Howard and Paul

Paul: [00:00:00] Hey Howard,

Howard: [00:00:01] Hi, Paul.

Paul: [00:00:02] how are you doing? I understand you're doing home repairs today. Not people repairs,

Howard: [00:00:06] We had to repair dark or damage to a wall to

Paul: [00:00:12] not because the dartboard was connected too tightly to the wall. This is literally darts related to the dartboard. So.

Howard: [00:00:17] absolutely the dark board stayed up.

Paul: [00:00:20] I, I, I was telling you before we came on that I've years ago, a friend of mine was playing darts and was, was as I'll, she'll say debauched teenagers. And he was reaching up for a dart and another deranged teenage friend of mine at the time, just hurled the dart in and,  just trying to be a goofy and I.

Guess, I'm not sure he was planning to have it happen, but the dart went right through the other, this other friend of mine's hand and pinned it to the dartboard, which was pretty exciting at three in the afternoon while skipping school. So.

Howard: [00:00:49] I'm never, I'm not quite sure when getting a teenager, a dark board appeared as a decent idea. I just don't recall that moment.

Paul: [00:00:57] yeah, it's maybe marginally better than lawn darts, but that's not much, it's not much of an improvement anyways. We'll stay away from darts today at all. Sharp objects  that


we're talking about. Metabolic syndrome. We started this conversation and described w w what exactly it is.

And this week, the plan was to finish up with talking about what we can do about it, because obviously that matters even more than what it is, but I thought maybe a good place to start is to talk, just to reminder a one Oh one X of exactly what metabolic syndrome is. And it's really just a basket of things, right.

That together.  Some, some, some loose set of things, indications that might suggest you have it, like abdominal obesity and so on. Right.

Howard: [00:01:49] right. If you have a beer belly, a little, a few extra pounds around your belly you're insulin resistant hypertensive, your triglycerides are high and your HDLs are a little low. You meet the definition of having metabolic syndrome.

Paul: [00:02:06] Just as an aside, I meant to ask you this last week and I was looking for some more stuff about it, but I didn't really find anything. I remember reading years ago, here it goes Paul, into some strange foray here. That it actually, when people say, well, I don't really have people are prone to say, when you talk about abdominal obesity as an indicator for metabolic syndrome and potentially being insulin resistant, which is obviously another one of the factors here they say, well, I don't have that much of a belly.

It's actually not very much. Abdominal obesity required to potentially be a risk factor here. We're not talking about people with an extra 70 pounds necessarily around them. Right.

Howard: [00:02:41] no, we're not.  We drew a distinction between I'll call it routine obesity and this toxic obesity with Abdominal fat. You don't need much fat around your organs to create a toxic environment, contribute the inflammatory mediators that they do to increase the risks associated with cardiac disease, dementia, stroke, et cetera.

Paul: [00:03:08] Yeah. And I think that's really key to understand, because there's always this sense. Well, yeah, I mean, I could have this, but look, I'm actually, I might have five pounds or 10 pounds or whatever, the carrying extra weight, but it's not that much. And the, the right, the correct answer is, well, it depends. And even at relatively small levels, it depends.

Where is it? Is it around the Oregon's? Is this.  Is this, is this really visceral fat or or always, or is it subcutaneous? And,  people are too quick, I think sometimes to just pass it off and say, well, this doesn't apply to me.

Howard: [00:03:40] sure. Well,  it's fascinating. I'll be in the office and then I'll ask someone if they have any medical problems. No, they don't. No, we're in a button-down shirt and I see a tiny little top of an incision where they had a median sternotomy and their chest was open. I'm like, what's that? Oh, I had an open heart surgery, you know?

So my vessels are fixed and it says here you're on some medications, right? I take them for blood pressure, but my blood pressure is normal on the medications. So they're not connecting the dots, which is also,  one of the things we tried to do last time is to all these dots for people.

Paul: [00:04:21] Yeah. And that's, that's really the key because otherwise, and we'll talk about this a little bit about it and what you can do about it, but otherwise there's a tendency to treat each of these discreet pieces as discrete pieces. And that's a bad idea because having metabolic syndrome is, is, is a risk factor for a host of different things.


And just to summarize, because we talked about it last week, but like type type type two diabetes, cardiovascular problems, arthrosclerosis. Yeah, the list goes on and on, right?

Howard: [00:04:56] Strokes dementia arthritis. I mean, they do affect tendons, muscles and joints as well. So it affects our entire body.

Paul: [00:05:05] yeah. It affects our entire body and it affects maybe that's just this before we go on. I mean, and in fact it's a huge fraction of the population. I,  something in excess of 60, 70% of the population has at least a couple of the markers of metabolic syndrome.

Howard: [00:05:17] Well, yeah, a tremendous number of people meet the clinical diagnosis of four for obesity. The precise number who meet the diagnosis criteria for med S Not exactly sure.

Paul: [00:05:31] Yeah. But at least for the, at least one of the major factors is a huge fraction of the population. That means it, which is at least concerning. So let's jump across and talk about what can be done about it and at a really high level. You can, you can bring let's first say one other thing before we get there, which is that in the you, I like your expression for this, but before we even think about what we're going to do about it, I think it's really important to say this is an AUC issue.

As you like to say, it's an area under the curve problem, what we're going to do about it and how effective that thing will be to some degree depends on how long you've spent in that condition, right. That area under the curve thing.

Howard: [00:06:08] great.  If you think about atherosclerosis and lipids, the longer your arterial walls are exposed to elevated lipids and inflammation, the worse the atherosclerosis is going to be. This is a disease that progresses slowly as are many of these diseases and they really. Creep up on us. And so the earlier that we have one of these light bulb moments and realize that we have an issue and we connect the dots, the better we are at minimizing the downside risks.

Paul: [00:06:41] Yeah. So again, another reason to be sensitized to this stuff and recognize that even though there are things I can do, if I've been, if I've been diluting myself or at least I'm aware of this for a long time as you're on and it's, it's probably. There's things you can do that to help mitigate the problem, but it's going to take longer than if it had never happened in the first place, or if you were, I don't know, 17, God help you or something. There's not a lot. Well, there probably are a lot of 17 year olds with metabolic syndrome who don't. I know. So, so let's maybe start off with the non magic side of things. The hard work side of things and the non medicinal things you can do. Cause we'll  break it out. There's,  there's some medicinal things and we've alluded to some of them already, but let's start off with the non medicinal stuff.

And these are all gonna sound really straightforward to people because we hear about it all the time and almost everything that you need to, you need to get more exercise, you need to eat better and so on. Right. These are the, these are the it's the same answers.

Howard: [00:07:35] It really is. And as we talked about previously I've had some success with people in obtaining one of those light bulb moments by trying to connect the dots. Now, when they're starting to see these pathways and you start to talk about what the road looks like in front of them, many people will buy it angle, understand and I'll start gently with them.

I'm like, look,  pick up a dumbbell and do five curls every day park in the spot. That's furthest away from the building and don't drive around to look for one closer. We can work on this.

  Paul: [00:08:19] I was at a, I was at a hiking trail yesterday, yesterday. I think it was going out for a run and I saw two people almost get into a fist fight. This is so crazy because before for going out into this hiking trail,  and go, and I don't know, a couple of miles or whatever distance they were going to go.

They were fighting for a parking place, nearest to the Trailhead when there were lots. 20 yards away. And I just shake my head,  peoples even when people's instincts are right, I'm going to, I'm going to go for a hike and so on. Is it really, is it really necessary that you then have some ,  knock down, drag out fight to see who can park closest to the trail?

And it's just remarkable to me, but it's turned it around, lose that instinct and it's w it's well, yet one more small step you can make towards. Make forcing yourself to be more active one piece at a time, whether it's at the grocery store or any, or a to help you out a trail head or somewhere else.

Howard: [00:09:17] right. 6,000 steps a day improves your all cause mortality risk. Yeah, it's not going to reverse metabolic syndrome in and of itself, but it's a phenomenal start and you'd be amazed at how easily it comes.

Paul: [00:09:32] Yeah. And I was looking at some of the numbers earlier today, just towards a reminder about how much exercise it takes to have a material reduction. If your, say your hypertensive leave, leave aside just a reduction in blood pressure, but a reduction in blood pressure as someone who's diagnosed hypertensive, it isn't very much, not very much, I mean, in terms of increased activity, but if you, especially, if you're starting from a sedentary base,

Howard: [00:09:55] Correct. If you get your heart rate up, as we discussed into the zone two range, which is not hard, you won't be sweating. You won't be winded. You won't be short of breath and it won't hurt. You're going to realize the benefits of exercise.

Paul: [00:10:12] . And it could be,  systolic might be five or six points down. I mean, it's not, it's actually it's material amounts for people, right. I mean, and it doesn't, and it starts at relatively low levels. This is a classic within reason, it's a classic dose response relationship to things like exercise and its impact on some of the markers of metabolic syndrome.

Howard: [00:10:31] right. People might laugh off a five millimeter mercury decrease, but it results in a very significant reduction in all-cause mortality risks.

Paul: [00:10:43] Yeah, and I I've argued because I've seen this happen with people I know who were hypertensive and began getting more active and actually gives fie people a feeling of control. And I think that's. Well, I think that's underrated as a factor here, because if you feel like the only things that can fix this, well, either that you're in, you're entirely in, you can't fix it, or it's drugs that leads to a feeling of helplessness, this learned helplessness problem.

And if you, if people learn that by being even modestly active, I can have an impact. I think that's hugely empowering for people. At least it has been for people that I've seen. It's been even small reductions that they can trace directly to their own activity is, are hugely important.

Howard: [00:11:22] no doubt. And  and you and I side differently on technology, but I've had some people buy,  an Omer own blood pressure cuff. Right. And I'm like, check it before you go out, go walk around the block and check it when you get back. And you gonna notice a difference.

Paul: [00:11:39] , no, no for sure. And a sustained difference. It's not just,  it's going to be good for the next hour or whatever is if you maintain this relationship with exercise, the impact in terms of those particular hypertensive markers are gonna are, are, will be sustained. And that's a feeling of empowerment, I think for people.

So, so exercise it's often called this  magic. Wonder drug, but it really is with prospective metabolic syndrome. It affects almost every marker that we've talked about, this rural fat hypertension some of the blood markers potentially it can be,  hugely swung by this. This is a, this is a really big insulin sensitivity.

I mean, that's true. We can trace that directly to exercise, right.

Howard: [00:12:17] correct.

Paul: [00:12:18] So these are all, these are all big deals. So exercise is one thing people can do, and everyone, everyone can start very modestly as you described. Another one that it's super important is sleep obviously. And I have a very fraught relationship with prescribing sleep to people because the next thing  and this is maybe a West coast, California thing, peoples are buying sleep trackers and stuff, and then they get ag and I started agonizing about the quality of their sleep and that makes their sleep worse.

But I'll. Do you mean leaving that derangement aside for a second? The relationship between sleep and some of the markers of metabolic syndrome is pretty clear.

Howard: [00:12:52] absolutely sleep will improve your insulin resistance improve your glycogen synthesis in it improves your immune health. It improves your blood pressure control. Sleep is an active process that your brain needs. And as I've sought to optimize my lifestyle for longevity, I've come to realize over the last five or 10 years, that sleep is such a critical importance is of such, such critical importance.

We need seven and a half to eight hours of sleep. You don't need less,  I don't care what you say.

Paul: [00:13:31] Yeah. Yeah, no, it's true. It's true.


But Hey, let me hit you while we're on the topic of sleep now, what's your, what's your number one. Best sleep tip. I always like to ask people this what's your best sleep tip.

Howard: [00:13:49] So I don't have one, so I won't, I won't eat within two hours of bedtime. Right. I want my blood sugar normal. If my blood sugar is high, when I go to sleep, I know I'm going to have a really. Bad nights, sleeping. I have to calm down, right? So if it's a stupid show or ch or a chill or a chill book I'm going to do that.

I'm going to decrease the lights in parts of the home, I'm going to get my circadian rhythm set to get ready to go to bed. So there are a few things.

Paul: [00:14:25] Yeah. I I'm a big fan of it. I've been converted to this over time that. It's more important that you w when you get to bed than it is about when you wake up. So if it means that I'm sleeping, I mean, to pick an extreme example from nine at night, until five in the morning and getting my eight hours that way, that's, that's what it is.

Right. But yeah, alternative of trying to convince yourself that if I go to bed at one in the morning, I'll somehow consistently sleep till nine or 10, maybe as a teenager, I did that, but it's not that easy now.

Howard: [00:14:56] I haven't slept till 10 since, since I was 13. Right.

Paul: [00:15:00] Right, right. But that's, but people are so resistant to the idea of the, I I'll talk to people and I says, what time are you?  What time you go to bed these days? Oh,  I try to be a bed by night. Really know your dog. If he will be a well, I'm getting ready by nine. No. Okay. What time are you actually at?

Well,  by the time I finished doing stuff and then I'll get in bed with a book around I on 10, 10, 15, and I said, and when do you stop?  Tweeting and stuff. Oh, well,  and the next thing  it's actually, it's 11 o'clock right. I mean, it's 11, 1130 before they're actually trying to drop off to sleep.

And then they're up again at five 30 or whatever it is, six o'clock in the morning. And it's like, dude, that's not what right.

Howard: [00:15:38] asleep is not a failure of something. Right. You're not failing at life because you go to sleep early.

Paul: [00:15:46] That's right.

Howard: [00:15:47] and if you're,  for those who have bought into optimizing their life for longevity and they're exercising and they're eating right, if you're not optimizing your lifestyle for the proper amount of sleep, then the end you missing a large contributor to your chronic disease risk.

Paul: [00:16:07] Yeah. Yeah, no, it's huge. It's huge. And I mean, it's without pay people suddenly stressing about sleeping cause that's becomes its own problem. I just, I just think it's one of the more remarkable up there with exercise wonder drugs.


let's jump over to diet here. I don't think there should be any surprises for people, but it's worth pointing out that,  the sugars, fats, alcohol, all these things  fructose, where did, where do we start?

These are all bad.

Howard: [00:16:38] Yeah. So  it, this is as a result of a caloric excess and then you bring in the insulin resistance. So your muscles can't store the glycogen. You still have you still have glucose that's that's floating around your blood. It hits the liver. The liver has to store it. It fills up it's.

Glycogen stores where it stores glucose. Now it turns it to fat. It processes that into triglycerides. It throws the triglycerides out into your bloodstream. That's why your triglycerides are high. And it just. Builds on itself. And then that fat will start to deposit. So we need to decrease our caloric burden.

And we'll get into this later, but we understand that clearly there's a genetic etiology to obesity and diabetes in many. Right. Obesity and subsequent type two diabetes. I need to clarify. So it's not as if you know that this isn't a fat shaming thing, you know that this isn't a,  a failure on your part.

There, there are a lot of people out there who really don't eat. A lot. And they can't lose weight and they're  stuck in this. And a lot of people on Twitter will scream. Ah, we didn't have any fat ancestors. Well, there was a different environment, right? That was a food scarcity environment. So our epigenetics didn't allow for that phenotype to be expressed.

But with 24 seven food availability, that phenotype is expressing itself now.

Paul: [00:18:12] Yeah. Yeah. We live in an obesogenic environment, as they say,

Howard: [00:18:15] Really do. And then you layer on the ultra processed foods and it makes the problem that much worse. So as you and I have talked about,  we need to rely on,  more fruits or more vegetable, certainly some fruits high fiber diets to pull out some fats lean

Paul: [00:18:36] do you, what's your view on, and this is getting down a nutritional rabbit hole. And so I'll, I'll confess that right away. But what's your view about the, the  the glycemic index with respect to certain fruits and things? How much, how much should we care? I mean, we, I think you were sent me something earlier about you had a banana or something and And you saw it, saw it immediately in, in on your blood glucose reading, but I mean, nevertheless, what's your view about that in terms of the trade off between the glycemic load of fruits or at least specific fruits and their utility as a, as a, as a S I won't say a superfood, but just as a part of your diet,

Howard: [00:19:12] So I do think that fruits have an important role, certain fruits, and I'll say in a good nutritional diet. What I worry about with certain fruits is not only the glucose, but the fructose, right.  Evolutionarily speaking, we don't have a need for fructose and our body just tries to dispose of it.

And if you look at the metabolism fructose, It ends in the production of uric acid and fatty acids. It doesn't unlike unlike glucose, which ends in hopefully just glycogen, but in some, it ends in glycogen and fat. So that's why some will use uric acid as a biomarker for your potential fat burden in your liver.

And now I fell D And so I do think that fruit does contribute somewhat to that. So I try to stick with blueberries and strawberries and less, less glut glycaemic fruits.

Paul: [00:20:13] Yeah. Yeah. Well, that's certainly my bias. And again, I came at this from a position of, I won't even say relative of absolute ignorance of decade or more ago where I just,  fruits or fruits or fruit. Right. So this whole idea of the, the, the differential loads was. I, I was, I had no idea. And so it's been a, it's been a learning exercise, but it's interesting to hear you say that.

So one thing as we're talking about the glycemic loads and so on, and we talked about this a little last time, but I got a question about it from someone who sent me an email after it, and that at risk of turning this to a, an ask me anything, what's your view on the, on oral glucose tolerance tests versus fasting blood glucose tests.

Howard: [00:20:52] Oh, there's no question. I mean, the OGT with measuring insulin levels will pick up an insulin resistant individual far sooner. I mean, perhaps it decades sooner than a fasting blood glucose level.

Paul: [00:21:11] So that was what I, that was my view. And that's what I, I said back to them. I said, I would talk to you, but I, I, so why do we insist on doing fasting blood glucose tests over oral to over the oral glucose tolerance test?

Howard: [00:21:23] Oh, I have no idea. I mean I'm an orthopedic surgeon for God sakes.

Paul: [00:21:29] I know. And I'm an idiot, but I mean, I have no idea. I was, I had no answer. That was the question he was asking. He was saying, my impression was, this is so much more sensitive and useful and there's so much noise and fasting blood glucose. Why do we not do? I mean, I literally, I think I told you this back in the fall, I had a, as part of some ridiculous insurance, I'll say scam, but I mean that in the nicest way possible they wanted me to do a fasting blood glucose for,  you do all these tasks and give them back the results and you get like a hundred bucks from the insurance company.

It's like, yeah, whatever. So yeah, you do these things and it's like, why are they making me do this? Because it's a ridiculously noisy signal. In the first place, leaving aside that I don't probably don't need to do it anyway, but I'll do it for cash because I'm greedy that way. So, but why aren't they making me anyways?

I just, this is maybe a topic for another conversation, but I had baffles me in medicine all the time. What I find when there's two or three different tests for this of the same condition or same marker and for whatever ridiculous reason we're doing one that makes no sense to me.

Howard: [00:22:31] Look, I,  we've talked about this online and offline a lot. Ma many doctors don't know about uric acid, right? They think it's a dead end product  period metabolism. They don't know about April OB LP, little a. How many friends,  are getting CAC scores with  cholesterol level of 200 to try and see whether they benefit from a stat and or not.

And,  look I'm. I'm not a population health expert. And granted all of this may function well for me as an individual and for assessing it in myself and my friends and those I love. And maybe it doesn't scale well on a population health. Level, but I do think that these are trends that are going to appear and are going to be traced and tracked and measured.

As we learn more, especially as we're going to discuss, we now have some medications that will clearly help people with insulin resistance, et cetera. So the more people that we can identify, the more that we can help.

Paul: [00:23:40] Yeah. Yeah, no, it's absolutely true, but I'll Cal Alan, my rant about tests. I just have a beard, my bonnet about it. So diet is the usual answers, right? Like Mo vegetables, fruits, high fiber grains, barley and protein, less of all that other garbage. And that should come as no surprise to people. But again, it's a dose response thing.

A people should be, I would be amazed the difference. But these, the effect that these things have at re even relatively modest changes, because it's, it's it, as I say it it's like a medicine, it's a dose response thing.

Howard: [00:24:15] people get scared, right? They think, Oh, I have to cut out a thousand calories. I have to lose 10 pounds. By Friday,  if they can cut the milk out of their coffee if they can skip a donut,  if they can skip an ice tea  just start to cut down on these little troublemakers as the weeks go on those hundred calorie savings really add up.


Paul: [00:24:48] So let's  quickly got a couple of other things that are more lifestyle related and then we'll jump over to medicine, others, the obvious ones smoking. I mean, I feel like it's crazy. This is 2021. Who do I need to say, why am I even talking about smoking? I was at a traffic light yesterday and every car around me had someone smoking inside.

I was like checking my, my, my phone to see if I had gotten to 1951 by accident.

Howard: [00:25:10] With the windows closed and their kids in the backseat.

Paul: [00:25:12] You it's like you were there. I just, my jaw dropped and I was, what crazy experiment are we running here? How is this possible in 2021? And yet here we are.

Howard: [00:25:22] Right.

Paul: [00:25:23] So anyways, well enough said out and you make a good point that that loneliness is a factor here.

And, and this is something that's obviously, we've talked a little bit about it in the context of the pandemic, but it's a longstanding and much broader problem that the, just the importance of being, being with friends and walking, it can give you, give you an, even an incentive to walk and socialize, right?

These things feed back on each other, which feeds back into some of the markers of metabolic syndrome.

Howard: [00:25:50] it really does. And  people who've written about the Mediterranean diet and its influence on longevity. Have clearly spoken to the fact that it's the Mediterranean lifestyle, right? These people are always out there meeting with their neighbors. They have large family and friends dinners. It's a, it's a lifestyle and being lonely and not having friends and not having people that you can speak up, pick up the phone and call or go out to dinner with and just to relax de-stress and share.

What's bothering you with is, is really quite a burden to carry.

Paul: [00:26:29] Oh, and I'm binge watching wine division chips is a bad idea. Let's just, this is just a really, I see this. This should be my whole prescription stop. Binge-watching one division with chips, my God, but anyways, get out and talk to people. So let's, let's jump over to the medicinal side of things. We've alluded to this already, but it's not that there's some, any specific medication that you, that addresses all of them.

Factors that are related to metabolic syndrome, but we do have some drugs that target specific aspects of it, right? Like Statens, for example,

Howard: [00:27:01] Sure so, well, we're going to target your LDL. So they're going to help to minimize your risk of cardiac disease. And if you have metabolic syndrome and an elevated. LDL then you're at very high risk because now you have both the LDL and the inflammatory burden from the metabolic syndrome. So you have both things that are necessary and sufficient cause heart disease, statins.

Aren't going to address your fatty liver and other things. But there are other medications that might.

Paul: [00:27:37] Well, so in that spirit, I mean, what others do you, do you like, do you likes the wrong word, but do you think are at least have some utility in here that are there typically medications, would you think of it typically through the lens of of medications that are appropriate for type two diabetics that help you manage blood sugar?

Is that the lens through which you'd look at it? Or how did, would you think about it?

Howard: [00:27:58] right. I think that helping people manage insulin resistance and the burden that comes with that will go a long way to helping Minimize the chronic disease burden of metabolic syndrome. So the SGL two eyes, and certainly the GLP one agonists really do seem to be making a big difference in people's lives.

This past week, the GLP one agonists were shown to decrease people's weight burden by I think, 16 to. 18% at a year. Really,

Paul: [00:28:34] Yeah.

Howard: [00:28:35] really remarkable.

Paul: [00:28:36] Yeah, no, sir. This is not a, this is not a wonder drug that's come out of nowhere. This has been a steady process of getting better at helping people manage their insulin resistance with a series of products here, but they can have, they can have real, real relevance and importance for people with metabolic syndrome.

Howard: [00:28:52] absolutely. And as we talked about there is a genetic basis for obesity and some of those obese. Patients will have metabolic syndrome. Some may not. They may benefit significantly from GLP one agonist going forward.

Paul: [00:29:10] Anything else? I mean, weight loss, drugs, or anything else that you think is interesting here or anything you've seen on the horizon or anything that you just heard people talk about?

Howard: [00:29:17] I think last surgery needs to be considered in this mix.  It. Especially,  for people with really morbid obesity and they've tried everything else. When all else fails and they've managed to start exercising and change their diet and they are just up against a wall and they're fighting their genetics.

Surgery is a good option for them.

Paul: [00:29:43] Yeah. Yeah, no. And it's, and, and obesity is such a, such a horrific marker here in terms of outcomes and long-term health with respect to this, with, to metabolic syndrome and just related, related inflammation problems. Anything else that you're seeing in terms of that has any utility out there with respect to medications or surgery?

I mean, I, I was, I was  banging my head, trying to think of some other things, and I ended up with. This spectrum of some surgery with respect to weight loss, and then some of the products aimed at type two diabetics and then Statens. And that felt to me like that was pretty much the universe.

Howard: [00:30:17] yeah, we're , we're  limited, right? It's diet, it's exercise, sleep, some medications maybe surgery. It's a lifestyle issue and you can't reverse 40 years of not paying attention to your lifestyle in In

Paul: [00:30:33] Three three quick pills. Yeah. Yeah. Well, and you can't reverse. I thought you were going to say you can't reverse 40 years of, of an obesogenic environment. I mean, this is the thing that I spend the most eyeopening for me with respect to what looking around and seeing people who appear to have some of the markers of metabolic syndrome is that I feel, I feel badly because I think it's really difficult to live.

In this environment where you're surrounded by this caloric overload on a daily basis. And not at least at the margin, because fall into some of these traps, whether it's some  caramel macchiato at the coffee shop of your choice every morning or something, but it's all of these things at the margin that are so cheap and easily available, that, that.

People it's really easy to fall into these, into these patterns of behavior that lead insidiously through this area under the curve that we've discussed two syndromes like this.

Howard: [00:31:28] Yeah, it really is a challenge. And again, I, I really try hard not to fat shame, not to blame it on eating. Too much,  it's more eating the wrong things. And I do clearly recognize that there is a genetic component and I don't lay fault or blame on people and really have to try and work with them hard.

  Paul: [00:31:59] .

 So much of it's just is the environment is the environment that, I mean, we just, the world we live in it's it's it's there. What was it? It was Yossarian , I think in catch 22, he was explaining something to one of the other pilots and it's part of, it's like, they're trying to kill me.

They're always trying to kill me. He was trying to explain what he wanted out of the army. Well, that's, this is the same thing they are trying. They're trying to kill you. So just be really careful about what goes into your mouth and you can see. Because they're, they're out there just like,  Yossarian's enemies, and they're trying to get you.

So anyways, that's that's metabolic syndrome. So I, I, I, I think we've covered most of what we wanted to something.

Howard: [00:32:34] I think we did. Thank you, Paul.