BIND: Benzodiazepine Induced Neurological Dysfunction

Benzodiazepines can feel like flipping a switch: panic quiets, sleep finally comes, your body unclenches. But what happens when that “off switch” starts rewiring the system you rely on to stay calm in the first place? Dr Andrew Rizzo joins me to dig into the biology behind chronic benzodiazepine use and why so many clinicians now recognize benzodiazepine-induced neurological dysfunction (BIND) as a real, patient-altering condition rather than a vague catch-all for “rebound anxiety.” 

We walk through the GABA receptor in plain language, including why benzodiazepines act as positive allosteric modulators, how the brain chases homeostasis by downregulating inhibition and upregulating glutamate, and why tolerance is structural not moral. Then we connect the molecular story to the clinical reality: why abrupt benzo cessation can be life-threatening, how seizure risk emerges, what “kindling” means for repeat withdrawal attempts, and why a slow benzodiazepine taper often takes months, not weeks. 

We also spend time on what patients and families actually need during recovery: validation, steady follow-up, and a plan that treats this like a fragile neurobiological injury. If you’re a clinician, a patient, or someone supporting a loved one, you’ll leave with clearer language, sharper warning signs, and a better mental model for why symptoms like photophobia, tinnitus, tremor, and cognitive fog can persist long after the last pill. 

Subscribe, share this with someone who needs it, and leave a review with your biggest question about benzos and withdrawal.

To contact Dr. Grover: ammadeeasy@fastmail.com

Transcript

Welcome And Key Definitions

SPEAKER_01 0:08

Hi, I'm Dr. Casey Grove. I spent years practicing emergency medicine before shifting my focus to addiction medicine. This podcast grew out of caring for patients, hearing their stories, and wanting to do better. Here we talk about recovery, medicine, and compassion. This is Addiction Medicine Made Easy. I am so happy to welcome Dr. Andrew Rizzo back to the podcast. As you may remember, he was the very sharp doctor that talked to us back in February about some of the unusual side effects and consequences of using cannabis. Well, he is here with us again today, and we are going to be talking about benzodiazepines, specifically a complication of chronic benzodiazepine use that we're learning more about as doctors, and it's called benzodiazepine-induced neurological dysfunction, also known as bind, B-I-N-D. The basic idea of bind is that benzodiazepines, which for many years were viewed as fairly benign medications, actually cause long-term neurological and physical symptoms such as insomnia, anxiety, poor cognition, and more. Dr. Rizzo will explain how and why this happens in detail in this episode. And a quick science alert: this episode is very science heavy. Here it comes. Watch out, here comes the science horn. A quick aside, my wife and daughter totally find that sound effect super annoying. Anyways, if you're not a clinician, we will break this down for you in a way that you can understand. Now, this episode is filled with so much great information, there's just only one issue with it. And let me tell you a funny story about this episode that explains it. So, my wife, the very lovely and beautiful and extremely intelligent Dr. Close, she and I were at an appointment going over our taxes. And since I am very plugged in with my email, I took a minute to see if I had missed any important emails, and I saw an email that said, Andrew Rizzo has joined your Zoom meeting, and I realized that, oh man, I hadn't put our podcast recording on my calendar. So I jumped in my truck and found a spot to record with Dr. Rizzo. He actually calls me out in this episode for being in my car during the episode. And because of this, I didn't have my usual audio equipment, so the audio came out a little weird. I tried multiple ways and times to fix it, and I couldn't quite get it right. Fortunately, it's only my voice that sounds weird and robotic. Dr. Rizzo sounds great. So my apologies. Now I mentioned this episode was very science-y, so let's go through a few definitions for the non-clinicians that are listening to help prepare for some of the terms used in this episode. Homeostasis is the body's ability to stay in balance and maintain all of its internal systems working correctly. Iatrogenic means that the condition was caused by the medical system rather than by a problem from the body itself or an infection, like a side effect from a medication, for example. Neuroplasticity is the ability of nerve cells and pathways in the brain to constantly adapt and rewire themselves as the brain learns and grows. Now, this one's a little more complicated. Receptor upregulation and downregulation. For this one, I'm going to make an analogy to help you understand it. Throughout our bodies, we have lots of chemical signals. These are molecules that our body makes, like insulin or adrenaline, and they act by binding to a receptor that is the same shape. So molecule A is the same shape as receptor A, so they bind and cause something to happen in the body. They cause the desired effect. Part of homeostasis, and now you know that term, is maintaining these chemical systems in balance, and one way the brain can do this is by adding or taking away receptors. Think of your brain's receptors like electrical outlets in a room that chemical messengers can plug into. When a chemical messenger or a drug or alcohol floods the brain repeatedly, the brain wants to stay in balance and so it removes outlets. In other words, there's fewer receptors and less response to those same signals. That's called downregulation. It's reducing the number of receptors. Upregulation is the opposite. There are more receptors, and you can think of it as the brain adding more outlets for chemical messengers to plug into. Okay, that was a lot. One final note, Dr. Rizzo and I talk about how hard it is to taper off of benzodiazepines, so we're gonna come back and do another episode in the future on that topic specifically. So with that, there is so much to learn from this episode, so let's get started. All right. Dr. Rizzo, how are you today?

SPEAKER_00 5:11

I am great. Thanks for having me back.

SPEAKER_01 5:14

So we are gonna talk about what I think is the bane of every addiction doctor's existence, which is benzodiazepines.

SPEAKER_00 5:22

Yeah, last month's podcast we did together on cannabis, I thought it was a really cool experience for me at least. And I thought we discussed some really impactful concepts that many providers, patients, and families struggle with comprehending. I plan on using our time together today to discuss a different drug of abuse and the one that I consider the most challenging to treat, and that's benzodiazepines. So, you know, whether we're managing the acute complications of benzouse disorder in my ED or trying to safely battle the chronic use complications in my detox facility, they are definitely also the bane of my addiction medicine practice too. So I'm I'm happy that you were able to reiterate that.

SPEAKER_01 6:02

Yeah, my my addiction practice in here in California, we have five physicians. We have another one joining next month. Yeah, we are all on the same page that man, we do not agree with long-term benzouse. Now, granted, there is probably a subset that needed under the care of a psychiatrist, and we're not talking about that. I think the way I say it to my patients is if you and your psychiatrist feel like your anxiety or whatever condition is so bad that you need a benzodazipine, that's your decision between you and them. But what I can tell you from what I see as an addiction doctor is long-term benzouse is not a good thing.

SPEAKER_00 6:39

I totally agree with you. So, my first exposure to the dangers of benzo use actually was like when I was in med school. And I remember my father would fill my grandmother's seven-day pill case as her mental state was slowly worsening into her late 80s and 90s. And despite my grandmother not remembering my name, she would immediately recognize when my father stopped putting the Larazipam tablets in the case. She would get so furious with him when she could not find those little yellow tablets. And considering that my grandma was put on Atavan by doctors in the 70s after she lost a teenage child, I think benzos truly were just a band-aid for my grandmother's griefs. But that wound never healed. And it definitely contributed to her agoraphobia and isolation within our family, and definitely contributed to her dementia also. This is kind of like the basis of why I really can't stand benzos for a lot of patients that really should have had different ways to handle things like grief and anxiety in their life. And I started really, as I was preparing for this recording, I listened to your September 1st, 2025 episode on benzos. And I would tell anyone listening to this right now, if you want a little bit of a foundation and a primer, pause this podcast, go listen to Dr. Grober's Benzo podcast on September and uh and then come back and listen to the rest of this. I think that'd be a really great way to combine these two podcasts together.

SPEAKER_01 8:04

So between the two of us, you seem to be the more organized one. So I know you have something you want to get started with. So what did you what did you have in mind for us to start with?

The Malpractice Hot Take

SPEAKER_00 8:14

Yeah, so uh one last thing before I start. You know, I I love working at a high watch recovery center in Kent, Connecticut, and South Brooklyn and New York City. What I say today does not represent my employers or my coworkers. Everything I say is just me. And I'm feeling a little extra spicy today. I know you said on our last podcast you like to start off with some of the main points. So I'm gonna start off with just one hot take, right? And so if you're a medical provider or someone who works in public health, I want you to listen very closely. Prescribing daily benzos to patients for anxiety is medical malpractice. Okay. And I know, Casey, you did say that 28 minutes into your benzo podcast episode, but I wanted to start off saying that. And prescribing daily benzos for patients for anxiety on a daily basis is medical malpractice. And I also want to let everyone know I'm using malpractice not from that medical legal triggering sense, but more from the Webster's dictionary sense. It's just improper and bad practice. It's something that we really need to work on actively on a regular basis.

SPEAKER_01 9:22

So if I could just add some commentary to that, I agree with you 100%. And I think we have to just be very clear about what we're referencing. So in 2026, if you are a new patient going to see your doctor for anxiety and all they offer you is benzos, that is very incorrect. I agree with you. Where I struggle, though, is I have plenty of patients who've been on them, like your grandmother's experience for years and years and years. And previously we didn't really realize how bad benzos were. So a lot of what we do now is try to convince people that there are other treatments for anxiety. So I just want to be really clear. If someone's listening and they're on a benzo and they're working with a doctor, that doesn't mean your doctor did something wrong. They may have made that decision 10 years ago before we knew a lot of this. But for any new patient that's coming to their doctor for anxiety, if they offer you benzos, I personally disagree with that decision. And Dr. Izzo, I'm assuming you do too.

GABA Receptors Explained Simply

SPEAKER_00 10:24

Totally correct. I yeah, I agree with everything you said. You know, the way we practice medicine 20, 30 years ago is very different than how we practice now. So it is hard to judge people, you know, that far in the past. But uh, yeah, the present day, we have a lot of information about benzos, and we really need to be um more cognizant about who we give benzos to and for very specific and sparing reasons. And also, to be honest, there's been a bunch of opioid lawsuits we've seen across the country to be who knows what the future brings with benzo-related lawsuits. So, for those who are not practicing in a safe manner, like just we all have to be just be careful of that. But let me defend my hot take, okay? So I want to start off on the molecular level to convince these listeners. And we just need to start at looking at the GABA receptor. So I think, Dr. Grover, this is where you press that button warning the listeners about like nerdy science stuff. I like to blather about. But anyone also who's near a computer or phone, if you find it more useful to open up a picture of the GABA receptor as I talk, I really find that might be very helpful because I will be talking about the GABA receptor and and to visualize it will really maybe help connect some of the points that I that I'll be making later on. So let's start with GABA, right? So that's so GAMA, amino butyric acid, it is the primary inhibitory neurotransmitter in our central nervous system. I love using analogies with my patients. So let's try to use an analogy. And Dr. Grover, with you being in a car, let's use a car as an analogy. Okay. So it is the brakes of our brain car. So GABA is the brakes to our brain car. When your brain is overstimulated, GABA is what slows the electrical firing down. Just like a car having two types of brakes, right? The standard brake pedal and the emergency brake, we actually have two types of GABA receptors and they do two different jobs. We have the GABA A and the GABA B receptor. But GABA A is the emergency brake. It is that fast-acting ion channel. When GABA binds to the GABA A receptor, a channel is going to open instantly, and negatively charged chloride ions are going to go into that neuron, so into that brain cell, and it's going to hyperpolarize that cell. And for those not in the medical field, that basically just means that that nerve cell is going to just stop firing. It's going to stop responding. This fast-acting GABA receptor is the primary target for so many things like benzos, Z drugs like ambien, and even alcohol. So, on the other hand, though, we have the GABA B, and that is more like our standard engine break. It's a G protein coupled receptor. It's slower. And instead of opening these chloride channels, it kind of triggers this cascade of events that eventually leads potassium out of our cell, blocks calcium from coming in. And it's something we can talk about on another day. But I particularly have a weird obsession with the GABA B receptor. And I would love to chat about it whenever I have the ability to. But however, for benzo use disorder, all our money is going to be on that GABA A receptor.

SPEAKER_01 13:34

Can I just make sure I understand you on this one?

SPEAKER_00 13:36

Yeah.

SPEAKER_01 13:37

So I actually didn't know any of this. So thank you for bringing this to at least my brain. The natural doubter chemical in our brain is GABA that I knew. I knew there was a GABA A and a GABA B, but I didn't realize that the GABA A is a lot more potent. And since benzos act on GABA A and people with anxiety and PTSD want to calm down as quickly as possible, is that why they like it so much?

SPEAKER_00 14:03

Correct. It's it's the response time to the GABA receptor is the quickest response times we're going to find in the world of the inhibitory neurotransmitters. Thus, it was a natural match where the scientists that created Bentos found this structure that's going to respond to it essentially immediately. And we're going to really go into more about the GABA receptor so that hopefully the audience or the listeners have a better understanding of really what makes that GABA A receptor so responsible for those clinical effects that we're going to be talking about and the complications leading to chronic use and abuse potential, et cetera, et cetera. Okay, cool. So GABA A receptors, it's a pentamer. So a pentamer is it's a receptor that's made of five different protein subunits and they're clustered together. And they have in the middle, it has this like central like tube, or we call it a chloride pore. And a standard GABA receptor, an A receptor, has two alpha subunits, two beta subunits, and one gamma subunit. And this is a typical receptor, and there are some variations. So we're just going to focus on the typical.

SPEAKER_01 15:15

If anyone hasn't Googled it, imagine you have basically five hot dogs and you tied them all together in like a little pentagon, and that's kind of what it looks like.

SPEAKER_00 15:25

Sometimes I feel like we we have similar brains, because I was actually going to use hot dog bun as more of the analogy, but I'm okay with hot dogs too. Maybe we're both hungry. And so this is kind of where it gets fascinating, right? So from a pharmacological standpoint, like the specific subunit actually dictates the clinical effect of that GABA receptor. So I'll give you a great example. There's 19 different subunits that make up the GABA A receptor. Now, if we hit a alpha one subunit, that is going to cause profound sedation, amnesia, and actually help with seizures. But if we hit the alpha 2 or the alpha 3 subunit, we're actually just going to get anxiolysis. We're going to get anti-anxiety effects. And this is an important concept to understand because the future of treating anxiety might rely on only hitting these very small subunits so we can avoid some of those negative side effects, but only hit some of the side effects we're looking to hit. Right now, the benzos essentially hit all of them. They're very sticky. And they just, as soon as they land near the receptor, they bind right between all the alpha and the gamma subunits, and they essentially force that GABA receptor to work overtime. So actually, before we add in the prescription pad, let's figure out how our brains handle natural GABA. Because natural GABA floats around in our bloodstream and in our brains all the time. And what's really ironic about it is actually GABA, the actual structure of GABA is made from glutamate. And the reason this is ironic is that glutamate is actually our main excitatory neurotransmitter. So I want everyone to take that analogy of the car and think of glutamate as the gas pedal, right? So GABA is the brake, glutamate is the gas. And the brain uses an enzyme. So it's called glutamic acid decarboxylase, or we typically I call it GAD or GAD, and GAD converts the gas pedal, glutamate, into the brake pedal GABA. And this is such an important concept to understand because when we withdraw from benzos, this all gets very severely disrupted and causes all of the bad side effects and the withdrawal side effects that we typically focus on when a patient comes to us in the world of addiction medicine. We can then actually naturally upregulate the system by doing things that are just otherwise really good for us, right? Like exercise, yoga, meditation. Nutrition is so important. There's so many cofactors. So vitamin B6, magnesium, they're all involved in this synthesis. And if we can naturally promote healthy gabergic tone, this will actually let our brain self-soothe. And this is often what I do with a lot of my patients who are struggling with trying to come off of benzos, is like really apply this holistic and daily life practicing changing environment that might actually give them enough to get through some of those really rough days.

SPEAKER_01 18:28

So can I just make sure I understand here? So normally, without any substances in our body, our brain works out a balance between the brakes, GABA, and the gas glutamate. When we introduce a substance, whether it's alcohol or it's a benzodiazepine, that balance is disrupted. And most of my patients, whether it's trauma or anxiety or insomnia, they like downers because it's that calming feeling. And so what you're saying is by taking a substance that disrupts that break gas balance, when we come off of it, we're all gas, which is why withdrawal is so bad. And it takes time for that to balance out, but doing healthy things for us makes that balance come back to normal. Or if we don't use substances, healthy life habits keep that balance as normal as possible. Is that right?

Tolerance Withdrawal And Kindling

SPEAKER_00 19:22

Yeah. And like I said, we seem to be on the same wavelength this whole day so far because this is exactly what I want to go into and talk about further. Um, I will also say that those healthy lifestyle changes, I wouldn't utilize them as the primary treatment regimen when you're coming off of benzos because of the dangers of that acute couple of weeks, if not months, while you're trying to get someone off of benzos. But I would say by integrating that into your daily routine, plus by working with a specialist like someone in addiction medicine to get you off of maybe an unhealthy habit or the addictive properties of benzos that might be negatively affecting your life, I would say that it would be really important to integrate that lifestyle with the slow tapering of the medication, working with a medical professional, essentially. Yes. So now I want to take that natural understanding of where GABA comes from in our body. And I really want to introduce the exogenous, powerful GABA-urgic drug like benzo. And like you said, it completely hijacks this delicate homeostasis system that we've worked so hard to try to develop. And in the clinical setting, whether we're managing acute toxicology in the ED or training fellows, teaching them about outpatient tapers, like we really always try to hammer home this concept of neuroadaptation. And the neuroadaptation is really what we're going to be talking about a lot in regards to what happens when benzos disrupt our bodies search for that homeostasis. So when you give a patient a pill, it artificially forces those chloride channels from the GABA receptor to open day after day. The brain recognizes that it's being artificially suppressed. So to survive, it adapts, it downsizes, it actually internalizes its own GABA-A receptors and simultaneously upregulates or increases those excitatory glutamate systems to fight through the days and days of over sedation while being on benzos. So you have a GABA receptor that is hiding the binding sites, and you have a body that is now creating more of that high energy, high agitation, high anxiety component to that glutamate system. So you have a double hit. The brain is effectively disabling its own natural ability to calm down. I was gonna say, this is not giving me a warm, fuzzy feeling. It shouldn't. This is a tragedy of the atrogenic cycle. We are causing this. Right? We prescribe a medication to fix a patient's anxiety, but chronic exposure structurally remodels their brain so that they can no longer regulate anxiety without a drug. The exogenous consumption doesn't just mask the problem. Over time, it fundamentally dysregulates the cure. That is patient harm. And that is now practice. So I really want to now actually explain on a molecular level what happens during the acute benzo consumption phase because I want to tie this all together, right? So when a when a patient takes that first dose of clonazepam or alprazzolam, the drug crosses the blood brain barrier. It finds that GABA A receptor. And the crucial point many of us don't realize is the benzodiazepines don't even directly bind to that GABA A receptor. They actually cannot open that channel by themselves. They're really considered positive allosteric modulators or PAMS. They bind to this specific allosteric site or this other binding site and they wait there. And they wait there until the brain's natural GABA comes along and it binds to their own active site. And you know what the benzos do? They act like a megaphone. They change the shape of the receptor. They dramatically increase the frequency of that chloride channel from opening. And the result is a massive influx of negative chloride ions leading to acute CNS or central nervous system depression or immediate relaxation. The patient feels that relief from the panic, they fall asleep, and the mechanism works beautifully. Wow, that's really nice, right? I'm trying to paint a little bit of a rosy picture.

SPEAKER_01 23:58

Well, I tell my patients, because they'll they'll come to me and I'm tapering them off of benzos, and they're like, Dr. Grover, does this mean I can never take a benzodazipine ever again? And I go, no. You know, if you need an MRI and you have horrible claustrophobia, sure, I'll give you a dose, no problem. If you're afraid of the dentist and you need a dental cleaning, I will use one here and there. That is okay. It's really, to your point, the daily use that is such a problem. And we can talk about the parallels to what the how opioids do this for pain, how opioids make pain worse in the long term. Similar idea. But yes, benzodinazipines are effective. And to your point, we have to understand what they do so we can really work to avoid patient harm. So your patient now is taking a clinazepam, they've relaxed, they've gotten through their MRI. What happens next?

SPEAKER_00 24:48

I told you I'm feeling spicy today. Yeah, so everything changes once we get to a chronic consumption state. And this is the trap. Like the trap is set. This is the trap. The brain is the master of homeostasis. It does not like being artificially forced into a suppressed, hyperpolarized state day after day, month after month. So it's going to fight back. And it's going to fight back with something called neuroadaptation. Now, the brain literally downregulates or decreases its GABA receptors. It pulls them away from that synapse, which is what I was mentioning before. And then it goes through a process called receptor uncoupling. Now, this is actually where the receptor, the GABA receptor, becomes functionally disconnected from that GABA site. The megaphone gets unplugged. This is the physiological basis of tolerance, and it's really unique to benzos. Not a lot of other drugs that I am aware of, and I don't actually can't think of any others that causes this profound uncoupling to a receptor like a GABA receptor. And this is why so many of our patients need higher and higher doses to achieve that same anziolytic effect. And it happens kind of quickly, right? The brain doesn't just blunt the brakes, it actually during chronic consumption, it also hits the gas. So we're trying to counteract this constant chemical sedation. The central nervous system is just going to upregulate and upregulate that excitatory pathway. And it's all based around that glutamate system that I mentioned. So the brain is now operating and functioning in this imbalanced state, and it's pretty fragile. And so this is where we get to that most dangerous phase, and that's that acute cessation or stopping taking benzos. This is where all the danger comes to a head. So I want to use that analogy of the car, and I want you to take that car that we're in, our benzo car, and we're driving it down a steep mountain, right? The brakes are worn out because we've downregulated our GABA. Our gas pedal is locked in acceleration because we've upregulated our glutamate. And now we're just lost control of that car. This is abrupt benzo cessation, right? When we abruptly remove an exogenous positive allosteric modulator like benzo's, that fragile equilibrium shatters. We are left with a brain that is massively upregulated, hypersensitive, and has literally no functional GABA left to stop anything. This is not a psychological craving. This is a profound, life-threatening chemical storm. When people say, Oh, I've heard that benzos are dangerous. I heard I can die from a benzo withdrawal. This is what we're talking about. This hyper excitable rebound manifests as severe anxiety, diaphoresis, tremors, and all types of sensory hypersensitivity. When it's left unchecked, it will lead to seizures because our brain's threshold is going to cross a point of no return. And each time our patients go through these withdrawals, we develop this kindling type of effect. And I feel like you've also talked about kindling in the past. And kindling is this process where every time we go through that withdrawal process, our bodies struggle with getting back to healing and finding that balance. And it makes it more and more challenging and the delta gets larger and larger. And basically the withdrawals become harder, longer, and more dangerous every subsequent withdrawal. And this is exactly why when we're managing these transitions in the clinical setting, we have to really respect that GABA receptor. We can't rush it, right? We have to slowly taper the medications, and we have to give our brain typically months to rebuild its own brace. And that's why ASAM and a lot of other professional societies really are starting to recommend a very slow and focused taper to get people off of benzo safely. And I think you've talked about in your practice before some of the challenges of getting people off of it, even when you're taking it, maybe a five to 10% dose reduction over a couple weeks at a time.

BIND And Protracted Symptoms

SPEAKER_01 29:01

Yeah, it's funny you mentioned that. I saw one of my patients, poor thing, horribly, horribly traumatized, pistol whipped by a significant other, threatened at gunpoint, on top of all the other trauma, came into my office yesterday morning in bad benzo withdrawal. And oh my gosh, she was in such a bad place. Hallucinating, shaky, sweaty, just looked awful. And I saw another one of my patients yesterday who was on benzos from her psychiatrist. And this is funny about doctors. They teach us how to start meds, but never how to stop them. Her psychiatrist put her on benzos and said, Oh, we can taper you off of this dose of clonazepam over two weeks. And she ended up in the ER three times for seizures. And so I just met with her and she has said so many times, Dr. Grover, thank you so much for actually knowing how to get me off of benzos. It's going to take us about four to six months.

SPEAKER_00 29:56

In your last benzo podcast in September, I think you mentioned about a patient that might have gone months without having any issues and all of a sudden, suddenly having a seizure. And I think that's something we need to remember because I really want to shift the lexicon from removing those phrases we use with other withdrawal syndromes like pause, right? The post-acute withdrawal syndrome or protracted withdrawal. We should really remove that from benzos and we should just replace it with bind because bind is that term that really fits everything that we've been discussing. And that's benzodiazepine-induced neurological dysfunction. This is a consensus term, right? This has been adopted by researchers and even patient advocacy groups. And it really accurately describes what's essentially an acquired yatrogenic brain injury. It's rather than just like the drug leaving our systems, bind is actually this de novo or like this new symptom creation that is not a return to the patient's underlying anxiety or insomnia. It's actually new symptoms based on the fact of their chronic benzouse. So we see sensory and motor changes, right? We see photophobia, phonophobia, tinnitus, parithesias, tremors. We see cognitive and psychological changes. We see that profound cognitive blunting that you've talked about in the past. We see memory deficits. We see that depersonalization and derealization. And we actually see a lot of intrusive ideations too, which is concerning considering the fact that these people are in a very vulnerable position when they're coming off of benzos. Right? People describe just like their brains on fire. They feel disconnected from reality. And there's a mechanism to this dysfunction. Like bind is basically a failure of neuroplasticity, right? Neuroplasticity, metaplasticity is such a hot phrase, not just in addiction medicine, but like in the wellness world and all over the place, right? But bind really means that our brains cannot find that neuroplasticity. We can't restore that balance. And after chronic exposure, the subsequent downregulation of GABA and the upregulation of glutamate causes failure. It's a failure to revert back to our factory settings. And this equilibrium is what we're chasing. And if it's structurally dysregulated, then our brain is going to be stuck. It's going to be stuck in a neurotoxic, hyper-excitable state that is essentially analogous to uh chronic traumatic brain injury, like CTE or TBIs, because it takes months, years, or maybe never ever truly going to heal. And once again, if someone comes to us for treatment in 2026 and they say, hey, Dr. Riz or Dr. Groover, I'm anxious. I suffer from insomnia. And the first thing I decide to do is throw 90 tablets of clonazepan at someone, that is now practice. Because I took someone who's struggling with an issue and I've just intensified that for essentially forever. This isn't about getting a substance out of someone's urine when we're trying to detox them. This is actively managing a really fragile and neurobiological injury. When a patient sits in front of you and they're terrified of their benzotaper, or they're exhausted by their symptoms they've had for over a year since their last dose of clonopin. Like we have to recognize as a society of addiction doctors that there's a molecular reality to what they are experiencing and not just a failure of willpower or behavior. Hopefully this makes sense. And if it doesn't, I'll I could try to explain some more stuff. But I really wanted to let everyone who's listening to this podcast try to understand not just the frustrations that we deal with on a regular basis dealing with benzo use disorder, but also sympathize to the people that are suffering from benzo use disorder and the families that are dealing with a loved one that's suffering from benzo use disorder. Because it can be really frustrating to think, hey, why is mom or dad like their behaviors have changed forever? Because it's easy to lean on that being a the behavioral source. But really, I want people to remember that there is truly a deep-rooted molecular and pharmokinetic change that occurs in our bodies when we're on benzo's for years. And we have to be patient. We have to be, we have to be loving and caring. And we have to realize that the people that we really care about who are suffering from this need way more time than we could ever imagine in recovery.

SPEAKER_01 34:18

So let me make sure I translate some of what you said. Because as I like to joke, I have to have four years of medical school just to be able to keep up with you. So the benzodazipines, as you've talked about, they make the brain's natural brakes work better. But it's like they make the wear and tear on the brakes happen faster. So over time, those brakes don't work as well. So the person needs more and more doses, higher doses over time. And then when people stop, the brain is just totally out of balance. And we'd expect like it should get back to normal pretty quickly. But because of how benzos work with these unique interactions with the brain that you've described, the brain's not right for months or even years and sometimes never goes back to its pre-benzostate. And this is what we're calling benzodiazepine-induced neurological dysfunction. And the brain controls all sorts of things in our bodies, how we move, how we talk, how we feel, our mood, our anxiety, all of that could be affected. So if someone says, I keep having these weird tingles in my hand, or I'm so sensitive to light, this could all be in this bind condition. And the way I said it to one of my patients, this is the one who they tried to quit benzodase beans over two weeks and she seized three times. This is not her name, but I said, Sarah, this is not a Sarah problem. This is a benzo problem. And she said, Dr. Governor, thank you so much for making me feel human. Because I felt like it was me. And I'm going to make one is maybe a bad joke here. But when my wife and I, the beautiful and incredible, amazingly intelligent Dr. Reb Close and I were starting, it was just her and I figuring out what to do in our practice. And we would say in the business world, keep your friends close and your enemies closer. It's the same with patients. If your patients are not doing well or they're struggling or they're making your job as a physician harder, they need more support. They need more frequent visits. They need a peer support. They need a sponsor. And I just feel like we can just say people coming off of benzos need some of the most support of any of our patients in addiction medicine simply because they can feel like it's a personal failure. And we're just finally now starting to understand these unique challenges with benzos.

Support Validation And Patient Dignity

SPEAKER_00 36:30

Dr. Gerber, you said a lot of really important points in that. And I will say, yes, your analogy and how you describe the um our car analogy is correct. I would say that in regards to brake pads, right, the benzos really help us wear out those brake pads way quicker. And some of our cars will never be able to replace those brake pads. And that is the concern for sure. Two is I think on our last podcast, it said you needed eight years of medical training to understand what I was saying. So now you said four years, so that's great. So you've like really improved your education over the last time we chatted. And then the third is you make me look bad with my wife because you bring up your amazing wife every episode. And like then my wife's gonna be like listening to this and say, like, well, why didn't you bring me up every episode? And I'm like, dang, you're so right. So I will say hello to my lovely wife. I also will bring you up in this, even though you're not in the medical field. I know you'll be listening to this. So thanks. And uh happy birthday, Ma. My mom's birthday is tomorrow. So she listened, she was the first person to listen to our podcast twice and was like, Yeah, listen to it two times in a row. I was like, mom, okay.

SPEAKER_01 37:33

So a funny story about why I speak about my wife that way. So I'm gonna bring up an uncomfortable topic, which is that in medicine, female physicians are treated different than male physicians. And so, so often we'll be going to an event and it's Dr. Grover and his wife. And I'm like, she has a medical degree. And one time we actually went to an event and I was like, oh yeah, my wife and I. And she was like, I do have a medical degree. So I just tried to be very clear that I want to honor her hard work in medical school. She trained before duty hour restrictions. And then I also am, I think my wife's number one fan. So yes, I always like to mention that she's beautiful and intelligent and a doctor. So there's a little bit of a story there. But yeah, I have to say, if there's one superpower that Dr. Close has as a doctor, it's to make people feel cared about. And it's really funny, she practices medicine in the jail and she gets in trouble with the deputies for giving the inmates hugs. You are not allowed to hug inmates in the jail, and she breaks that rule all the time. So she's too busy to listen to this. But I think to your point, our benzo patients need so much support, and making them feel safe and human makes their benzo taper easier because they know they have a safe place to land.

Clinical Takeaways And Fellowship Plug

SPEAKER_00 38:46

Casey, I like you a lot and you seem like a really good guy. I'd love to summarize for my listeners who are probably wondering why we're off on a tangent, but I'd really like to summarize what we talked about today, and I'll let everyone get on their merry way. But I really just wanted to just touch on the core clinical takeaways. So, you know, first is benzozepine withdrawal is fundamentally different uh from any other withdrawal in the drugs of abuse that we typically treat. So abrupt cessation does not just cause discomfort to our patients. It really does trigger a profound chemical imbalance uh between the GABA system and that unchecked, upregulated glutamate system. It's life-threatening and it can drastically lower the seizure threshold. So please, for someone who's listening to this, never recommend going cold turkey, never stopped abruptly. We need to slowly get you off of benzos if you feel that you have a problem, or as a medical provider, if you think one of your patients has a problem, we really need to slowly get someone off of them in the safest way possible. And Sam has a lot of really good guidelines on that if anybody needs to look them up. Second, tolerance is structural. It's not just behavioral, right? So when a patient requires higher doses, it's because their brain is actively down regulating those GABA receptors and uncoupling from the benzoallosteric sites to survive that constant suppression. So they're adapting to that chemical environment we prescribed. Third, recognize bind, right? So benzodiazepine-induced neurologic dysfunction is real. And when a patient presents months after cessation with things like photophobia and cognitive blunting and tremors, and don't casually dismiss this. It's failure of neuroplasticity. So the brain takes a painfully long time to rebuild its inhibition. And because of that, our jobs are to validate that injury and provide supportive care while our patients heal. And finally, prevention is our most powerful tool. As subscribers, we are the gatekeepers. We have to understand how rapid neuroadaption occurs. And we need to be very careful when we prescribe any benzos by limiting their duration and really actively helping our patients utilize those natural mechanisms to upregulate their own endogenous GABA. And I think if we if we really follow these or recognize these four main points, I think we're doing a good job. I looked at the recent statistics that actually benzo prescription patterns in America has dropped over the last eight to 10 years. I do have a little bit of a concern. The largest prescribing group is a group within 65 and older. And because of that, I mean, we're increasing fall risk, uh, dementia concerns and the morbidity that comes along with that, and also the resources from our healthcare system and the strain it does put on local healthcare systems. So just we should all be cognizant of the elderly patient that is struggling with benzos. And I kind of just want to end off this episode to remind residents and students and even attendings interested in addiction medicine to apply for an addiction medicine ACGME approved fellowship. Addiction medicine is the coolest field, right? I think Keesy and I will both agree it's it's like the coolest field, and it needs more of us to grow every day. And 50% of the spots were unfilled this year. Like that, that to me just boggles my mind. And it's not too late to find a program for July 1, 2026. If you're a resident and you're you don't know what you're going to be doing at the end of your residency, you can contact a group like ACAM or go onto the Match website and you can look for the programs that had open spots and reach out to the coordinators and the fellowship directors directly. Because we just need more of us out there to help the growing population that's struggling with addiction. And I really hope that we get more really awesome doctors out there and PAs and NPs to help fill those gaps across the country where people are really suffering the most.

SPEAKER_01 43:07

And a huge thank you to Central Coast Overdose Prevention for supporting this podcast. And always remember treating addiction saves live.