Bonus Episode: Can Your Cholesterol Be TOO Low? Why Starting is Hard, & Your Cardio Time-Hack

0:01 [SPEAKER_00]: Hey, it's Jordan from Barbell Medicine. [SPEAKER_00]: Now this episode preview is from exclusive content that regularly goes out to our Barbell Medicine Plus subscribers. [SPEAKER_00]: In addition to exclusive content, Barbell Medicine Plus subscribers get early access to episodes and products, at free listening, discounts on products and services, and the ability to ask Dr. Barakie and I questions, all for about the cost of a cup of coffee each month.

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0:38 [SPEAKER_00]: Welcome back to the Barbomedicine Plus, ask us anything. [SPEAKER_00]: I'm Dr. Jordan Vigamam, and today we've got a jam-packed episode diving into everything from the philosophical debates of lipidology to the psychological friction of getting off the couch. [SPEAKER_00]: First up, we're asking the question that apparently keeps at least two doctors up at night.

0:56 [SPEAKER_00]: Is there such a thing as, quote, too low of a cholesterol level? [SPEAKER_00]: We'll break down the genetic and clinical trial evidence to help you understand the core debate. [SPEAKER_00]: Is it about a minimum biological threshold or is it all just a function of lifetime exposure? [SPEAKER_00]: Then we'll shift gears to the gym and we'll tackle supersets, triceps, and giant sets.

1:13 [SPEAKER_00]: If you're short on time, is it a good idea to string together three or more non-overlapping exercises? [SPEAKER_00]: We'll give you the take home advice on how to be efficient without sacrificing your gains or hogging all of the gym's equipment. [SPEAKER_00]: On the mind body connection, we're dissecting a fascinating question, does acupuncture do anything?

1:30 [SPEAKER_00]: We'll talk about the difference between no-susception and pain, and whether measuring brain activity under anesthesia is a valid way to prove an effect, ultimately clarifying how much of acupuncture's benefit is truly physiological, versus a powerful placebo effect. [SPEAKER_00]: And finally, we're tackling two major life challenges.

1:47 [SPEAKER_00]: One is behavior change. [SPEAKER_00]: If you ever noticed that you've had a feeling of dread before starting the task, is it laziness or is it psychological inertia? [SPEAKER_00]: And then too, how to do cardio in a time crunch? [SPEAKER_00]: What to do if you only have two 30 minute sessions a week and you've hit a plateau?

2:01 [SPEAKER_00]: We'll explain why intensity is one of the major factors for progressive overload and give you two strategies to facilitate that. [SPEAKER_00]: Plus we'll touch on the nuance of mono and saturated fats in your diet, the difference between writing a template in coaching people 101, and a look on ADHD meds and exercise programming.

2:18 [SPEAKER_00]: But without further ado, I do have to introduce the second most handsome doctor in North America, Dr. Austin Baraki, what's going on, man? [SPEAKER_01]: Hey, I'm doing okay. [SPEAKER_01]: As we were chatting before getting started, I'm traveling for work at the moment, and so I'm working with a little bit of a different set-up in case people, I don't know, detect a difference in the voice or the audio quality or something like that.

2:38 [SPEAKER_01]: But yes, I'm away attending on the hospital wards. [SPEAKER_01]: in West Texas at the moment, so not at home in my usual set-up, but things are going okay at the moment. [SPEAKER_00]: Yeah. [SPEAKER_00]: Austin, nothing's happened to his vocal folds. [SPEAKER_00]: Nothing's happened to his oral fairings.

2:54 [SPEAKER_00]: His intact, it's just, you know, the audio is going through the iPhone 16, which it has a decent microphone on it. [SPEAKER_00]: So we'll see if my audio engineering stuff is up to snuff and, you know, if we get a bunch of, we get a bunch of hatecoms on this episode. [SPEAKER_00]: Like he ate it, man.

3:12 [SPEAKER_00]: I don't know what I don't want to tell you. [SPEAKER_00]: Like it just, yeah, I can deal with the critics. [SPEAKER_00]: That's okay. [SPEAKER_00]: So yes, like in Austin's DMs, if you don't like his sound, he'll, he really appreciates that. [SPEAKER_00]: All right, well, let's dive in because we do have a lot to get to today.

3:24 [SPEAKER_00]: So first up, is there such a thing as too low of a cholesterol level, specifically LDL and apolipoprotein B? [SPEAKER_00]: So the question is, hi, docs. [SPEAKER_00]: I have two doctors in my life, my PCP and my cardiologist who cannot seem to agree on whether there is such a thing as an LDL or apob level that is too low in the context of primary prevention.

3:47 [SPEAKER_00]: I reviewed what I could of the literature and honestly it seems as much of a question of epistemology and risk management as science or medicine. [SPEAKER_00]: One doctor argues that the evidence from clinical trials and from people born with certain genetic mutations shows that levels at or lower than that of a neonate are at least not harmful.

4:05 [SPEAKER_00]: The other argues that we don't have multi-decade evidence of what happens when we reach those levels in humans through medical interventions rather than genetic mutations. [SPEAKER_00]: Without making this about my specific case, [SPEAKER_00]: How do you think about an issue like this? [SPEAKER_00]: I actually thought this was a very interesting question.

4:22 [SPEAKER_00]: It's not new, but it's a different take. [SPEAKER_00]: Because we've gotten questions before. [SPEAKER_00]: I don't think on the AMA, but elsewhere, hey, look, can cholesterol be too low? [SPEAKER_00]: Or look at this study. [SPEAKER_00]: It shows that there's increased mortality when cholesterol levels are too low.

4:36 [SPEAKER_00]: And we'll get to why you can see some studies like that. [SPEAKER_00]: But it's never been specifically about [SPEAKER_00]: April, like a protein B, and it's also never kind of introduced this other wrinkle where it's like, hey, look, what about, do we have multi-decade evidence that lowering this through medications, you know, actually provides the same benefits as some of these genetic mutations.

4:54 [SPEAKER_00]: So the premise as I understand it is this, and then get you to confirm that we're talking about the same thing. [SPEAKER_00]: apoliper protein B or apob is a structural protein that's found on potentially atherogenic lipoproteins, making it a critical measure of total particle count. [SPEAKER_00]: We're talking about the stuff that carries cholesterol around in the body.

5:14 [SPEAKER_00]: So when discussing lipid lowering achieving ultra low levels of circulating LDL also means achieving ultra low levels of apob. [SPEAKER_00]: So this debate, if it were a debate, centers on whether the human system requires some minimum amount of circulating LDL particles for health, or if you can just go as low as you want, and maybe that's even better.

5:37 [SPEAKER_00]: And then we also have to define like what is ultra low in this case. [SPEAKER_00]: And so, [SPEAKER_00]: we could define that as something below 40 milligrams per deciliter, which approaches the levels that are seen in newborns. [SPEAKER_00]: They're usually born with like 20 to 40 milligrams per deciliter, which is during the period of most active brain development and growth.

5:54 [SPEAKER_00]: Does that seem like a reasonable kind of interpretation of what we're talking about here? [SPEAKER_01]: Yeah, totally. [SPEAKER_01]: This is analogous to other, you know, context where I've gotten this the same question and so I'm I would say relatively familiar with this this question and the conversation and back and forth and debates around it among the, you know, clinician community and certainly among the Twitter sphere.

6:16 [SPEAKER_00]: Let's say totally. [SPEAKER_00]: Okay, before we dive into the different lines of evidence and ultimately get to like an answer here. [SPEAKER_00]: So if there's two doctors, one's a PCP and one's a cardiologist, do you want to pin one of the opinions on one of the physicians like which opinion is attributed to the PCP and which ones are attributed to the cardiologist and your best guess?

6:36 [SPEAKER_01]: Yeah, my prediction here is that the cardiologist is the one who is more comfortable with the lower ApoB or LDL cholesterol targets and the primary care physician might be the person who's more concerned that, quote, we don't have multi-decade evidence of what happens when we reach those levels through pharmacologic intervention rather than genetic mutations.

6:54 [SPEAKER_01]: That's my guess in my prediction. [SPEAKER_00]: Yeah, I'd say that I'd be in agreement there. [SPEAKER_00]: All right, so let's start off with this genetic evidence. [SPEAKER_00]: So we're talking about like loss of function type mutations. [SPEAKER_00]: And I know that you've talked about this a number of times.

7:06 [SPEAKER_00]: So I'm going to let you kind of go off on this king. [SPEAKER_00]: Like when we talk about genetic evidence, loss of function, like what specifically are we talking about? [SPEAKER_00]: Like what are we losing function in? [SPEAKER_00]: And like what happens? [SPEAKER_01]: Yeah, I think that without diving into a full exposition of the physiology of circulating LDL and APOB, it is important to understand as we've talked about in other contexts that it matters how you got there.

7:31 [SPEAKER_01]: We've talked about that with blood pressure, for example, it matters how your blood pressure got high or how it got low. [SPEAKER_01]: And to some extent, there's actually also some similarity here, but understanding the physiology of [SPEAKER_01]: where do these APOV particles come from?

7:44 [SPEAKER_01]: They're synthesized, produced, and excreted from the liver into the bloodstream. [SPEAKER_01]: They circulate throughout the body. [SPEAKER_01]: And then they are also cleared predominantly by the liver as well, but also to some extent in some other tissues. [SPEAKER_01]: And so the amount that is swimming in our blood at any given time that might be detected when you do a blood draw.

8:03 [SPEAKER_01]: That's just a snapshot in time. [SPEAKER_01]: is going to relate to the difference between how quickly are these particles being produced and succeeded from the liver into the bloodstream versus how quickly are they being cleared from the bloodstream. [SPEAKER_01]: So there are kind of two angles that you could look at to get a sense of where is this person ultimately settling out, so to speak.

8:25 [SPEAKER_01]: And so when we look at [SPEAKER_01]: For example, lifestyle things that can impact these blood levels causing them to rise, a lot of it ends up having to do with impairment in their clearance, they're not as efficient and as effective at getting this stuff out of the blood. [SPEAKER_01]: So on the other hand, when we see patients with certain genetic mutations and mutations not like the cool X-man kind that give you superpowers, but side of those mutations can be good or favorable, right?

8:54 [SPEAKER_01]: They're not all that I only say that because mutation kind of tends to have a negative connotation to it, but in this situation, when people have what's called that loss of function mutation in a gene called PCSK9, that leads them to be [SPEAKER_01]: They can produce it just fine, but it is rapidly cleared so that it doesn't stick around in the bloodstream that long and when LDL cholesterol and these APOB particles don't stick around in the bloodstream that long.

9:22 [SPEAKER_01]: They don't have that much of an opportunity to get into the walls of our blood vessels and cause problems. [SPEAKER_01]: And yes, for anybody who is like upset with me right now, I also recognize that there are other contributing accelerants to the process of atherosclerosis, things like smoking and inflammation and insulin resistance and things like that.

9:40 [SPEAKER_01]: But, [SPEAKER_01]: When we look at what is the composition of plaques in arteries, it is not made up of cigarettes milk. [SPEAKER_01]: There is lipid lane plaque cholesterol that got there one way or another, and it could have been accelerated by these other risk factors, but we also know that patients who just have isolated severe high blood cholesterol levels, they tend to develop rapidly progressive early or premature at their sclerosis.

10:04 [SPEAKER_01]: So, people who have these kinds of gene mutations, specifically the example we're talking about is this PCSK9 loss of function, they are super-efficient clearers of ApoB particles out of the blood. [SPEAKER_01]: What's the effect of this? [SPEAKER_01]: Is that they live with super-low blood levels of LDL cholesterol, super-low blood levels of ApoB?

10:24 [SPEAKER_01]: Almost like they're living on a drug that mimics that effect called a PCS K9 inhibitor. [SPEAKER_01]: And then what's the downstream effect of that? [SPEAKER_01]: Is they have a dramatically lower lifetime risk of developing atherosclerotic cardiovascular disease? [SPEAKER_01]: and the amount of that risk reduction is going to be in proportion to how much lower their blood levels are because as we've talked about elsewhere, this is a phenomenon that relates to the cumulative lifelong exposure, how high and for how long.

10:52 [SPEAKER_01]: And so when you're born with low levels and you live most of your life with low levels, you're going to end up being at very low risk. [SPEAKER_01]: The question or the implication with respect to this question, asker's scenario, though, [SPEAKER_01]: Even though these people are born with low blood LDL and APOP levels, and they live with those for a long time, is there some sort of severe off-target harm that they suffer from.

11:14 [SPEAKER_01]: That would be indicative of their levels being, quote, two low. [SPEAKER_01]: For example, do they have a way higher rate of developing early cancers, or dying from rapid early onset dementia, because that's often a concern from people that like, [SPEAKER_01]: to low I might at higher risk of developing dementia or something like that and that just doesn't really seem to pan out in this patient population.

11:36 [SPEAKER_01]: Again, I will recognize that not for two people at a given blood level of LDL cholesterol, they might have gotten there by different ways and so it's worth examining what happens when we get there by different ways because are all these centers the same ultimately or are there some variations.

11:52 [SPEAKER_01]: And so when we look at other gene mutations, for example, when you're unable to produce ApoB particles or familiar hypo beta lipoproteinemia or to impress you with my pronunciation there, that's less of an issue related to hyper-efficient clearance of these particles and more of an issue with [SPEAKER_01]: your ability to produce them, those beta lipoprotein particles that would get secreted on those particles, you have a limited ability to do that.

12:19 [SPEAKER_01]: Now, when people have two defective genes with that, that leads to a severe impairment in their health because they have limited ability to package, [SPEAKER_01]: all sorts of things on these lipoprotein particles. [SPEAKER_01]: There's a lot of other things besides just cholesterol on them, and so they end up requiring other treatment approaches relating to their dietary fat intake and fat soluble vitamins and lots of other things.

12:44 [SPEAKER_01]: This is also a super tiny fraction of this population. [SPEAKER_01]: But more often, these people have heterozygots, meaning they have one defective gene and one normal gene, and these people also live with very low blood levels of LDL cholesterol, because they're just not as good at producing these circulating particles.

13:02 [SPEAKER_01]: But they tend to not have symptoms or complications, as a result, similarly, would you expect to find, for example, [SPEAKER_01]: that they get very early onset dementia because everybody, if you go on the internet and you read about this stuff, you see people say, well, your brain is mostly made of cholesterol, cholesterol super important for your brain.

13:18 [SPEAKER_01]: If you lower your blood cholesterol, you're going to get dementia without recognizing that there's all sorts of physiology that they don't know. [SPEAKER_01]: In terms of the blood brain barrier and lipid trafficking in and out of the brain that more so doesn't tend to happen, then does and things like that.

13:31 [SPEAKER_01]: And so you would predict, or people who are of that belief might predict that those with very low levels are going to be prone to all these things, which also isn't really what we end up seeing. [SPEAKER_01]: So that's the at the approach to this question from the genetic side of things.

13:46 [SPEAKER_01]: This person said that their physician was questioning, well, is it safe for reasonable or appropriate to extrapolate what we see in the genetics and areas to people who don't have those genetic things, but we achieve a similar result through the use of medicines that might be stated the started later in life.

14:02 [SPEAKER_01]: which is sort of a valid question, I think. [SPEAKER_01]: But the thing is, is that many of these drugs that we have end up in one way or another mimicking the effect of one of these gene mutations and ultimately people end up getting exposed to it for a smaller fraction of their life compared with if they're born with it.

14:19 [SPEAKER_01]: But we can still look at the trial data anyway to approach this question as well. [SPEAKER_00]: Yeah, yeah, like just if you look at the genetic data alone, you're like, okay, so apparently there's not some like unknown risk or unknown risks of hearing low LDL level low apolipoprotein b otherwise it would have shown up in these these people who live their entire life.

14:40 [SPEAKER_00]: their tire lives with low LDL, low APL protein B. So from the start, you're like, okay, I'm getting kind of convinced. [SPEAKER_00]: I'm feeling like pretty okay about this, but maybe it's different if you use a medication to get there or a number of medications there. [SPEAKER_00]: Right.

14:56 [SPEAKER_00]: And so fortunately, this has been investigated a number of times. [SPEAKER_00]: And so we just a brief review of some of the longest term data that we have on this. [SPEAKER_00]: So first up is the Fourier trial. [SPEAKER_00]: This is a study on a PCSK9 inhibitor. [SPEAKER_00]: And effectively, [SPEAKER_00]: this was done in people with high risk of cardiovascular disease.

15:19 [SPEAKER_00]: And it found that reducing their LDL levels produced a persistent cardiovascular benefit. [SPEAKER_00]: They also extended this study for 8.6 years of the average follow-up there. [SPEAKER_00]: And that established a strong dose-dependent relationship between lower LDL levels and a lower risk of heart disease.

15:41 [SPEAKER_00]: In a dose-dependent relationship, [SPEAKER_00]: the more reduction in adverse cardiovascular outcomes. [SPEAKER_00]: And this relationship held true down to levels less than 20 milligrams per decelerate, decidedly lower than the neonatal level. [SPEAKER_00]: And there was no statistically significant increase in serious adverse events with lower LDL levels, including like neurocognitive decline, which was actually tested.

16:07 [SPEAKER_00]: So that's one study, that's the Fourier trial and the Fourier extension on that. [SPEAKER_00]: The Improved Safety Analysis followed all of patients treated with azetamide and Symbestatin. [SPEAKER_00]: Again, these drugs together would lower LDL a bunch and it showed no increase in adverse events in patients achieving LDL levels less than 30 milligrams per deceler over more than six years of follow-up.

16:31 [SPEAKER_00]: And then finally, the Ebinghouse study specifically evaluated cognitive performance in patients achieving LDL levels below 25 milligrams per desoliter using PCSK nine inhibitors and reported no change in cognition. [SPEAKER_00]: Now, like full disclosure, if you're looking for multi-decade evidence 20 years, 30 years, 40 years.

16:54 [SPEAKER_00]: Fair enough, we don't have that data. [SPEAKER_00]: A data does not exist, it perhaps it will, you know, these longitudinal studies going out further further into the future will be, probably be retired by the time that stuff gets, gets published, but we have robust evidence showing that there's a dose-dependent relationship between LDL lowering and reduced heart disease risk, whether or not you got [SPEAKER_00]: Also, there's no apparent harm that's been identified in these data sets related to just low LDL levels or low apolipoprotein B levels.

17:34 [SPEAKER_01]: So like, I want to point out one very important caveat here, not not even necessarily caveat, but just something to hammer this home because [SPEAKER_01]: Again, having observed and been part of enough of these arguments at this time, I already know that there are going to be people who are, well, maybe not among our listenership so much, but if you put this out on the public feed, maybe maybe listening, who say, but I heard about this study or I read this study that showed that people with lower levels of cholesterol had a higher risk of death.

18:01 [SPEAKER_01]: Right, this is vandied about all the time. [SPEAKER_01]: And I'm not intending to be dismissive of that, but rather to help to clarify why that observation is so frequently made and why it does not directly inform our opinion and recommendations here. [SPEAKER_01]: So when we take patients and do a randomized and prospective study, meaning we take a group of patients at the start and we randomize them some to lower their blood cholesterol levels, for example, using statins or PCSK non inhibitors or a ZMI, or inclercerin, or whatever, you know, then pedoic acid, whichever of the agents you want, and the other group to get placebo or to not have their blood lipids lowered, and then we follow them forward in time.

18:40 [SPEAKER_01]: What do we end up seeing? [SPEAKER_01]: reliable, consistent, essentially predictable impact on their heart disease risk over time based on the degree of blood lipid lowering and the amount of time that it is lowered for. [SPEAKER_01]: What types of studies show us that other finding, where people with lower blood cholesterol levels have a higher risk of death?

19:02 [SPEAKER_01]: There are a few different study designs that tend to show us this. [SPEAKER_01]: One is retrospective studies. [SPEAKER_01]: The other are cross-sectional studies, for example, which are both different forms of observational data where you're not taking people randomizing them and following them forward in time.

19:18 [SPEAKER_01]: And some prospective studies, but that are a prospective cohorts where you're observing them going forward. [SPEAKER_01]: You're not taking a group and randomizing them to intervene on their cholesterol levels. [SPEAKER_01]: Rather, you're taking them from the start and seeing, well, people who have lower versus higher, what happens to them over time.

19:34 [SPEAKER_01]: And this is where we have to come back to that same question of, it matters how you got there. [SPEAKER_01]: Because we also know that blood cholesterol levels can be impacted by other things, [SPEAKER_01]: But if you have malnutrition, if you have cirrhosis, if you have certain types of chronic inflammatory diseases, if you have advanced cancer, these are all things that can lower your blood levels of cholesterol.

20:00 [SPEAKER_01]: It can incidentally also lower all sorts of other things. [SPEAKER_01]: It can lower your testosterone. [SPEAKER_01]: It can lower your thyroid hormone. [SPEAKER_01]: It can lower your hemoglobin levels. [SPEAKER_01]: It can lower tons of things, right? [SPEAKER_01]: And so when we see people, this like you shaped curve of people who tend to die more when they have low blood cholesterol levels, [SPEAKER_01]: That is never what we see in prospective randomized trials where we take people and we randomize them this group is going to actively lower their blood cholesterol whether through lifestyle or medicines or anything else versus not.

20:31 [SPEAKER_01]: But in observational data sets where there is some form of what we call an unmeasured illness phenomena where the group that at baseline or at the start is starting out with the lower levels of data. [SPEAKER_01]: They quote unquote so to speak. [SPEAKER_01]: Those people tend to have more cancer, more illness, more disease.

20:48 [SPEAKER_01]: And of course, we're going to be at high risk of death from those very things. [SPEAKER_01]: If, and this is the final point I'll make here and then we can move on because it's so important. [SPEAKER_01]: If, in fact, we saw that those who had the lowest levels of blood cholesterol did have that high risk of death.

21:02 [SPEAKER_01]: If that was a robust finding, then what would we see when we actively lower those levels using medicines like Stance and PCS K9, if there's people who would be dying left and right, way higher rate, compared with those who had higher blood levels. [SPEAKER_01]: What would then our clinical guidelines say?

21:20 [SPEAKER_01]: Definitely don't use these drugs. [SPEAKER_01]: They're contraindicated. [SPEAKER_01]: As has been the case in many other contexts when we did studies of one drug versus another and the people that got the drug died more. [SPEAKER_01]: We stopped using that drug. [SPEAKER_01]: This has happened many times throughout medical history.

21:33 [SPEAKER_01]: And then we would also actively recommend people use strategies to raise their blood cholesterol levels to get up to that sweet spot on the U-shaped curve. [SPEAKER_01]: we would have to see that that fits in the randomized perspective data, that is not what we see. [SPEAKER_01]: It's only in these flawed observational studies where there is some other phenomenon that is driving the low level versus the high level contributing to that risk of death.

21:57 [SPEAKER_01]: So that's just a super important phenomenon because it is going to come up for the rest of time. [SPEAKER_01]: You're going to go out there, you're going to see these arguments and you're going to see someone saying, what about this paper, people with low levels died more? [SPEAKER_01]: Well, they had other reasons to die more.

22:09 [SPEAKER_01]: It wasn't because [SPEAKER_00]: Yeah. [SPEAKER_00]: Yeah. [SPEAKER_00]: And this is analogous also to like when you see those as not the same exact studies like the same papers, but similar observational data where people with a lower BMI on average higher all cause mortality than those with a BMI that's consistent with the obesity that could occur in that definition.

22:29 [SPEAKER_00]: And it's like, yeah, if you have cancer, if you have some sort of like severe medical condition that is causing the low BMI in the short [SPEAKER_00]: I mean, I don't know that we needed a study to tell us that, but apparently we need some nuance and how these studies are communicated so that people don't take that to me.

22:49 [SPEAKER_00]: Oh, well, I should just have a BMI of 30, a blood cholesterol, LDL level of 200, and I'm good to go. [SPEAKER_01]: It's like, yeah, same thing with A1C, hemoglobin A1C measurements for diabetes control. [SPEAKER_01]: Right? [SPEAKER_01]: You're going to see the lowest, a, and A1C of like 3%.

23:01 [SPEAKER_01]: Yeah, you probably probably die in more compared with, you know, and that doesn't mean we recommend people, you know. [SPEAKER_01]: get their A1 sees up and their weight up and their cholesterol up and their blood pressure up. [SPEAKER_01]: I'll tell you who my most worried is going to die very soon.

23:14 [SPEAKER_01]: The person with the lowest blood pressure in the room. [SPEAKER_01]: This is just over 30. [SPEAKER_01]: I'm about to go to a code blue on them, right? [SPEAKER_01]: That doesn't mean that we want to actively raise people's blood pressure up to the highest level. [SPEAKER_00]: Yep. [SPEAKER_00]: Yep.

23:25 [SPEAKER_00]: Exactly. [SPEAKER_00]: No, it's a good point. [SPEAKER_00]: One last little piece of nuance I want to get you to weigh in on this. [SPEAKER_00]: So a hemorrhagic stroke, so bleed. [SPEAKER_00]: There's some signal in meta-analysis of intense LDL lowering trial, suggesting a small possible increase risk of hemorrhagic stroke.

23:44 [SPEAKER_00]: The evidence for this risk appears most strongly for statins, whereas non-statin therapies like PCSK-9 inhibitors, [SPEAKER_00]: have not really shown that the clear consistent safety signal, even though they do achieve ultra low levels of LDL, and this is my estimation largely outweighed by the reduction in ischemic strokes, so lack of blood flow to a particular area of the brain.

24:06 [SPEAKER_00]: Do you agree with that take? [SPEAKER_00]: Do you think, I mean, how do you parse this out? [SPEAKER_00]: I imagine you don't do much counseling on this specifically, but it's in your brain somewhere. [SPEAKER_01]: Yeah, I mean, I've been hearing about this for many years. [SPEAKER_01]: I remember first learning about this going through medical training, and I remain unsure of what to make of it.

24:21 [SPEAKER_01]: I will say, you know, the person who asked this question specifically said, without making this about my specific case, but I think that having a specific case in mind is really important when it comes to discussions of how aggressive ought we be when managing these things. [SPEAKER_01]: because the types of patients in whom I'm even, you know, entertaining the idea of being this aggressive are people who are at very high risk.

24:45 [SPEAKER_01]: It's not just your run of the male primary prevention, you know, because in general, I don't necessarily do a ton of the, like, aggressive optimizing for all comeers where it's like, if you want to live to be 200, I want to get your lipids to undetectable. [SPEAKER_01]: When you have no family history or otherwise, totally healthy, like I think it's generally.

25:02 [SPEAKER_01]: overly aggressive and overkill for a lot of people unless they specifically for whatever reason are highly motivated to do that. [SPEAKER_01]: But if I have, for example, somebody who is maybe in their 40s or 30s who already has clinical evidence of atherosclerosis, who has family history of early heart disease, who has elevated lead but protein little A.

25:19 [SPEAKER_01]: maybe who has, you know, all sorts of other high-risk features. [SPEAKER_01]: Yeah, that's the situation where I'm going to be counseling and talking about what are our options to be more aggressive here. [SPEAKER_01]: And then we're weighing, what is an almost certain risk of you having a heart attack or an eschemic stroke?

25:34 [SPEAKER_01]: First is like a maybe the data on this isn't super clear relating to the risk of hemorrhagic stroke and it's only through this like one way of managing this [SPEAKER_01]: And so, ultimately, I don't, this doesn't tend to come up terribly often, and additionally, even for my very, very high risk patients, I'm not routinely saying, I need to get your LDL or APB to be like, undetectable.

25:57 [SPEAKER_01]: If I can get it down like, well, below. [SPEAKER_01]: D, milligrams per desolator, if I can get it down into, say, into the 30 range of, I'd be like content with that for the vast majority of these, again, ultra high risk patients, not everybody, not all commerce, not routine primary prevention.

26:13 [SPEAKER_01]: But I'm not saying that I need to push you way lower than that. [SPEAKER_01]: And if I did measure somebody's LDL cholesterol, or their APOB, and it was like 10 milligrams per desolator or five, I'm also just kind of reassessing and thinking, like, do I need to be this aggressive with this person?

26:29 [SPEAKER_01]: Am I getting them increment, you know, how much of incremental benefit do I think this is having would it be reasonable to back off and let them settle out maybe around like say 30 or and that's not based on any evidence just to be clear it's just like a feels thing because a lot of people get kind of spooked around around those kinds of levels.

26:46 [SPEAKER_01]: So I don't really think it's a, I don't like removing this conversation outside of the risk context of a particular person because that's where I really anchor these conversations is if the higher your risk is at the start, the more aggressive I think we can justifiably be and. [SPEAKER_01]: We might then accept some theoretical risk of some of these things happening, given that you have a near-certain risk of having an atherosclerotic event.

27:10 [SPEAKER_01]: Whereas if you're not as high of risk, then maybe we don't need to be quite as aggressive and then we can just avoid this conversation altogether. [SPEAKER_00]: Yeah. [SPEAKER_00]: Yep. [SPEAKER_00]: So just to summarize heart disease risk reduction involves targeting multiple risk factors.

27:24 [SPEAKER_00]: So not just cholesterol levels and lipids, but also blood pressure, insulin resistance, smoking, inflammation, etc. [SPEAKER_00]: The goal for all of these risk factors though is the same. [SPEAKER_00]: Minimize lifelong exposure to all of them. [SPEAKER_00]: And depending on your personal risk profile, you may want to be more aggressive towards one or more of these things depending on the individual.

27:46 [SPEAKER_00]: So yeah, to your point, it's helpful sometimes to actually have a specific case to really highlight like, well, look, your 10-year or 30-year risk is X. If we did this intervention, it would now be Y. And is that worth it to you at based on your goals, preferences, et cetera? [SPEAKER_01]: So [SPEAKER_01]: Yeah, yeah, and I do these kind of consults with people all the time, so if somebody's struggling with this or they want to tie breaker opinion on their head from their physicians, I'm happy to help.

28:14 [SPEAKER_00]: Uh, next we're moving on to behavior change, uh, the question is, hello, guys, is it normal to not feel motivated to do a task before doing it, and is it normal for people to usually get the motivation retroactively, they get the inclination after starting? [SPEAKER_00]: I feel like the answer is yes, but for some reason, I feel like asking, uh, is mostly a sanity check.

28:35 [SPEAKER_00]: This can relate to exercise, study, socializing, really, anything, I think. [SPEAKER_00]: Uh, to answer simply, yep, pretty normal, man, uh, the initial feeling of like, dread and procrastination or heavy resistance that accompanies the thought of initiating, it's any sort of like taxing task, call it like physiological inertia.

28:54 [SPEAKER_00]: It's like an inherent friction in shifting from an established behavioral state, right, or quote, like resting state to a new one or one requiring more effort. [SPEAKER_00]: It's not [SPEAKER_00]: laziness. [SPEAKER_00]: But there are multiple like inputs here that prevent people from starting.

29:10 [SPEAKER_00]: They want to be more focused. [SPEAKER_00]: It's like a perfectionism trap. [SPEAKER_00]: They have anxiety about, oh, what's it going to cost me in terms of effort to start this thing or do this thing or like finish this thing. [SPEAKER_00]: Some thought that this is like a human attempt to quote, conserve resources against like higher energy type outputs.

29:28 [SPEAKER_00]: And basically your prefrontal cortex is predicting how much effort you are going to need to put out to do the thing and the prefrontal cortex may not be aligned with reality so it could be, you know, a little an over-exuberant response here and it tends to be higher for novel tasks or tasks where you're uncertain hey look how much energy is actually going to take how many resources actually going to take so you have this higher projected cost.

29:53 [SPEAKER_00]: higher psychological inertia and then you get a predictable response avoidance. [SPEAKER_00]: But yeah, when you initiate the change you start, you get like kind of like a almost an expectation violation. [SPEAKER_00]: You get some real feedback like what is this really going to be like that supersedes your previous predicted projections.

30:10 [SPEAKER_00]: So taking action actually interrupts this sort of negative feedback loop and gives you like a cognitive relief from these perceived barriers. [SPEAKER_00]: It updates your forecast. [SPEAKER_00]: The trick is to minimize this perceived cost of initiation. [SPEAKER_00]: I don't have any Jedi mind tricks to trick your prefrontal cortex.

30:30 [SPEAKER_00]: It's way more advanced and evolved than anything I can come up with off the fly. [SPEAKER_00]: But I do have a few tips here if there was an initiation protocol. [SPEAKER_00]: bypass this inertia, the psychological resistance to starting and do like a micro start. [SPEAKER_00]: Just five minutes.

30:54 [SPEAKER_00]: You set a clock for five minutes, commit yourself to starting for five minutes, and you give yourself full permission to stop, right? [SPEAKER_00]: You can start badly incorrectly, but you just got to start. [SPEAKER_00]: There's actually an effect, I think it's called like the zygermic effect.

31:08 [SPEAKER_00]: It's a psychological phenomenon where people remember unfinished or interrupted tasks better than completed ones. [SPEAKER_00]: And so you get this like push to close the loop. [SPEAKER_00]: So you just got to start and then your brain starts working. [SPEAKER_00]: It's like, okay, I got to get back to that.

31:20 [SPEAKER_00]: I got to start. [SPEAKER_00]: So just give yourself permission to start. [SPEAKER_00]: And even if it's you start wrong, at least you started. [SPEAKER_00]: Um, and then the last thing I'd add here is more of like a concern, like, if this is something that you're consistently dealing with, uh, and you try to start, but like, you don't get any retroactive like motivation or enjoyment out of not only starting, but even completing a task, I would recommend seeing a healthcare professional, because there may be something else going on here and, uh, these sort of like podcast bro suggestions are probably insufficient for behavioral change.

31:54 [SPEAKER_00]: Maybe maybe something else is going on. [SPEAKER_01]: Yeah. [SPEAKER_01]: Interesting topic. [SPEAKER_01]: I appreciate you doing a bit of a dive on it. [SPEAKER_01]: I don't have a ton to add towards this in terms of recommendations or advice outside of a book recommendation. [SPEAKER_01]: And going through Steve Magnus's book, do hard to answer.

32:10 [SPEAKER_01]: Get gets at a lot of these topics and the kind of the the sports psychology around it, which was a super interesting one. [SPEAKER_01]: So I would recommend that for anyone interested. [SPEAKER_00]: All right. [SPEAKER_00]: Next question, a few left here. [SPEAKER_00]: How to improve cardio when you have limited time.

32:33 [SPEAKER_00]: This, I'm a recent barbell medicine plus subscriber and I'm loving it. [SPEAKER_00]: Thank you. [SPEAKER_00]: Happy you're here. [SPEAKER_00]: I'm coming out of 10 years of a very sedentary lifestyle due to mismanagement of career and family stressors. [SPEAKER_00]: Also, I have neglected cardio, my whole life, I'm 40 years old.

32:47 [SPEAKER_00]: You guys have convinced me to do better. [SPEAKER_00]: A few months ago, I started jogging, easy and into it by going at a very slow pace. [SPEAKER_00]: Due to my own excuses, I can only reliably get two sessions a week for cardio. [SPEAKER_00]: About 30 minutes each, occasionally I can get a third session in.

33:01 [SPEAKER_00]: My current strategy has been to pick a jogging pace. [SPEAKER_00]: I think it can sustain for the 30 minutes. [SPEAKER_00]: This has been okay and working. [SPEAKER_00]: I've gone from a 13 minute pace down to a 1030 to 11 minute pace, but I stagnated. [SPEAKER_00]: Would you recommend a different strategy with the time constraints I've given?

33:19 [SPEAKER_00]: Great question. [SPEAKER_00]: I think this probably applies to a lot of folks, whether they want to admit it or not, but first off, like, congratulations. [SPEAKER_00]: Going from 10 years of being insufficiently active to reliably, not only lifting, assuming you're doing lifting, but also doing the cardio.

33:35 [SPEAKER_00]: That's awesome. [SPEAKER_00]: Nice, nice work. [SPEAKER_00]: Yes, as far as the plateau and the stagnation you describe, that is completely normal and almost expected, because where's the progressive loading here, right, like going faster, yes, does increase the, you know, it catches the stress of the workout back up to your new found fitness.

33:56 [SPEAKER_00]: That's great, but [SPEAKER_00]: It may be insufficient for driving further adaptations past a certain point. [SPEAKER_00]: It seems like what you're experiencing. [SPEAKER_00]: So given the time constraint of only two, maybe three, 30 minute sessions per week, increasing the work out duration or the frequency is not really something we can do.

34:16 [SPEAKER_00]: So the only really viable vector for progressive loading is going to be intensity. [SPEAKER_00]: And this bears a discussion like, well, why? [SPEAKER_00]: And like, what do? [SPEAKER_00]: for conditioning in the current physical activity recommendations they basically equate one minute of moderate to vigorous activity to two minutes of vigorous conditioning.

34:43 [SPEAKER_00]: And so this is born out in the physical activity guidelines they recommend 150 to 300 minutes per week of moderate to vigorous conditioning or 75 to 150 minutes of vigorous intensity conditioning. [SPEAKER_00]: They ultimately recommend 500 to 1,000 meta-met minutes per week where every particular activity has a specific met cost.

35:07 [SPEAKER_00]: The faster you go, the more muscle mass you go, are using, harder it is, tend to use more met's, cost more met's. [SPEAKER_00]: And then the longer you do it, you multiply it at the time, but what you do that activity for, you get the met minutes. [SPEAKER_00]: So currently, at your current pace, it's approximately six and a half minutes per minute.

35:25 [SPEAKER_00]: And you're doing on average 30 minutes twice per week. [SPEAKER_00]: So 60 minutes total. [SPEAKER_00]: So you multiply those things together. [SPEAKER_00]: And you get about 390 met minutes per week. [SPEAKER_00]: So it's not bad. [SPEAKER_00]: But I think it should be higher to be consistent with the current guidelines, the minimums.

35:39 [SPEAKER_00]: And also, again, to improve your [SPEAKER_00]: So we need more intensity, which actually may be even more beneficial. [SPEAKER_00]: So a new study that came out, we'll talk about this on one of our upcoming podcasts. [SPEAKER_00]: Effectively, they use the UK BioBank data. [SPEAKER_00]: It's like hundreds of thousands of data points here.

35:59 [SPEAKER_00]: To show, we'll look. [SPEAKER_00]: with respect to cardiovascular disease, to type two diabetes, to all cause mortality, is it really just a one to two ratio between moderate type of conditioning to vigorous intensity conditioning? [SPEAKER_00]: They found actually we may have been underestimating the power of vigorous intensity conditioning.

36:20 [SPEAKER_00]: So for all cause mortality, one minute of vigorous physical activity is equivalent [SPEAKER_00]: For cardiovascular disease mortality, they found that one minute of vigorous conditioning is equivalent to approximately 7.8 minutes of moderate intensity conditioning and for type 2 diabetes, one minute of vigorous conditioning is equivalent to approximately 9.4 minutes of moderate intensity conditioning.

36:51 [SPEAKER_00]: I suspect, you know, there's not a bunch of statistical analysis that's gone on to create these numbers, but ultimately with this tells me, there are a few different things. [SPEAKER_00]: One, this is mostly based on accelerometer data and so I suspect when people are doing moderate intensity stuff.

37:08 [SPEAKER_00]: It's just not that hard. [SPEAKER_00]: It's not that taxing for them. [SPEAKER_00]: And so the results are kind of predictable. [SPEAKER_00]: They're just not getting as much of the exercise derived benefits because they're not doing enough exercise. [SPEAKER_00]: But if you're doing bigger stuff, almost certainly it's hard enough.

37:21 [SPEAKER_00]: And so yet, you get a bigger effect, especially on like a per time basis. [SPEAKER_00]: It's just more than what we thought. [SPEAKER_00]: So... [SPEAKER_00]: This gives me a rationale to increase your intensity to ultimately get you what you want to go. [SPEAKER_00]: So the way I would do this, I would think about one sort of high intensity interval training work out.

37:48 [SPEAKER_00]: So this would be like three to five minute long intervals at a faster pace than you're running now, interspersed with one to two minutes of brisk walking in between. [SPEAKER_00]: and you kind of repeat that. [SPEAKER_00]: You get to go faster. [SPEAKER_00]: So it's kind of more intense on average than just doing 30 minutes at the same pace.

38:05 [SPEAKER_00]: So I would do something like that. [SPEAKER_00]: If you're running, for example, at a 10 30 to 11-minute pace right now, we're talking about like a nine-minute pace. [SPEAKER_00]: So you don't have to sprint. [SPEAKER_00]: We're not doing a three-year-five-minute sprint. [SPEAKER_00]: But something a little faster than what you're doing right now, and you're going to walk in between those three to five minute intervals.

38:20 [SPEAKER_00]: I would start at three minutes. [SPEAKER_00]: I gradually build up over time. [SPEAKER_00]: The second workout. [SPEAKER_00]: There's second 30 minute session would probably actually include some sprint intensity training, which I just call surges, right? [SPEAKER_00]: Some people call them strides, whatever.

38:33 [SPEAKER_00]: So this would look something like, start a 10 minute run at your current pace, 10 to 11 minute per mile pace, and then you're going to do five to 10 second surges. [SPEAKER_00]: every minute on the minute for a couple sets. [SPEAKER_00]: And these five to 10 second surges are pretty hard, right?

38:49 [SPEAKER_00]: You're going to go pretty fast. [SPEAKER_00]: It's it's sprint realistically is what it is. [SPEAKER_00]: But it's only for five to 10 seconds. [SPEAKER_00]: I would start it actually five seconds and then go up a little longer. [SPEAKER_00]: I would not go longer than 10 seconds for this particular application.

39:00 [SPEAKER_00]: I would just add more. [SPEAKER_00]: more of the email work. [SPEAKER_00]: So I would start with like, you're going to do five of these surges every minute on the minute, like total. [SPEAKER_00]: So five totals set the surges and then over the course of weeks, you can increase that up to maybe like 10 total surges.

39:15 [SPEAKER_00]: And then you're going to finish with another 10 minute run at the pace you started at. [SPEAKER_00]: We're just elevating the intensity of the total workout. [SPEAKER_00]: And I would adjust the run pace, what you're doing for the the periods that you actually are are running not sprinting to be about 80 to 85% of your max heart rate.

39:33 [SPEAKER_00]: That gets you out of zone two and more decidedly in a zone three, although again, the zone ranges for heart rates are a little squishy and very amongst individuals. [SPEAKER_00]: But that would tell me that you're for sure in the vigorous zone and you're probably going to get more out of your workouts that way at some point.

39:49 [SPEAKER_00]: there's going to be a limit on how much intensity we can actually tolerate. [SPEAKER_00]: And at that point, we got to get back to scheduling. [SPEAKER_00]: Or maybe it's fine. [SPEAKER_00]: Maybe you're meeting the current physical activity guidelines, your health is reasonably well and you can just leave it, maintenance mode.

40:03 [SPEAKER_01]: Yeah. [SPEAKER_01]: I love this. [SPEAKER_01]: Obviously, you know, I've been doing a lot more running alongside time on the stationary bike of late alongside my lifting and things are going pretty well. [SPEAKER_01]: So getting into this topic and some more depth is is cool. [SPEAKER_01]: I agree with your recommendations here of incorporating more intensity, especially now that [SPEAKER_01]: This individual is past the initial phase where he did this kind of intro ramp up of doing 30 minute low intense super low intensity and then his pace is gradually improved that shown us not only that he's gotten some initial party respiratory adaptations, but also importantly some muscular skeletal adaptations like his.

40:44 [SPEAKER_01]: bones, joints, muscles, tendons, ligaments can tolerate doing this now, whereas it would have been not a great idea for us to recommend that he jump right into some sprint interval training if he was just like, hey, I'm now decided to start doing this, what should I do? [SPEAKER_01]: That's what that would not be the time to introduce that kind of thing.

40:59 [SPEAKER_01]: So now that he's built up some tolerance for this, I think it's a great time to introduce a little bit of intensity. [SPEAKER_01]: given the constraint that he is essentially volume limited by duration. [SPEAKER_01]: There is a reason though that the fittest runners, those who are able to maintain the fastest basis for the longest distances and things like that, they tend to do a massive amount of trading volume.

41:20 [SPEAKER_01]: So, ultimately, that is the biggest, most powerful lever if you want your, you know, aerobic fitness, running economy, things like that to improve the most over the long term. [SPEAKER_01]: But if that's not a high priority for you, and you're more just trying to get generally healthier within the time constraint or the volume constraints that you were effectively putting on yourself.

41:36 [SPEAKER_01]: Yeah, intensities the next thing to lean into, and you have prepared yourself to do this. [SPEAKER_01]: Starting at the lower end of those intensity targets that Jordan mentioned are, is going to be wise, but you should do great with this, I think. [SPEAKER_00]: Yeah, that's some idiot arguing with me on Twitter and at X about this.

41:53 [SPEAKER_00]: I don't know if you remember the post I made about zone two cardio. [SPEAKER_00]: Like what is it really and like why it might probably doesn't matter for most folks? [SPEAKER_00]: The whole point is like when people talk about zone two cardio they're referring to this five zone model of exercise intensity and you can attribute or demarcate these different zones by heart rates.

42:12 [SPEAKER_00]: You could do a by blood lactate levels by [SPEAKER_00]: Carbon dioxide, there's a number of different physiological parameters that you can sort of draw your lines in the sand. [SPEAKER_00]: They don't all align as well as we'd want them to, and it varies significantly from individual to individual.

42:28 [SPEAKER_00]: Where there's just, look, you're this heart rate, but your blood lactates this. [SPEAKER_00]: It's not as clean as we want it to be. [SPEAKER_00]: And so I made this post, mostly informational. [SPEAKER_00]: And then at the end, I was like, hey, look, if you're only doing 150 minutes a week of conditioning.

42:43 [SPEAKER_00]: I don't think it matters if most of that zone 2 is just not enough total training volume for me to really be concerned about fatigue management in that case. [SPEAKER_00]: It's just the volume's not high enough. [SPEAKER_00]: I don't want you to do at 150 minutes for sprint intensity training either.

42:57 [SPEAKER_00]: I wouldn't go that far, but if it's zone 3 or zone 4, I don't know that I care. [SPEAKER_00]: If you're a strength athlete, trying to maximize your 1 or max, sure, different thing. [SPEAKER_00]: Anyway, this idiot was like, [SPEAKER_00]: If you ever run a marathon and I'm like no dude, I'm trying to develop 800 pounds.

43:13 [SPEAKER_00]: Of course, I haven't run a marathon because I don't that's not my goal. [SPEAKER_00]: And he's like, see, you don't know what you're talking about. [SPEAKER_00]: I'm like, that's an interesting point to make, but he's like, no, no, people should just be low and slow and do hours of that per week.

43:25 [SPEAKER_00]: And I'm like, hey, look, yes, if you want to maximize your aerobic fitness, you're going to need to do a lot more total training volume. [SPEAKER_00]: And yep, a lot of that is going to be low and slow, zone one zone two, and some exposure to this higher intensity stuff, maybe about 20% of your total training volume.

43:40 [SPEAKER_00]: Sure, no argument there. [SPEAKER_00]: And he's like, good. [SPEAKER_00]: I win. [SPEAKER_00]: And I'm like, But what if somebody only has like 60 minutes a week to train? [SPEAKER_00]: you want them to just like walk for the 60 minutes because that is not sufficient to generate the sort of training load that we want for the minimum physical activity guidelines of the 500 to 1000 minutes per week, even though I have problems with metabolic equivalents as a measurement of that.

44:05 [SPEAKER_00]: And he goes, well, you just want people to do more exercise then. [SPEAKER_00]: I'm like, you're not getting it. [SPEAKER_00]: What if somebody can't do that? [SPEAKER_00]: Time is a huge barrier for most people when it comes to exercise. [SPEAKER_00]: So what if somebody can't do that?

44:16 [SPEAKER_00]: And he goes, what do you, everyone should just do crossfit then? [SPEAKER_00]: I'm like, oh, I'm not talking of crux. [SPEAKER_00]: Like, like, can you just acknowledge that if somebody has a limited amount of time to train? [SPEAKER_00]: that modifying intensity is a viable way to increase the training load to get the effects that we want on health.

44:34 [SPEAKER_00]: And he's like, and no, people should just walk more. [SPEAKER_00]: I'm like, I got to, I got to, I got to, I have to, cool, you're right, you're probably right, carry on. [SPEAKER_00]: That's just it. [SPEAKER_00]: Yeah, I'm going to go long off. [SPEAKER_01]: Yeah. [SPEAKER_00]: Totally.

44:45 [SPEAKER_00]: So we do have some resources on this in our in the show notes. [SPEAKER_00]: So we have our heart rate maximum heart rate calculator and our zone calculator. [SPEAKER_00]: So if you want to know zone one zone two zone three zone four zone five some some estimates for those targets for you.

44:59 [SPEAKER_00]: You can check that out linked in the show notes. [SPEAKER_00]: Also what is high intensity interval training. [SPEAKER_00]: What is sprint interval training. [SPEAKER_00]: It should you do them. [SPEAKER_00]: We have a article on that by Dr. Baraki. [SPEAKER_00]: the new nature article where they're sort of comparing like what is the effect of X amount of volume of moderate intensity cardio versus vigorous intensity cardio where I got those numbers from that new paper.

45:18 [SPEAKER_00]: It's open access. [SPEAKER_00]: It's linked in the show notes and then also the physical activity compendium. [SPEAKER_00]: They just updated this last year. [SPEAKER_00]: So it's effectively the metabolic cost of every activity that you can think of. [SPEAKER_00]: That's I'm, I'm exaggerating a little bit, but not by a lot.

45:35 [SPEAKER_00]: They have a bunch of very specific things in there. [SPEAKER_00]: Like walking uphill backwards with the pack on you or walking on an unstable surface compared to like on concrete, also some weird sexual stuff in there. [SPEAKER_00]: But I want to draw the listeners attention to the following.

45:51 [SPEAKER_00]: When we're talking about 150 to 300 minutes per week of moderate to vigorous physical activity, we're talking about cardio. [SPEAKER_00]: Talking about, we're not talking about lifting. [SPEAKER_00]: We're not talking about taking the weights off the bar. [SPEAKER_00]: We're not talking about, you know, strongman stuff.

46:04 [SPEAKER_00]: We're not talking about CrossFit, whatever, because similar to how we've talked about like cholesterol levels, BMI, blood pressure. [SPEAKER_00]: It matters how you get there. [SPEAKER_00]: It's not just an [SPEAKER_00]: your exercise physiology class would like to have a word about how you got your elevator heart rate.

46:25 [SPEAKER_00]: So anyway, the physical activity compendium can be useful if people are like, well, is this moderate to vigorous activity or is this vigorous activity on average? [SPEAKER_00]: It can be useful for that and that's linked in the show notes too. [SPEAKER_00]: Art that is a wrap on this free sample of our bonus content that regularly goes out to our Barbel Medicine Plus subscribers.

46:44 [SPEAKER_00]: Again, to join head over to barbelmedicine.com slash plus and sign up to be a barbel medicine plus member today that's barbelmedicine.com slash plus. [SPEAKER_00]: Thank you so much for listening, we'll catch you guys next time.