Statins, Muscle Mass and Strength: A long-term trade off?

What if a lower LDL comes with a quiet cost to your strength and resilience? We dig into a massive biobank analysis linking long-term statin use with declines in grip strength and appendicular lean mass, then connect the dots to sarcopenia, mitochondrial function, and the daily choices that shape metabolic health. Strength is more than performance; it predicts independence, glucose control, and longevity, which is why any therapy that erodes muscle demands a closer look.

We walk through the study’s design, what “appendicular lean mass” really measures, and why the findings held even after adjusting for lifestyle and genetics like SLCO1B1. From there, we peel back the LDL-centric mindset and focus on terrain: insulin, inflammation, triglycerides, HDL, and LDL particle quality. You’ll hear why refined carbs, seed oils, and chronic inflammation push lipoproteins in the wrong direction—and how protein-forward meals, resistance training, and lower insulin load tip the balance toward larger, less atherogenic particles with benefits that extend well beyond a single lab value.

We also compare statins with hydrophilic options, alternate dosing strategies, and newer PCSK9 inhibitors, clarifying where they may fit for secondary prevention and where big questions remain—especially around muscle preservation and all-cause mortality. CoQ10 gets a fair review: low risk, mixed evidence, and not a proven fix for long-term function. Most importantly, we share practical steps to protect your muscle: track grip strength, prioritize 1.6 to 2.0 g/kg daily protein, lift two to three times per week, walk after meals, and align circadian rhythms with sleep and sunlight. Medications can lower numbers; only your muscles move you through life. Let’s make treatment plans that respect both.

If this conversation helped you think differently about risk and resilience, follow the show, share it with a friend, and leave a quick review so more listeners can find thoughtful, evidence-informed health guidance.

For slides, open source references and video go to: www.thehealthedgepodcast.com

Transcript

Framing The Statin–Muscle Question

SPEAKER_00 0:00

Welcome to The Health Edge, translating the science of self-care. I am Mark Pettis and with my friend colleague John Bagnulo. John, good morning, my friend.

SPEAKER_01 0:10

Hey, good morning, Mark. Great to see you, bud.

Study Design And Methods Explained

SPEAKER_00 0:12

Great to see you, as always. We have a nice paper that looks at the longer-term effects of statin use on two really important attributes of health that we have talked about on podcast recordings in the past, John. And these two attributes relate to strength, muscle strength, and muscle mass, fat-free mass, lean body mass, as it's often sort of referred to. And we have talked about, John, many times how strength, something that can be assessed with a hand grip, continues to be one of the best predictors of longevity and health span, quality of life. And we've talked a lot about how lean body mass, muscle mass, is critical when one looks at the epidemiology of sarcopenia, loss of muscle mass, loss of functional capacity, and the extent to which sarcopenia is a huge predictor of poor metabolic health, chronic complex disease, shortened life expectancy, and worsening health span, just diminished quality of life across the board. And sarcopenia, as we have reviewed, is really epidemic in our society right now. And so when you see a paper like this that looks at people over several years that have been on statins and goes on to measure uh kind of a before and after uh strength via hand grip and muscle mass, and you see very significant declines over time that were not seen in the non-statin users, it really gets your attention. And so uh uh this will be a fun paper and very, I think, meaningful paper to review, John.

SPEAKER_01 2:31

Yeah, absolutely. Um, you know, as you said, this isn't something that is new to the conversation that you and I often have, whether it's you know in a recording or offline, you know, we we look at cholesterol, I think, differently than a lot of uh healthcare professionals, clinicians, researchers. Uh it's you know, its role in the body is so diverse and critical, right? And I I think that we could extrapolate these findings. Obviously, we we don't have that that data or that evidence, but we know that with the loss of muscle mass and with a loss of strength, we also see a typically a concomitant loss in bone density. We often see a loss in mitochondrial function, right? Or the the strength of ATP production, energy production at that that individual, that sarcomere unit, that that fundamental unit of the of muscle. So yeah, I mean this is I think a really especially the first study we're gonna talk about. That's a powerful, that's a powerful study. Uh, you know, when you look at 170,000 plus participants, you follow them. It's that's that's pretty remarkable. So yeah, it's a good time to probably dive into that.

Key Findings On Strength And Lean Mass

SPEAKER_00 3:51

Yeah, let me I'm gonna pull up some slides here. And I do apologize to those that are listening to this podcast. Uh, the slide deck, the video will be available on our website, the healthedgepodcast.com. Also, we have a YouTube channel. Uh, so for those who want to go back and look more specifically at some of the slides that we're sharing. But this is the study that we're looking at. Uh, this was published uh very late in 2025. So this is a very recent paper from Sweden. Uh, and uh this is an observational study, and we frequently up top uh talk about relationships that are drawn from these studies are uh correlations, they're not necessarily cause and effect, but uh, from what we know about the mechanisms of statin on mitochondria, muscle function, uh, it the the wide body of research looking at how statins can disrupt mitochondrial function and ultimately muscle function uh is a pretty solid context upon which this observational study sits. So this this has some some deeper context to it. But the study is called statin use, is associated with a decline in muscle function and mass over time, irrespective of the statin pharmacogenomic score. And we'll we'll talk about what that's statin pharmacogenomic score is, but that's a really important aspect to the uh study design. And uh this was a study, again, that looked at almost 300,000 participants from the UK Biobank. We've reviewed many papers that have come from the UK Biobank, uh, kind of like our national health exam and nutrition survey uh in the US. And again, they looked at individual uh grip strength uh using a you know a hand uh uh dynometer and uh the appendicular lean mass, and we'll talk a little bit more about that. But this really looks at arms and legs where most of our muscle mass resides and measures uh muscle mass in those areas um using bioelectrical impedance. And then typically, as you see, uh they collect data and people on statins over a period of time, and average uh time here was five, six plus years, uh, and they correct for other factors that could influence differences in these findings, right? So they adjust for demographics, lifestyle, other health factors in an effort to better isolate the effect that the statins are having. And these were uh, you know, one nice thing about these Biobank or NHANES study is they do give you a nice cross-section of your general uh public. Uh so here you're looking at uh mid-late 50s, uh 46% were male. Uh and that essentially uh was the cohort that was examined here. And uh again, just very by way of understanding the methodology, this appendicular lean mass measures the total amount of fat-free, bone-free tissue, which is of course primarily muscle in the arms and legs. And because it accounts for over 75% of the body's skeletal muscle, it is a very good measure uh of strength, mobility, metabolic health, which is which is key. We we we drive this home with almost every podcast how metabolic health just connects to virtually everything. And and metabolic health is is within the realm of every human being uh if if they have a good roadmap for how to achieve that. And so um you'll see appendecular lean mass used in many papers that measure sarcopenia strength. Uh and again, these are um typical uh uh measures and standards. Uh and then you know, just we'll sort of cut to the chase, John. We'll just go through these and then we'll just start talking a bit more. Uh so what they showed over time was that uh continuous statin use was associated with a decline in muscle function and mass, over a 25% decline in grip strength, and 73% decline. These are that's a pretty wow, think about that. 73% in appendicular lean mass compared to people who never use statins. And this, and we'll we'll come back to this. This was irrespective of this pharmacogenomic score, uh, which looks at an individual's genetic susceptibility to statins. We we there are a few genes that have been identified that uh associated SNPs, or what we would call polymorphisms of those genes, can interfere with an individual's ability to metabolize statins, so they might be at greater risk of uh muscle uh disruption. And it's important to look at that because if you see differences uh in uh muscle mass strength, and more of these individuals have the genetic predisposition, then uh you know you're looking at a a bit more of a complex gene-drug interaction, which obviously not every user of a statin will have. Uh, and so it's it's important that they corrected for that. And again, what they found when they looked at these SNPs is that they were pretty equally represented. In other words, they did not significantly influence uh the rate of decline.

SPEAKER_01 10:31

And that's really important, right, Mark? Because we hear, at least I hear so often, that well, the only real concern with long-term statin use would be in a you know, small percentage of adults who have one of these genes that you know make that less compatible as a as a treatment. But you know, this really speaks to that. That no, it's not it's not a small subset of the human population that has to be concerned. It's you know, if you're dealing with almost 300,000 people and you're seeing that after five years, users are losing 73% of their muscle mass, that's you know, those findings are powerful. They should be a you know, should be a game changer, right? For how statin use is how it's uh how prevalent it is, I guess I would say.

Genetics, Myopathy, And Drug Choice

SPEAKER_00 11:15

Yeah, it certainly changes the longer-term value proposition, right, John? Because if you're by extrapolation altering muscle mass and strength in a way that will influence metabolic health, and the very reason for your being on a statin is because your your your metabolic health may not be good to begin with. Right. Uh uh and you you can begin to see how um you know the unintentional long-term consequences of that can be very significant. And uh and we won't we don't have to go down the road of you know uh statins and we we've we've talked a lot about the clinical outcomes, there are just so many studies, uh, but the there really is no mortality benefit uh to statin use. Uh no one would question that if for secondary prevention for an individual that's had a prior heart attack or some type of cardiovascular intervention, you don't have to treat as many people to see a reduction in subsequent heart attacks. Um and there's value to that, surely, but the mortality benefit, I think people are often surprised. I think they are too meaningful mortality benefit. I think some of the studies that have been done suggest an extra day of life. Uh, you know, and I guess if you do something special with that extra day, maybe it's worth it. But uh, you know, it's it's you know, while there's some value to statins, I'm not going to dismiss that in my perspective, John. I think this is yet another reason to be really uh discerning over the the long term.

SPEAKER_01 13:06

Um it's a cost-benefit ratio, and I just think the cost is far greater than people really appreciate.

SPEAKER_02 13:13

Yes.

SPEAKER_01 13:14

While the benefits are, I think, you know, very, very, very small.

SPEAKER_00 13:20

And if you look at these pharmacogenomics, uh, just to give people uh a sense of what we're talking about, the the gene that has been most widely studied uh is is this SLCO1B1 uh gene. Variations in this gene do affect how liver takes up statins, and and particularly some of the uh more widely used uh statins early on, like symvastatin, uh with a with a very strong risk of muscle pain and what we might call myopathy. And muscle pain doesn't, in the short term, doesn't equal uh necessarily reduction in lean body mass. You know, most of the data looking at myopathy just looks at these short-term effects. Which are significant. I've had them uh when I've uh been on statins, and I also have this uh gene mutation. Um and uh so these are really important uh effects. Not that everyone needs to have this gene measured. I generally don't recommend people do it routinely unless they're on a statin and and if they're having any muscle symptom, I will I will recommend they get it. Um uh uh we do know that there are some other genes that are less prevalent but can also affect uh the risk. And uh I think for the the importance of this from my perspective, John, is that if uh an individual and the clinicians involved in their care um are committed to statin use, there are some statins that have a lower uh risk of uh disrupted muscle function, uh like resuvastatin, which is the generic, also known as crestor, um uh pravostatin, pravacore. These are a bit less impacted by this gene mutation. So for the clinician and for the individual, uh, it might affect the type of statin that they decide on. It certainly would affect the dosing of that statin that they decide on. Um but there's no question for some, uh, particularly in the absence of a prior cardiovascular event or multiple risk factors like diabetes and smoking, and you know, the things that we talk about, uh, you know, having this gene mutation and not tolerating statins would make me a bit skeptical that any statin would be met without some problem short or long term. But the, you know, I just want to give people sort of the current, I think, uh, standard of care. And so, you know, some statins are less likely to cause myopathy uh due to differences in how they're metabolized. And uh, these would be the hydrophilic, these are more water-soluble, yeah, and and pravastatin, also known as pravocol, and rosuvastatin, also known as crestor, uh, would fall into those um hydrophilic categories. So you might tolerate those after not having tolerated um things like uh symvostatin or a torvostatin, which is also Lipitor, probably the most widely prescribed drug uh in America. Uh and so uh, you know, these are really important issues. And and I know that there are people who struggle with these side effects that I think get underreported. And uh you, as you know, John, I it's not easy for some people to have these conversations with their not at all.

SPEAKER_01 17:26

Yeah, not it's not easy at all.

Mortality, Benefits, And Tradeoffs

SPEAKER_00 17:28

It's so um the dogma is so um strong. Yeah, and it and not, you know, and and and there is some evidence for for certain individual cost-benefit analyses, but the um, you know, I I find people sometimes either uh suffer uh unnecessarily or they may just stop their drug and never never tell their doc because they're you know, it's you feel self-conscious. It's kind of thing, right? You're not you're not a good patient. Uh so and then the last thing I I would just touch on here, John, that we've talked about and that comes up frequently in consultations that I have done in the past, I'm not doing as many these days, is uh, you know, is does taking, if if you're committed to a statin and and you feel it is a it's the best choice, uh, would CoQ10 um help mitigate or diminish the risk of muscle function? And all of the research that I've reviewed only looks at this short-term. None of them have looked at long-term issues that this paper addressed, reduction in strength and muscle mass. Um, and this paper did not specifically look at concomitant CoQ10 use. So um, but um, what you will see from what has been published is that uh CoQ10 comes in two forms. Right? The reduced form is ubiquinol, and uh that tends to be better absorbed, a bit more bioavailable than the uh less expensive form, the ubiquinone, regular CoQ10. Uh that so people often recommend ubiquinol because of its better bioavailability, but when you really look at the the data, uh the data's really been less convincing. Um, you know, despite higher absorption rates, you know, there are some meta-analyses and a few randomized controlled trials have not consistently shown that CoQ10, in either form, significantly reduces statin-associated muscle symptoms. Some people do derive benefit, and it may be that those are people that have a this genetic predisposition. I don't think the the research is clear on that. Um and my uh in my opinion, and I I think um what you'll see just in terms of consensus for what that's worth, is that uh there doesn't appear to be a real harm or downside uh to CoQ10. Um and it I don't think it takes long to see whether it might mitigate those those muscle symptoms. And so um uh you know, recommending it and trying it while on a statin, I think is a completely safe thing to do to see how you might respond while on a statin. Uh, but it's it's certainly not a slam dunk in terms of uh mitigating those effects. And again, these this that research looks at short-term effects. You're put on a statin, you're also put on coQ10 two months later. How you know what are your muscle symptoms compared to those who get the statin without coQ10? And so that that's what most of these randomized trials have looked at. They tend to be short-term. So um it's a it's an interesting topic, right, John? Only because so many people take these meds. These are the same people who are at risk of sarcopenia and and uh the same people that have disrupted metabolic health. So this is again an example of the many shades of gray that this topic presents itself with. Yeah. I will not be framed uh in that way generally with the prescriber.

Lipid Quality, Insulin, And Inflammation

SPEAKER_01 21:27

Yeah, you know what's what's great. Thank you for that that overview. I it was awesome. Uh, you know, especially the pharma, you know, genetic component to that, which is like I mentioned earlier, it's what people often refer to as well, that's where you're gonna run in possibly you're gonna run into issues with statins. But you know, I I think you have to look at this as we're we're taking a just yet a different angle or perspective to the broader topic, which is lipid management, the different ways to manage the different. Types of lipids and where is the where's the greatest value for you know for managing lipids? Is it total cholesterol? And I think that's what I would come back to this with. The question is, well, we know that these statins can have some modest benefit, but I would say, Mark, that more of that is probably the like the modest anti-inflammatory benefits that that a patient would get from using a statin, especially something like Crestor. You know, there's an anti-inflammatory component there that I think is where the benefit comes into play as opposed to the lipid lowering or cholesterol lowering effect. And I, you know, when I when I think about cholesterol, you know, again, you and I talk about this all the time. I don't, I never look at like the total cholesterol as being a an a core component to the discussion about what has to be managed, right? I I think it's the way the cholesterol is packaged by the body. Like I think, you know, this would hopefully for our listeners help clarify some of this. And the body is going to package that cholesterol into one of several different types of packages. And and the one we're trying to we're trying to avoid are the really small, dense packages. And in in as you and I always talk about, that's that's more of a function of the quality of carbohydrates in a person's diet, their insulin levels, right? I mean, and if you can produce a shift with respect to lipid metabolism, if you can, that cholesterol in the body, if you can make it of a different, like qualitatively a different package, that, in my opinion, Mark, is that's where the greatest efficacy is in treatment. So, what can we do to make the LDL packaged in these large buoyant versions as opposed to these small dents? And I don't, you know, statins, to my understanding, I haven't seen a study that has shown that statins change things on that qualitative level. And statins, you know, they lower you know serum cholesterol levels, but they're not really changing per se what the liver's doing with you know all of the different versions of cholesterol that it's that it's attempting to package. So, you know, that would be an important question I would have. I I don't know if we can answer it yet, but is there any shift towards larger, buoyant, more type A LDL molecules with statin use? And I haven't seen anything show that. And I think that's really where the that's where the gold is, so to speak, with lipid management. It's just changing the qualities of those as opposed to taking this quantitative approach where we're treating all we're treating all LDLs equivalently. And it's just, and then the other question I had for you, Mark, is well, I don't know if we have an answer for this one, but you know, the the newer generation cholesterol-managing drugs like Rapatha, right, that are working on a different mechanism, but have been we've been told that they're much safer, much fewer downsides. I just don't know if, you know, do we know that yet? You know, how will that affect muscle strength, muscle mass with you know this type of a with this type of uh analysis? I don't I don't know that we have those that data, right?

SPEAKER_00 25:18

I'm unaware of that data being out there, John. I certainly think of statins as just wholesale uh uh uh inhibitors of of cholesterol production and all its various packaged uh uh formats. And and that is important because, yes, it it is very effective at lowering LDL. Uh it it it'll manifest as reduction in the number of LDL particles, uh, which is you know an important, uh it'll reduce APOB, which is certainly an important biomarker and uh and a uh uh kind of a surrogate for small dense LDL. Um but it also reduces HDL cholesterol, uh, which I you know people people often think of as the good cholesterol. Uh and I'm unaware of any data suggesting that you'll see a shift as part of those mechanisms from small dense to the more large buoyant um uh LDL patterns.

SPEAKER_01 26:32

So that's all it's always been explained to me by by researchers that that really is a function of insulin more than anything else.

PCSK9 Inhibitors And Open Questions

SPEAKER_00 26:41

Yes. And that's and that's certainly what you see in um low carb, very low carb, ketogenic nutritional interventions is is not only will you see a reduction, usually in LDL, yes, a small percentage may their LDL might go up uh because eating more fat is just central to a ketogenic, low carb, very low carb plan. But what you see is obviously a dramatic drop in triglycerides, increases in HDL, that, as we talk about all the time, John, are very associated with better cardiovascular outcomes. And then you will tend to see, regardless of the LDL level, a shift uh from the small dense um particles to larger, less atherogenic particles. And so there you're getting a global reduction. Um in if we add uh you know a HOMA insulin score to that, uh, you know, an A1C, you could take blood pressure, you could take any cardiometabolic measure and generally see significant improvements. So one intervention is giving you global improvement, another is focusing on one isolated variable. And you know, I've come to just uh realize that you know there is a point beyond which what has been published, John, for many will lead to the conclusion that anything you do to lower LDL, regardless of the mechanism, regardless of what might be other unintentional consequences, uh, and there is some research suggesting we've looked at this, John. People can go back and look at some of the papers we've reviewed looking at insulin resistance, which tends to go up with statin use. Uh, you know, we're talking about muscle function. Uh so it um I think the school of thought around anything that lowers LDL is is worth doing no matter what, uh, will continue to be the case in the traditional, certainly cardiology community, and uh for those that sort of um accept um what have been guidelines that haven't changed much in in many, many years. So uh, you know, whether whether uh that's the right thing to do or not, uh, you know, uh people have to just really understand their unique risks and and hopefully have a relationship with someone they trust to help them sort of quantify that risk-benefit analysis. I think Rapatha, uh, you know, which which for those that may not be familiar, these PSK9 and inhibitors, you know, they they tend to affect the removal of LDL, while statins affect the production of cholesterol and LDL. Uh Rappatha enhances the clearance or the elimination. And um so if someone, and again, this is in my opinion, John, if somebody is looking at secondary prevention, maybe they're intolerant of a statin. Um Rapatha, if nothing more, then lowering LDL particle number, small dense LDL particle number uh would would be the rationale for that. You know, that the the research that's been published would suggest some benefit in reducing events. Um, but mortality is not one of those events that I've seen. And so I do think it there is this, there's still this tendency to just get caught up in LDL and uh lower is better under any circumstance.

SPEAKER_01 30:46

And you know, we've talked about we've we've talked about papers and we've you know we've shared them, especially the more recent ones that were been published in the BMJ. Really large, large numbers, again, of participants, UK biobank data. You know, people over the age of 55, if they have a an LDL of 130, uh, they live longer than those who have an LDL of 100. I mean, that's been really you know well reported, those studies. Uh you know, I you're hundreds of thousands of participants now. And there's three to you know, three or four studies that would, again, would make this this this approach, this notion that LDLs can't be too low. They they would make a clinician really question that if they look closely at those papers. But for whatever reason, Mark, it's hard to explain the the dogma around cholesterol and not and also you know, forget the LDL conversation. We I think a lot of people need to be better versed in understanding the difference between cholesterol-sulfate, which is formed when we're out in full spectrum light, and we get that sulfation taking place with UVB light. It's a very different version of cholesterol than the non-sulfated version. And, you know, I think that you look at the differences in everything from immune function and the role that cholesterol-sulfate plays in that, differences in heart disease as you get to more equatorial regions where people are outside in the sun more. But again, this is this is somewhat theoretical. We have these associations, and there have been other, you know, researchers have put this link between sunlight, cholesterol sulfate, and how various you know, systems, organ systems function much more ideally with cholesterol sulfate and how it's far less athrogenic. The liver does very different things with it. But um, there's just so many layers to this that at this point in time, with you know, several decades of research and looking at the effects of statin use and then trying to you know better appreciate some of this you know, biobank data from the UK and and European studies, which has now been done with the Dutch. It's not just, you know, it's not just the UK, there are other populations, European, albeit you know limited to European populations, but they're showing that lower LDLs, you know, to your point, that people aren't they're not necessarily benefiting, they could be at a greater risk for all-cause mortality, just because of how important it is for not only muscle function and maintaining muscle mass, but also for the immune function. I mean, our body needs cholesterol and it needs a significant amount of it to be available as part of a normal immune function, as part of a normal, you know, phospholipid bilayer, mitochondrial membrane. It's it's just it's ubiquitous in terms of where it's needed and having an ample amount of it is if it's not there, there's gonna be a downside.

Lifestyle Levers That Shift Risk

SPEAKER_00 33:48

Yeah, I mean, that is a holistic biopathy perspective, John. I I'm sometimes intrigued by how uh much we lose that perspective when we really get honed down on one particular molecule or family of molecules. Uh, it there's no biologist worth their salt that that wouldn't be quick to acknowledge. Cholesterol is one of the most important molecules in human biology. And uh LDL is an important uh immune um um uh tool, an immune sort of messenger. Uh and and you touched on a bit ago, John, about the importance of inflammation and and statins have non-LDL lowering effects on inflammation. And might that be uh more of a meaningful target? Uh, you know, a study done some time ago, I think it was done at the Brigham and Women's Hospital in Boston, the Jupiter trial, yeah. When um uh Rosuvastatin crestor was coming to market, uh they looked at these were individuals that had a pretty high burden of cardiovascular disease. So this was secondary prevention. And the greatest effect that those taking resuvastatin had were those that had a high high CRP associated with that higher LDL. You did not see the same degree of cardiovascular protection with a similar LDL level, and those that had a normal CRP. That was a really fascinating study, and it got a lot of attention back then. But it it it it does, I often look back on that trial, John, as one of the early indications of the importance of inflammation. And I think you and I would agree that inflammation and insulin resistance are like, you know, they're they're bound at the hips.

SPEAKER_01 35:53

Yeah, absolutely.

SPEAKER_00 35:54

Uh, if the focus is more on that, um, you're likely to be getting more to the root cause. And certainly a higher LDL can be seen with greater burdens of inflammation as LDL responds to whatever that inflammatory insult might might be. And so um anti-inflammatory principles that we talk about all the time, be it nutritional movement, full spectrum light, right, mind-body techniques, um uh anything you can do to lower insulin and inflammation, independent of LDL, is likely where I think the research would suggest you're gonna get the biggest bang for the buck. Uh, and when you can do those things through lifestyle, you're not you're not looking at myopathy. You're not, you don't have to ask the question, is you know, how strong am I going to be 10 years from now? Uh I'm really happy that my LDL is 50, uh down from 160. Uh, you know, my every doctor I know thinks I'm like the best person on the on the planet, uh only to you know confront very significant quality of life and possibly metabolic disruptive issues on the road. So it is, I don't know how far we've come, John. I I think that the the average consumer does seem so much more skeptical. Uh you know, if the the you know, not to get too into the rabbit hole, but the pandemic, I think, you know, uh uh created a lot of distrust around medical establishment and you know, these authoritative uh structures, people, the you know, the the the the uh organizations, and and I think more people are just skeptical now and uh discerning. And I I applaud that. To me, that that's the that's the signpost that people are beginning to say, you know what, there's more to this story. And um uh and and that's ultimately where the truth is revealed, right? It's in your own experience. Uh you want to be informed, surely. Um but uh get as many perspectives as you can because it uh yeah, we're still pretty locked into this LDL paradigm. And and for some, that again, that you know it's it's worth paying attention to, but for the majority, uh I think it's it continues to be overstated in my head.

Practical Guidance And Closing Notes

SPEAKER_01 38:36

Mark, one of the best pieces of advice is that you ever gave me when we first met was you said, John, question everything. And I and I do, uh, and I think people are in general doing that more. And then I add to that question everything, and if it doesn't make sense biologically, I think you need to question it the second and third time as well. You know, that then then the deep dive, at least that's what I do. I if something like lowering cholesterol in the body, you know, again, just shutting off production of one of the most biologically important molecules for overall health, it just biologically doesn't make sense. And you know, to the point that you made about insulin and inflammation, and if we add the infection burden to that, those three eyes, insulin, inflammation, and infection, and usually two of those three are tied together. If we focused on those, I I it wouldn't be, you know, again, it wouldn't be even remotely comparable the results you would produce in terms of risk reduction as opposed to this, you know, lipid lowering. And it's really just a theory, the the lipid, it's just a theory at this point, but people think it's it's established. It's it's it's very theoretical. And that's why, you know, as you mentioned earlier, you don't really see the you don't see the significant reduction in all-cause mortality. You don't really see even some of the benefits to these lipid lowering events with cardiac events. Some of the studies really, you know, don't show any results there as well. So I I think it's a fascinating topic. And I am also, I'll I like to end on a positive note. I'm also encouraged by the number of people who question statin use, who now understand seed oils have their downsides, even though they get that, you know, the heart endorsement on them, right? I you know, there's some really encouraging signs uh where people are a little more conscious and are making empowered decisions.

SPEAKER_00 40:41

Yeah, I I I think that's a great, a great note to to close on, John. And uh just you know, for those, if you're taking a statin and you've been on it for a while, please don't just stop it. Some some medications should not be just discontinued. Uh but if you're if you're on a statin and you've had muscle symptoms or or you know, if you just get a simple hand grip and work on that, um, you know, if you if you start just feel yourself dropping off the curve in terms of your strength and and and your your muscle mass, that's really uh good conversation to have with your provider. What might the alternatives be? Um really important to be getting enough protein, right? It it again, if you're sort of committed and on a long-term course of statins, we know that, and again, giant, we we talk about this all the time, but getting some resistance work a couple days a week, making sure you're getting sufficient protein, things that you can do to support your muscle mass and metabolic health, um, you know, at least a gram and a half. Yeah.

SPEAKER_01 41:51

Maybe more.

SPEAKER_00 41:52

Maybe more per day, and maybe more, right? Closer to two. Uh, so you know, be be generous with the protein throughout the day, get more resistance work, get get more sunlight to sulfate your cholesterol. Uh, and you know, that's a good thing to be doing under any circumstance. But in in particular, if you're on a statin, anything you can do to really help your muscles uh is going to be critical because it it's it would seem clear that many will have disruptions down the road with this. So um great topic. Uh yeah, thank you, Mark. It was awesome. Thank you. We will put um uh some of the references that we've noted in the slide deck, all of this can be found on our website, um the health edge podcast.com. And John, until we uh connect again, great to see you.

SPEAKER_01 42:50

You as well, buddy. See you next week.

SPEAKER_00 42:52

Take care.