The Impact of Addiction on Brain Development

Foreign. I'd like to welcome everybody to today's presentation on the impact of addiction on the child's brain. We're doing this in honor of Children's Health Day and also the last day of Recovery Month for 2020. I am your host, Dr. Donnelly Snipes. We're going to explore briefly brain development and what they call critical periods and the impact of exposure to alcohol, opioids, nicotine, cannabis and stimulants on the fetal brain. The impact of exposure to alcohol, opioids, nicotine, cannabis and stimulants on the developing brain. So we're going to talk about the fetal period as well as the developing brain. I want you to think of the brain kind of like a bonsai. And if you have ever done gardening, then you may be aware of the different periods of growth in a plant. When the plant first emerges from the seed, it's new green growth. And during this period it is really susceptible to wilting, it's susceptible to wind, it's susceptible to getting stuck, stepped on. There's a lot of, you know, danger. It is very fragile in this period. And that's what we're talking about in the fetal and child and adolescent brain. All the way through age 24, the brain is still growing. So if you liken it to a, to a plant that would be sort of like the softwood and the new green growth, it is very susceptible to problems. If you want to take it further and think of a bonsai tree, when you prune a bonsai, you are telling it to grow in certain directions and if you prune it in one area, then it won't grow there, it'll grow shoots somewhere else. When the brain is exposed to toxins of, of any sort, it's sort of like pruning that branch and it may go a different direction. And it's important to remember that during this period of brain development there's lots of cell differentiation and lots of stuff going on. And if the brain gets blocked in one place, it may say, okay, well I won't develop those dendrites, I'll go over here. So you, you are going to end up with a character characteristically different looking brain. Most drugs of abuse easily cross the placenta and can affect fetal brain development in utero. Exposures to drugs can have long lasting implications for brain structure and function. These effects on the develop, these affect the. Sorry, I can't talk. Developing nervous system because when the brain is young, it hasn't developed its homeostatic regulatory mechanisms. So when it is inundated with toxins. When it becomes excitotoxic, for example, it can't protect itself, just like the little sapling can't protect itself from gale force winds. Therefore, when the developing brain is exposed to drugs, it often differs from the effects on mature systems. Once the brain has developed its resources to protect itself, it. The. It doesn't. The. The drugs don't have the same intensity of effect and may actually have completely different effects on the brain. In the fetus, drugs can impact blood flow to the placenta. So if a mother is taking something that is going to either dilate or constrict blood vessels, that's going to impact the blood flow to the placenta as well as everywhere else in the person's body. Drugs. We know from other studies and other classes that drug use, you know, in infusing your body with extreme amounts of what your brain perceives as toxins, and the withdrawal period, when all of a sudden all those go away, that activates the HPA axis and it increases stress and increases stress hormones, which actually, like cortisol, act directly on the neurological mechanisms of the fetus. So what happens to mom happens to fetus, and we do need to be sensitive to that. Critical early events. There are a lot of periods during brain development that it's really important to be aware of. And from conception all the way through age 24, the brain is much more susceptible to injury. However, there are certain critical periods in development where there may be more injury. The neural tube is closed around day 22 of embryonic life and neurogenesis. Most people don't even know they're pregnant at this point. And there is another period when neurogenesis is theoretically complete, which is at 16 weeks, you've got, you know, 22 days, which, again, most people don't know they're pregnant, and 16 weeks, which is four months, you know, kind of into that second trimester. During the second half of gestation, nerve cells in the brain are generated and migrate to the appropriate brain regions. So basically, in the first half of gestation, if you want to oversimplify it, the shell of the brain is kind of created and, and all of the stuff that's needed for brain functioning is moved in during the second half of gestation. All of that stuff is essentially unpacked and put away. If you want to think about it that way. Elevated prenatal psychological or, and or biological stress signals repeatedly have been linked to HPA axis dysfunction and fearful temperament, as well as internalizing and externalizing behavioral problems in childhood. And Adolescence, even if the parent is not ingesting illicit substances. You know, it is possible with extreme stress even that that influx, that constant high level of glutamate and norepinephrine and is going to impact the environment in which the baby is growing and it's going to impact brain development. Affected regions are associated with higher order cognitive functions, including reasoning, planning, attention, working, and recall language, and social and emotional processing. So pretty much a lot of our higher order things, breathing's not, not impacted very much, But a lot of the things that make us human are impacted as a result of prenatal stress. One thing I found interesting was the developing organism has been found to make adjustments based on its predicted postnatal environment. So if the environment in which the baby is forming, the fetus is forming, is saturated with stress hormones, then the brain is going to prepare for an environment in which it's always going to be saturated with stress hormones, which is kind of interesting. Fetuses exposed to an improvised impoverished intrauterine environment will prepare for and perhaps thrive in a postnatal environment of nutritional skill scarcity. So if the baby is not getting enough nutrition, and we know a lot of people who abuse drugs also have poor nutrition, if the baby has, if the parent has poor nutrition while the baby is in utero, then that baby is going to potentially prepare for nutritional scarcity, which may mean dialing down that base metabolic rate. That same fetus, if it is instead born into an environment of nutritional abundance because of these developmental adjustments, is now potentially at an increased risk for obesity, diabetes, and cardiovascular disease. It's going to gain weight faster and potentially easier than its counterparts because the body learned, the brain learned when it was in utero, that nutrition was scarce and it needed to conserve energy. I thought that was fascinating. So think about whatever is happening in the uterine environment is a practice run, a staging, if you will, for what the fetus expects when it's, it's born in, into the world. So it's going to prepare for that, it's going to create the receptors and, you know, eliminate certain receptors based on what it anticipates the environment being based on the environment that it's growing up in. So if it grows up in a healthy environment, it's going to be prepared for a healthy environment. If it grows up in an impoverished environment, it's actually already going to have the survival adaptations in some ways to survive a little bit better in an impoverished environment. People who are pregnant show a decline in physiological and behavioral responses to stress during the third Trimester, including a reduced cortisol response, decreased blood pressure, heart rate, and catecholamine responses to both psychological and physical challenges. I thought this was fascinating because the body is preparing that fetal environment, it doesn't want the fetus to experience stress. So during the third trimester, interestingly, that cortisol response is dampened. Injury occurring at specific stages of postnatal life can dramatically reshape the underlying circuit development, which becomes increasingly more difficult to correct later in life. Stuff that happens during the fetal period can sometimes be ameliorated if you work with children, especially if you work with very young children. You probably already know about the Early Steps program. This is an invaluable program to identifying children who, for whatever reason, may have developmental delays. I worked with Early Steps as initially as a parent, because both of my children were micro preemies and they needed additional, you know, services in order to help them catch up to, you know, other children of their, of their age, so to speak. But when children are born, we can't undo everything. If there are certain types of brain damage, it may not be completely reversible, but a lot of stuff, because the brain is so malleable at this point, a lot of things can be greatly improved upon, and that's important. The earlier we intervene, the easier it is to correct it. Using. Instead of using the bonsai analogy, let's think of another analogy. Think about clay or concrete. You know, the earlier you try to make a change in the shape or smooth out a, a problem in the clay or in the concrete, the easier it's going to be to fix. If you wait until that concrete has hardened or until the, the clay has been put in the kiln, it's going to be dagum, next to impossible to effectively fix. The brain's physical structures are set at around age six. Wow. Okay. So the physical structures aren't even set until the child is entering first grade. So let's think about how the prenatal environment, as well as the antenatal environment, you know, up to age 6, can be so powerful on the child's brain development. That includes nutrition, as well as exposure to things like secondhand smoke. During adolescence. You know, the physical structures are set during adolescence. Different parts of the brain form hundreds of millions of connections. So this is when everything starts to, well, connect. You know, think about, if you are a city planner, this is when we are laying out all the roadways to figure out how you're most efficiently going to get from one place to another. Frontal cortical development. We Talk about the prefrontal cortex a lot in my classes. And frontal cortical development comes later, is actually the last thing to develop and likely contributes to refinement of reasoning, goal setting, impulse control, and evaluating long and short term goals. Think about our drinking age. It's 21. Think about when youth often start smoking and experimenting with drugs way before 21. Remember that, that is during that period when the brain is still extremely malleable, when it's going to react much stronger because it doesn't have its homeostatic mechanisms solidified yet, it's going to react much stronger to the assault from alcohol or, or other drugs, you know, all the way up to age 24. So even people who are legally drinking and legally smoking are potentially causing significant changes in their brain structure. Just putting that out there. Alcohol Alcohol exposure appears to affect the timing and pattern of nerve cell generation, both delaying the process and altering the number of cells that are produced. Babies that are born to people who consumed alcohol while they were pregnant have smaller brain sizes. Early heavy exposure leads to the most severe outcomes and is associated with mental retardation, sensory deficits and motor problems. Now we think about fetal alcohol spectrum disorders. It's important to understand that they don't know, unfortunately, they don't know how much alcohol or the timing of alcohol ingestion. They don't know when it is most significant or most likely to cause fetal alcohol spectrum issues. They found fetal alcohol spectrum issues in children who were born to parents who only drank, you know, maybe one drink a day or some who only drank during the first trimester when they didn't know they were pregnant. And they've also found other children with FASDs who were born to parents who drank a whole lot more. And then there are some kids who are born to parents who drank who don't end up with an fasd. So they're not exactly sure when or how much. But the guideline is not don't drink when you're pregnant. Unusual cell formations can be seen in many areas of the brain, including the hippocampus, which is responsible for learning, memory and the fight orf flight response. The cerebellum, which is responsible for motor activity, and the neocortex, which is responsible for sensory perception, motor activity and spatial reasoning. Now, it's been a long time since most of us have had, you know, biophysiology. So, you know, I, I, I will put next to the brain structures what they're basically responsible for doing on most of the slides. So you don't have to try to remember what, what was the hip, hippocampus responsible for? But let's think about these really quick. If a child has unusual cell formations in the hippocampus, for example, which impact the child's learning, memory and fight or flight or emotional regulation, what is that going to look like in terms of mental health and behavioral issues? And what may need to be addressed in early steps and in early intervention in order to make sure that that child can learn, develop memory and, and regulate emotions. The cerebellum, the motor activity. A lot of times we see hyperactivity as a result of the damage caused by fetal alcohol exposure to, to alcohol and the neocortex. Sensory perception. What you hear, what you see, what you smell can be impacted. And for a child, that could mean that it becomes much more potent and overwhelming, or it may be much duller. But we do want to recognize that alcohol potentially affects most higher order areas of the brain. Nicotine, you know, this is another one of those legal drugs. And when I talk about nicotine, I'm spilling specifically using that word, not tobacco, because nicotine is extremely toxic to the brain and it is one of the most addictive drugs out there. And this includes nicotine from nicotine replacement therapy and from, you know, vaping that is just theoretically, quote, pure nicotine. We want to recognize that it's not just tobacco, but it's nicotine as well that affects the fetus. Nicotine readily passes through the placenta like most other drugs. But fetal concentration of nicotine is significantly greater than that achieved by the mother. So if the mother drink, drinks, sorry, if the mother smokes 1 milligram of nicotine, it will be potentially 1.25 or 1.55 milligrams. You know, I'm, you see what I'm getting at in, in the fetus, it's going to be much more potent in a much smaller, much more vulnerable organism. Exposure to nicotine through maternal consumption, either through smoking, vaping, or nicotine replacement therapy, or even secondhand smoke. And that's not just the occasional walking by it, smoking, somebody smoking outside of a store. But if you're in a household where other people are smoking and you're smelling it, you're getting that secondhand smoke, you know, several hours a day. You know, that can disrupt the choliner, cholinergic system, which is a key modulator of brain development. It also alters what they call synaptogenesis, which is the formation, genesis, formation of synapses, neuronal migration. So moving those neurons around to Start forming the neural networks and neurotransmitter release. We know when we're dealing with people who have depression or schizophrenia or other issues that a lot of those problems can be traced back to imbalances in neurotransmitter systems. Well, we also know now that nicotine alters the formation of synapses, neuronal migration, neurotransmitter release, and brain development. Newborns exposed in your utero to nicotine tend to be more irritable, have poorer attention, exhibit hypertonicity, which they tend to be stiffer, increased tremors and startle responses and, and poorer self regulation than unexposed infants. So they tend to be much more hypervigilant, if you want to think about it that way, much more irritable. Children exposed to nicotine in utero show increases in externalizing behaviors as young as 18 to 24 months. So they looked at children who were 18 to 24 months, you know, preschool age, daycare age, and found that those children had much more difficulty with emotional regulation and tended to be much more impulsive and externalizing. They tended to do more biting, hitting, yelling, as opposed to withdrawing. For example, A study of 3 year olds exposed to tobacco in utero, now notice this, this particular study looked at tobacco. A study of 3 year olds exposed to tobacco in utero determined that increases in oppositional were correlated, interestingly enough, with third trimester exposure. You know, a lot of times we're taught well, you know, the really dangerous period is the first trimester. That's not exactly true. There's a lot of stuff going on in the first trimester and the danger of miscarriage is much higher in the first trimester. But brain development goes, as I said, all the way through age 24. Children age 6 and younger exposed prenatally had decreased receptive language skills. So they had a harder time learning and understanding what's being said and an increased likelihood of ADHD. 16 to 18 year olds that were exposed in utero, so we're now looking at, you know, 18 years past exposure, exhibited cognitive deficits. Interestingly, this effect appears to be withdrawal induced. A lot of these children became smokers themselves. They started self medicating at a, a lot of them at a much earlier age. So when they weren't, when they didn't have the nicotine in their system, they had cognitive deficits and increased impulsivity. Prenatal exposure to nicotine greatly increased the risk of later tobacco use and the development of substance use disorders. When that brain chemistry is altered, when those receptors are altered. When the dopamine system is altered, the. It's sort of priming the brain to want, need, crave whatever words you want to use. The influx of external stimulation, it's prepared for those exogenous substances to come in and assault it. If you want to think about it that way. Now remember, when we're dealing with humans, we can't say that every three year old exposed to tobacco in utero is going to have this. We see a greater likelihood, a greater correlation, not necessarily causation. And they did not examine in that particular study, Pat, whether the teenagers were living in a household with smokers. My guess is they probably were. And it's important to recognize that, that children growing up, I grew up in a household, this was, you know, way back when when people still smoked in restaurants and everything with a mother who was a chain smoker. And so I was exposed to it consistently. And when we, now we know that when we look at children who are exposed consistently to nicotine, secondhand smoke at home, that they often have withdrawal type symptoms when they're at school, when they're several hours removed from nicotine exposure, which is kind of interesting. Cannabis has also been legalized in a lot of places. Now remember cannabis, we're talking about marijuana with THC in it. We're not talking about CBD oil, we're talking about substances with thc. THC can cross the placenta with reasonable efficiency. Endogenous cannabinoids, that's the cannabinoids that your brain produces, it's itself are crucial for proper development in utero. We are starting to learn more and more about these cannabinoid receptors in our brain and that they're responsible for a lot of stuff, just like serotonin is and, and we can't ignore them. And we're starting to see how these cannabinoid receptors are involved. You know, we've known for a long time that cannabis can help address nausea, for example. And we're starting to learn how it these cannabinoid receptors impact people's mood and their physiological functioning. But in utero, cannabinoids assist in proper fetal development. Exogenous cannabinoids, that means anything that you're taking in from the outside, such as marijuana, often alter those fetal growth trajectories because they're getting too much, it's coming in and the little fetal brains going, whoa, you know, you're overwhelming me with too much of this stuff. It's a tidal wave. And so the brain starts to adapt to try to protect itself, which means when the marijuana is not being ingested exogenously, that the amount that the brain produces endogenously, then the amount the brain produces itself is insufficient because the body has adjusted to having too much coming in. Newborns exposed to marijuana exhibit sleep disturbances, altered responses to visual stimuli, increased startles and tremors which often persist through age three. Now the interesting thing, or the positive thing, if you want to embrace the dialectics here is it seems to dissipate after age three. But we do want to recognize that there are changes that occur and impact the, the young little person up to age 3 which also impact the caregivers because it probably means the child is more irritable, more demanding sometimes and, and may not sleep as well. Prenatally exposed school aged children exhibit deficits in executive functioning and verbal and memory tasks. Executive functioning, remember is decision making, planning, impulse control, you know, all that prefrontal cortex stuff. Six year olds showed attention deficits, elevated impulsivity, hyperactivity, still problems with short term memory and verbal reasoning. Think about how important it is for a six year old to be able to sit in class and pay attention to, not impulsively get up, walk around the room to remember things, you know, short term memory, learning what the teacher's saying and verbal reasoning. Our classrooms, our American school system is based on verbal auditory learning. So if the child is having difficulty processing this, what does that mean for their abilities to succeed in the classroom environment? Elevated levels of D2D dopamine receptor transcript in the amygdala of males, not females, just males, suggest the potential for altered emotional regulation in males that are exposed to cannabis in utero. They are starting to examine sex differences in the effects of, of a lot of drugs on people. Even in their 20s, exposed individuals will still have deficits in working memory and impulse passivity. Let that sit with you. Now, going back to what Pat asked earlier about nature versus nurture, even in their 20s. Now does that, does this apply to everyone or only children who did not have a responsive healing environment in their early child and toddlerhood? I don't know. Prenatally exposed children were also more likely to experiment with marijuana at an earlier age and use more frequently? Again, the brain has been primed to have to be inundated, have those cannabinoid receptors inundated from exogenous cannabinoids. So this is a form of self regulation, if you want to think about it that way, because the brain is waiting for it. Some studies have shown that exposure to THC during the Second trimester may also result in increased heroin seeking behavior in youth, which is interesting. Now, there's a lot of possibilities and correlations there. It doesn't mean for sure, but it is one of those things to kind of take in mind, keep in mind opioids. Now, a lot of, I don't know what it's like now, but when I was pregnant with my children, the doctor didn't have a problem with opioids, so to speak. He was like, nah, it's not a big deal. It's not going to harm the fetus. You know, obviously taken as prescribed. But, you know, now we're learning that that may not be the case so much, especially if you're taking it long term. Opioid receptor expression and endogenous opioid concentrations. Remember, that's the opioids the brain produces itself in the fetus and neonate differ from that in adults. So the way the brain handles opioids and the amount of opioids in the neonate's brain differ from that of adults. Exposure to opioids in utero and childhood may have more distinctive effects compared with adult exposure. Just like any other drug at the pre and elementary school ages, prenatally exposed children show motor and cognitive impairments, inattention and hyperactivity. These are important targets for clinicians who work with toddlers and early school age youth to recognize that there may be some impairments there and figure out how to mitigate them as much as possible. Deficits in spatial learning and memory may be tied to hippocampal cholinergic alterations. Some of these alterations, like I said, we may be able to help the child work around, you know, after a stroke, for example, we know that people who have a stroke who lose the ability to speak, speak, may be able to learn how to speak and communicate again, even if that portion, a portion of their brain is completely harmed. It's important to recognize that's even more possible in the developing brain to help the the brain basically do a workaround. But it's important that we step in and provide this nurturing, healing environment as quickly as possible. The American College of Obstetrics and gynecology in 2012 recommended opioid maintenance therapy. That's medication assisted therapy. Think buprenorphine as the first line of treatment for opioid dependence during pregnancy. Since illicit opioid use is associated with poor prenatal care, nutrition and poor fetal health. When the fetal brain is exposed to opioids and then goes through withdrawal and exposed to opioids and then go through withdrawal that is extremely traumatic on the tissues and the structures of the brain. So it is better in this case to make sure that the environment, that the host, the parent is able to access prenatal care, has good nutrition and that, you know, if the, if the child has to be exposed to opioids, that it is at a steady, low dose like buprenorphine, in order to prevent those withdrawals, those ebbs and flows that can be so incredibly damaging. Prenatal buprenorphine may produce fewer neurobehavioral problems than methadone. Naltrexone exposure. Now, naltrexone, remember, is the one that prompts opioid withdrawal. Okay, it's the opposite. Now, trexone exposure during pregnancy often should be avoided as it significantly impacts the endogenous opioid systems in the child's brain in utero. We know that those systems are there. They're there for a reason. The body needs them. The fetal body needs them to grow. So if the, the mother is taking naltrexone, it may essentially shut off those endogenous opioid systems in the fetal brain and they're not sure what the impact is. Now, some parents opt for naltrexone therapy, and that is an option out there, but generally it's not the first line recommendation. Stimulants, and we're talking about amphetamines, methamphetamines, Adderall, any of those, you know, high intensity stimulants. I'm not necessarily talking about caffeine unless you're, you know, way overdoing it. Stimulants affect the serotonin system and activate the reward system by triggering a massive release of dopamine. This can be especially problematic to the fetal brain in the second trimester. Brain changes in exposed neonates include abnormal brain development closely resembling that in oxygen deprived infants, including altered density in the white matter. So the brain is of a smaller size and it has altered density in remember, the brain has white and gray matter. So there are significant actual physical structural changes that represent basically asphyxia. The brain was being starved of oxygen. That's not good in any situation. There are decreases in sizes of certain brain regions, including the putamin, which is involved in learning, the hippocampus, which is involved in learning and memory and correlated with poorer sustained attention and verbal memory. Now, you may not remember the difference with white matter and gray matter and all that stuff, but suffice it to say that there are more than 100 disorders associated with Problems in the white matter. All of these disorders have a uniting thread or commonality that they are associated with cognitive dysfunction and emotional dysregulation. Prenatal amphetamine exposure was associated with externalizing behavior problems. And at five years, a lot of children who are exposed in utero to drugs have externalizing issues. So emotion regulation is going to be really vital for everybody. You know, for the parent who may be having difficulty dealing with feeling overwhelmed with a cranky, colicky infant, to the child, you know, when they start to get a little bit older, where we start teaching them even from a young age, they don't hit, they don't throw, they don't bite. What do they do? We can't just say don't do that because they've got to have something. They're, they're externalizing, they're communicating something. So how can they communicate their distress in an appropriate fashion? And, and that's a huge target for young children. Maturational changes are regionally age and sex dependent and occur in different brain regions at different times. As I mentioned earlier. The prefrontal cortex, for example, is the last area to fully develop. So it is, has a longer window of vulnerability during adolescence. There are also numerous alterations in dopamine pathways. What do we associate dopamine with? Mostly addiction. Dopamine is your perseveration neurochemical. It says, I want to do that again. Let's, let's do that again. That, that was really awesome. Dopamine triggers an increase in endogenous opioids, which you know, is where your pleasure comes from. Dopamine imbalances are also associated with things like depression and schizophrenia. So altering these dopamine pathways can be really bad mojo. Early mid adolescent exposure to drugs. So we're out of the fetal period, we're into the child period. Early and mid adolescent exposure may be especially likely to affect social behavior, reward sensitivity and affect regulation. So think about what's going on with the child at this point in time. And they are, you know, going through changes, they're going through puberty. And when we talk about early and middle adolescence, we're really talking about pre pubertal exposure. And during this time, it seems like the brain areas that are most susceptible are reward, which is dopamine, and social behavior, which also includes oxytocin and affect regulation. Late adolescent exposure so we're thinking post puberty, you know, 13, 14 on to 24 may be more likely to disrupt cognitive task issues because of the more slowly developing prefrontal cortex systems. So by after puberty pretty much. Not completely, but mostly the area that's going to be most malleable is that prefrontal cortex where we have impulse control, problem solving, reasoning, all of those things. The most common alterations reported across substance use substances used are in the frontal lobe, which is the last region to complete development. Adolescence is a time of neurobiological development and increased propensity to seek out novel stimulation and engage in risk taking behaviors which can alter development. Know think back to that bonsai tree. This is the time where certain receptor pathways if you. I'm greatly overgeneralizing and oversimplifying, but certain pathways are going to get pruned back and others are going to proliferate. The frontal loes that executive functioning and the limbic and hippocampal circuitries, which is where we do learning and emotion regulation. So combine emotion regulation and impulse control. Those are two biggies that are still vulnerable to exposure to physical and emotional stressors during adolescence. Well, if you've been around an adolescent, you know that impulse control, decision making and emotion regulation for any adolescent is challenging. But when those areas of the brain are not working as well as hoped, it can be even more challenging. Unfortunately, due to the high rates of alcohol and drug co use including marijuana, nicotine and other substances, researchers have really had difficult time figuring figuring out abnormalities caused by any one substance in particular. So alcohol and cannabis have a lot of overlap, partly because alcohol and cannabis are usually strongly linked and often frequently used together. Studies that have demonstrated timing specific exposure effects with different patterns of lasting consequences after exposures during early and mid adolescence as opposed to late adolescence include long lasting social anxiety and and increased risk of later alcohol use disorder. So pre adolescence, you know that early mid adolescence, pre puberty, there's a much greater chance of developing long lasting social anxiety and increased risk of alcohol use disorder. Heavy alcohol drinking, even in children and adolescents. I mean, I hate to say children, but children do drink. Heavy alcohol drinking reduces the rate of brain growth in proportion to the amount of daily consumption. So a child who maybe goes to a party, you know, they're in high school, they go to a party, they have a wine cooler or a beer or something on a weekend, they're not going to have near the impact on their brain development. And as a youth who is drinking a six pack every day, alterations were reported. And this is going to sound like old hat by this point in the structure of the frontal lobe affecting emotional expression, problem solving, memory, language and judgment. The temporal lobe, which impacts their ability to process affect and emotions and language. And again, that auditory learning, which is what we do. You're doing it now. You, you did it in college, you did it in high school. People who have deficits in auditory learning really struggle in our culture because of the way we teach and parietal lobe, which again is language processing. So we see these alterations in current adolescent alcohol and cannabis users. Adolescent marijuana and alcohol users who were abstinent showed persistent alterations in the thickness of the frontal anterior cingulate cortex, the frontal cortex, which is involved in attention, reward seeking, decision making, impulse control and emotion regulation. So they had alterations actually in the structure, in the density of their prefrontal cortex. Adolescent marijuana users also showed deficits on behavioral tasks of working memory, long term memory, attention and impulse control. So think about when you used to have to study for that exam. You know, hopefully you remembered stuff throughout the semester, but long term memory helped you succeed in school and a lot of other things. Short term memory, you know, that helps you with cramming the night before. But we use both of those, you know, even well, you know, throughout our lives, adolescent alcohol users showed poorer performance than non drinkers on tasks of attention and executive functioning, Self awareness, inhibition, working memory, emotion regulation, motivation, planning and problem solving. A lot of that is that frontal cortex development. Youth and adolescents who use nicotine show brain volume alterations relative to the nicotine dependence severity. So how many milligrams of nicotine are they exposed to per day? Now, you would be shocked, and I don't know the numbers right off the top of my head, but the amount of nicotine that a youth can get or a person can get from one of the cartridges used to vape with is significantly higher than a pack of cigarettes, for example. So a lot of youth are ingesting a whole lot more nicotine than even, you know, youth back in the 70s and 80s when, you know, smoking was heavy. So it's important to recognize that, that although vaping may be seen or perceived as being less harmful, in some ways it's more harmful. And nicotine is also associated with altered attentional processing, especially during withdrawal. Think about people that you've known or yourself. If you have stopped smoking, you know, that withdrawal period, even if you're smoking and you've gone four or five hours without a cigarette, how does that affect your attention? How does that affect your irritability? So nicotine exposure by vaping, by smoking, by nicotine replacement therapy, or by secondhand smoke, you know, anytime that organism is getting dosed with nicotine, at a certain point, you know, when they leave that environment or when they're not being exposed anymore and they're going to go through a detoxification period, if you will. And that often results in withdrawal type symptoms, especially, you know, cognitive difficulty focusing, difficulty with attention, and irritability. Like a bonsai tree, there are times when the brain is developing and much more malleable. You know, once the bonsai grows and it has that hard wood, you know, it's got a branch, it's a lot harder to shape the direction that's going to go. But if you prune it, when it is still in that softwood or that green growth stage, you know, the plant adjusts and starts growing, you know, different ways. We see the same thing in tomato plants, but I'll spare you that analogy. The brain begins development in the first trimester and continues until 24 years of age. During adolescence, different parts of the brain develop at different times. This is kind of akin to different branches of the bonsai tree. An insult to the immature brain can cause much more dramatic changes because of its malleability. So like I was saying, a sapling is going to be more easily damaged by hail or strong winds or the cat stepping on it than something that has bark around it that is protected. All drugs appear to alter parts of the brain associated with learning, memory, emotion regulation, planning, problem solving, and impulse control. So, you know, that was kind of a downer presentation. The positive positives that, you know, I can take out of that is that the research shows that in a lot of cases, early intervention is able to help that malleable brain regrow. You know, think about a tree that has, or, you know, a bonsai, something that has been disrupted in one area. It doesn't kill it off. It sprouts a new branch somewhere. It figures out a way to continue to survive, to continue to thrive. So even if, and we don't know for certain, there haven't been enough studies done on, you know, postmortem, on the brains of people that were exposed to drugs in utero or later in life to know for, for certain how persistent these changes are in the density of the gray and white matter and the, and the neuronal density. But we do know that with, you know, early intervention, the brain can be coaxed to learn new ways of functioning, and the child can develop the emotion regulation and the attentional skills necessary, or at least much better skills than the child would have had initially. If this podcast helps you help your clients or yourself, please support us by purchasing your ceus at Allce Dot com or getting your agency to sponsor an episode. A direct link to the on demand ceus for this podcast is at allce.com/podcastce. That's allce. Com podcastce. To sponsor an episode of Counselor Toolbox and reach over 50,000 clinicians per week, go to Allce. Com sponsor. Thank you.