Neurobiology of Addiction | Quickstart Guide

A one-hour clinical primer by Dr. Dawn‑Elise Snipes on the neurobiology of addiction. Covers how tolerance forms (receptor desensitization, compensatory neurotransmitter changes), withdrawal physiology (HPA-axis activation, post-acute withdrawal syndrome), and the roles of major neurotransmitters. Reviews how common substances (alcohol, stimulants, benzodiazepines, opioids, cannabis, nicotine) alter neurochemistry, the medical risks during detox (e.g., life-threatening alcohol withdrawal, Wernicke’s encephalopathy), and practical implications for treatment and early recovery (symptom timelines, monitoring glucose/medical comorbidities).
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Foreign.
I'd like to welcome everybody to today's presentation on the neurobiology of addiction. And I am going to try to.
Make this less dreadful than it actually sounds.
So let's just get started and get into it. Please feel free to ask questions in the chat room.
I will answer them as I can, and if I don't have the answers, I will look them up for you.
In this class, it's really basic.
We're going to be talking about how tolerance develops and discussing the impact of addictive substances and behaviors on the brain and body. We're not going to go deep down into it because guess what, we've only got an hour, so we're really going to be hitting the highlights. But I think it's important to recognize and to help clients recognize the, the impact that not only addictive substances, but addictive behaviors have on the.
Have on the body and on the brain and that they are enduring.
Just because you went through detox or just because you stopped doing it for two weeks or, you know, a week or whatever, doesn't mean you're not going to experience some withdrawal symptoms for a while because the brain has to recover. In substance abuse treatment, we call this the post acute withdrawal syndrome.
Briefly, for those of you who are.
Not super familiar with addiction and tolerance, let's talk about tolerance.
The brain is really cool because it.
Knows that we need a certain balance of neurochemicals in our body. And everybody has a slightly different balance.
But the brain tries to maintain homeostasis in the body.
Just think of it like running a warm bath.
And when you run a warm bath.
You know, what, what are you doing? You are turning up the hot, turning up the cold, trying to get it so it's just right. And that's what the brain wants to do.
When you take drugs or experience stress, it increases levels of certain neurotransmitters. If you are taking stimulants or experiencing.
Anxiety or anger or anger, any of.
Those stimulatory feelings, it's kind of like.
Turning up the hot water. If you are using depressants like benzodiazepines or opioids, or you're just feeling depressed, it's like turning up the cold water.
So you know, when you're taking a.
Bath, if you, you know, suddenly ramp up one or the other, it's going to make the bath so it's uncomfortable.
To normalize the chemical levels for the.
Breath br in the brain for survival.
The body or the brain balances the temperature. So, and it does this Two ways. It increases the secretion or receptor activation.
Of the opposite neurotransmitters. So if you are taking a depressant, for example, like alcohol, when we first drink it, it has depressant effects. And guess what to regulate for that, the body starts increasing its production of our excitatory neurotransmitters, glutamate and stuff, because it says, we don't want to get slowed down that much. We need the, you know, hello, you know, warm it up a little bit.
And it can also reduce the activation.
Of the targeted receptors, which is really what we talk about when we talk about tolerance. So if you're flooding your brain with dopamine all the time, eventually the brain is going to say, okay, dopamine receptors. When the dopamine gets there, it has to reach this much higher threshold in order to activate you. If you want to think about it in terms of a door, because a lot of people talk about receptors in, in terms of a lock and a key.
When the body becomes sensitized, instead of.
Being able to knock lightly on the door and get it opened, the body says no, if somebody wants this door open, they're going to have to pound the heck out of it. You know, they're going to have to hit it with their fist and make a really loud noise. Same sort of thing, you know, it's not, doesn't exactly translate, but same sort of thing with tolerance, those targeted receptors become less sensitive and they start ignoring the light knocks on the door and they wait until there's, you know, a pounding to get the same high.
The person either needs more of that.
Same substance, so more cocaine, more benzos, more whatever, or something completely different, you know, which is, you know, people can combine different substances in order to, you know, hyperactivate and get more dopamine into the system. And dopamine and our endogenous opioids are really what we typically talk about in terms of addictive substances.
Now you're going to learn throughout the.
Presentation that there are a ton, well, not a ton. There's about half a dozen neurotransmitters that are involved in just about every addiction addictive process. So it's not just dopamine.
And we want to look at these because it also gives us some clues as to what the person might be.
Self medicating, whether their GABA is too low or their serotonin is too high or, you know, whatever. It's not an exact science, you know, it really is not. But it does help us understand what's going on with the clients. And it may help the client understand. Understand where their cravings are coming from. Because when they are, when their body becomes desensitized to the influx of the chemical. So the dopamine, for example, you know, the body says, we're not going to open the door unless you're pounding on it.
Well, then the per. When the person is not pounding on.
The door, when the person is not flooding their system with. With opioids, then the door's not opening, so the opioids aren't getting through, which means there's. There. It's creating a deficit on the other side of the door. So what happens? The body starts craving and it says, hello, you know, we need to get some of that stuff through here. The brain's function. And again, it's really cool how it does it. It's frustrating that it takes so long to fix it, but it's really cool that the brain automatically kicks in when it senses it's getting too hot or too cold and tries to regulate by controlling again the activation of those targeted receptors or increasing the production of other brain chemicals to balance it out.
Withdrawal triggers opposing physiological and psychological symptoms.
Well, the psychological is because of the physiological. When you're taking, for example, cocaine, let's take a stimulant. Since we've been talking about opioids. When you're taking cocaine, you are ramping up your system. You are flooding it with dopamine and excitatory neurotransmitters. You are, you know, turning up that heat really, really high. So the body says, oh, my gosh, I can't run that hot. That is too hot. We're going to burn up. So I need to start letting fewer of those excitatory neurotransmitters through, you know, turn down the temperature a little bit that way. But I also need to start secreting compensatory neurotransmitters to try to, you know, blunt it out, to try to put out the heat.
So when people are in withdrawal, the.
Brain has not gotten the message yet that there aren't going to be any more assaults that you aren't. You've turned down the hot water, and so it's expecting more hot water, is expecting more heat to come its way. So it's going to keep producing those compensatory neurotransmitters, and it's going to keep the sensitization of those receptors higher for longer.
It takes a little while for the brain to go, oh, the assault is over.
I don't have to compensate anymore. I can go back to normal or whatever that is for that person.
So withdrawal.
When people start experiencing their withdrawal symptoms, what you're seeing is the excess of the toe, all of the opposite neurochemicals. If the person was taking system depressants, then you're off often going to see, you know, diarrhea, you're going to see anxiety, maybe high blood pressure. You're going to see a lot of those excitatory symptoms.
The chronic administration of drugs disregulates the stress response.
And the hyp book that hypothalamic pituitary adrenal axis or the HPA axis, and we talk about the stress response system or the HPA axis a lot in my classes.
And it's important to recognize that anytime you are altering those, the homeostasis of.
The neurotransmitters in your brain, that is considered a stressor. And during withdrawal, when the brain feels like it's, you know, it's needing something that it's not getting, then that triggers.
The HPA axis that triggers the stress response. And they found that there are certain responses common for all drugs of abuse.
And alcohol, including an activated HPA axis response, which, as you know, when the.
HPA axis kicks off, it releases cortisol.
Adrenaline, glutamate, norepinephrine, all of your fight or flight chemicals, which can often prompt feelings of anxiety or agitation in people.
Repeated cycles of addictive behaviors.
When you keep doing it, you know, once, if you just, if you don't drink very often and you go out and you drink alcohol and maybe you get buzzed or whatever, you, you drink enough that it alters how you're feeling, then you may have that anxiety or agitation when you start to sober up. But if you are habitually drinking alcohol or using cocaine or opioids or whatever, then the body says, okay, you know, I just, I'm coming to expect that you are going to. The brain says, you are going to assault me. You know, you are going to turn up that temperature or turn down the temperature, depending on what you're taking every single day. So I have got to be prepared for that.
So it blunts the HPA axis response.
Just like it blunts the response to the substance, it also blunts the stress response. And a lot of times when people come into detox, they talk about being sick and tired of being sick and tired. It doesn't matter whether they were taking opioids or cocaine or methamphetamine or, or.
Cannabis, whatever it is.
A lot of people when they show up to detox, they are tired. And that is one of the symptoms that we see in people who experiencing something called hypocortisolism. Basically, the brain has experienced stresses so many times and that stress response that it started to say, you know what, I can't be this stressed out. I can't run this hot. Because every time we're stressed, it's turning up all those excitatory neurochemicals.
This leads to something what that I call flat or furious.
And it's an exaggerated response. So the body is just kind of in this blunted state, not really reacting. Think like Eeyore as a result of experiencing so much over stimulation of that HPA axis. It's just, it's kind of holding on for all it's worth. It's like, I'm not going to respond to anything but the most urgent emergencies now. But when it finally does get stimulated, it goes from, you know, 0 or negative 2 to 150, like that. So there's an exaggerated response. Where it would normally have gone from, you know, 0 to 10, it goes from 0 to 100. And that's the body's way of going.
Wait, put on the brakes, we're not doing this again. The reduced sensitivity of brain systems involved in the experience of pleasure or reward is also, you know, a sign of.
Tolerance and something that the brain does.
In order to try to protect itself.
You know, it's weird to say that the brain thinks it can't be this happy all the time, but it can't be flooded with that imbalance in neurochemicals all of the time.
So let's talk about some of these neurochemicals. Serotonin is responsible for your mood.
We know that people take SSRIs, NRI s and D.
Antidepressant medications in order.
To help their mood.
Now, serotonin is interesting because too much serotonin produces anxiety.
Too little serotonin, people experience feelings of depression.
Now is that because of the serotonin levels or is that because of the.
Levels of other neurotransmitters that are affected? Because serotonin is out of whack, we don't know. Which is part of the reason it's so difficult for doctors right now to identify which type of medication will be will be best. I mentioned just a minute ago, SSRI is your selective serotonin reuptake inhibitors. They mainly act on serotonin. And then serotonin's availability affects the availability of just about everything else. But SSRI is just act on serotonin.
SNRIs act on norepinephrine.
So it increases the levels of norepinephrine and, and directly and then indirectly serotonin.
And then sndri.
Ss, NDRI affect the, or increase the levels of serotonin, norepinephrine and dopamine. So it's kind of like throwing the kitchen sink at it. But not everybody needs more dopamine, or at least not to that degree. So some people respond better to certain medications than others. Which, when your patients are on antidepressants, you know, it's important to know whether what type of antidepressant it is so you have an idea about what's going on. And if you see some side effects, if it doesn't seem to be working for them, then you can advocate for them to advocate or with them to advocate with their doctor for maybe an alteration to a different type of medication or to consider a different one in that family.
Anyhow, serotonin regulates mood, heart rate.
When you have, especially if you have too much serotonin, your heart rate may go up.
Blood pressure, it can go up as.
Serotonin levels go up.
Pain threshold, nice thing, pain, pain threshold.
Goes up as serotonin levels go up. As serotonin levels go down, pain threshold goes down.
Memory. Now here's where we get a little wonky here.
Serotonin itself affects those things, but it also affects the amount of dopamine, plus or minus. There are multiple different types of serotonin receptors out there. So depending on which serotonin recept serotonin receptors are being activated versus blunted, you're going to have different reactions in terms of the release of dopamine and glutamate. So not all serotonin is created equal. Just to add a little kink in the into the works.
Serotonin, interestingly enough, also aids in wound healing. So in early recovery people, or even.
In active addiction, people may have a more difficult time recovering from wound healing because serotonin is actually found in platelets that can increase skin development. You know, the knitting together back of wounds.
As, as my doctor says, dopamine is also involved. And this is the one we generally.
Talk about in terms of addictive behaviors.
But attention, memory and motor control are.
All directly affected by dopamine. People with ADHD tend to have insufficient levels of dopamine. People with restless leg syndrome or Parkinson's disease often have insufficient levels of dopamine. Because your dopamine goes down throughout the day, which is why symptoms of RLS And Parkinson's are often worse at night.
Motivation.
And also I should note that when.
People are, have symptoms of schizophrenia and.
They'Re taking antipsychotics or atypical antipsychotics, that reduces dopamine. So they may start having issues with restless leg syndrome or, or something like that. And that's, that's a difficult little thing to balance.
If they're taking.
Any medication for restless leg syndrome, then that's also increasing their, their dopamine levels, which may affect their mood symptoms. And you know, if they have any psychotic symptoms, it may, it may affect those.
Dopamine is also known for affecting our motivation. Now we used to call it the.
Pleasure chemical, but they found that that's not really actually accurate anymore. Dopamine is more involved in what I call perseveratory behaviors.
It's the.
I want to do that again. That was really fun. Let's do more of that. You have a lot of other chemicals like your endogenous opioids that provide the pleasure aspect of it. Dopamine is your going after it, your motivation, your determination.
Dopamine is also responsible for arousal. When we are an energy, both sexual arousal and, and energy. When people are taking antipsychotics, what do.
We often see as a side effect? A lot of times they are feeling exhausted, and this is a side effect of lowering dopamine levels. When people are depressed and, and you know, one of their symptoms is extreme fatigue. You know, that could be because of low dopamine, because we know that serotonin levels affect levels of dopamine.
And dopamine is also involved, just like serotonin, in our pain threshold.
So as serotonin goes down, dopamine goes down. As dopamine goes down, pain threshold goes down.
When people are in early recovery, if.
They have been ramping up their dopamine.
With addiction, addictive behaviors, then they may.
Experience temporarily more pain. Their pain threshold may be lower. What normally wouldn't bother them too much may feel more painful to them because their body is, you know, relying on external sources of stimulation for dopamine. So it's, you know, not getting as much through naturally takes a while for.
The body to realize, oh, you want.
Me to do this by myself again? Okay, I got it.
Norepinephrine is another chemical, and it's an excitatory neurochemical.
It also helps us with focus and concentration.
Interestingly enough, it's also involved in tear.
Production, blood pressure immunity. It reduces digestive activity and increases blood glucose.
When that HPA axis is activated.
It Secretes cortisol and norepinephrine.
Shortly thereafter, norepinephrine tells the body, hey, we need to fight or flee. So you need to put some blood.
Sugar into the system so we have some energy to run on.
And it also reduces digestive activity because.
Now'S not the time to rest and digest. Now's the time to fight or flee. Well, all that works well in a well functioning system. But if somebody happens to also have diabetes, in addition to addiction, or in addition to even, you know, chronic stress, that keeps that HPA axis activated, in addition to generalized anxiety disorder, we're going to see that they have high, higher levels of norepinephrine more often. That HPA axis is activated more often, which means they're gonna have dumps in blood glucose more often. And people who have diabetes know this just by virtue of the fact that they know that stress makes it more difficult to control their blood sugar.
We wanna be on the lookout for this with clients in early recovery.
A lot of people in the US have pre diabetes or undiagnosed diabetes. We know that people who have been engaging in addictive behaviors often have not.
Been taking the best care of themselves physically.
So they may not have gone to the doctor or they may have overlooked symptoms. So we do want to make sure that we are keeping an eye out for any underlying physiological pathology that might show up during that early recovery period. But we do know that during detox and for people who do have diabetes, during post acute withdrawal syndrome, that first year or so, it is more difficult for them to regulate their blood glucose, so they will need to be much more attentive to it.
And acetylcholine, this isn't one we talk about a lot, but it is an important one.
It's involved in cognition, another one that's involved in tear production, bowel functioning. When acetylcholine gets out of whack, people may experience symptoms of irritable bowel syndrome. It helps regulate dopamine and serotonin. When acetylcholine is in the system, it increases dopamine and reduces serotonin, which is kind of interesting because we know that serotonin increases dopamine. So it's almost like they kind of.
Work against each other.
But the system knows how the system works. Recognizing that acetylcholine is involved in alteration of dopamine and serotonin and noting its connection with irritable bowel syndrome is important to know. Because if somebody starts having IBS symptoms in detox, early recovery, keeping an Eye on that. You know, it could just be, you know, the initial week or two. Some, some substances, when you detox, your, your GI system just goes completely haywire for a little while. Opioids are a particular example.
But after you get through that initial.
Acute detox period, if they're still experiencing irritable bowel syndrome or symptoms, it's certainly worth having them go to the doctor and get that looked at.
Glutamate is our main excitatory neurotransmitter. It is used in the Krebs cycle to produce energy.
It is involved again in dopamine release and memory.
You know, it doesn't have its fingers in quite as many things as far.
As body systems as some of the other ones do, but it is, if we don't have that, there is no get up and go. Glutamate is basically our gas, if you want to think about it that way. Or it makes the gas available, I guess, would be more accurate.
GABA we know as our body's main.
Calming chemical. It's our natural volume, if you want to think about it that way. It's involved in REM sleep. It opposes glutamate and reduces tremors. A lot of your benzodiazepines are mimicking or activating gaba. The REM sleep is something to pay attention to. If somebody's not getting good sleep, they may not have adequate levels of gaba. GABA is made, you have glutamine, which is broken down to make glutamate, which is your excitatory neurotransmitter, which, lo and behold, is broken down to make gaba.
So if you don't have enough glutamate.
You'Re not going to have enough GABA because you don't have enough raw materials to make it, which is kind of an interesting quandary sometimes to look at. If people are using a lot of stimulants, then the body may turn down the amount of glutamate that is being made available, loosely speaking, which means they won't have as much glutamate to work with to break down to make gaba. Gonadal hormones, your testosterone, your progesterone, your.
Estrogen, interestingly enough, are also affected. Gonadal hormones are affected.
Affect libido, you know, when your estrogen or testosterone is out of whack, then you're probably not going to have as strong of a libido. And you will find out shortly that alcohol actually influences the levels of estrogen and testosterone in the human body.
The availability of serotonin is affected by.
Levels of testosterone and estrogen.
When those levels are not right, then.
You'Re going to have differing levels of serotonin availability.
Additionally, just to put another kicker in there, when we are under stress, when.
That HPA axis is regularly activated or when it becomes blunted, that affects our level of gonadal hormones because the body.
Says, you know what, there's a lot.
Of stress out there. There's a lot of fighting or fleeing going on. Now is not the time to reproduce. So libido tends to go down. Levels of testosterone and estrogen tend to get altered as well in response to stress itself. We know that people who are, you know, experiencing addiction, experiencing, you know, problematic use of substances or even behaviors are often experiencing chronic, ongoing stress. Whether it's because they are, you know, withdrawing and then, you know, they need to use again in order to feel normal, quote, unquote, or whether it's because they start to sober up and they look around and life is not being kind and they see all the devastation caused by their addiction and they get stressed out, or they just don't have the coping skills to deal with life on life's terms.
You know, it could be a variety.
Of things, but I have yet to meet someone who is presenting for treatment who isn't experiencing or hasn't been experiencing pretty high levels of chronic stress for quite some time.
So let's talk about specific substances. Alcohol is one of the most studied.
So there is the most information about that.
And I will note with our neurotransmitters. Neurotransmitters occur throughout the body, and there.
Is no way currently to measure accurately the level of any neurotransmitter in the brain.
You can do urine tests and measure.
The levels of neurotransmitters in the body, but we don't know how much of, you know, the serotonin that we measure in your urine is actually, you know, able to get to and cross into your brain and stuff. There is no way to know how well those brain synapses are functioning and how well they are stocked, if you will, with neurotransmitters. So please do not be fooled with claims that peop people can take a urine test and identify which neurotransmitter levels are out of balance. All that tells you is throughout their whole body, what might not be in balance.
Also, there are only currently alcohol and.
Cocaine that have medicate and opioid, I'm sorry, alcohol and opioids that currently have medication approved Treatments, cocaine, cannabis really don't.
Nicotine does.
But as far as the substances that we typically talk about, so I guess it would be alcohol, opioids and nicotine have like FDA approved treatments.
So we'll talk a little bit about those.
But there are neurochemical correlations between, you know, what's going on with people who are recovering from detoxing from cocaine and who are detoxing from cannabis. We need to recognize that they do impact neurotransmitters. And just because we don't have a specific drug we can throw at it doesn't mean that it doesn't directly impact neurotransmitters.
So anyway, alcohol affects the endogenous opioid.
System, which is our feel good system.
Gaba, dopamine, serotonin and glutamate.
So wow, alcohol affects everything.
Alcohol consumption results in the release of.
Endogenous opioids, which is what gives us that pleasure feeling and dopamine, which makes us want to do it again.
They found that in order to block.
This reaction, naltrexone has been helpful because it blocks those opioid receptors. So that is one treatment that they are exploring for alcohol abuse.
With chronic alcohol consumption, the body adapts.
By reducing the number of GABA receptors. Remember, this is the one that helps us calm down. It's our natural valium to counteract the continuing alcohol induced GABA increases. When we initially drink alcohol, remember, it's.
A depressant initially and it causes GABA.
To increase in our system.
But the alcohol leaves our system really fast and the body has ramped up.
The amount of glutamate it's producing to balance out the gaba. And so then we start feeling anxiety and people start feeling that tightness in their chest, their blood pressure goes up.
Alcohol inhibits glutamate at lower doses.
When it's having the, when it's creating the glutamate in our system or the GABA in our system, when we initially drink, inhibits glutamate, promotes gaba. That's a great thing. At higher doses, when you start to become severely intoxicated, the body goes, whoa, that's too much gaba. We need to start balancing it out. So think, think of that bath again. You know, you are turning on way more cold water and the body's going, we can't be that cold. We can't be that, you know, depressed. So I need to turn up the glutamate, turn up the hot water to keep us from dying, which is a good thing.
And baclofen has been found to be.
Helpful in dealing with the symptoms of GABA receptor dysfunction.
Alcohol also inhibits glutamate at lower doses.
Promoting relaxation, which, you know, we talk about.
At higher doses, the increased glutamate receptor.
Activity can be problematic, again causing that anxiety effect that people experience. Remember, alcohol detox can be life threatening for people whose bodies have adapted enough that when they stop using the alcohol and it leaves their system, their glutamate levels can be so high, as well as other neurochemicals, their blood pressure can go skyrocketing, which can trigger a stroke and all kinds of other problems. So don't fool yourself that just because alcohol is legal, it's not a dangerous detox.
Alcohol also increases serotonin levels. Interestingly, patients with alcohol dependence have lower levels of serotonin. Okay, well that makes sense.
When they drink alcohol, it increases their serotonin. So the body says, hey, I don't need to produce that crap anymore. You're going to give it to me normally.
You're going to be artificially ramping it up.
You know, that's. You see where I'm going with this?
And so you. Less serotonin naturally is going through because the body's expecting you to turn that.
Dial up and just really dump serotonin periodically.
So people who are alcohol dependent, their body has adapted to that excess serotonin.
By not letting as much through, by not secreting as much. And when they start to sober up, guess what? They have lower levels of serotonin. They start to feel symptoms of depression.
And alcohol reduces testosterone levels and increases estrogen levels.
Reduced testosterone reduces serotonin levels. So people may experience symptoms of depression, lethargy.
Increases in estrogen are associated with increases.
In general of serotonin and increases the feelings of anxiety.
So it's interesting to kind of think.
About, well, if the opposite happens during withdrawal, you know, people's estrogen levels may be low, their testosterone levels may get higher. So what does that mean in terms of their mood, in terms of, you know, things that might trigger relapse? Alcohol causes brain damage, just no two ways about it. Through toxic metabolites, which cause neuron, neuronal damage. So that's one thing you're just, you know, poisoning your brain.
It also reduces brain derived neurotrophic factor.
Or bdnf, which is necessary for neuronal survival. I kind of think of it like food for food for the neurons. You know, if they don't have it, they can't continue to survive and grow or Oxygen for the neurons, whatever you want to think about it as, it.
Also causes excitotoxicity due to increases in glutamate.
And we see this in people who are exposed to trauma, who are exposed to chronic stress, and people who regularly ingest alcohol. All of those ramp up that HPA axis, ramp up the levels of glutamate, and basically make it too hot. It's, it's too excitable, too much glutamate in the system, so it becomes toxic and you start killing brain cells. Which is why people who have alcohol dependence often show, or even PTSD often show reduced hippocampal volume, because some of those neurons are just are dying because of the excitotoxic environment.
Alcohol also inhibits amino acid metabolism. Amino acids are the building blocks, the.
Protein building blocks that our body uses to make the neurotransmitters that we need to function. The dopamine, the norepinephrine, the glutamate, all of those things are made from amino acids.
So if our body can't break them.
Down, then it doesn't have the building blocks and it can't build those amino acids. So, yeah, we're going to feel kind of crappy.
Another thing alcohol does is inhibits the.
Absorption of thiamine, which is one of your B vitamins.
You might think, well, B vitamins, they're water soluble, not a big deal. It's a big deal. Thiamine deficiency can lead to alcohol related.
Dementia, also known as Wernicke's encephalopathy, which is a medical emergency. Okay. Do not confuse this with anything.
A lot of times people with early.
Signs of Weirnicki's encephalopathy look like they're intoxicated. They have difficulty with motor coordination and gait, their memories confused. They seem like they've got a little bit of dementia or something going on, kind of, or like they are severely intoxicated.
If somebody you're working with, even if.
They don't identify as having alcohol dependence.
If they have recently stopped drinking, they're.
Trying to self detox or, you know, they went on a bender last weekend and they are, it's Monday morning and they're in your office and they're still sobering up a little bit and they're, they start to evidence those symptoms. It's essential to get them to the emergency room. You know, just eating a good diet ain't gonna do it. Um, if they actually do have alcohol related dementia, they're gonna need the doctor to give them intravenous thiamine in order to get those levels back up.
If it's left untreated, it can lead.
To Korsakoff syndrome, which is, you know, more problematic and can be long lasting, which is what we actually call alcohol related dementia.
But if left untreated, it can also.
Cause death in up to 20% of cases. So I know I'm harping on this, but it is really important to recognize the symptoms of Wernicke's encephalopathy in any of our clients, even the ones that don't identify as alcohol dependent. And if they start having symptoms of cognitive confusion, cognitive decline, especially if it's conv. Combined with some, you know, difficulty and coordination, we do need to pursue that in conversation with them to make sure that they are not in danger.
Stimulants affect the brain by building up dopamine and serotonin. They block the reuptake. So dopamine and serotonin stay in that.
Synapse for a little bit longer. So we get to sit there and bathe in it, which, which again, the longer our neurons bathe in something, the more that potentially gets absorbed into the system.
Concentration, memory, energy, perseveratory behaviors and motivation, vasodilation.
So our blood pressure, basically immunity and pain management are all impacted again by dopamine and serotonin.
Low dopamine is associated with restless leg.
Syndrome, fatigue, Parkinson's and movement related issues.
Remembering that every substance alters the level.
Of dopamine and serotonin. So we do need to help patients.
Be prepared for this.
So if they start experiencing, you know, some mild panic attacks, if they start experiencing more anxiety, we can help them prepare for those things and understand what's going on and forecast a little bit whether this is a post acute withdrawal thing or if it's going to be.
Also.
Associated with, you know, long term anxiety or something.
A lot of times the brain does.
Mostly recover from the assaults, but it takes time, like a couple of years. And yes, Carl, dopamine is also associated with adhd.
Alteration of nerve cell structure in the nucleus accumbens and prefrontal cortex in the brain is also associated with continued cravings. So stimulant use, especially, you know, chronic stimulant use, actually causes changes in the cell structures which can persist for years.
After somebody quits using, which is one of the reasons they hypothesize, and that.
People, even after the stuff's out of.
Their system and they've been living a recovery lifestyle for a year or two years or whatever, they may still have occasional cravings.
Benzodiazepines increase gaba. Increased increases in GABA causes increases in dopamine.
We feel relaxed, we feel good. It's great.
It also alters serotonin levels and decreases norepinephrine. These are all things that we would.
Expect in an antianxiety medication.
However, detox from it is going to look the opposite. So you're going to have reductions in.
Dopamine, you're going to have reductions in gaba, you're going to have increases in norepinephrine. So you'll see a lot more anxiety, agitation, GI disruption as the HPA axis ramps up into high gear. Because it is getting the message that there is a stressor out there. There's, you know, glutamate levels are going up and there's, there's a problem.
Opioids activate dopamine and serotonin and also mu.
Opioid receptors.
One of the side effects of taking.
Opioids, you know, whether you're taking them by prescription or otherwise, is slowed gastric motility or constipation and potentially reduced blood pressure and slowed respiration. We know that opioids have depressant effects.
It also reduces gaba. Interestingly enough, when opioids reduce gaba, it.
Produces an increase in dopamine because gaba. Well, you're not interested in all the, how all of it happens. You can read about it if you click on the links.
But the opioids reduce gaba, which allow.
More dopamine to be released into the system, which is why people often feel more energetic when they take opioids, because the reduced GABA means that they're also having more stimulant, more glutamate, more, more norepinephrine activity and that increased dopamine. So you can combine energy with dopamine and woohoo, you got a party.
Cannabis is one that we don't talk about a lot. And when we talk about substance misuse.
And substance abuse, we often talk about your, your methamphetamines and your cocaines and those things.
But cannabis does affect the brain. The THC and cannabis.
Now remember that CBD oil or CBD technically is not allowed to have more than 1 to 3% THC in it. So it has very little THC. But cannabis itself has higher levels of THC. THC binds to the endogenous cannabinoid receptors. And the ones where we're talking about mainly are the CB1 receptors. This inhibits GABA, which increases dopamine. Okay, so people who, when they take cannabis, sometimes you may have talked to somebody who got particularly strong marijuana, and when they used it and they ate it or they smoked it or however they took it, they felt like they were having a panic attack or their heart was going to beat out of their chest. Well, GABA was inhibited and glutamate increased, which caused that reaction, but it also increased dopamine.
At low doses, cannabis increases serotonin, so.
They have found that it can help some people feel better, but at high doses, it actually reduces serotonin. So you need to find that happy medium. If you're talking about thc, it has.
Been shown, you know, and we know.
This to reduce nausea due to serotonin activation.
But chronic use, and this is interesting, may result in dysfunction of CB1 receptors.
You know, the brain thinks that it's getting too much because anything we take orally or we snorted or whatever is.
Going to be at much higher doses.
Than our brain normally produces it, whether it's melatonin or serotonin or any of those things where anything that we take in artificially is at much, much higher doses. So as with everything else, the CB1 receptors may desensitize or become less sensitive, which reduces the flow of blood with glucose and oxygen to the brain, which can result in attention deficits, memory loss, and impaired learning ability. Some people believe that this can be reduced as the body gets used to not having the influx of the THC anymore. Some people have been found to experience ongoing problems with attention and memory. So the research out there is a little bit contradictory about how much, for how long produces these effects. But we do know that in some people it can happen.
Nicotine. Nicotine imitates acetylcholine. It increases dopamine, gaba, norepinephrine, and serotonin.
So nicotine just kind of throws the entire kitchen, kitchen sink at you. Now, why is nicotine important and the same thing with cannabis? As Tequila points out, cannabis is sometimes called the gateway drug.
Well, nicotine kind of can be too, because when people are taking these drugs, they.
And even alcohol, you know, your legal substances.
They are altering the levels of.
Neurochemicals in their brain. So somebody may have, maybe in. In detox, they may be trying to sober up. But if they're still smoking, they are still using or, or dipping, they are.
Still using drugs that are altering the.
Levels of neurotransmitters in their brain. And when they do that habitually, what's going to happen? They're going to develop tolerance Once they develop tolerance, what's going to happen? They're going to have to have something stronger in order to get the same relaxation response.
Maybe they're not even trying to get.
High, but they're trying to feel, quote, unquote, normal.
And so nicotine actually can be, as.
Can cannabis, can be a stepping stone to harder substances or to more problematic substances because of that, that tolerance effect that people experience.
Addictive behaviors add stress to the body.
There's just no two ways about it.
When you are flooding your body with.
Way more than it wants to have and go back to that bath again, you know, if you're sitting in the.
Bathtub and all of a sudden you.
Turn off the cold water and you turn the hot water on full blast.
You know that's going to hurt. It's an assault to your skin. Same sort of thing happens when you.
Are ingesting or engaging in some sort of behavior or ingesting some sort of substance that increases those chemicals in your brain.
You're either basically turning the hot water.
Up full bore or dumping a whole bunch of ice in, or turning the hot or turning the cold water up full, full bore.
Either way, you are significantly altering the.
Temperature of the bath and it's going to get uncomfortable. And in order to be able to tolerate it, in order to be comfortable, what are you going to do?
You're going to try to balance it out.
Your body does the same thing with the neurotransmitters.
When it perceives that it is a.
Toxic environment in your brain, it's going.
To try to balance it out because your brain wants to live. When those neurochemicals start getting altered, though.
When your serotonin goes down too much, people are going to feel depressed, depressive symptoms. So if they've been doing addictive behaviors, a lot of them increased dopamine and increased serotonin. So in that detox period, guess what? They're going to have low dopamine. So low perseveration, low determination, and low mood.
We want to recognize that a lot.
Of these mood symptoms occur during detox as a result of changes in the brain. It's not just somebody being poochie because they can't have their drug of choice. There are actual changes and lasting changes in the brain that, you know, they last for months. You know, hopefully not longer than a year. Pause usually only lasts for about a.
Year, but they are real.
And somebody who is experiencing extreme depression or extreme anxiety or even not extreme, may feel bad enough that it triggers an addiction.
Relapse Somebody who is anxious all the.
Time or feeling like Eeyore all the time, you know, is going to have a really hard time staying sober.
The brain survival response is to adapt.
To protect from overstimulation.
Once it becomes sensitized to excessive levels.
Of a neurotransmitter or hormone, it may become hypo reactive. So remember, it's, it's kind of like knocking on the door. Initially, you just need to knock lightly on the door. But then eventually the person on the.
Other side of the door, if you.
Will, gets tired of everybody knocking on their door. So they only answer it if somebody's like, banging on the door if there's an emergency. Same sort of thing with our brains. When our brain becomes hyper reactive, it says, I just can't, can't do it anymore. Can't let that through there because it's.
Getting.
Is getting too hot or I'm getting too tired.
If the levels of the neurotransmitters are increased enough to trigger a response, then the response may be exaggerated.
So they're flat, they're just going along, you know, whatever.
But if they finally get enough that passes that threshold and it actually triggers.
The HPA axis, they go from flat to furious.
During withdrawal, early withdrawal, the brain has.
Not yet gotten the message that there's.
Not going to be any further assaults. I'm not going to keep turning up.
The temperature randomly on you.
So the compensatory responses dominate. So if the body's still afraid that you're going to turn up that hot.
Water, ramp up the temperature, it's going to keep that cold water flowing because it's expecting another burst of hot water.
And it takes a while for the.
Brain to get the message that, okay, we're safe, and to start rebalancing and becoming less hyposensitive.
During the first one to two years of recovery. It's vital for people to understand that the injuries or adaptations in the brain so they can expect and mitigate physical and psychological symptoms.
If they understand what's going on, that is half the battle. If they recognize that, okay, you know, my body is trying to rebalance itself and find that, you know, happy temperature. It's easier for them to say, okay, this is hopefully a temporary thing, and to plan for it, to notice it, and to do something about it.
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