disorder is the most stigmatized health condition in the world, and it's still related to this idea of perceived cause and control over the disease. And anyone living with addiction who feels stigmatized are going to be less likely to seek treatment, less likely to stay engaged in treatment, and more likely to feel isolated and stuck in a pattern of unhealthy behaviors. A person-centered focus and operating from a trauma-informed lens is probably one of the easiest changes in mindset that can be very helpful in combating stigma in both the justice involved and individuals who are living with substance use disorder. And that simple change in mindset of going from what's wrong with you, which can be a very default thought when we're sitting across from someone who is different from us or we don't understand, but if we shift our mindset to what's happened to you and embrace the understanding that the reason someone is sitting across from us is because we are all a product of our experiences, our environments, the things we've been exposed to, the types of role models and lessons that have been reinforced in our lives growing up. And shifting that to something that's inherently problematic with you as a person and shifting it to what has happened to you that is has influenced where you are today is much more effective in ensuring that the person-centered focus doesn't get lost, but it also becomes very effective is in understanding what has happened to people is important for us to help figure out because that's the only way that we can address needs, introduce resources and treatment and things that will be effective to helping somebody in the long run. It's also important if you're working in this population to keep in mind that there is often a perception bias. Patients who improve leave and are often forgotten. Patients who do not improve return frequently and those are the ones that we tend to remember. It can lead us to think that most patients do not improve, but that is contrary to the scientific data that's out there and the recovery and successful treatment rates that do exist. This slide helps illustrate the hierarchy of stigma and OUD recovery compared to the effectiveness of some of the treatment modalities. And what's really interesting is the the top of the list for stigma, right, medication-free, abstinence-only, is often the preferred method of recovery and the further down the list that you go, the more stigma that we see often being associated with those types of medication-based pathways. But interestingly enough, when you look at the science and the data and the research outcomes that exist, the further down on this list that we go, we actually see an increase in effectiveness where medication-free, abstinence-only is actually the least effective when you start looking at long-term outcomes. And the other options on the list have an increase in effectiveness the further down the list you go. And so I think it's very important to try and combat stigma with some of the evidence and science that's out there that supports that not only are medication-based pathways effective, they're actually more effective than some of the preferred pathways of abstinence-only that still exist out there. So the primary goals of treatment with medications focus on stabilizing functioning by reducing and eliminating withdrawal symptoms, craving, and recurrence of use. Very often we hear medications for opioid use disorder being described as just swapping one addiction for another, replacing one drug with another, and I think this chart that is presented here is very helpful in kind of addressing some of these myths and providing a more appropriate mindset for what's really going on here. So I encourage you to pause on this slide and make sure to read and understand the differences between somebody who is actively in substance use, engaged in drug culture, and taking a drug to get high versus somebody who is in a recovery mindset, is taking a medication under the care and treatment of a medical provider, and is using this medication to get healthy and well. Let's discuss what it means for medications to be considered evidence-based OUD treatment. The three FDA-approved medications for OUD include methadone, buprenorphine, and naltrexone. Medications for OUD are at least twice as effective as abstinence-only for sustaining recovery. There's abundant evidence that medications reduce opioid use and opioid use disorder related symptoms, that being on medications increase length of time in treatment, they lower the risk of overdose mortality, that taking medications is associated with a reduced risk of infectious disease transmission, and we also see a reduction in criminal behavior associated with drug use when someone is on medication-based treatment strategy. How medications for opioid use disorder work in the brain? Methadone, buprenorphine, and naltrexone all have an impact on the effects of opioids and opioid receptors in the brain, and these medications create stability and consistency. Now they do so in a little bit different way. So the opioid receptors in the brain that have previously been occupied by whatever substance was leading to opioid use disorder, methadone, buprenorphine, and naltrexone are going to take over these opioid receptors and create their own functioning on these receptors. They do so slightly differently because methadone is a full agonist, so it's going to fully occupy that receptor while also creating kind of a blocking effect tolerance from other opioids. Buprenorphine does not completely bind or fill, it has what we call a sealing effect, meaning that you're not going to fully activate that receptor no matter how much of that medication is introduced into the system. And naltrexone is considered a non-narcotic because it doesn't do anything to activate the receptor, it blocks the receptor and is a barrier to other opioids. So let's break down what each of these categories means in a little more detail. An agonist activates a receptor, so when a chemical fills or binds to that receptor, it's going to cause an action. In this case, with opioids, the action that they're causing is analgesia or pain relief. Heroin, oxycodone, hydrocodone, morphine, opium, fentanyl, and others are short-acting agonists, meaning that they will fully fill that receptor and activate it, but their effect is also going to wear off very quickly over time. Methadone is also a full agonist, the difference being here that it is a long acting agonist, meaning that it is going to fill that receptor but it's not going to wear off as quickly, and this is going to become very important in understanding how medications are different than the substances that may have been causing the substance use disorder. A partial agonist, or sometimes called a partial agonist slash antagonist, basically just has combined agonist and antagonistic properties, meaning that from an agonist side of things, it is going to activate the opioid receptors but it's going to do so to a much lesser degree. It has what's called a ceiling effect, meaning that there is a limit or a plateau of how much activation is going to occur on that receptor, meaning that at some point, the more medication that's being introduced is going to stop having an effect on that receptor and you will only ever reach partial activation of that receptor. The antagonistic properties of the medication also means that simultaneously, it is blocking that receptor and having an impact on the effects of any other opioids that may be present. So it's doing kind of a dual work of partially activating that receptor but then also partially blocking anything else that may be in the system. So buprenorphine is a partial agonist and it has that ceiling effect, meaning that there's only so much that can be activated, but it's also blocking the effects of other opioids. An antagonist blocks receptors in the brain. If you're blocking the receptor, you're preventing other chemicals from binding and attaching to those receptors and therefore you're preventing an action which means that no effect is going to take place. This includes naloxone and naltrexone. What's also interesting about antagonists is while they do block the receptors, they will only block an empty receptor, meaning that if the receptor is already empty, then it just closes and puts a lid on that receptor so nothing else can enter or bind to it. However, if there is something already on and attached and binded to that opioid receptor, an antagonist is first going to kick everything off and then it will put a lid on it and close that receptor. And so antagonist medications include naloxone, which we often know as brand name Narcan, and naltrexone, which is more commonly understood as the extended release Vivitrol. This slide visually represents the opioid receptor activation and I think it's very helpful in starting to highlight the mechanisms of why methadone and buprenorphine are very different behind the scenes when compared to heroin, fentanyl, or any of your other short-acting opioids. As represented by that red line, that heroin or fentanyl is going to have a very sharp and dramatic increase of the opioid receptor activation, but it's also paired with a very significant and drastic decrease that happens relatively quickly. And therefore, in active use, you're trying to recreate that spike and avoid that decline over time, so it's a lot of up-down, up-down. It's unstable. It actually tells your brain and your body that you're in crisis because it's not stable or sustainable, and therefore your brain and your body prioritize seeking out that substance rather than doing some of the regular routine operations that it needs to do to be able to maintain healthy behaviors and healthy conditions behind the scenes. So the difference in methadone and buprenorphine is that, first and foremost, you don't have that immediate spike. Because these are longer-acting medications, they take a little while to build up, but it also means that they're more stable and consistent over time. And once you meet that maintenance-level dosage, you're creating that very kind of plateaued, you know, stable and consistent environment. And what that also does is tells the brain and the body that it's not this crazy, chaotic rollercoaster ride that needs to be sought out and maintained, but instead it creates stability and consistency so then the brain and the body can kind of resume back to business as usual and start reprioritizing all of those routine functions that kind of got hijacked and reprioritized when we had just short-acting opioids in the system. And so methadone and buprenorphine are not just replacing one substance with another. It very much is an entirely different environment that's being created behind the scenes. So just because all of these substances and medications are sharing the same opioid receptors does not mean that the experience is equivalent to each other. You can also note that naltrexone is at the bottom there. There is no opioid receptor activation because it is an antagonist so all it does is block the receptor. It does not activate it, but you still are creating that stability, consistency, and predictability over time, which is why all three of these FDA approved medications are much more effective for treating OUD and they are not just swapping in another opioid to replace the opioid that was there before. Identifying and screening for OUD can happen in a lot of different ways, the most common being brief screens that are utilized by multidisciplinary staff and the goal is to have a question or a couple of questions to identify individuals with a history of substance use disorder and if they screen positive then they get referred to clinicians for additional assessment both for the diagnosis of opioid use disorder as well as the appropriateness of any types of treatment plans. If you're looking for basic signs or symptoms of withdrawal you're essentially looking for symptoms that resemble a flu-like illness and depending on the particular substance the symptoms may have varying periods of when they first emerge as well as how long they last. You're short-acting opioids like heroin or your prescription painkillers usually 8 to 24 hours after that last use you'll start to see withdrawal symptoms emerge and they're going to last for an average of up to 10 days. You're longer acting opioids such as methadone and even buprenorphine to a certain extent you're not going to see that instant withdrawal kick in it usually takes a few days for withdrawal symptoms to emerge however once withdrawal starts you usually see that they start to fade again within that period of 10 days give or take depending on the individual. There are a variety of tools to clinically assess withdrawal the most common being the clinical opiate withdrawal scale or the CALS score and this helps categorize the withdrawal state by taking into consideration the patient's symptoms and behaviors and providing a numeric score of where someone is in that timeline of withdrawal. It's important also keep in mind that if withdrawal was precipitated or brought on suddenly by the introduction of an antagonist like naloxone into the system you're likely to see a more severe syndrome that can occur with more extreme and aggressive symptoms that may be presented. These types of assessments are really important especially if you're looking to introduce a medication like buprenorphine that is that partial agonist partial antagonist because it helps assure that somebody is in that appropriate window of time where the introduction of a medication will be helpful rather than the introduction that could be precipitating withdrawal and so there is kind of an important timeline to keep in mind if we are entering into a partial agonist treatment plan. Toxicology and other tests are also supportive of clinical assessment and diagnosis of opioid use including the ability to rule out withdrawal from other substances as well as identify if polysubstance or combination of substances are at play. The amount of time that substances will show up in a urine drug screen are variable. It's also important that certain substances have to be specifically tested for and may not be included on your regular drug screen kits with fentanyl still being less common and having to be specifically tested for. It's also important to mention that positives for other substances alongside opioids does not hinder starting a medication-based treatment for OUD. It should be addressed and assessed maybe in other treatment planning and goal setting but is not a reason not to consider a medication-based pathway for OUD. Methadone and buprenorphine will not show positive on an opiate test screen. They need to be specifically tested for so that's also a useful tool because it's able to distinguish if somebody is taking a medication-based treatment or if somebody is still using other types of opioids. They do not read the same on a urine drug screen. It's also important that if they're not specifically tested for most will not be able to see if somebody's on methadone or buprenorphine with a standard drug screen. There's other tools and tests that are available that can also be helpful and should be done if you're looking at treating the whole person. Opioid use disorder is treated with long-acting opioid agonists or partial agonists. Buprenorphine can be utilized in the acute withdrawal stage. It's important to keep in mind that there is the potential for buprenorphine to exacerbate withdrawal because of its partial antagonistic effect and that's why a clinical guideline such as the cow score has been developed to assist in initiation and timing of the introduction of this therapy. Treating opioid use disorder, the same treatment strategy applies to patients who are undergoing withdrawal kind of naturally from the inability to obtain and take opioids as well as to someone who maybe has had precipitated withdrawal from an antagonist such as naloxone. So it doesn't matter how we got there if somebody is entering withdrawal then they have the ability to be treated with medications for OUD. Of course it's important to recommend psychiatric evaluation just to assess and rule out any other medical health concerns that may be going on. Now let's transition some of our conversation to justice involved populations. In justice populations there's something called the age crime curve that is just looking at rates of criminal behavior usually pulled from arrest data and the age of the individuals that are engaging in this behavior over time. And for the most part there's this curve where there's kind of a peak in late adolescence early adulthood and there's almost what you would think is a maturation maturing out of criminal behavior over time. Other researchers though have looked at this kind of general curve in the population and says that it's actually not just one curve but there's very two distinct category groups that are emerging that produce this general age crime curve. The first group being what we would call the adolescent limited and this is where there's going to be that peak of delinquent behavior in early adolescence young adulthood and a sharp decrease and desistance from that behavior over time. The other group though is that we have is the lifetime persistent and the biggest factor that kind of distinguishes who's in that adolescent limited of you know kids being kids making bad choices you know not having a fully developed brain yet types of behaviors versus those that kind of maintain and persist in criminal behavior over time. You'll also see in the lifetime persistent group that it's not this big peak of kind of in and out of adolescent delinquency that is happening but instead it's kind of a low and slow burn over the course of a lifetime and the biggest difference here is that the majority of people involved in both substance use and delinquent behavior persist in this lifetime persistent category and it's really important to keep in mind that substance use is the most important modifiable risk factor meaning that if we can have an impact on substance use we can absolutely have a much more tangible impact on preventing this lifetime persistence from being the pathway that somebody is on over the course of their lifetime. So by fixing substance use we're going to have an impact on the delinquency that often co-occurs with it. So what's the importance to justice professionals for understanding addiction? Well the biggest being that there is huge overlap in the prevalence of substance use and criminal behavior and there's a ton of research out there but a rough generalizing of some of the trends is that around 80% of individuals who are justice involved are there as a result either directly or indirectly because of alcohol or drugs. Around two thirds of the population is going to test positive for substance use and arrest and 63% of persons in jail, 58% of persons in prison would meet the clinical criteria of having a substance use disorder and it really is variable depends on the region depends on the study but anywhere between 17% and 81% are finding themselves in acute withdrawal at the time of entry into the justice system and requiring detox or medically managed withdrawal services. So the importance of identifying substance use disorders in the justice system is that scientific research has consistently supported that screening and treating substance use disorders while a person is involved in the justice system is effective in approving long-term outcomes. So if you're early detecting SUDs you're helping to save and rebuild lives you have the ability to reduce recidivism and of course promoting public safety and public health that go hand-in-hand with improving individual outcomes. Screening and assessment can also support diversion of individuals from an overburdened justice system and so treatment is a viable pathway and has been shown to be effective for many justice involved candidates. It enables alternatives to incarceration being appropriate and effective and it also helps support the decisions about immediate medical needs, release planning, what goes into community supervision. Generally speaking if we want people to be successful we have to make sure that we are assessing and understanding what and how substance use may be playing a role with that individual. So substance use public health and community roles are constantly shifting as well. Really in the last decade we've seen courts and law enforcement drastically changing their roles. We've seen the expansion of specialty courts. We've seen law enforcement paired sobering centers. We've looked at mental health divisions within law enforcement entities but jails and prisons have been a little slower to adapt and it's unfortunate because often jails and prisons are still the largest mental health provider in these justice settings and many of the correctional settings medication assisted treatment or medications for OUD are still largely absent but we are seeing growth in that category so we are seeing progress and movement but we're well under a threshold of what we should be seeing for access to that type of care in these settings. Addiction is a chronic medical condition therefore a person does not stop having a medical condition just because they've been incarcerated. It's also important to be mindful that non medically trained criminal justice professionals should never make medical or medication based decisions related to treatment of a medical condition. Research in justice involved populations have repeatedly shown that recurrence rates upon release are very concerning. Within the first two weeks of release an individual is 40 times more likely to overdose with fatal overdose being the leading cause of death after release. This rate stays tenfold higher even up to a year after release and part of what's going on is that low tolerance that's happening after a period of non-use creates a greater risk if an individual goes out and does use. When we look at the percentage of justice involved individuals that are receiving medication-based treatment for opioid use disorder that number has remained relatively consistent at less than 5% of the population. Recidivism is reduced when medication treatment is introduced with justice populations. There's a lot of studies and data to support that there is both a reduction in post-incarceration deaths from overdose among individuals who are receiving medications for OUD well incarcerated in correctional facilities. We also know that untreated OUD is going to contribute to a return to the same behaviors and activities that likely led them to be justice involved in the first place. Reincarcerations, other risky behaviors, and generally just all of these other risk factors are what's out there if we don't create change by introducing medication-based treatments in this setting. Well litigation has not made its way to every individual state yet there is a large and growing body of legal precedent that is emerging throughout the rest of the country. Back in 2019 the United States Court of Appeals for the First Circuit up in the New England area established precedent that individuals incarcerated must have a right to treatment including medication-based treatment during their incarceration period. So even though every state has not had litigation reach them yet more and more states are finding that these types of litigations are occurring and are being ruled in favor of providing medication for a medical condition well incarcerated. In addition to overdoses post-release we're actually also seeing a spike in overdose events during the incarceration period. It appears to be on the rise so looking at data you know from 2009 to 2019 we're seeing a lot of increases in mortality rates in prisons and in jail settings and unfortunately this surge is outpacing the same increases in trends we're seeing in the general national drug overdose rates and so it also is despite a decrease in the number of those being incarcerated for drug crimes which altogether that really just means that there is very much diversion of illicit substances into the correctional settings and we need to have better responses for those that are dealing with opioid use disorder and need access to appropriate care to decrease some of these mortality rates in these settings. Naloxone is approved by the FDA to reverse overdose by opioids. There is a variety of brand names out there most common being Narcan but there are others and there are other similar medications different from naloxone that are opioid reversal agents. Generally speaking though they're administered by injection or nasal spray the nasal spray becoming the more common possibly just because of ease of use and comfort level is is greater for most individuals. The naloxone as an antagonist has the greater affinity for those opiate receptors in the brain so they're going to clear out that receptor right if it's got any other opioids on those receptors it's going to knock them off and then it's going to block that receptor. Just keep in mind naloxone is very short-acting it is a temporary effect meaning that as the naloxone wears off it's very likely that opioids are still present in the system and if they're still present at a high enough rate they can rebind to all of those receptors and potentially put someone in a subsequent overdose situation. So it's very important to administer naloxone and follow through with any medical evaluations. Naloxone does save lives it's very effective at reversing overdoses and saving lives. Unfortunately though it's not a fix-all it is an acute intervention it is not treatment and once somebody has been subject to an opioid poisoning event once they are at an increased rate that it may happen again with especially if there's no intervention or treatment that's made available to the individual for long-term care. Diversion is a concern that's always brought up if you're providing a substance or a medication to one part of the population and wondering how much of that substance is going to be diverted to other members in that population. And the research and evidence that's out there looking at buprenorphine in incarcerated settings is finding that non-prescribed buprenorphine is actually already pretty widely available in these settings. A recent study who screened individuals leaving incarcerated settings shows that as many as 81% reported buprenorphine being very or somewhat easy to get in those incarcerated restricted settings. And the best and easiest way to decrease diversion is to increase legitimate access to treatment with these medications because over and over the research shows that when you increase access to care then diversion of those types of medications decreases substantially. It's important to stay solution focused when implementing such a change as introducing medications for opioid use disorder in a justice setting. What can be viewed as very intimidating and challenging and inherently having a lot of barriers to the implementation, a different perspective will also show that these barriers actually have very achievable and effective and sustainable remedies that can be implemented and put into place to help make this transition as feasible as possible. The good news is if you're trying to implement mood strategies in your correctional setting there is a lot of support and guidance out there about how to do so effectively. From publications from SAMHSA to Correctional Health Care to legal guidance, legal action centers, your American Correctional Associations, there's a lot of information that's already out there. There's a lot of kind of best practices, how-to guides, evidence-based resources, as well as strategies that have already been implemented and employed elsewhere that are being used as case studies of how to repeat and implement in various settings. Please take a moment and complete the opioid response network evaluation survey link below. Grant funding has provided this training to you free and at no cost and is tailored to the request that was submitted. Your feedback on this training is very important in order for this type of work to be able to continue and be made available to individuals seeking out information and education. Please scan the QR code or click the link below to access the survey and please be as open and honest as possible on your feedback so that future trainings can incorporate those comments. Thank you very much!

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