Lisinopril | Blood Pressure Medication
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And you can stop worrying about what your kids get their hands on. Start shopping at thrivemarket.com slash podcast for 30% off your first order and a free gift. Welcome everybody to another episode of Dr. Matt and Dr. Mike's medical podcast. I'm your host, Dr. Mike Todorovic. And I'm joined by my co-host...

The one and only Matthew. How are you, Matthew? Well, my doctor said recently at a consultation that I have high blood pressure and short-term memory loss. Oh, wow. Sorry to hear. Well, at least I don't have high blood pressure. Great.

All right, Matt. Which goes well with today's topic. Oh, it does. Well, you're right because today's topic is a drug known as lisinopril. Lisinopril, shall we spell it for the audience? L-I-S-I-N-O-P-R-I-L. Lisinopril. And it's what we call an ACE inhibitor, right? So we know that because all ACE inhibitors end with a suffix, pril. Wow. Which I believe...

is a systemic naming pattern for this class of drugs done by the International Non-Propriety Name and In System or INN, the IN. Sorry, the... The IN system. What's the IN system? The International Non-Propriety Name. Oh, so you mean that, for example, when a drug is made and a company markets it, they give it...

their own name. Yeah, like a brand name. And this is the generic name? I think along those lines. So basically everything that comes off the back of future developments of ACE inhibitors, they will always end with Pril. Okay. So is lisinopril a brand name or a generic name? Generic. Generic name. Okay. So we're talking about lisinopril, the ACE inhibitor, which means we obviously have to talk about ACE at some point.

Let's just... For everyone to... So that they're all on the same page, why would somebody be prescribed lisinopril as a drug? Yeah, so... One second. That's okay. Are you okay? Have you been taking lisinopril? Yes. No, I haven't, but that's something we'll come back to. Regarding the cough. You know what? Later on, cough, and I'll say it again, and it'll be a good lead into... It'll be a good... Yeah, good joke. Next time you cough, I'll be aware. So the question I asked Matthew is...

What or why would somebody be prescribed lisinopril? Primarily for central hypertension, which is hypertension with an unknown cause. That's essential. That's essential or primary. Okay. So this would be the majority of people with hypertension? Yes, that's correct. I can't exactly remember the number, but it's somewhere in the region of 90-ish percent of all people.

which just means a chronic high blood pressure state. Yeah. These people have what we call essential or primary hypertension, which is there's no real objective reason for it. There's theories that it's probably due to something, right?

But it's not like a secondary cause like you have narrowing of the renal, like the renal stenosis. Yeah. Or you have a tumor in your adrenal gland. So this drug's obviously going to drop blood pressure. All right. So that would be its primary use. Oh. But there's also if you had congestive heart failure. So this is where your heart's not working as it should. Yeah. Not pumping.

pumping blood out. Therefore, it's not delivering the amount of blood to the body that's required. By taking a drug like this, it takes some pressure off the heart. Stress off the system. Yeah. Okay, okay. And then the other one, sometimes it would be used in the short term if a person's just had a MI, myocardial infarction. Right, again, to take stress off the system. Yeah. Because it's going to reduce pressure. Probably. I think it may also have an effect on even...

Blood flow to the heart itself. Right. All right. Okay. So are we going to begin by talking a little bit about the history, its discovery, how this drug came about? Well, I think you should maybe preface it with...

The system behind it because it's an ACE inhibitor. You're right. But the system that it works in is the RAS pathway, which I know we've done podcasts on before, but let's just do a quick overview of that because then the drug itself fits into that pathway.

system, that pathway. Okay. All right. So this drug is what we call an angiotensin converting enzyme inhibitor, an ACE inhibitor. So we need to talk about where ACE sits within a very interesting and relatively complex pathway called the renin-angiotensin-aldosterone system, the RAS. Now, this RAS system, it is controlled predominantly by the kidneys.

And it's the kidney's way of maintaining blood pressure long-term. To itself. Would you say it's to itself? Well, I would say that it is being selfish because I always ask my students, why would the body hand over control of long-term blood pressure to the kidneys, right? You'd think it would be the heart or the brain or something else. And the answer is because your kidneys need to filter your blood every single day, every single minute, 120 mils per minute, it must filter every

And to maintain this,

rate of filtration, which we call the glomerular filtration rate, it needs constant blood being supplied to it, which is regulated by the pressure. So if blood pressure drops, kidneys filter less blood, to put it simply. So yeah, it makes sense that the kidneys would be in control of it. Because if you go one day without filtering your blood, you end up not filtering the 180 odd liters of blood you need to filter throughout that day. It'll be something significantly less. And that means you could potentially accumulate toxic byproducts.

Right, or metabolites. So just, I don't know if I'm asking this question too early. I reckon if you have to ask that question. All I was going to say is when we think of this system, we always think it's a system that's just made by the kidney for the body.

But more recent developments has been that all tissues kind of generate this pathway. Yep. Or its own kind of paracrinal, the local regulation. But then I'm just wondering, as the kidneys just become...

not the gatekeeper, but kind of the overseer of this process because it's not only benefited itself, but then the whole body. And so it kind of becomes this- Major regulator. Yeah. Yeah. Yeah. I would say so. So let's talk about what this system is, how it works. So firstly, if there is a drop in blood pressure or a drop in blood volume or a stimulation of the sympathetic nervous system, which is your fight or flight system, these are the three major triggers that,

Or even a drop in sodium in your blood as well. So if any of these things drop. Okay, so we got, say them all again. Drop in blood pressure. All right. Drop in blood volume.

A drop in the amount of sodium that your kidneys are filtering, right? And also a stimulation of your sympathetic nervous system, which is your fight or flight. So these are the major stimuli to your kidneys to trigger this system. This system, right. And because it's called the renin-angiotensin-aldosterone system, that's the order in which these chemicals are released. So all of these will trigger the kidneys to release a chemical called renin.

And what renin does is it's an enzyme, it's a hormone that can jump into the bloodstream and it will come across a chemical called angiotensinogen, which tends to be produced by the liver and just gets- It's always there. Into the bloodstream. Yep.

So in the bloodstream, renin will meet angiotensinogen. Now we've said before in podcasts that if a chemical ends in O-G-E-N, it means it's inactive. So it needs to be activated. And often if you chop off that O-G-E-N, you get the active form. So angiotensinogen needs to be activated into angiotensin.

Which kind of isn't that active, to be honest. No, very true. But that's what renin does. It chops the angiotensinogen into angiotensin into a more active form. Kind of like you in the office, you know, active but doesn't do much. Yeah, people think I'm active, but I'm just sitting there. And then angiotensin will be floating through the bloodstream. And when it gets to predominantly lung tissue,

There's an enzyme produced in higher quantities at the lung tissue, which is ACE, which is what we're talking about today, angiotensin converting enzyme. So it makes sense. It converts angiotensin and it converts angiotensin, which you could call angiotensin 1, into angiotensin 2.

And it's this angiotensin two, which is the you of the relationship where... A productive one. I don't do much. You do everything. And one of the things that you do do... Is raise blood pressure. Is increase blood pressure. Make you pee less? Me personally? So...

Angiotensin II, now it's been produced or converted into angiotensin II by ACE. Angiotensin II does all the work. So it is a generalized vasoconstrictor. So it goes to the blood vessels of the body and constricts them.

It also goes to the kidneys because remember the kidneys started this whole process because it was worried it wasn't getting fed enough. Tells the blood vessel leading into the kidney to dilate to get bigger so more blood goes in and tells the blood vessel leaving the kidney to constrict. Now I'm not talking about the renal artery and renal vein here. I'm talking about the arterioles that are feeding. Going to the nephron. That's right. That's not feeding the oxygenated blood to the kidneys but providing the kidneys with what's required to be filtered. Okay.

So that's the afferent arteriole coming in, it dilates that, and the efferent arteriole going out, it constricts that, which increases the pressure at the kidney itself to increase filtration, which is what we wanted. So it increases blood pressure through vasoconstriction of the peripheral vessels of the body. It increases renal perfusion, but angiotensin II also goes to the...

adrenal gland and stimulates the release of aldosterone and aldosterone goes to the kidneys nephron this specifically the nephron uh zac nephron and distal distal convoluted tubule yeah distal convoluted tubule probably a little bit of the collecting ducts as well and tells it to throw sodium back in the blood back in the blood because wherever sodium goes what follows

Water, usually water. Water, yeah. So I always think about when you eat something salty, you get thirsty. So wherever the salt goes, the water follows. And what that means- Or during this, when it's very humid, your salt shaker fills with water.

Okay. Do you notice that? It clumps up. It does. It clumps up. So salt back in the blood, water back in the blood and bananas into the urine. Okay. Just wait. Ed, yep. Everyone's thinking, what's he talking about? And you're right. He has no idea and neither do I. When the water jumps back into the blood, that increases your blood volume, which was one of the triggers for this pathway and therefore also increases the blood pressure. Okay.

Now you said it throws bananas back in because generally when we throw the sodium back into the body, it swaps it for? Potassium. Potassium, yeah. So that's one of the roles of aldosterone. So if you stimulate this pathway, you pay out potassium, right? So-

Did I cover that part? Great. In this case, we've got lisinopril, which blocks ACE. So if it blocks ACE, you're not converting the Dr. Mike into the Dr. Matt, the inactive to the active form, which means you don't get any of these things happening. You don't get the generalized vasoconstriction. You don't get the increased perfusion of the kidneys. You don't get the aldosterone released. You could argue that

Angiotensin 2 also triggers ADH, antidiuretic hormone, also known as vasopressin in the US, to be released from the hypothalamus. That also increases water back into the body. So in a way, it's very similar to aldosterone. But yeah, with an ACE inhibitor like lisinopril, none of these things happen. So it keeps blood pressure and blood volume low, which is probably what we want when we have essential hypertension or congestive heart failure. Now, history, going to history.

Yeah, well, the history for leucinepril isn't overly amazing or great. Okay, so it's like the history of Matt Barton. That's right. But it's, I don't know, what would you call it? It's brother? It's grandfather? I don't know. What are we talking about? The first ACE inhibitor. Yeah, okay. Which was captopril.

Captopril was the first ACE inhibitor, which- Sounds like a superhero. It- Captopril. Captopril, which is not really used that frequently anymore because you have to take it three times a day for it to be effective. And functions similarly to lisinopril. Yeah, it's still a pril. It's still an ACE inhibitor. Okay. But it's shorter actin, shorter half-life.

Probably has a more side effect profile. So you need more. The captopril isn't commonly used anymore today. Whereas leucinepril, planopril are the more common derivatives or siblings. You said that all of the ACE inhibitors have pril as a suffix. Do you want to tell us why that's the case? All right. So we go to the history of trying to understand how to control blood pressure. Yeah. And go into what you said. When did you say? 1800s?

I didn't say anything. Okay, didn't say any numbers. Okay. Well, anyway, they understood that... I can talk about a bit of the back... Do you have any... Yeah, absolutely. Okay, so maybe just mention that quickly. When they started to understand that endotensin 1 and 2 and ACE were starting to play a role... Sure, sure. So they knew about blood pressure, high blood pressure. They knew that it could affect the heart. And then they started to link...

disease with high blood pressure and heart disease. And they didn't realize, oh, there's a relationship between the kidneys and the heart, which we've just explained as the RAS system, right? Now, this was first observed by somebody called Richard Bright in 1836. And he related hypertrophy, so increased size of the heart itself, the heart muscle, to increased resistance to blood flow in the small vessels, right? Yeah.

Then in 1868, George Johnson was looking at nephritis and he had a look at all these fibroid alterations in the renal blood vessels. And he said that they were due to an quote unquote impure condition of the blood, but he didn't know what it was. So something in the blood is changing the vasculature and was also responsible for hypertrophy within the heart.

Then in like 1872, we have F.A. Muhammad using a primitive smigmograph, so blood pressure, Bezira, if that's how you want to do it. And they first described high blood pressure in 1872. He also linked left ventricular hypertrophy to hypertension and said it was due to nephritis.

Which is probably true, but not in those direct ways. That's right. Now, the thing is, obviously, if the kidneys are being alterated, it's altering the amount of renin being released. So potentially more renins released, more RAS, more high blood pressure and alterations to blood vessels and heart structure.

But it wasn't until the end of the 19th century, so late 1800s, that Tegersted, a Finnish professor of physiology, which is what I am too, Matt, but not as smart as this guy, working at the Karolinska Institute, which is a great research institute.

And his assistant analyzed the effect of renal extracts on arterial pressure. So what they found was that there was a compound in rabbit renal tissue. So they'll take it out, smush it up and inject it into the vasculature. And they found that this increased blood pressure. Wow. And they called it renin. Because? Because renal. Just a chemical from the renal system. Yeah. So the Latin for kidneys is renin.

Renal. Or I think the Latin for kidneys is renin.

Okay. So renin, they just said, yeah, this came from the kidneys. We're going to call it renin. So that was the first thing they found. So that was the very beginning of them understanding that, oh, this renin can increase blood pressure. Now they didn't know that it was not happening directly because that renin then has to trigger angiotensinogen to turn into angiotensin one. And then we need ACE to turn angiotensin one into angiotensin two. And then we need angiotensin two to also stimulate aldosterone. So there's this cascading pathway, but that happened earlier.

as the years progressed. Do you have any more information on those subsequent years? Yeah, I don't have any information in terms of when they discovered these enzymes like ACE and renin. Well, you just did renin, but ACE in terms of turning one into two and then how two had an effect throughout the body. However, I do know around the 1960s there was a group in the UK called

I think it was led by John Vane. And he was looking at means of controlling blood pressure through the possibility of manipulating ACE. Surname Vane. V-A-N-E. Nomative determinism is what that is. His name is determined his job.

I don't know about you, but the number one thing I look forward to when I return from traveling is a good night's sleep in my own bed. That has never been more true than it is now that I have a Sleep Number smart bed. I get so sore after traveling on planes, but after literally one night in my Sleep Number smart bed, my body feels restored, rested, and relaxed. The fact that my bed actually listens to my body and adjusts to my needs to keep me sleeping soundly all the way through the night is worth it alone.

to mention my husband and I never need to argue over firmness because we can each dial in our own sleep number setting. Why choose a Sleep Number smart bed? So you can choose your ideal comfort on either side. And now, for a limited time, Sleep Number smart beds start at $849. Prices higher in Alaska and Hawaii. Exclusively at a Sleep Number store near you. See store or sleepnumber.com for details.

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A postdoc from Brazil. What's a postdoc? A postdoctoral scientist. Okay. Someone's just finished it. So, Sergey Ferreira. Oh, of course. He started those chocolates. The chocolate company Ferreira Rocher. Makes total sense now. Chocolate causes blood pressure. No. There you go. It was known that in Brazil you got bitten by a...

Brazilian pit viper. Right. Which I think, at least according to some of the sources I looked at, was common in cane field workers. Well, I mean, that makes sense. They would get bitten and then they would...

I didn't see die, but they would collapse, like have a syncope event, and then they would have super low blood pressure. So they faint from low blood pressure. Yeah, yeah. As a result of the Viper bite. Not because they're freaking out. Probably that as well. Well, they probably did the opposite. Yeah, they would increase blood pressure. A fight and flight would actually go up. But anyway, they found that something with the Viper venom was causing a drop in blood pressure. Right. Now-

Sergei Ferreira took that molecule, which they then called bradykinin potentiating factor, BPF. Why? Why? Why? Because the venom would potentiate bradykinin, which I guess they've then understood what it was at that point. Can you explain to us what it is? Bradykinin, well, again, it's a series of proteins that I think the...

Helokinin pathway, which comes from the liver, usually becomes activated inflammation. And then bradykinin, as an example, can help with vasodilation of blood vessels, but it can also kind of sensitize... Nociceptors? Yeah, which kind of gives you the pain associated with... Well, it at least plays a role in the pain associated with inflammation. So it's pro-inflammatory, pro... It's...

Pro pain? It was known to be a vasodilator. Okay. So they took, well, Sergio took that to the UK hospital

And they wanted to figure out whether this could play a role with ACE. Right. And blood pressure. So what made the, oh, okay. Because, so you'd think it would be the opposite, right? Considering that ACE helps increase blood pressure and bradykinin reduces blood pressure. Right. Right. But I think they realized that the, if you were to, in hip, no, ACE would,

would decrease the levels of bradykining. That makes sense because it wants to increase blood pressure. So what this lab group was doing, I don't know what animal, I'm guessing it possibly was, unfortunately, cats and dogs. And they would put these chemicals. Do you have a Google alert that just says research cat dogs and then whatever research comes up in cats and dogs? I think it was just the period of time we were in. Maybe.

So they were putting these chemicals upstream to the lung and then recording what's coming out the downstream of the lung. So for instance, they would put angiotensin 1 in and it would come out as angiotensin 2. Oh, because of the ACE in the lung. But they didn't know ACE, the whole role of it at that point. Put angiotensin 2, it comes out as angiotensin 2. So it's already been generated. It's not going to get modified any further by something in the lung.

Now, if you put angiotensin 1 in with the venom, it would still come out as angiotensin 1. So that would... Can I just... From basic reasoning, my thought would be then the venom is inhibiting ACE. It's inhibiting whatever's in the lab that's converting. That's right. And then that kind of allowed them to postulate that it has an effect. So...

ACE is working as an enzyme that cleaves a protein to another type of protein. So you're saying that this Brazilian pit viper was the world's first ACE inhibitor? Yes, to some degree, yeah. The first prill. That's right. What would you call it? Would you call it viper prill? I like it. What would you call it? Snake a prill? Venom a prill? Yeah. Venom a prill.

Pitpril. Pitpril. Because it's the pit viper. Yeah. Anyway. I like viperopril. I can't even say it. What the lab group. The researchers. Yeah. What they postulated was the venom isn't perfect in its inhibition, but it's doing a role of some kind of stopping the enzyme to turn one thing into the next thing. Sure. Now, they already knew that there were some enzymes in the digestive system that did this.

One being carboxypeptidase, is that right? Which is released by the pancreas and then kind of doesn't,

chop up proteins that you eat in your food into individual amino acids, but it chopped it into chunks at certain amino acid residues, right? I think, and this is just from memory because I taught it not too long ago, is carboxypeptidase chops the carboxyl end of amino acids that are bound together. So it chops the carboxyl end, the carbon dioxide ends.

COO or COOH and chops them off. So that's how it makes bigger chunks of protein or peptides into amino acids or at least smaller peptides. Okay. Yeah. So with the combination of the venom and their understanding of the carboxypeptidase system already, they postulated that an ACE inhibitor would work in the same way. So they already theoretically...

Figured it out before they just like came out with a drug. Does that make sense? And they knew that a venom, if you just swallowed it, it would be deactivated. So it wouldn't actually work. So they, you couldn't really give blood pressure medications by injecting people. I mean, you could, but it's not overly convenient or people won't enjoy it. So they were trying to come up with a venom alternative that can be taken orally. Okay.

And so they worked off the carboxypeptidase kind of same system, but they worked with different residues. And the thing that they came up with was a slight modification that ultimately led to the inhibitor. And the reason why this is the theory, it's not 100%. Like it's a bit like... But most things you say, yeah. It's a bit like...

When we spoke about aspirin, where did the name etymologically come from? This is a strong theory that Capdo, which is the first ACE inhibitor, was to capture the enzymes binding site more strongly than the venom. And so that's where Capdo came from. The Pril part was, I think, the proline lysine end. And that then became Pril. So Capdo Pril was the first ACE inhibitor. And it did it by competitive inhibition. Yeah, that's right.

And so it was effective through a carboxyl group with a zinc-binding sulfur-hydro group. That's the technical part. You got that everybody? Yeah. Does that make sense now? But as I said, catapril wasn't overly effective because you needed to take a lot of times a day. So then they kind of developed siblings of it, like lanopril, in today's case, lazinopril, which lazino is just another term where the proline is...

swapped for lysine. Yeah. And the lysine is a linsinopril. Cool. That's the naming of it. No, that makes sense. So...

We've spoken about the drug itself. We've spoken about the history of the drug. We've spoken about its mechanism of action, blocking ACE, and by doing so, ultimately reducing angiotensin II, stopping its ability to be a potent vasoconstrictor, stopping the release of aldosterone, which causes sodium and water retention, and therefore you get blood vessels relaxing and widening, so you get vasodilation, you get reduced blood pressure, and

You probably also get less fluid retention maybe because you're not holding on to all the sodium. So some of that sodium will be peed out and some of that water will go with it. So it might lead to a little bit of some reduced fluid retention. So therefore, it's obviously going to be prescribed for things like hypertension, heart failure, post-myocardial infarction. What about...

I know that one of the side effects, Matt, is a persistent dry cough, right? Yeah, a persistent dry cough basically. Can you explain – because the other side effects are things like hypotension, low blood pressure, that makes total sense. Dizziness or lightheadedness, which makes total sense because of the hypotension. Hyperkalemia, which is high potassium levels, that makes sense because we said that normally aldosterone –

holds the sodium in the body so the water follows in the body and then swaps it for potassium to be peed out. But in this case, it's stopping that. So the potassium stays in the body and the sodium leaves so you can get hyperkalemia potentially. So that

Fries.

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But the persistent dry cough, I just can't seem to see where that fits in. Yeah, it's thought that it fits into the bradykinin effect. So as we spoke about earlier, bradykinin is... And that's probably another effect of what we're seeing with the ACE inhibitors. It's not only stopping the production of angiotensin 2, which has all those downstream effects, but it's also...

allowing the increase of production of bradykinin because you haven't got the ACE to break down bradykinin. So there's more bradykinin in the vasculature of the lung. It's thought that that buildup is the irritant effect within the lung that causes the cough. So would you say that bradykinin is the equivalent in the opposite direction to angiotensin 2? Is sort of like it's...

equal because Brady Kahn and his drop vasodilating and angiotensin two is vasoconstricting. Are they sort of the homeostatic balances of each other? Um,

I don't know. Okay. That's just a question. I'm sure that they're not exactly equivalents because we know angiotensin II does a bunch of other things. But my thought would be bradykinin is there to maybe counteract the angiotensin II. And that makes total sense that if you're now blocking angiotensin II, it gives bradykinin the chance to be the most potent activator here. And it's the... Did you say why cough? What does it do to the airways to make you cough? I would imagine the bradykinin is just...

As we see bradykinin in inflammation within a tissue that is sensitized in C-fibers, which are the nerve fibers which kind of tell you something is painful.

That is the sensitization. But in your airway, you don't have really pain receptors, but you have irritant receptors. Right. And one of the side effects of activating irritant receptors is to cough. Okay. Yeah, that makes sense. So that could be anywhere from 5% to 20% of individuals with taking the medication like an ACE inhibitor would develop a cough. When you look at leucinepril, at least a study that I looked at,

When we looked at side effects, the most common side effects, which range between 3% to 10% of individuals taking lisinopril, it would be more likely causing things like dizziness and headaches as the most common symptom. Yep. Or should I say side effect? Whereas cough is somewhere in the range of 1% to 3%. But I believe...

the cough effect can diminish over time. Right. As you, I assume... I guess desensitise to it. Yeah. Okay. So the bradykinin stimulates nociceptors. It stimulates the... That's the thought. It sort of irritates the airways, stimulates the possibly C fibres of the nociceptors and you end up getting some, oh, there's an irritation in the airways, the reflexes to cough to get it out even though there's nothing there to get out. That's the theory. I don't think it's been objectively proven but that's the closest...

we've kind of come up with for an explanation. Cool. Now, what else do you have about ACE? But that would be, I mean, when you have primary hypertension, the ACE inhibitors would be generally the first line of medications. Okay. A reason for discontinuing an ACE inhibitor would be a cough. And so then it would lead into the cousin of ACE inhibitors being the angiotensin 2 receptor blockers.

I guess the reason that they aren't quite as effective as the ACE inhibitors for blood pressure regulation, but they do have a benefit of not having a cough associated with them. What else? What else about lisinopril? Anything else you'd like to highlight?

No, I think we've covered pretty much everything we need. We've gone to the history, we've gone through the naming, we've gone through its clinical indication. There are others sometimes that's used preventatively with people with diabetes. It's used as a medication to prevent neuropathies and nephropathies. Okay. But primarily you would say it is an antihypertensive drug. Cool. And then side effects. Some people will also develop...

more allergic kind of reactions to it, angioedema, those kind of things. But that can happen with a lot of drugs. I would say the most common side effect associated with it is the cough. Right. All right. I think that that's not bad for an ACE inhibitor. You did pretty well. I did very well, but you did pretty well.

Matthew, thank you for helping me understand this in April. We will meet again at some point in the future if you care to join me for another episode. I'm Dr. Mark Todorovic and that's Dr. Matthew Barton and thank you for listening to Dr. Matt and Dr. Mark's Medical Podcast.

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I can't tell you how often I hear, oh, I'm a little OCD. I like things neat. That's not OCD. I'm Howie Mandel and I know this because I have OCD. Actual OCD causes relentless unwanted thoughts. What if I did something terrible and forgot? What if I'm a bad person? Why am I thinking this terrible thing? It makes you question absolutely everything and you'll do anything to feel better. OCD is debilitating, but it's also highly treatable with the right kind of therapies.

Regular talk therapy doesn't cut it. OCD needs specialized therapy. That's why I want to tell you about NoCD. NoCD is the world's largest virtual therapy provider for OCD. Their licensed therapists provide specialized therapy virtually, and it's covered by insurance for over 155 million Americans.

If you think you might be struggling with OCD, visit nocd.com to schedule a free 15-minute call and learn more. That's nocd.com. Hey, guys.

Have you heard of Goldbelly? It's this amazing site where they ship the most iconic, famous foods from restaurants across the country, anywhere, nationwide. I've never found a more perfect gift than food. They ship Chicago deep dish pizza, New York bagels, Maine lobster rolls, and even Ina Garten's famous cakes. So if you're looking for a gift for the food lover in your life, head to goldbelly.com and get 20% off your first order with promo code GIFT.