GABA: Positive Psychiatry's Unsung Key To Quieting Mental Static

Your brain doesn’t just need more “happy chemicals.” It needs stability. We zoom in on GABA, the primary inhibitory neurotransmitter, and make the case that it’s one of the most overlooked keys to calm, clarity, resilience, and true mental health.

We break down the neurobiology without the fluff: how GABA is made through the GABA shunt, how GABA-A and GABA-B receptors shape phasic and tonic inhibition, and why the excitatory-inhibitory balance between glutamate and GABA forms the functional backbone of the brain. From there, we connect the science to lived experience through the idea of “network flurry” the noisy, overdriven brain state that can show up in major depression, generalized anxiety, panic, PTSD, chronic stress, and the feeling that your mind simply won’t shut off.

We also get practical about treatment. We examine how benzodiazepines and Z-drugs amplify GABA-A signaling, why they can bring fast relief, and why tolerance, dependence, sedation, and cognitive effects can work against long-term flourishing for many people. We clarify what gabapentin and pregabalin actually do (they are not direct GABA receptor drugs), then explore the emerging promise of neuroactive steroids like allopregnanolone and medications such as brexanolone and zuranolone for rapid antidepressant effects, including postpartum depression.

To round it out, we highlight non-medication tools that support GABA function: mindfulness meditation, prayer, yoga, structured breath work like box breathing, exercise, and nutrition that supports healthy neurotransmitter synthesis. Let's hink differently about anxiety, depression, sleep, or stress.

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Transcript

Why GABA Matters In Psychiatry

Rakesh Jain, MD, MPH 0:05

Hello and welcome back everyone to Positive Psychiatry with Rakesh Jan. I am your host, Rakesh. And on this episode, we're going to talk about GABA. Yes, we are, because that's the one neurotransmitter that I just don't think we have addressed adequately in the field. And folks, before we go any further, perhaps we should take a minute to look back in the history of our field, our field of traditional psychiatry, where we do, I think, a pretty doggone good job at, you know, reducing symptoms and reducing mild or moderate or severe psychopathology. But we don't talk about positive psychiatry as much with our patients as we should, and we certainly don't talk about it with ourselves. And if we don't have that goal in mind, then the odds are obviously pretty strikingly high that we're not going to take our patient to full flourishing, right? Anyways, I'm going to get off my soapbox right now and let's dive into this beautiful neurotransmitter, GABA. And let's let's work hard at understanding the importance of this unsung hero of positive psychiatry. That is GABA. Okay, so to truly appreciate the power of GABA, we first do have to spend a few minutes trying to understand its complex

GABA Shunt And Brain Wiring

Rakesh Jain, MD, MPH 1:46

neurobiology. And we have to start with this stark and undeniable fact about the brain's cellular composition. So the monoamining system, which we spend an enormous amount of time talking about serotonin, norepinephrine, dopamine. In fact, if you take all of them together, they account for only 1 to 2% of all the synaptic connections in the entire central nervous system. Yes, you heard me correctly, just 1 to 2%. Think of those as neuromodulatory systems, much like you know, fine-tuning dials in a massive instrument, which is great, of course. But the instrument itself, the brain, the structural bedrock of all neural communication, is in fact, you know, primarily glutamaturgic, the primary excitatory neurotransmitter of our brain, and GABA-ergic, the primary inhibitory neurotransmitter of our brain. So between glutamate and GABA, they run over 80% of all the circuitry in the human brain. 80%. And GABA is synthesized within these inhibitory interneurons. And it is built through a very elegant metabolic pathway that we call the GABA shunt. And this process begins with either glucose or glutamine, which is then converted into glutamate. That's right. For GABA to be created, glutamate has to be first created. And then a whole bunch of enzymes and our neurons, particularly the glutamatoric acid decarboxylase, also known as GAD, steps in. And what that does, it will cleave a carboxyl group from the glutamate and transforms the highly potent excitatory glutamate molecule into the world's greatest inhibitory neurotransmitter, GABA. And you and I may want to think about GABA as the brain's primarily stabilizing force. Think of it as the mama energy of the brain, if I may use that as a metaphor. And once we synthesize GABA, it's packaged into the synaptic vesicles. And there, when an action potential fires down the neuron, most likely into neurons, calcium rushes into the terminal and causes these vesicles to fuse with the presynaptic membrane. Now, what happens then? Well, guess what? We get a literal shower, a thunderstorm

GABA A Versus GABA B

Rakesh Jain, MD, MPH 4:42

of GABA. And when that happens, oh my goodness, then GABA binds to two different families of receptors. Each one has its own unique timeline and mechanism. One of them is called GABA A receptors. Now these are ionotropic receptors. We're going to talk much more about the GABA A receptors in a few minutes. But we simply can't afford to ignore the GABA B receptors because they're the metabotropic receptors. They are slower. But slower doesn't mean not valuable. They have a sustained timeline. And GABA B receptors are G protein-linked coupled receptors and they act to their own downstream second messenger cascade. So when the GABA B receptors are activated, they offer a prolonged stabilizing hyperpolarization. So think of the GABA B receptors as the calm grandmother energy, stabilizing energy of the human brain. Now GABA A receptors, these are quick, faster, ionotropic. As I said before, they are fast because they're ligand-gated ion channel receptors, which is a whole bunch of words. But essentially what it means is when GABA comes to the receptor, it triggers an instantaneous shift that opens the channel, the channel that's inside these five subunits that come together to form the GABA A receptors. And they're usually two alpha, two beta, and one gamma, or one delta subunit. We'll talk more about that later, but just think of it as a five-leafed flower, five different petals that are closed. And what GABA receptor does, it creates an opening of this channel. It allows for chloride, which as you know is negatively charged to go right into the postsynaptic neuron. So this causes a hyperpolarization, a fancy way to say that it makes that particular neuron fire less. This is called phasic inhibition. And it's really important because, you know, just like kids in a kindergarten class, you simply cannot let them run around crazy, right? You have to be able to control them. That's why GABA is the adult in the room, the teacher, the hall monitor. And without that ability to control, my goodness, the brain would be in so much trouble with both neurological challenges and psychiatric challenges.

Clearing GABA And Balanced Inhibition

Rakesh Jain, MD, MPH 7:42

I should also say that once GABA has done its work, then it has to be eliminated. We can't have it hanging around, right? We don't want that. So after this happens, what we have is a clearing of the GABA, and it is cleared by these special transporters that we call GABA transporters or GAT transporters. And they come in different forms: GABA transporter one, two, and three. And these are found both on neurons and surrounding astrocytes. And once this GABA is picked up by the GAT transporters, they're broken down. They are broken down by GABA transaminase. And by doing that, what it does, it ends the action of the GABA. That's important. So in the brain, what GABA does is a really lovely combination of phasic inhibition and tonic inhibition. And as you will see in psychiatric disorders, we really do need the help of both of these two kinds of actions from our magnificent, hardworking, but underappreciated GABA. Well, folks, now that we have mapped out the cellular machinery of GABA, and we appreciate that, boy, it's hardworking. It with glutamate forms about 80% of the backbone of the human brain. And we think of it as the single greatest of all inhibitory neurotransmitters. And those of us interested in positive psychiatry would appreciate this fact that life isn't all about doing the right thing. It's also about not doing the wrong thing. That's why an inhibitory neurotransmitter, in fact, does have a profound role to play, not just in psychiatry, but also in positive psychiatry.

Network Flurry And Mental Illness

Rakesh Jain, MD, MPH 9:46

Let's now talk about a concept called network flurry. So, in a perfectly healthy, thriving brain, the relationship between glutamate and GABA is like a masterclass in harmony. Everybody's getting along well in this household. Glutamate provides the necessary drive and spark and signal transmission that we need for learning and memory and mood and cognitive action. But you know what? GABA provides structure, focus, containment. So think of GABA not as a like a wet blanket that smothers brain activities, but rather as a highly sophisticated director of traffic. It is controlling traffic in a bustling metropolis like Houston or Dallas or New York. And like a good traffic cop at a busy intersection, GABA directs these neuronal networks to prevent overstimulation and congestion and chaos. See? GABA is not a wet blanket. It's not a party pooper. In fact, it is a harmony creator in the human brain. And you know, in things like depression in particular, or bipolar disorder, or even things like postpartum depression, it is the presence of chaos in brain circuits that leads to challenges, but also things like stress. Without a formal disorder, stress is a real problem. Guess what? This flurry of neuronal activity is often because GABA isn't containing the human brain's circuitry appropriately. So without GABA, folks, the brain circuits do begin to fire out of control. We see this breakdown in disorders that we call major depression. And you know what? Tools such as the magnetic resonance spectroscopy studies, they show significant reduction in GABA concentrations in the prefrontal cortex and the anterior cingulate cortex in major depression. No wonder the symptoms of major depression are rumination and sadness. And the same thing happens with GAD, generalized anxiety disorder and panic disorder. We see widespread down regulation of GABA A receptor binding. Same sadly is true in PTSD. So when GABA levels drop or its receptors become desensitized, the excitatory inhibitory balance tips dangerously towards hyper excitation, and the brain loses its ability to filter out background noise. This state of chaotic hyperarousal is what I'm calling network flurry. So network flurry is the biological opposite of psychological flourishing, which is of course a central component of positive psychiatry. So when a patient is trapped in this state, their prefrontal cortex is completely overwhelmed by like a nonstop storm of bottom-up stress signals from an overactive amygdala because, well, the traffic cop is not working. And the traffic cop, of course, is CABA. So these individuals are not able to access their executive function. They cannot do appropriate cognitive appraisal. And they certainly don't build resilience, right? They get trapped in survival mode, exhausting their metabolic reserves, just trying to manage this inner noise. And this is probably why these traditional monoamine treatments often fall short, because if a patient's brain is locked in a severe state of network flurry, simply increasing synaptic serotonin or norpinephrine or even dopamine. It's like trying to adjust a radio station when the speakers are already blown out by static. See, clinical practice connects with neurobiology. So for us to create a space for true healing and positive psychological health, we have to quiet the static first. We have to intentionally restore this excitatory inhibitory balance. We have to calm down this network flurry. We have to do that. And GABA, of course, is the way to go. So, going forward, we will dive into the psychopharmacology of GABA. We will explore how our traditional medications affect this system. We're going to analyze the pitfalls of old school approaches and look at the cutting-edge novel agents, both medication and non-medication. Both of them are novel appropriate ways to enhance GABA functioning in a brain that is locked into this flurry that we just talked about. Okay, let's continue our conversation, and we are now going to talk about the foundational neurobiology of the excitatory inhibitory balance. We gotta

Benzodiazepines Benefits And Hidden Costs

Rakesh Jain, MD, MPH 15:18

talk about this. So for decades, when we wanted to target the GABA system, we reached just primarily for one class of medications, benzodiazepines. And the generation before us, folks, who didn't have benzodiazepines, they reached for barbiturates. Both of them may have different names, but essentially they work through the same mechanism. So to understand how benzodiazepines work, we have to look closely at the structure of the GABA A receptor pentomere. Now, this word pentomere is beautiful, which literally means five different petals, subunits of the GABA A receptor that come together to create this receptor. It's beautiful actually. If you get a chance to look at it, it's worth looking at and really appreciating the glory of nature to create such a complex and beautiful receptor and to give each human being billions of them. How lucky we are, right? So benzodiazepines don't bind at the same site as the brain's own GABA, but they bind to a distinct and specialized site location. We call that allosteric. It sits between the alpha and the gamma subunit. Okay? So benzodiazepines officially technically they're called positive allosteric modulators. They do not directly open the chloride channel on their own. They don't. Instead, when we have endogenous GABA receptors bind to their own site, the presence of benzodiazepine increases the receptor's ability to signal to the GABA. So it kind of enhances GABA's functionality, the GABA that we produce in our own brain. So this mechanism is actually quite effective at providing rapid relief from things like acute pain or muscle spasm. But it does come with a heavy, heavy clinical cost that, you know, kind of runs counter to the goals of positive psychiatry. Because benzodiazepines are non-selective. They are pretty indiscriminate. They bind to alpha-1, alpha-2, alpha-three, alpha-5 subunits. That's a problem. Because that leads to sedation, amnesia, well, even dependence. So that's a bit of a challenge, isn't it? So because of this lack of selectivity, chronic long-term benzodiazepine use, while it is appropriate for about 10% of patients, for about 90% of patients, it's not appropriate. It's like using a sledgehammer to drive in a nail. That's not appropriate. And the brain, if it's overexposed to benzodiazepines, responds to this continuous, heavy, heavy stimulation by downregulating its own GABA A receptors. It says, hey, I don't have to do my job, somebody else is doing it. So our own GABA system weakens and weakens and weakens. Weakens so much that without the external benzodiazepine, I can no longer sleep or control my own anxiety. See the problem? So from a positive psychiatric perspective, benzodiazepines, not for everybody, thank God. And we should make sure that people who need benzodiazepines are not denied them. That's a really important thing to remember. But for a lot of patients, they actively impair the very mechanism that's required for long-term psychological flourishing. That's the problem. They can impair neuroplasticity, they can impair long-term potentiation in the hippocampus. So if a patient is taking high doses of benzodiazepines, it's going to be really important for us to appreciate do they really need it? Is it helping or are they trapped? Are they trapped in the benzodiazepine loop? And perhaps help them overcome it. I also want to alert you that the Z drugs, we know them well, right? Zolpidem, Zopiclone, S Zopiclone. Well, they have different names. They're called Z drugs. But the thing is, they bind to the exact same benzodiazepine site on the GABA receptor. They just show a greater selectivity for the alpha-1 subunit. But they're not all that different. And they certainly can help initiate sleep. They really can. But they carry a risk of tolerance and dependence and cognitive disruption. And what worries me from the perspective of positive psychiatry is in fact can weaken the brain's own innate system to create normal, healthy sleep. So we should perhaps now talk about some other options that are not without their own problems, but that have been forwarded for clinical

Gabapentin And Pregabalin Explained

Rakesh Jain, MD, MPH 20:34

use. And those are the non-benzodiazepine GABA A modulators and medications with novel psychopharmacology. So thankfully, there have been progress. There have been progress. And we have this group of medications that we call GABAPentenoids. And there's two in particular that are quite famous now, right? GABAPentin and pregabalin. Neurontin and Lyrica are their trade names, and very often we call them by that. But despite their names, GABA pentenoids do not bind to GABA A or GABA B receptors, and they don't even interfere with GABA reuptake. In fact, their primary mechanism of action is to connect to what's called a voltage-gated calcium channel. It's known as alpha 2 delta subunit of the voltage-gated calcium channels that live on the presynaptic excitatory neurons. So, no, they don't bind at all to GABA A or GABA B receptors, but to a very different location, as I said, to a completely different location, which is the presynaptic excitatory neurons. So by binding to this specific subunit, GABA pentenoids, the ones that we've talked about, reduce the inflation. Of calcium into the presynaptic neurons. And that leads to the dampening of these activities that are often provoked by things like, say, glutamate. So, from an excitatory inhibitory perspective, GABA pantonoids do not push down the GABA break. Rather, they gently lift the foot off the glutamate gas pedal. Did you notice a significant difference? Yeah. So this subtle shift effectively lowers and creates the same situation where we have reduced glutamatergic tone so the GABA that wasn't functioning can rise. And that, from a therapeutic perspective, is often used in generalized anxiety disorder and fibromyalgia. But let's be careful. Let's be careful. Over time, what we have discovered is GABAPentinoids themselves have their own challenges. Weight gain is one of them. Excess sedation is another one of them. And what's rapidly emerging, not just here in the United States of America, but all over, is an increasing true addiction to both GABAPentin and Bregabeline. We have to keep in mind that when we intervene in this manner, addiction is in fact a possibility.

Neurosteroids And Rapid Antidepressant Effects

Rakesh Jain, MD, MPH 23:29

So now we come into this fascinating new world of neurosteroids, which I think represent a major frontier in modern neurobiology. What are neuroactive steroids? We should first talk about this molecule called allopregnanolone. Yes, say that five times, folks. And the neurobiology supporting its role in health and illness is actually quite well established. So allopregnalolone, it's a metabolite of progesterone. You know, women produce it, and so do men. So do men. They're synthesized directly within the brain. It's not just the gonads, it's not just pregnancy. It's directly synthesized within the brain and functions as an incredibly potent positive allosteric modulator of actually not just one kind of GABA A receptor, but two kinds of GABA receptors, synaptic and extrasynaptic. Really an important point. And unlike benzodiazepines, which require a specific gamma subunit configuration, neurosteroids in fact bind to a distinctly different site located in the intersubunit interface between alpha and beta subunits or directly onto the delta subunit contained in extrasynaptic receptors. My goodness, that's a lot of big words I'm throwing out. But it's important. We appreciate a few salient things. We already produce neuroactive steroids, NASs, men and women. We already produce it. We have been doing it since the advent of time. Point number two, these neuroactive steroids have a clear and impressive role in the human brain, which is to act on GABA A receptors. And two kinds, unlike say benzodiazepines or Z drugs, they work on both, both intrasynaptic and extrasynaptic GABA A receptors. So by doing this, neuroactive steroids powerfully enhance the tonic inhibition. Tonic means longstanding. Phase means temporary, right? A phase. We're going through a phase, temporary. But tonic is sustained, stabilizing force that regulates the overall excitability of the entire neural networks. Oh my goodness. Now we are talking, right? So this brings us to some of the more exciting recent breakthroughs we have had in psychiatry, in mental health, which is the arrival of neuroactive steroids called brexanolone and xoranolone. I am certain you've heard about them previously, but if not, we're going to have a quick conversation about them. So these groundbreaking agents, they have demonstrated very rapid and profound antidepressant effects without ever acting on serotonin or norpinephrine or dopamine. And in fact, the FT has approved them for postpartum depression and even for major depressive disorder in countries around the world. By directly restoring the health of extrasynaptic GABA A receptors and by rapidly re-establishing the healthy excitatory inhibitory balance, these substances, these neuroactive medications, can lift a patient out of a severe acute depressive state, sometimes within hours, within days, rather than weeks or months. And what about sexual dysfunction? None noted. What about weight gain? None noted. And of course, the beautiful thing about these medications is additionally that it is episodic treatment. It is not continuous treatment. You can imagine that's music to anybody who's interested in positive psychiatry. Well, as clinicians, we're always interested in precision phenotyping, right? We really don't want to treat every patient presenting with depression or anxiety with the same broad brush approach. That's why a considerable amount of progress is being made with GABA-specific medications, both for postpartum depression and God willing, even in major depression.

Spotting GABA Deficit In Real Life

Rakesh Jain, MD, MPH 28:27

So let's think this out. How does a GABA urgic deficit present clinically? Well, we don't have a blood test or an imaging that can show us that, but you know what? We have something as good. We have the ability to talk to and observe our patients. Well, patients who live in a continuous, unremitting state of anxious arousal, they may have such a challenge. So patient presenting with a lot of muscle tension or racing pulse, an inability to settle down, maybe sleep-onset insomnia where the mind races the moment the head hits the pillow? How about profound hypersensitivity to sensory stimuli? How about becoming easily overwhelmed by emotions, loud noises, bright lights, chaotic environment? What about this hyperreactivity to minor stresses, moving immediately from states of calm into full-blown fight or flight response? What we may want to do in such individuals in such clinical presentations is to remember that, hey, I need to think about excitatory inhibitory balance. How do I non-pharmacologically, that's always the first opportunity, the first way to go? But how do I, if I'm going to use pharmacology, how do I think this out? How do I reduce the network flurry? How do I restore the brain structural stability in terms of network functioning with healthy excitatory inhibitory balance? How do I do that? So when then it's appropriate to not use the classic medications, SSRIs, SNRIs, because they don't make sense, or to augment them with something that establishes EI balance would be the right way to go. The truth is, true flourishing requires this kind of integrated approach. When we do use pharmacology, we really should not rely on what's comfortable to us. Rather, we should rely on what is our understanding of the patient's symptoms, what might be the underlying neural architectural difficulties, and how do I fix that so the patient's own natural flourishing state is improved.

Meditation As A GABA Training Tool

Rakesh Jain, MD, MPH 30:56

We definitely need to talk about non-pharmacological options because GABA is one of those beautiful neurotransmitters where non-pharmacological techniques definitely work. Mind-body interventions have become very popular in the last few years, and I am super stoked about that. That's a good thing. Because from a GABA perspective, that's exactly the right way to go. You know, traditional ancient cultures have known this even without having an MRI. They've known this for a long time. Meditation and prayer. Yeah, lifestyle interventions have been part of every ancient culture and religion I've ever encountered. You know what? They were right. So we may have advanced functional neuroimaging today, but essentially, all we're proving is what has been known for a long time. We should really carefully examine the data on the neurobiological mechanisms of mindful meditation and even formalized therapies called mindfulness-based stress reduction or or even MBCT, mindfulness-based cognitive therapy. I've been very lucky that that I've been exposed to both of them. I've actually received formal training in both of them, and I encourage you to do the same. It's very hard to be a quality clinician, even a clinician who primarily prescribes medications, to do all the right things by our patients unless we allow ourselves and give ourselves the opportunity to really learn other forms of treatment. So when our patients engage in focus attention or open monitoring meditation, whichever kind, functional neuroimaging reveals a significant and pretty quick localized increase in regional blood flow within the prefrontal cortex. But it's not just that. It's not just that. It serves as the primary gatekeeper to the thalamus. It's a shell. You don't get to come into the main part of the thalamus unless this gate opens or closes. So when we have an individual engaging in mindfulness-based or meditation or prayer-based interaction with themselves, what happens is there's a highly coordinated release of GABA quick. And the surgeon GABA acts like a massive volume control dial and filters out distracting sensory noise that dampens overactive emotional circuits and brings a sense of not just emotional calmness, but biological calmness and cognitive clarity. The beautiful thing is if one keeps practicing this, there are significant long-term neuroplastic effects of this practice. And we know based on studies of long-term Buddhist practitioners during meditation, there is an increase in high amplitude gamma band oscillations, which comes to us thanks to appropriate GABA functioning. So by regularly engaging in mindfulness, which we really ought to encourage our patients and to be quite honest, each other to engage in. We're not just inducing a temporary state of relaxation. We're actively training and strengthening our GABA circuitry. It's a gift that never stops giving. It helps the brain build its natural resilience to stress and to hyper-arousal.

Yoga Breath Work And Vagal Calm

Rakesh Jain, MD, MPH 35:15

I think we should also talk about another highly potent non-pharmacological intervention that targets the GABA system. That's yoga and structured breath work. Yep, I said it. And here I am, a psychopharmacologist, talking about yoga and structured breath work. But I have to. I have to. And you and I have an obligation to offer our patients, if you're interested in positive psychiatry, to offer them interventions that have minimum side effects that they can use on their own and use it to improve not just their symptomatology, but their wellness. A positive psychiatry practitioner embraces all of these techniques. We should appreciate that 80% of all the vagal fibers are afferent. In other words, in other words, they carry sensory information from the body back into the brain. So when I'm using things like breath work or yoga, 80%, 80% of my vagal nerves are in fact bringing those signals up into my brain. How is the body not profoundly important in this entire process, right? So when the nucleus tractus solitaris, also known as NTS, is activated through yoga or breath work, which very often go hand in hand. Guess what? The sympathetic fight or flight response centers in the human brain that are predominantly noradrenergic, they have more GABA signaling on them. GABA is inhibitory. So when GABA signals, those overactive neurons just chill out. They fire less. When they fire less, of course, the individual is less anxious, feels not just better, but feels more in control of their life. And elements of positive psychiatry go up. So I would say if you're interested in GABA and you're interested in positive psychiatry, what you already are quite interested in is self-empowered wellness. And you already are interested in teaching patients how to implement these techniques. More power to you. You might want to start out by recommending something as simple as boxed breathing. You know what that is. Four second inhale, four second hold, four second exhale, four second hold. Four four four four. Even that done for a minute or two, my goodness, it's a kappa prescription. And once the patient is able to gently move into other elements, maybe just 15 minutes of yoga, particularly Hatha yoga, which is gentle, mindfulness-based yoga. And when they're ready, when they're ready, we move on to maybe mindfulness-based stress reduction. But baksh breathing is, in fact, a very important way to get people started. Can we look at a couple more things before we end our conversation about GABA and interventions?

Exercise Nutrition And Lasting Balance

Rakesh Jain, MD, MPH 38:50

We should absolutely highlight the importance of exercise and diet, particularly exercise. So physical exercise enhances glutamatergic tone and gabergic tone. It's the only intervention we know where both are in fact elevated during exercise, and this elevation of both of them, in fact, restores the excitatory inhibitory balance. Exercise is really a powerful way to improve the tone of our GABA A receptors, both intra and extrasynaptically. There's no doubt that nutrition plays a role as well. No, we can't directly take GABA supplements. That's not all that effective. Some, but not all that effective. But a healthy diet, particularly rich in vitamins, because multiple B vitamins are involved in the cycle involved in appropriate synthesis of GABA from glutamate. So poor nutrition? Sorry, that will lead to poor creation of GABA. So there's no specific GABA-ergic diet, but just a healthy, well-balanced diet rich in plant foods, that is the way to

Integrating GABA Into Positive Psychiatry

Rakesh Jain, MD, MPH 40:15

go. All right, folks, it's time for us to integrate all that we have learned together. We really have gone talking about GABA, perhaps the most under-discussed of all neurotransmitters, the mother energy of the human brain, the wise neurotransmitter of the human brain. I'm so glad we had a chance to dismantle some of the old reductionist views of GABA. It's just a simple chemical sedative. And we have talked about its essential foundation in excitation and inhibition. It is the biological bedrock upon which positive mental health is built, upon which emotional agility is found, psychological resilience is built. And of course, optimum positive psychiatry is practiced. So I would encourage you folks to keep learning about GABA, but more importantly, not just learn about it, but start considering it as an element in both your pharmacologic and non-pharmacologic interventions that we offer our patients. We cannot always control the external events in our lives, that is true. We can't control the complex world around us. Also true. But through this rigorous evidence-based practice of positive psychiatry, we can absolutely optimize GAPA, glutamate, this excitatory balance. We can quiet the inner static, we can re-establish our core neurobiological balance, and we can sure as heck unlock our true positive potential. Oh man, I really enjoyed this conversation with you, GABA. It's an important, important neurotransmitter, so please keep learning, keep growing, and keep striving for positive psychiatry. This is Rakesh Gen signing off. And I'll see you next time on another episode of Positive Sachi. Bye-bye.