Discover How Dopamine Impacts Serotonin, Hormones and Happiness

You. I'd like to welcome everybody to today's presentation on dopamine. I'm your host, Dr. Donnelly Snipes. Today we're going to discuss what dopamine is and its function, how it interacts with serotonin, norepinephrine and gaba, the symptoms of excess and insufficiency, and what people can do to help their body balance dopamine and get it into the right level for them. And, and I've said this before, I'm going to say it again. It's dangerous to think that we can monkey with the system, that we're just going to randomly increase one neurotransmitter and not affect all of the others. So, and, and we're going to talk about that some today. For example, when we work with people who have psychotic disorders and they take antipsychotics, it acts on some of the dopamine receptors and has create certain side effects that can be problematic. One of those side effects is actually preventing them from getting good sleep. And as a result, there's more stress and it throws other things like estrogen and testosterone out of whack. So it's interesting how it all works together, and I'm not going to talk about it a whole lot today, but it's important to remember that all of your neurotransmitters, your dopamine, norepinephrine, serotonin, acetylcholine, gaba, glutamate, and there's others, but those are the big six interact with cortisol. They interact with your thyroid hormones, they interact with your gonadal hormones, including oxytocin, estrogen, testosterone, progesterone. And if you've been with us through this entire series, you know that each one of those chemicals, if you will, or substances, has dramatic effects on mood. And if one goes wonky and it causes another to go wonky, then you have this cascade effect of wonkiness, if you will. So let's talk about dopamine. Dopamine is a neurotransmitter located throughout the body, including the brain, the immune system, the kidneys and the pancreas, just like all of our other neurotransmitters. It's got his grimy little mitts in everything. However, dopamine does not cross the blood brain barrier. So its synthesis and functions in peripheral areas, which means throughout the rest of the body, are largely independent of its synthesis and functions in the brain. Now, this is unique with dopamine, so that's just a unique thing to, to Recognize. So if somebody takes a dopamine pill, it ain't gonna do anything for them. It is dopamine synthesized from L dopa and it's your main motivation chemical. It gives motivation salience to things. When our dopamine is adequate and we do something that's pleasurable, then dopamine helps us process that memory and say, that was awesome, let's do it again. If it was problematic, dopamine says, let's process that memory and not do it again. I, I'm not going to come back for this one. Dopamine can reduce insulin production and increase food intake which impact serotonin levels, which is kind of in interesting. When your insulin gets low, your body says, oh my blood sugar is low, I need to eat. And when people eat it increases dopamine and serotonin levels. I am not prescribing by any means randomly self medicating with food or something else that might, might increase dopamine. But we have seen that, that your comfort foods, your high fat, your high sugar processed foods tend to cause a spike not only in blood sugar, but also in dopamine and serotonin. You have serotonin, I'm sorry, you have dopamine and serotonin in your gut where they play a role in digestion. If your peripheral dopamine levels are low, then you're going to have more difficulty with digestion. Dopamine reduces gastrointestinal motility and protects the intestinal mucosa. We talked in the serotonin video about how a lot of the intestinal mucosa is made from 5ht which is a precursor to serotonin. But you know, we also have to recognize that there are other things at play. So if the gut is upset, it could be that serotonin's low and that 5ht barrier is getting too weak. It could be that dopamine is lower and the intestinal mucosa is not being protected as much. Another take home from this is if the gut is upset, it's not absorbing the nutrients. No matter how well you're eating, it's not absorbing the nutrients it needs to make the hormones and neurotransmitters and everything else to heal the body. Dopamine reduces the activity of lymphocytes and reduces inflammation by suppressing pro inflammatory cytokines. Let's think about this. Dopamine is our motivation chemical. Dopamine spikes when the stress response goes off. Fight orf flight. And dopamine says I'm really motivated to protect myself. All Right. Well, that makes sense. If you're in pain, if you've got a lot of inflammation, you're not nearly as effective at fighting or fleeing. You're in pain. So part of the stress response is a reduction of inflammation. Now, cortisol is the main chemical involved in suppressing inflammation during the fight or flight response. But dopamine does do a little bit too mood. Well, dopamine impacts mood. If you're not motivated then to get off the couch, then you're not going to be ex exposed to anything that might trigger feelings of happiness. It helps with coordination and muscle movements. We see that people with restless leg syndrome have problems with their dopamine. We see people with Parkinson's disease have problems in their dopaminergic system. Generally, when we start seeing muscle tremors and things like that, dopamine is getting too low. When people have psychosis, dopamine is getting too high. What we struggle with sometimes is if you have somebody who has psychotic features with their mental health diagnosis and they develop restless legs or Parkinson's, then you're kind of scratching your head. And I actually did have a client that struggled with that at one point. The antipsychotic medications actually reduce the dopamine too much. But so the doctor really struggled trying to find the right balance of medications. So she didn't have restless legs and she also wasn't actively psychotic. Dopamine impacts learning, attention, and memory. It gets its grimy little me m m into our prefrontal cortex. Motivation. Again, let's think motivation. What's it doing up here? It's motivating you to pay attention to something. And if you're not motivated to pay attention, then you're probably not going to learn very well. Dopamine also, as I mentioned, helps with motivational salience and it helps filter the things that are important to remember and the things that aren't so important to remember regulates the flow of information from other areas of the brain, including problem solving in the frontal lobe and the thalamus. And it also impacts wakefulness. If you've worked with people who are on antipsychotics or have Parkinson's disease, they often are sleepy. And part of this is attributed to people not being able to get good sleep and people not feeling as. As motivated. They're. They're sleepy all the time. When going to talk about the sleep issue in a minute. There are many subtypes of receptors for all of your different neurotransmitters. And you can't just say dopamine and where you're talking about everything. Just like you can't say cannabinoid receptors and think you're talking about just one thing. THC acts on one type of cannabinoid receptor. CBD acts on another type of cannabinoid receptor. And these receptors are in different places in the body and brain and serve different functions. D1 receptors, dopamine 1 receptors prepare the set of possible appropriate responses. It helps the person figure out, all right, what are my options here? D2 shapes and selects from this initial response set framework. So. So somebody can think about all the possibilities, but then deciding whether they're going to fight, flee, fawn, freeze, or forget about it is sort of a D2 thing. D1 is the most abundant dopamine receptor in the central nervous system. It regulates neuronal growth and development and mediates some behavioral responses, stopping right here, regulating neuronal growth. That's really important in addictions and in other diseases where neurons are actually dying. Neuronal growth, or what we call neurogenesis, is really important. When people's dopamine levels are low and those D1 receptors aren't getting stimulated, then the brain doesn't know that it needs to build new neurons. An agonist increases and an antagonist decreases. Parkinson's disease medications are dopamine 1 agonists. It increases the activity of the dopaminergic system. Turkeride is an example of a dopamine 1 agonist. It has been used as a treatment for hypo hyperprolactinemia or hypoestrogenism, or pcos, polycystic ovarian syndrome. Why am I bringing that up? Well, you may be working with a client who has low estrogen, and they may be developing symptoms of pcos. It's important to recognize that when the person's level of estrogen is lower than what the body thinks it should be, then you're going to have some side effects. So dopamine agonists can increase dopamine and also increase estrogen levels. It's also used for pulmonary arterial hypertension. Now, this isn't your normal high blood pressure medication. This is specifically in the pulmonary arteries. Not as common, but you could see it in a patient. When we take the clinical assessment, we ask about what medications they're on. If you don't know what a medication is, that's fine. Some doctors don't even know all the medications that they're. They. That patients are on that were prescribed by other doctors. You can look it up when they leave, but it's important to understand how medications people are on for different disorders may be impacting their neurotransmitters, their hormones, and their mood and cognition. As a result, D1 agonists are serotonin receptor antagonists. All right. Remember I typically said that when serotonin goes up, dopamine goes up. Well, with D1 agonists, we see serotonin being antagonized or reduced. Oh, my gosh. So if somebody's taking a D1 agonist for PCOS, then their serotonin may start getting low. That's interesting. 5H2A receptor antagonist. 5H2A is one of your serotonin receptors, interfere with the heightened state of dopamine activity and may be useful in the treatment of psychosis, alcohol and cocaine dependence. Five H2B antagonists have previously proposed, been proposed as treatment for migraine headaches and heart disease. If you've got somebody on migraine medication, it's going to affect their serotonin levels. A5H2B antagonist, it's going to reduce the activity of the serotonin receptor, but that's also going to act to increase the D1 dopamine 1 receptor activity. So dopamine may increase, and you may be going right now, well, that sounds great. Who doesn't want more dopamine? You don't. Too much dopamine can contribute to adhd, like symptoms, diabetes, difficulty concentrating. Remember that Goldilocks principle that we've talked about? Too little is bad, too much has side effects. You want it to be in that sweet spot. D2 receptors. Schizophrenia can be attributed to an imbalance in dopaminergic pathways that signal D2 and D1 receptors. This is called the dopamine hypothesis. We have found over the years that this is overly simplified. There are other things that are going on in schizophrenia, but we do know that just like in addiction, dopamine does play a role. Most antipsychotics are antagonists, so they reduce the activity of the dopamine 2 receptor. It says, no, we don't need that going on right now. Addictions, any addiction, whether you're talking about sex, drugs, gambling, impacts the D2 receptors more than others. And that's important to recognize because remember, if the D1 receptors are being addressed or whatever, then the D2 receptors may not necessarily be active. Parkinson's disease is characterized by dopaminergic neuronal degeneration and especially D2, and requires a dopamine agonist. We want to increase the activity of the dopaminergic system In Parkinson's disease, since they're losing neurons, then we're, we need to try to increase the activity of that system and like turn up the volume, if you will. D2 receptors are responsible for stimulating the dopaminergic transmission in obese individuals and may perpetuate pathological eating as a means to compensate for decreased activation. So what does that mean? That means in people who are obese who eat for non hunger related reasons, they may have a dysfunction in their D2 system. Notice I'm not saying just emotional eating. When the body's deficient in D2, it registers that as a problem. It says we're running low, running low, running low. Need to do something which may motivate somebody to eat. Because eating especially those comfort foods can increase the activity of the dopaminergic system. They may not be feeling emotionally bad. They may be, you know, just literally motivated to eat in order to get those levels up in their brain. Major depressive disorder patients have shown decreased dopamine in the central and basal nuclei of the amygdala. Remember, that's our fear processing of postmortem depressed patients who committed suicide compared with control subjects. So they have less dopamine in their fear processing area, which is, you know, just one of those interesting facts that is out there. It's not something we're going to be able to specifically address and say, well, let's pump up the dopamine in the amygdala. We can't do that with any accuracy right now. Dopamine depression and post acute withdrawal. 2/3 of patients are not achieving remission from depression with current antidepressants. And a lot of patients, and we talked about this before class today, a lot of patients who are in early recovery from addiction, and I use that term loosely to represent the first two years for a lot of people are not going to feel themselves, they're not going to achieve full remission of their mood symptoms with selective serotonin reuptake inhibitors. Because no matter how much you crank up the serotonin, if the dopamine receptors aren't there, no matter how much you crank up the dopamine, it's just got nowhere to go. So recognizing that low dopamine is potentially causative in people with depression and pause and recognizing what might be causing that for the individual and, and we really need to take a close look at the symptoms and not worry so much about the neurotransmitters. I know you all are here because you're interested in the neurotransmitters but it's just not that easy. It's not that easy to there. There's no pill that we can give somebody that's suddenly going to make them motivated. Anhedonia, or the lack of pleasure contributes to the persistence of major depressive disorder. Depression and anhedonia have been shown to be associated with reduced dopamine response to reward. Well, that makes sense. If there's half the neurons there for some reason, and I'm over generalizing, but if there's fewer neurons or if the dopamine system isn't being responsive, it's being lazy, then yeah, you're not going to feel very motivated, which, you know, kind of explains it. If the dopamine system is not responding, then the motivation is going to be low. So you may see a reward and be like, yeah, that's cool, but whatever. Most antidepressant treatments do not directly enhance dopamine. We know this, which may contribute to residual symptoms including impaired motivation, concentration and pleasure. Now remember, you have your SNDRI's, your selective SSNDRIs, selective serotonin, norepinephrine, dopamine reuptake inhibitors that people can take, tricyclic antidepressants and MAOIs. Your old fashioned antidepressants increase serotonin, norepinephrine and dopamine but have significant side effects. I, in 25 years of practice, I have not seen someone, I've not worked with someone who was on an maoi. They're that rare. Now. It could happen, but I wouldn't expect it to happen. In clinical practice today, the latest generation of antidepressants like wellbutrin or bupropion can be considered norepinephrine and dopamine reuptake inhibitors. Most doctors are going to start somebody on an SSRI that's just standard protocol right now. That's what the American Psychiatric association recommends as the first line pharmacological treatment. But then if they're not responsive to that, they may switch over to an ndri. Norepinephrine dopamine reuptake inhibitor. Let's think about that again. Is this going to work? Is this going to be the magic bullet? No, it's not necessarily. For some people, it'll do wonders. For other people. It's not that they don't have enough norepinephrine or dopamine going into the system. It's not that it doesn't stay there for long enough. It's that the receptors are just not there or they're Lazy. So there's a problem later down in the system and, and we need to figure out what that is. It's important that we encourage patients when we're working with them. If they're not feeling better, they've been on three different antidepressants and they're still not feeling better. Okay, well, let's, let's look at what we're missing. Let's take a look at the broader picture. And one of those broader pictures, as I've been harping on for two months now, is going to the doctor and getting a full blood panel, making sure their thyroid, their gonadal hormones are well balanced and healing that HPA axis, that stress response. Because if cortisol is out of whack, then the whole system's going to be out of whack. If estrogen or thyroid hormones are out of whack, the whole system's going to be out of whack. And no MA, no amount of SSRI or SNRIs are really going to impact your thyroid levels. So we need to be cognizant. I worked with one woman, and this is kind of unrelated, but whatever, who was showing signs of severe clinical depression. And one of the first things I do with all of my patients is I say let's go to the doctor and get a full blood workup done to make sure we're not missing anything physiological because talk therapy isn't going to fix that. Turns out she was dangerously anemic. They admitted her to the hospital and put her on an IV because she was that anemic. And as soon as they got her, her iron levels stabilized, she started feeling remarkably better. And, and that's why I think a multi disciplinary approach is so important. I wouldn't have thought about anemia causing that significant of depression, but it did. Dopamine can decrease inflammation. We talked about that. Dopamine excess may cause vitamin B6 deficiency. Well, how do you get dopamine excess if you, if it doesn't cross the blood brain barrier? You may not get dopamine excess in the brain unless you're taking a medication for that. But if you're trying to increase peripheral dopamine, you actually can increase, you can increase peripheral, you know, in your body dopamine, which can cause a B6 deficiency, which again will impact your body's ability to, your nervous system's ability to effectively function. Now here's an interesting little tidbit. When dopamine interacts with norepinephrine, norepinephrine is inhibited. So when dopamine goes up, dopamine or norepinephrine is kind of suppressed. And you're thinking, okay, well, that's interesting. And again, this is just in certain areas of the brain. Now, why is that important? Melatonin release is primarily controlled by the suprachiasmatic nucleus, which drives circadian rhythm. The circadian rhythm of melatonin secretion from the pineal gland. All right, that's not anything that we're surprised by. However, what you may be surprised by is norepinephrine plays a direct role in stimulating melatonin release from the pineal gland. If dopamine's too high and it's suppressing norepinephrine, then guess what? People may not be getting good sleep. High dopamine can impair norepinephrine activity and contribute to insomnia. Both dopamine D1 and D2 receptor mechanisms are important in mediating anxiety. Dopamine antagonists have been reported to be associated with social anxiety disorder symptoms in patients treated for Tourette syndrome and schizophrenia. Okay, well. Hm. Patients with social anxiety disorder are commonly given SSRIs. SSRIs are your first line psychopharmacology, psychotherapeutic agent for anxiety and depression. They've show been shown to be effective and safe, you know, blah, blah, blah, according to the powers that be. You can argue those points if you want, but that's just what is being published. However, if appears that SSRIs are not effective if the patient is on current dopamine antagonists. So if somebody's on a dopamine antagonist medication, like an antipsychotic, and they're feeling anxious and they're given an ssri, it actually doesn't do much good. So they're finding there's competition with. When those. When they're on those medications. We're not prescribers, so you don't need to worry about prescribing. But if you have a patient who is on dopamine antagonists and they have social anxiety and they're not feeling any better from the ssri, well, the research says that makes sense. So we may need to look at some other alternatives. We may need to encourage them to advocate for. For themselves with their physician. Dopamine agonists, things that increase dopamine, can stimulate oxytocin release. All right, so let's go back here for a second. Social anxiety is very common, and if somebody has low levels of dopamine, then SSRIs don't seem to work. All right, that takes us up to dopamine agonist. So let's increase the dopamine. Well, that's not so good if you're working with somebody who has adhd, Tourette's, or schizophrenia, because we're trying to lower their dopamine. But dopamine agonists can stimulate oxytocin release. All right, so it sounds like that's an impossible quandary. It does, but we may get there. Disruptions in dopamine function can indirectly impact oxytocin pathways involved in disorders like anxiety, autism, addiction, and depression. So what they figured out is if you can't increase the dopamine because, you know you're trying to decrease it for other reasons. Intranasal oxytocin has actually been shown to be quite effective for addressing a lot of the symptoms, especially related to anxiety and social anxiety that we see in people who have. Who are on dopamine antagonists. Disruption of the dopaminergic system as a result of addiction is also known to markedly reduce oxytocin levels. So dopamine goes down, oxytocin levels go down. Right. Remember, oxytocin is our bonding hormone, our desire to interact with other people hormone that goes down. You know, do I really want to go out and spend time with my friends, or do want. I just want to sit at home and drink? Well, when your oxytocin goes down, that's not a really hard decision. So it's important to recognize that the impaired social, emotional functioning in addiction is. Is partly due to reduced oxytocin as a result of the destruction of some of those dopamine neurons. Huh? Hallelujah. Oxytocin is also one of those chemicals that is responsible for increasing motivation to interact with others. When you are working with somebody who's in early recovery and they just have no motivation to go to meetings and they don't really want to be around other people. Is that low dopamine or is that low oxytocin or. Or both, but that those are things that we need to consider. There are ways to increase oxytocin, being around people, doing nice things. Intranasal oxytocin. I didn't find any studies that specifically addressed social apathy and intranasal oxytocin in post acute withdrawal. But it might be something to explore in terms of ptsd. Yep. PTSD messes with your dopamine levels, too. Chronic or complex stress can lead to excessive dopamine release initially. And. And remember when we talk about combat stress or complex stress disorder or. Or Adverse childhood experiences this chronic stress. Initially the stress response dumps dopamine and glutamate and all those other stress chemicals to give you the energy to fight or flee. Makes sense. However, at a certain point the dopamine actually may become. Dopamine levels actually may become depleted. You've secreted so much so quickly that you ran out in the storehouses. Likewise, you may see dysfunction in the system because you secreted so much for so long that those dopamine neurons, just like an addiction, start to become resistant to being activated. They start sort of turning off and in some cases dying off because of over stimulation. And they found that this depletion of dopamine or reduction in dopaminergic activity has been does contribute to the symptoms of PTSD and cptsd. Hypodopaminergia or low dopamine levels is associated with an increased risk of developing ptsd. And that was actually shown I, I talked about it in a couple of videos that I did on ptsd. People who had adverse childhood experiences or complex post traumatic stress who already had low levels of dopamine were more likely if they were exposed to another trauma to develop post traumatic stress as people compared to people who had adequate levels of dopamine and were exposed to that stressor. So what does this mean in recovery? When we think about addiction and I know we've got some addiction counselors in here, when you've got somebody in early recovery, they are more susceptible to traumatic injury because their dopaminergic system is not working quite as well. Basically. Remember there's that acute stress when the initial stress, when, whenever that was, whether it was when they were six months old or 60, there's that acute stress, the stress response, the HPA axis activates and cortisol's released your stress hormone if you will, that increases dopamine and norepinephrine release. Norepinephrine helps you with attention, with focus, with energy and dopamine helps you with motivation. These are all things we want. We when we're trying to avoid that hungry lion with chronic stress, dopamine and norepinephrine and this is overly simplified, become depleted due to high utilization and and I'm not going to go through it again, but there are multiple ways that that dopaminergic system can become inefficient and ineffective. But when that happens, people develop symptoms like depression and anxiety. In other videos I've talked about the Flat to the Furious and when people undergo chronic stress and the stress response remodels like this, when things become miscalibrated, when there's no major stressor going on, they tend to feel apathetic, anhedonic, flat. And when something does trigger them enough to start the stress response, they have this tsunami of stress chemicals that are released and they become furious and, or frantic in most cases. Occasionally you'll have somebody who's so depleted that there's just nothing that's going to get them up off the couch. They're just like, screw it, whatever. And that's a very dangerous place to be when somebody doesn't have the motivation to protect their own survival. Stimulants, whether we're talking Adderall or meth, stimulants, increase brain dopamine. Genetic differences that alter the expression of dopamine receptors in the brain. So the way you're wired in utero can predict whether a person will find stimulants appealing or aversive. Well, score technically. There are tests that can be done to see if somebody is going to be more prone to the rewarding effects of stimulants. If you are a parent who has recovered from amphetamine addiction or methamphetamine addiction, and you want to know if your child is susceptible, one aspect of that susceptibility is genetics. Now remember, it's not all genetics. It's in genetics and environment, the whole nature, nurture thing. But there are genetic tests that can be done to determine whether the stimulants will be as rewarding for them as it was for you. Now remember, even if they don't have that gene mutation or expression, they still may develop an addiction if the environment is bad enough or conducive to developing addiction. But this is one way we can explore stimulant users. People who use cocaine, amphetamine, methamphetamine, exhibit lower striatal dopamine, D2, D3 receptor availability. Remember I said there's all kinds of do dopamine receptors out there, so they have lower receptor availability. Differences in the D1 receptor were found to modulate responses to opioids. So no matter what's going on with your D2 and your D3, that's not going to impact whether or not you find opioids rewarding or not. But, but we do know that there are certain expressions or polymorphisms, if you will, of the D1 receptor gene that make opioids way more rewarding to certain people than others. And I think we've all known people who can take pain pills, for example, after they have Surgery or something. And they're just like, yeah, whatever takes makes me sleepy. Could take it or leave it. And then there are other people who take it. And it's just like this feeling of elation and, and part of that is neurochemical and is due to the expression, the way that their D1 receptor genes are expressed. Chronic elevation in dopamine triggers a wide ranging set of structural changes in the brain that are responsible for the behavioral abnormalities which characterize an addiction. When you use, your brain's flooded with dopamine and serotonin and all kinds of other stuff, cortisol, when those receptors are constantly bombarded and overloaded, your brain says, this is not healthy. So it starts shutting down those receptors. It says, no, we're not going to let as much through. And that's what we call tolerance in addiction. And that, and that's again due to those, that chronic elevation of those hormones and neurotransmitters in terms of structural changes. We see the pruning of neurons. We see shrinking of certain areas of the brain as a result of neuronal death. Dopamine plays a role in depression along with serotonin, norepinephrine, gaba, estrogen, testosterone, progesterone and oxytocin. We need to remember this. Now what is, why do I have the plus next to testosterone? To remind myself that when dopamine goes up, testosterone typically goes up. So if dopamine is low, testosterone tends to follow suit. And we have seen in people as they age, testosterone levels tend to drop, estrogen levels tend to drop. That's just part of aging. Which means that it's possible that dopamine levels may also tend to drop some. And remember, dopamine is responsible not just for motivation, but also for learning, for memory, for cognition. And this partly explains, partly explains why as we get older, those changes in gonadal hormone levels are also impacting our neurotransmitter levels, which make it more difficult for people to think of things, to retrieve memories, to put words together. So older people tend to be slower in responding. It doesn't mean they've got dementia. It just means their brain is slowed down a little bit. The dopaminergic system is modulated by several neurotransmitters, including glutamatergic neurons and GABAergic fibers. Glutamate is our main stimulant chemical. GABA is our main relaxation chemical. GABA is made by breaking down glutamate. So you've got, you know, they're buddies Changes in The Glutaminergic and GABAergic or Dopaminergic System influence anxiety like or depressive behavior. And I'm just kind of driving home that point that if dopamine, if the dopamine system is thrown out of whack, it's going to impact the glutam, glutamine and GABA system as, as well. You can't alter one without out altering their buddies. Dopamine dysfunction is linked to certain symptoms of depression, such as low motivation. Serotonin is involved in how you process your emotions, which can affect your overall mood. But remember, dopamine plays on motivational salience. So your overall mood and how you process that emotion is going to inform dopamine about whether this is a good thing or this is a bad thing or something to not even pay attention to. Both dopamine and serotonin are involved in sleep inflammation, appetite and energy levels in terms of dopamine insufficiency. And I have direct and indirect because remember, it could be that there's a dysfunction in the dopamine system somewhere, not making enough, not squirting it out, not leaving it in the synapse long enough, not receiving it, or not sending it. So it could be dopamine or it could be that some other neurochemical or hormone is too low, which is naturally dragging down dopamine. However, symptoms of dopamine insufficiency include muscle cramps, spasms, tremors, aches and pains, restless legs, adhd, loss of balance, constipation, difficulty eating and swallowing, weight changes, gastro, gastroesophageal reflux, trouble sleeping or disturbed sleep, low energy and inability to focus, moving or speaking more slowly than usual, feeling demotivated, hopeless, inexplicably sad or tearful, mood swings, anxious, suicidal thoughts or self harm, low sex drive, hallucinations, delusions, lack of insight, loss of coordination, and addiction to particularly stimulants. But in some cases, remember, opioids can also be triggered by the way it, the way they act on other dopamine receptors. Now the things that I have bolded on here, these are all symptoms of depression. And that's why it's so difficult to ferret out what, which system is malfunctioning. So what do we do to increase it? Foreign, we're not going to be able to take a pill. Well, there are some medications that actually do increase dopamine, but they are medications. You're not going to find anything over the counter that is going to effectively increase dopamine levels. Past what your body normally can do. Cocaine and amphetamines, nicotine stimulants and MDMA all will increase dopamine levels in the brain. Okay, so we do know that that will happen. Like I said, this is not something over the counter. Well, nicotine kind of is, but that's very small in its effect compared to cocaine and ADHD medications, et cetera. Medications for Parkinson's and restless leg syndrome are designed specifically to increase dopamine. Opioids may increase it. Dopamine reuptake inhibitors, and this is actually a, another medication that's used for adhd, Methylphenidate, in order to help the body heal. How do we do this naturally if we're not going to start pumping people full of drugs or encouraging them to talk to their doctor about getting drugs? All right, so how, what else do we do to help the body balance itself? Recalibrate all of its internal machinery, Decrease sugar and caffeine to reduce dopamine flooding? There was a thing for a while. I haven't heard of it much in the past few months, but the dopamine detox and there's something to be said for this and, and I'm not saying I'm. You don't want to get rid of all dopamine, but if you are regularly flooding your brain with dopamine, whether you're day trading or you're involved in some high stress occupation or addictions or something else, you're flooding those, those circuits and some of them are bound to short out. So the dopamine detox says let's take a break and quit flooding the circuits and let everything dry out a little bit so we don't over stimulate. And there's something to be said for that. There's something to be said for unplugging, so to speak, and giving the brain a chance to relax. Going along with that is reducing your stimulants, reducing your caffeine and your sugar. That can help. They have found that it for people who are trying to reduce sugar and, and, or caffeine. Chromium can help with sugar cravings and has been shown to help a little bit with mood in people with depression. Am I prescribing that? Absolutely not. What I'm saying is there are things that patients can talk with a nutritionist or their doctor about to help them get past the sugar cravings. If they're one of those people who just, you know, they're regularly chowing down on Skittles and whatever else. The sugar withdrawals can be pretty Poignant because as the sugar detoxes from the body, the dopamine levels are going to go, go down precipitously, which is going to trigger those sugar cravings. The body says, out of balance, let's, you know, do what we need to do to increase it. Again, get sufficient quality sleep and set your circadian rhythms. And I have like three videos on sleep hygiene and the importance of sleep hygiene. When you don't get enough sleep, your body already perceives that as a stressor and triggers the stress response and increases dopamine. When you don't get enough sleep, you are have more difficulty typically controlling intrusive thoughts, which adds stress, which triggers the stress response, which increases dopamine, which floods the system sufficient. When we're sleeping, and especially when we're getting good deep sleep, our brain clears out adenosine. They found that people who are on antipsychotics tend to not actually get nearly as much deep sleep. So when they wake up in the morning, they still have adenosine residue. If you want to think about it as a factory, it's kind of like still having trash all over the aisles in the factory makes it hard to get around on your day. So a lot of people who are on antipsychotics tend to feel very foggy in the morning because they're not getting that deep sleep. They're also missing out on the time when the body restores and rebalances. But basically, it's important to have people work with their physicians, work with a sleep specialist if needed to get sufficient quality sleep. That's just, that's imperative to maintaining balance in the system. Exercise increases hormones that increase dopamine. All right, not everybody wants to go to the gym. I get it. Any kind of exercise, moving your body, gardening, playing tennis, walking the dog, playing with the kids, whatever it is that you like to do that moves your body and increases oxygen. And if it gets you outside and get some vitamin D, that's a bonus. But that will help increase dopamine, decrease chronic stress. Chronic stress keeps that HPA axis activated, which eventually will lead to dopamine insufficiency. So decreasing that chronic stress. Have patients make a list of all of their stressors, just everything, and then go through and figure out which stressors they can let go of or they can address to free up energy that they can use to move toward their rich and meaningful life. Some things that we stress over this chronic stress is stuff that we don't need to stress over or triggers that we don't need to see. I have all but sworn off social media and especially the, the Twitters and the Facebooks and those sorts of things because I found them to be too triggering. There were, there was just too much vitriol and it was just nasty and it was stressed me out. I'm like, why are people so ugly to each other? So I quit. And I have been. I've had more energy. I've been immensely happier since I did that. But being on social media is not important for me in order to move toward my rich and meaningful life. So that was one of the things on the list that I saw that I said, hey, we can cross this one off. And all of a sudden I had one less stressor. Stress is a part of life. We aren't going to be able to get rid of everything but helping people figure out, you know, are there things that I'm stressing over or doing that are. That's depleting my energy and stressing my body that I don't need to do? Remember, stress is not just mental, it's physical as well. L phenylalanine is converted to L tyrosine, which is converted to L dopa, which is converted to dopamine. All right, well, great. Thanks for that chemistry lesson. Aspartame. Now, we still have aspartame in a lot of our diet sodas. Aspartame is made by joining together the amino acids aspartic acid and phenylalanine. The consumption of aspartame can elevate the le. The levels of phenylalanine and aspartic acid in the brain, thus inhibiting the synthesis and release of dopamine, norepinephrine and serotonin. I've talked to a lot of people who drink a lot of diet soda, and when they stop drinking diet soda or they switch to something that sweetened with something else besides aspartame, they get incurred incredible headaches. And part of this is because of the sudden jolt to the brain of the change in the levels of dopamine, norepinephrine and serotonin. It goes away, but, you know, it's one of those unpleasant sort of detox things. Now you can increase tyrosine by eating bananas, almonds, apples, watermelons, cherries, yogurt, beans, eggs and meat. Tyrosine, the amino acid can cross the blood brain barrier. If your reason for not having enough dopamine is you're not giving your body the building blocks it needs, well, here you go. Try eating some of these things. You can go online These are not the only foods that have tyrosine in them. If you don't like any of these, find something you do like and encourage people to experiment for two weeks. Try eating something that's high in tyrosine at each meal and see if they find that it helps their mood. Probably not going to hurt anything if it doesn't. Okay, no harm, no foul, but at least you ruled that out. Adequate levels of vitamin D, magnesium and omega 3 essential fat fatty acids may also help to raise dopamine levels. Remember, food is broken down in a chemical process in our body and in order for that process to take place, in order for the dopamine to be assembled, if you will, it requires all of these vitamins and minerals and other things to sort of act as spark plugs, if you will. That's why we can't just say take tyrosine and you're going to be good. The diet needs to be well rounded and zinc deficiency is also implicated. Too little zinc may increase dopamine synthesis, but it contributes to ADHD like symptoms. And zinc is necessary for other activities in the body. Too little, no good. Too much, no good. What's the sweet spot for that particular person? People who drink green tea have been shown to have increased levels of the precursors to dopamine, ginkgo, Sammy and ginseng. Ginseng have been implicated or shown to increase the precursors to to dopamine. Now remember, a lot of this stuff cannot cross the blood brain barrier and act act on the dopamine in the brain. It may act on the peripheral dopamine, reducing inflammation, those sorts of things. It's also important to recognize that some of these things like Sammy are thought to be, if you will, sort of like herbal antidepressants. What does that mean? That means they will interact with the other, other medications people are taking. And if somebody has bipolar disorder, taking something like Sammy could potentially trigger a manic episode. So it's really important. Remember, mania is one of the symptoms of too much dopamine. So if somebody has bipolar disorder, they take Sami for their depression, they may suddenly have too much dopamine and trigger a manic episode. Kava also increases dopamine, which is interesting because a lot of people think of kava as an anti anxiety medication, but, or herb, but it is. I mean they've shown repeatedly that dopamine increases oxytocin, which may help reduce anxiety symptoms. Clary sage, bergamot, lavender, lemon and rosemary, among others are essential oils that have been shown in multiple peer reviewed studies. On PubMed to increase levels of dopamine in the body. Now remember, we can't measure the levels of dopamine in the brain in humans, because you just can't. The best they can do is measure blood plasma levels, which is your peripheral dopamine levels. Inhalation of essential oils can communicate signals to the olfactory system and stimulate the brain to exert neurotransmitters like serotonin and dopamine to further regulate mood. So the studies mainly looked at what happened in rats because rats brains are apparently as pretty close to ours, which anyway, so they do know what happens in the rat's brain. And from anecdotal reports with people, seems like some of these essential oils can be effective at increasing motivation and dopamine levels. How do essential oils actually work? Because that's the question. Question I get a lot. Tiny molecules of essential oils are dissolved in the nose as it stimulates the olfactory receptors, activates its cells that carry signals from the essential oil sent to other areas in your limbic system, in your nervous system. And, and the limbic system is the primal brain responsible for memory, instinct and mood. Which is why when we smell something, it often triggers memories. You know, it's just going into that limbic system and going oh, brownies for me when I smell pine saw, it reminds me of my grandma's house. You know, it's just one of those almost instant connections. The olfactory system is the only sensory mechanism that involves the limbic system and amygdala in its primary primary processing pathway, which is interesting. So your sense of smell is the only sensory mechanism that involves the fear processing area and the memory, instinct and mood area. So when you smell smoke, there might be fire. Symptoms of excess dopamine include ticks, addictive, pleasure focused behaviors. Now if you don't have enough dopamine, you may engage in addictions. But when you are in addiction, then you typically have excess dopamine when you're using. Hypersexuality, mania and paranoia are also symptoms of excess dopamine. In people with bipolar disorder, Hypersexuality is a very common symptom, sometimes prodromal symptom to a manic episode. How to decrease dopamine. Most antipsychotic drugs are dopamine antagonists. Okay. Anti nausea drugs are also dopamine antagonists. Oh, okay, so let's think about that again. You have a patient who is, oh, they get so car sick and they're going on this long trip and they take an anti nausea drug, Won't call out a name. And when they do, they just their level of depression and motivation and everything is just oh my gosh, crap. And and I can tell you it happened for me. And, and I didn't know why I would take the anti nauseam medication before we would head into Washington D.C. when we lived in Virginia and by the time we would get there I would just be miserable to be around. And lo and behold, it was monkeying with my dream dopaminergic system. And you know, that's probably not a good thing. Helping people understand this. If they have to take the anti nausea drug, okay, help them recognize that it may also impact their mood and potentially have them talk with their doctor about if there are other things that they can do to medicate the side effects or to address the nausea and reduce stress. Well, going back to anti nausea drugs again, generally people take these when they're getting ready to go on vacation so their loved ones may get really offended if they get to the their in laws house and the person who took the drug. Anti nausea drugs is just poochie, you know, depressed, unmotivated, blah, blah. So it's important to educate people and I've gone over my time, I apologize. Dopamine, Its function is for pleasure and motivation. Symptoms of excess psychosis, ticks, tremors. Decrease it with antipsychotics, but also reducing stress. Reducing that HPA axis can reduce stress. Symptoms of too little dopamine include depression, Parkinson's, anxiety and difficulty with problem solving. How do you increase it? Naturally effective diet, especially tyrosine and hydration, exercise, sleep, some essential oils and norepinephrine, dopamine, reuptake inhibitors. Alrighty. Well, thank you all for being patient with me. I'm sorry, I got off on a little bit of a tangent and ran over my time. What questions do you have about dopamine? And I know there were a bunch of questions. I'm going to kind of scan through here real quick. I know Adriana was trying to address them as much as possible. Thank you, Lisa Hazel, you are so kind. Unfortunately, there are no new treatments for methamphetamine right now. Hey Shyman, it's always good to see you. Prometh. I'm not sure I understand the question. Is dopamine related to crashes. And yes, new life low dopamine is a risk factor for ptsd. It won't cause it. It just makes you more prone to develop PTSD symptoms if you're exposed to a trauma. It. And for those of you who have questions about pause. I Do have a vid, A video specifically? Actually, I have a couple videos specifically on pause or post acute withdrawal syndrome. Because it's important to understand that in post acute withdrawal for most people, all of their neurotransmitters are out of balance for them. Their thyroid may be out of balance for them. Their gonadal hormones may be out of balance for them. We also need to consider the impact of, on a different note, the impact of hormones on people who are undergoing gender transition therapy. We need to consider the impact of a lack of hormones on people who are going through andropause or menopause and how the gonadal hormones impact mood and cognition and whether that's something that they want to consider talking about with their doctor. Yes. Partly mobile phones partly increase. If you're on your mobile phone and you are getting stressed out, that increases dopamine. Or if you're just, you know, just loving it. Whatever you're seeing on tick tock or whatever, you're increasing dopamine, which is potentially suppressing norepinephrine, which is suppressing melatonin release. So it's going to keep you awake. Additionally, mobile phones, you put out blue light which tells the pineal gland it's not time to go to sleep. So putting a sleep filter on your mobile phone can help with that. But most sleep specialists recommend turning off the mobile phone at least an hour before bed. Yes. Therapist talks. It is definitely possible to get 31 credits in addiction studies. We have over 500 courses at all CEUs. A lot of them, not all of them are presented from a co occurring perspective. I do have the entire 400 hour plus curriculum on all CEUs that I use to train people who are wanting to become addiction counselors. So it's definite. I have at least 400 hours of addiction specific counseling. All righty everybody. Thank you all for being here. I appreciate it and I will see you next Wednesday.