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Barbell Medicine Podcast

Menopause Part 3: Body Composition, Bone, Brain, & the Fitness Changes (The Data vs the Influencers)

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<p>Most women in 2026 are told menopause affects everything, the weight, the belly fat, the bones, the heart, the brain, and that the fix is hormones, supplements, and a proprietary protocol. The data tell a different story. Menopause does some of it, but not all of it.</p><p><br></p><p>In this episode, Dr. Jordan Feigenbaum and Dr. Austin Baraki, with OB-GYN Dr. Loraine Baraki at the clinical handoffs, put real numbers on what menopause actually changes, e.g. body composition, the cardiometabolic shift around the final menstrual period, bone, cognition and sleep — and on the single biggest modifiable lever against what actually kills postmenopausal women.</p><p><br></p><p>This is Episode 3 of Barbell Medicine's four-part menopause series.</p><p><br></p><p>Timestamps:</p><ul><li>01:23 Intro </li><li>02:45 Body composition & the SWAN study </li><li>04:16 How much weight gain is really menopause?</li><li> The answer: about 1.5 kg Subcutaneous vs visceral fat</li><li> Why waist beats weight (and body-fat %) </li><li>17:21 Does menopause crash your metabolism? Clinic: MHT for body composition </li><li>23:51 Dr. Loraine Baraki — MHT, weight & testosterone </li><li>27:29 The cardiometabolic shift: cholesterol at the FMP </li><li>30:18 Insulin resistance & metabolic syndrome </li><li>33:12 Blood pressure & 10-year heart risk </li><li>34:54 Clinic: the "estrogen crisis" lipid panic </li><li>39:13 Bone: the advice vs the data Why DXA misses most fractures </li><li>41:24 LIFTMOR: lifting heavy with low bone density </li><li>44:47 The LIFTMOR results </li><li>46:53 Lifting vs Pilates, and falls </li><li>52:17 Clinic: "Should I be deadlifting?" </li><li>56:14 Cognition & brain fog </li><li>57:50 Why brain fog is mostly a sleep problem </li><li>59:17 Clinic: brain fog, night sweats, broken sleep </li><li>1:03:06 Depression & dementia in midlife </li><li>1:05:43 Does hormone therapy protect the brain? </li><li>1:08:53 Clinic: "Am I getting early dementia?" </li><li>1:13:19 Dr. Loraine Baraki — the timing hypothesis & the brain</li><li>1:16:15 What actually kills postmenopausal women </li><li>1:17:31 Fitness: the biggest mortality lever </li><li>1:20:21 Strength, power & grip </li><li>1:25:15 Clinic: where to start when you're overwhelmed </li><li>1:30:41 The detraining problem </li><li>1:32:38 Trained vs untrained: what's recoverable </li><li>1:34:53 The actual plan </li><li>1:39:48 Takeaways</li></ul><p><br></p><p>Resources:</p><p><br></p><p>Subscribe to BBM Plus for the full unabridged Direct Line: barbellmedicine.supercast.com/</p><p&… Medicine coaching and templates: barbellmedicine.com/</p><p><br&… book pre-order: barbellmedicine.com/shop/learning/signal/</… composition & metabolism</p><p><br></p><p> Greendale et al., SWAN body composition, JCI Insight 2019: <a href="doi.org/10.1172/jci.insight.124865"; rel="nofollow">doi.org/10.1172/jci.insight.124865</a>&l…; Lovejoy et al., visceral fat across the transition, Int J Obes 2008: <a href="doi.org/10.1038/ijo.2008.25"; rel="nofollow">doi.org/10.1038/ijo.2008.25</a></p>…; Pontzer et al., daily energy expenditure across life, Science 2021: <a href="doi.org/10.1126/science.abe5017"; rel="nofollow">doi.org/10.1126/science.abe5017</a></…; Karppinen et al., metabolism in midlife women, Eur J Prev Cardiol 2023: <a href="doi.org/10.1093/eurjpc/zwad177"; rel="nofollow">doi.org/10.1093/eurjpc/zwad177</a></p… et al., lipid changes & the menopause transition, JACC 2009: <a href="doi.org/10.1016/j.jacc.2009.10.009"; rel="nofollow">doi.org/10.1016/j.jacc.2009.10.009</a>&l… et al., menopause & metabolic syndrome (SWAN), Arch Intern Med 2008: <a href="doi.org/10.1001/archinte.168.14.1568"; rel="nofollow">doi.org/10.1001/archinte.168.14.1568</a>…; El Khoudary et al., AHA Scientific Statement on midlife women, Circulation 2020: <a href="doi.org/10.1161/CIR.0000000000000912"; rel="nofollow">doi.org/10.1161/CIR.0000000000000912</a>… et al., SWAN bone loss across the FMP, JBMR 2012: <a href="doi.org/10.1002/jbmr.534"; rel="nofollow">doi.org/10.1002/jbmr.534</a></p>&l…; Siris et al., undiagnosed low BMD & fractures (NORA), JAMA 2001: <a href="doi.org/10.1001/jama.286.22.2815"; rel="nofollow">doi.org/10.1001/jama.286.22.2815</a><…; Watson et al., LIFTMOR, JBMR 2018: <a href="doi.org/10.1002/jbmr.3284"; rel="nofollow">doi.org/10.1002/jbmr.3284</a></p>&… et al., EFOPS 16-year, Menopause 2017: <a href="doi.org/10.1097/GME.0000000000000720"; rel="nofollow">doi.org/10.1097/GME.0000000000000720</a>… et al., MEDEX-OP, JBMR 2021: <a href="doi.org/10.1002/jbmr.4334"; rel="nofollow">doi.org/10.1002/jbmr.4334</a></p>&…; Sherrington et al., exercise for preventing falls, Cochrane 2019: <a href="doi.org/10.1002/14651858.CD012424.pub2"; rel="nofollow">doi.org/10.1002/14651858.CD012424.pub2</a&g… Position Stand: Osteoporosis and Exercise, Med Sci Sports Exerc 1995;27(4):i–vii (no DOI)</p><p><br></p><p><br></p><p>Cognition & mood</p><p><br></p><p><br></p><p>Greendale et al., SWAN cognition, Neurology 2009: <a href="doi.org/10.1212/WNL.0b013e3181a71193"; rel="nofollow">doi.org/10.1212/WNL.0b013e3181a71193</a>… et al., sleep in midlife women, Obstet Gynecol Clin North Am 2018: <a href="doi.org/10.1016/j.ogc.2018.07.008"; rel="nofollow">doi.org/10.1016/j.ogc.2018.07.008</a><… et al., Harvard Study of Moods and Cycles, Arch Gen Psychiatry 2006: <a href="doi.org/10.1001/archpsyc.63.4.385"; rel="nofollow">doi.org/10.1001/archpsyc.63.4.385</a><… & Kravitz, mood and menopause (SWAN), Obstet Gynecol Clin North Am 2011: <a href="doi.org/10.1016/j.ogc.2011.05.011"; rel="nofollow">doi.org/10.1016/j.ogc.2011.05.011</a><… et al., Lancet Commission on dementia 2024: <a href="doi.org/10.1016/S0140-6736(24)01296-0" rel="nofollow">doi.org/10.1016/S0140-6736(24)01296-0</a></p><p><br></p><p><br></p><p>Shumaker et al., WHIMS (estrogen+progestin & dementia), JAMA 2003: <a href="doi.org/10.1001/jama.289.20.2651"; rel="nofollow">doi.org/10.1001/jama.289.20.2651</a><…; Espeland et al., WHIMS (estrogen-alone & cognition), JAMA 2004: <a href="doi.org/10.1001/jama.291.24.2959"; rel="nofollow">doi.org/10.1001/jama.291.24.2959</a><… et al., KEEPS-Cog, PLoS Med 2015: <a href="doi.org/10.1371/journal.pmed.1001833"; rel="nofollow">doi.org/10.1371/journal.pmed.1001833</a>…; Henderson et al., ELITE (timing hypothesis & cognition), Neurology 2016: <a href="doi.org/10.1212/WNL.0000000000002980"; rel="nofollow">doi.org/10.1212/WNL.0000000000002980</a>…, hormone therapy for primary prevention, JAMA 2022: <a href="doi.org/10.1001/jama.2022.18625"; rel="nofollow">doi.org/10.1001/jama.2022.18625</a></… & mortality</p><p><br></p><p> Mandsager et al., cardiorespiratory fitness & mortality, JAMA Netw Open 2018: <a href="doi.org/10.1001/jamanetworkopen.2018.3605"; …

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[SPEAKER_01]: Last episode, we walked through 2,000 years of people in positions of power, mostly men, telling women to hold back when it came to exercise. [SPEAKER_01]: And the moment that the science finally corrected the record, today we pick up where that left off. [SPEAKER_01]: What does men upause actually do to a woman's body?

[SPEAKER_01]: Now most women in 2026 are getting told that it does everything. [SPEAKER_01]: The weight, the belly fat, the bones, the heart, the brain, the fix is hormones, supplements, and obviously a proprietary protocol. [SPEAKER_01]: The data tells another story. [SPEAKER_01]: Menopause does some of it, for sure.

[SPEAKER_01]: But there are a lot of other factors in play, such as decades of detraining, imperceptible changes in eating habits, and age-related differences too. [SPEAKER_01]: Today, we put numbers on the difference. [SPEAKER_01]: The body composition, the cardiometabolic shift around the final menstrual period, what happens to bone, cognition, and sleep, and the biggest tool that we have to fight against what actually kills postmenopausal women, which is in a hormone.

[SPEAKER_01]: Now, by the end of this podcast, the woman from last week, the one at the Dumbbell Rack, holding the five pounders, she'll have a much clearer picture of what changed because of menopause, what didn't, and what she can do about both. [SPEAKER_01]: I'm Dr. Jordan Fuygenbaum, and this is the Barbell Medicine podcast.

[SPEAKER_01]: And to help us walk through why 50 years of clinical advice told women not to lift heavy, what men upholst actually does to your body composition and your brain, and the single lever that drops mortality more than any pill on the market, it's the second most handsome doctor in North America, Dr. Austin Baraki, what's going on, man?

[SPEAKER_01]: Hello. [SPEAKER_00]: I'm feeling good. [SPEAKER_00]: This is a broad topic that we're tackling over the course of many weeks and again, happy to help dive into it with the assistance of my better half once again. [SPEAKER_01]: That's right. [SPEAKER_01]: And speaking of, if you're new to the show, two things, one, this is Barbell Medicine.

[SPEAKER_01]: We are physicians who've been in the health and fitness space for almost 20 years now, which is scary to say. [SPEAKER_01]: We try to translate clinical research in the language that a non-clinician can use as well as, uh, you know, serve our clinicians in the audience. [SPEAKER_01]: But number two, this is episode three of our menopause series episode one walked through the transition itself and the 20 plus year correction on hormone therapy.

[SPEAKER_01]: Episode two covered the history and today we talk about what actually changes during menopause. [SPEAKER_01]: on the next episode episode four, that'll be lifestyle and training prescription, what to actually do. [SPEAKER_01]: Each episode does stand alone, but if you have time, maybe pause this one, go back to episode one.

[SPEAKER_01]: All right, Dr. Barack, let's start out with body composition, and we'll begin with the question that women probably hear about most frequently, what menopause does to body composition. [SPEAKER_01]: They've probably heard all sorts of numbers thrown around and you have to, but the actual study that gives answers to this question, most carefully, is the swan body composition study.

[SPEAKER_01]: And I think the answer, it gives is different from what most women have been told. [SPEAKER_01]: So swan is an acronym and it stands for the study of women's health across the nation. [SPEAKER_01]: This is a prospective group of about 3,000 women across seven different sites in the United States.

[SPEAKER_01]: and they were followed yearly with serial dexus scans, which stands for dual energy x-ray absurdometry, which is basically a fancy way of saying x-ray technology to tell you different body composition levels and they did that for over 10 years. [SPEAKER_01]: So this is from UCLA, Greendale and colleagues and they published their analysis in 2019.

[SPEAKER_01]: If menopause itself were the primary reason that women gained weight in the middle and during midlife, you'd expect body fat to start piling on quickly when the transition hits. [SPEAKER_01]: You'd expect it to keep piling on across the postmenopausal years and account for most of what a woman gains between ages 40 and 60.

[SPEAKER_01]: Now, the swan data shows something different, menopause does add something to this curve, but it's more of a small bump on top of a much larger trend that's more about aging and behavior across these years and across several decades, several decades. [SPEAKER_01]: So, Austin, before I give the answer to what this study found, [SPEAKER_01]: Imagine this, a patient walks in, she's 51, very menopausal, and she's gained eight kilos over the last six years.

[SPEAKER_01]: Her menopause coach that she found on Instagram tells her that this is hormonal, that estrogen and progesterone changes are the reason and that the only fix is menopausal hormonal therapy plus a proprietary supplement stack, predict for me, going in, what proportion of her eight [SPEAKER_00]: Yeah, it's an interesting question because there are two ways of looking at it.

[SPEAKER_00]: One is how much of this weight gain is directly attributable to any degree of hormonal decline, or if you wanted to take the extreme stance like estrogen deficiency. [SPEAKER_00]: So to speak, because that could be evaluated, that could be tested. [SPEAKER_00]: And if true, then replacement or delivering, giving the woman that hormone back.

[SPEAKER_00]: should either reverse that trend or should mitigate it from happening in the first place. [SPEAKER_00]: So that is in fact a testable hypothesis. [SPEAKER_00]: The other way to look at it, and this is the I suppose more charitable way, and if I were the person making those kind of claims, I might pivot and make the claim in this way to say, well, a lot of the changes that happen around midlife lead to a lot of unpleasant symptoms, and those unpleasant symptoms can then lead to a cascade of downstream consequences.

[SPEAKER_00]: So for example, having [SPEAKER_00]: You know, hot flashes can make it really unpleasant to stay as active to be outside to be doing things throughout the year. [SPEAKER_00]: The night sweats can disrupt your sleep, make it more difficult to recover, can make you feel terrible, and have less energy and motivation to do the physical activity, might increase appetite, things like that.

[SPEAKER_00]: So there's a lot of indirect, plausible indirect ways that there could be some impact here. [SPEAKER_00]: But I think that if the question was, this is, if she's saying purely directly hormonal and the way we reverse it as by giving the hormones back, that is, to my understanding, not well-supported by current evidence looking at this as far as the direct impact of the hormonal decline throughout the menopausal transition on total body weight gain, total body fat gain.

[SPEAKER_01]: Yeah, I think you hedged that appropriately with the general thing. [SPEAKER_01]: So to me, there's really three predictions here, possible. [SPEAKER_01]: One would be if it's purely hormonal, you would predict, well, look, none of this is, or a very small fraction of it's going to be related to the changes in hormones.

[SPEAKER_01]: If it's indirect, you're allowing for a greater proportion of that. [SPEAKER_01]: And then the third one would be effectively, [SPEAKER_01]: because the indirect changes are so large. [SPEAKER_01]: And cause all of these downstream behaviors and experiences and symptoms, whatever, then all of it is actually related to menopause.

[SPEAKER_01]: So you can't be wrong if you hedged it three different ways. [SPEAKER_01]: There you go. [SPEAKER_01]: Yeah. [SPEAKER_01]: All right, well, here is what Greendale found. [SPEAKER_01]: The rate of fat gain doubled during the perimenopausal transition. [SPEAKER_01]: A typical woman was gaining about a quarter kilogram a year before the transition, and that went up to about half a kilogram a year during it.

[SPEAKER_01]: The pattern held across every different ethnic group that swan tracked. [SPEAKER_01]: The doubling lasted for about three and a half years, basically the window around the final menstrual period, and then the rate slowed back down. [SPEAKER_01]: So that totals about [SPEAKER_01]: across three and a half years.

[SPEAKER_01]: That's what menopause itself does to body composition for the average woman. [SPEAKER_01]: Based on the best study that we have with thousands of women followed across their actual menopause transition. [SPEAKER_01]: Now, if you compare that against the actual midlife, weight, curve, or weight trajectory, [SPEAKER_01]: Well, the average U.S. woman gains 10 to 15 kilograms of total weight between ages 30 and age 60.

[SPEAKER_01]: The Perry menopausal acceleration accounts for 1.5 kilograms of that on average. [SPEAKER_01]: Whereas the other eight to 13 kilograms result from the interaction of aging, behavior, sleep, reduced activity and dietary patterns that sort of predate and outlast the transition. [SPEAKER_01]: So you weren't wrong [SPEAKER_01]: But I think the next question is, where does the fat go, right?

[SPEAKER_01]: And subcutaneous fat, this is the fat that's primarily under the skin you can pinch it. [SPEAKER_01]: It's generally less metabolicly active. [SPEAKER_01]: And so you can think of it as sort of maybe cosmetically something that you don't want to see. [SPEAKER_01]: But I would view this as maybe the safest kind of body fat.

[SPEAKER_01]: Agreed. [SPEAKER_01]: This real fat is the fat that is packed around your internal abdominal organs. [SPEAKER_01]: This is more metabolically active and more strongly linked to disease. [SPEAKER_01]: Telling the two apart requires a CT scan because you can't really pinch your visceral at a post tissue.

[SPEAKER_01]: Sometimes this is called belly fat, but even that can be misconstrued where you have some subcutaneous belly fat, and this is deeper. [SPEAKER_01]: Again, you can't really see it. [SPEAKER_01]: And so you use a CT, usually at the level of the lower spine, which can measure each kind of fat separately.

[SPEAKER_01]: So this study was run by love joy and colleagues at Pennington Biomedical in Louisiana. [SPEAKER_01]: They took 156 women in their 40s and 50s and followed them yearly for four years with cereal, dexa, again, that's at X-ray technology, and abdominal CT scans. [SPEAKER_01]: 38 of the women transitioned to postmenopause during the follow-up and the remaining women [SPEAKER_01]: what they found.

[SPEAKER_01]: Only the women who became postmenopausal saw a significant rise in visceral fat on the order of 40% over the years around their final menstrual period. [SPEAKER_01]: The premenopausal throughout group, those who didn't transition, did not show a comparable visceral fat increase whereas the transition or group, that was 38 women, [SPEAKER_01]: So the sample size is relatively modest, but again, they found that they had an increase in this real fat and this has been replicated in other studies with similar directional results.

[SPEAKER_01]: Now, I said earlier that subcutaneous fat, the fat you can pinch is probably the safest kind of fat. [SPEAKER_01]: This real fat, again, you can't pinch this, is associated with worse cardio metabolic outcomes, which is the fancy way of saying stuff related to your heart, related to how you process sugar in your blood and things like that.

[SPEAKER_01]: And it is, to my mind, the second most dangerous type of fat. [SPEAKER_01]: The first most dangerous fat is upstream. [SPEAKER_01]: in the liver. [SPEAKER_01]: And so the way I think about this is that if you're liver, which is not supposed to have much fat in it, gets full of fat, that spills over into the visceral fat compartment again, packed around your organs.

[SPEAKER_01]: And if that gets full, it can go elsewhere to your muscles for example, and get a deposit of there. [SPEAKER_01]: And then so those to me are the top three, like most dangerous types of fat you can have. [SPEAKER_01]: And then finally, in a distant fourth is subcutaneous fat. [SPEAKER_01]: Um, that's my current understanding of how this thing works and each of these sort of ectopic depots or storage sites, liver, visceral, intra-muscular, all contribute to insulin resistance and subsequently cardiometabolic disease.

[SPEAKER_01]: For our purposes, the practical point is that the kind of fat menopause ads is on the wrong side or the dangerous side of that overflow pattern. [SPEAKER_01]: We discussed this more in our article and podcast on why your waste matters more than your weight, the signs of visceral fat, and those are all linked in the description.

[SPEAKER_01]: But one interesting thing here is that you might not be able to pick this up with just a waste circumference test. [SPEAKER_01]: While waste circumference is reliably correlated to visceral adipose tissue, it's still a crude measurement. [SPEAKER_01]: And that's really the problem here.

[SPEAKER_01]: I think the R value, which basically tells you how well these things are correlated where like an R value of 1 would be a perfect correlation. [SPEAKER_01]: I think it's in the mid-7's, like, 0.77 or something. [SPEAKER_01]: So it's pretty good, but if we're just talking about, like, a couple hundred grams of change or, you know, less than that, your waste or comforts may not actually change where this can actually increase visceral fact can actually increase which can be problematic.

[SPEAKER_01]: Austin, is that something that you are actively measuring? [SPEAKER_01]: Are you sending people for CTs or DEX scans to check yourself? [SPEAKER_00]: Yeah, I mean, I just had this conversation actually with a woman yesterday because we're in a wait management context. [SPEAKER_00]: We're in the Perry Menopausal stage of life and her first question was, [SPEAKER_00]: You know, what do you think my target weight should be?

[SPEAKER_00]: And she's been tracking her body fat percentage on these types of body composition scans. [SPEAKER_00]: What do you think my body fat composite percent should be? [SPEAKER_00]: And so I essentially, you know, had this whole conversation where I said, well, [SPEAKER_00]: If the big picture goal here is, you know, optimizing your health.

[SPEAKER_00]: We're thinking about health consequences and preventing complications down the line. [SPEAKER_00]: We have a wide variety of different measures and tests and things like that that we can use. [SPEAKER_00]: And your absolute body weight. [SPEAKER_00]: not the most useful number to me. [SPEAKER_00]: There might be a range of healthy weights where you could be, but of course you can have different compositions.

[SPEAKER_00]: Even body fat percent does not tell me a whole time, because it doesn't tell me where is that body fat? [SPEAKER_00]: Is it around the hips and legs? [SPEAKER_00]: Subcutaneous compartments generally healthy or quote unquote? [SPEAKER_00]: Or is it in the abdomen in the visceral compartment, a little bit less healthy, or the much more concerning that site?

[SPEAKER_00]: And so then I said, [SPEAKER_00]: You know, she's been expressing some concerns because getting these body composition scans required like a fair amount of travel for where she lived. [SPEAKER_00]: They were expensive and so I said, well, a waste measurement is not going to be a perfect way to assess this, but it'll get as much closer.

[SPEAKER_00]: And so I would track a waste measurement and set a waste measurement target for you. [SPEAKER_00]: before I ever thought about setting a body fat percentage target for you or a single body weight target for you. [SPEAKER_00]: I think that those are progressively less useful for predicting your health outcomes.

[SPEAKER_00]: And so, you know, if the waste measurement was around 34 inches for this, you know, for this particular patient, maybe aiming for a 31 inch waste measurement. [SPEAKER_00]: I would at least feel more confident that we have substantially reduced her visceral fat if that change were to take place.

[SPEAKER_00]: Is it quite as good as maybe deliberately quantitating all of the visceral fat? [SPEAKER_00]: No, but I also don't routinely do that in practice either. [SPEAKER_00]: I use a set of other measures. [SPEAKER_00]: So one could be waste measurement. [SPEAKER_00]: The other could be other markers that would be reflective of the consequences of visceral fat.

[SPEAKER_00]: So what is the lipid panel look like? [SPEAKER_00]: What are the triglycerides look like? [SPEAKER_00]: What is the glucose look like? [SPEAKER_00]: A1C or other markers of insulin resistance? [SPEAKER_00]: Because if I see all of those things present, it's almost a safe assumption that there is some degree of visceral fat liver fat muscle fat contributing to those things.

[SPEAKER_00]: Whereas if all those things look fantastic, blood pressure, blood lipids, insulin sensitivity, or fantastic waste measurement is where I want it to be, there's really not too much more use of quantitating somebody's visceral fat with a CT scan. [SPEAKER_00]: And in fact, there's a downside of, hey, we're going to radiate you to tell me like, hey, you're actually don't have that much visceral fat.

[SPEAKER_00]: We're doing great. [SPEAKER_00]: So, [SPEAKER_01]: Yeah, yeah, the middle seabirds are kind of not worth it. [SPEAKER_01]: Exactly. [SPEAKER_01]: I had the same conversation with a man, same thing, he asked me, you know, what should I target weight be? [SPEAKER_01]: And, you know, I said, well, look, I'm happy to provide you with the target weight, but I have to also tell you, it's maybe the least useful information, because it doesn't tell me about your body fat, what kind it is, and where it's located.

[SPEAKER_01]: And so I started thinking about this hierarchy of like, [SPEAKER_01]: Maybe medical metrics that we can use here. [SPEAKER_01]: Weight is probably the least useful. [SPEAKER_01]: Yes. [SPEAKER_01]: EMI comes right after that, because it does now, it gets, okay, to height. [SPEAKER_01]: And we have some pretty good evidence for most groups of people that once you're above 30, that tends to be associated with caring too much body fat, which certainly includes liver, this real adipose tissue, and the muscle.

[SPEAKER_01]: But it's not perfect. [SPEAKER_01]: Okay, and so then you can have like a waste or conference and like, okay, we're getting better a body fat test depending on what kind of body fat test if it's it's it's it's not great, but like if it tells you how much body fat someone's carrying and where they carry it, I fear yes, yeah agree and so then finally you get to like, yeah, we got a whole body CT and now we know where everything's that.

[SPEAKER_00]: Well, I think that that's also where, you know, you've done an episode before on that body roundness index. [SPEAKER_00]: And I think that it's trying to take these like, you know, non-radiation involving non-invasive measures and try to turn them into some higher fidelity kind of version of the waste measurement that can maybe capture some of that a bit better.

[SPEAKER_00]: You know, and we're all using different tools that trying to examine the same problem. [SPEAKER_00]: If I have somebody whose waste measurement is already either borderline or in a concerning range, and they have other evidence of kind of metabolic consequences, then I already know what I need to know and we know what we need to do.

[SPEAKER_00]: If all those things look great. [SPEAKER_00]: then we also know where we're at and what we need to do. [SPEAKER_00]: If there's some conflicting measures, like if somebody has a healthy appearing waste measurement, but they have evidence of metabolic consequences, then there might be some value in trying to look at things in a different way.

[SPEAKER_00]: So, it's a matter of using the tools to answer the primary question instead of just wanting the data for the sake of it. [SPEAKER_01]: Yeah, so I basically told them I was like, look, I want your body weight to be [SPEAKER_01]: the number that has somehow arrived at this wacer conference, and you have to figure this weight tight ratio, which is about 0.5 or less.

[SPEAKER_01]: But not less than 0.4. [SPEAKER_01]: Yeah, and he's like, what do you think that's gonna be? [SPEAKER_01]: I'm like, well, that's, yeah, came in more challenging. [SPEAKER_01]: But yeah, yeah, we would recommend reading our article and listen to our podcast on why you're waste matters more than you're wait because I talk about all of that there.

[SPEAKER_01]: So we know that menopause adds maybe the metabolically harmful kind of fat. [SPEAKER_01]: But the bigger question, at least to me, and probably from most women, is what does it do to your metabolism? [SPEAKER_01]: Right? [SPEAKER_01]: Because you hear this all the time that look. [SPEAKER_01]: Once you, it's going to be different when you're older, especially when you go through menopause, your metabolism is going to crash and then you're going to store all this body fat, particularly in the abdomen.

[SPEAKER_01]: Well, we've got some data on this. [SPEAKER_01]: Dr. Herman Ponzer's international team published the biggest study ever done on this question in the journal Science in 2021. [SPEAKER_01]: They used doubly labeled water, which is the gold standard way to measure how many calories someone actually burns a day.

[SPEAKER_01]: And they did this in over 6400 adults across 29 different countries. [SPEAKER_01]: and importantly, they corrected for body size. [SPEAKER_01]: So they could see if metabolism actually changes with age once you account for the fact that bigger bodies burn more energy. [SPEAKER_01]: We also did a podcast with Dr. Ponser.

[SPEAKER_01]: 10 out of 10 will recommend. [SPEAKER_01]: He also wrote the book, burned, which I thought was pretty good. [SPEAKER_01]: So. [SPEAKER_01]: If it were true that menopause slows metabolism, we would expect the curve of energy expenditure to inflect sharply downward during age 45 to 55 in that window, but as it turns out, based on the most rigorous methods of measurement performed by Dr. Ponser and his research group, it doesn't.

[SPEAKER_01]: Total energy expenditure, when adjusted for body size, stays relatively constant [SPEAKER_01]: Now after 60 it declines to buy about 0.7% per year on average with no sign of a menopause specific dip. [SPEAKER_01]: Now, that study was not in just menopausal women or people during that period of menopausal transition, but there was a subsequent study in 2023 by Carponin and their research group that looked specifically at resting metabolic rate in bedlife women and confirmed the same pattern.

[SPEAKER_01]: What drives the decline in resting metabolism is aging with no real menopause-specific signal on top of it. [SPEAKER_01]: So Austin, imagine a patient she's 49 perimenopausal. [SPEAKER_01]: She's gained eight kilograms over the last five years. [SPEAKER_01]: And again, she's been told by her menopause coach.

[SPEAKER_01]: This is all estrogen. [SPEAKER_01]: Deficiency and her metabolism has subsequently crashed as a result. [SPEAKER_01]: She's asking you to prescribe menopausal hormonal therapy, specifically to reverse the body composition change. [SPEAKER_01]: Walk me through that visit and what you actually say to her.

[SPEAKER_00]: Yeah, there's probably going to be a familiar theme to some of our other patient scenarios. [SPEAKER_00]: And this is less hypothetical than one that I see pretty frequently. [SPEAKER_00]: And so getting a sense of where these beliefs came from and validating the challenge that this woman is going through.

[SPEAKER_00]: And really, I'm trying to see, is there any other compelling indications or justifications to prescribe menopausal hormone therapy that I'm seeing? [SPEAKER_00]: Are there any other, [SPEAKER_00]: over to like the textbook science of estrogen deficiency. [SPEAKER_00]: We went through a lot of those on our last episode because there are kind of categories of symptoms.

[SPEAKER_00]: There are the things that are very specific, suggestive of estrogen deficiency that are very likely to respond to estrogen therapy. [SPEAKER_00]: There are those that could be related, but can also be related to other things. [SPEAKER_00]: And then lastly, there are those symptoms that are really unlikely to be related and are more likely to be related to other things.

[SPEAKER_00]: And I view this as kind of a flu-espectrum of sorts. [SPEAKER_00]: And I am very open to, again, I describe this as sometimes coloring outside the lines when it comes to rigid clinical practice guidelines if I think something is safe and has a reasonable potential to benefit the person.

[SPEAKER_00]: But if they have rock solid, regular menstrual periods, no other symptoms whatsoever of estrogen deficiency. [SPEAKER_00]: And purely the only issue that has happened. [SPEAKER_00]: is some weight gain over the past five years. [SPEAKER_00]: I am gently redirecting the conversation, probably a bit away from menopausal hormone therapy as the key to improving that particular aspect that we have much more effective strategies for this.

[SPEAKER_00]: Now, here's the other side of that coin and somebody could plausibly make this case. [SPEAKER_00]: It's like if the person is absolutely locked in on this as the only thing that [SPEAKER_00]: they believe is going to help them. [SPEAKER_00]: I really like the way that you have framed some of the study.

[SPEAKER_00]: I think you did this more for me than for our audience, where you set it up as terms of like, if this were true, what might we expect from this study? [SPEAKER_00]: And then you look at the study results, right? [SPEAKER_00]: And so, [SPEAKER_00]: If hormone therapy were otherwise safe in this person, we could say, like, if this weight gain were purely hormonally mediated, if that was a thing, and it is safe to try.

[SPEAKER_00]: And we wanted to give it a three-month trial, four-month trial, six-month trial. [SPEAKER_00]: What degree of weight loss should we expect to see? [SPEAKER_00]: And then if we do that, and more likely the person does not spontaneously lose all of that weight, then that might go to challenge the hypothesis that this weight loss was purely hormonal.

[SPEAKER_00]: course, this assumes a lot of things about how scientifically rigorous the person's mindset is towards this sort of thing. [SPEAKER_00]: But I think in general, trying to do a comprehensive assessment of all of the potential reasons to prescribe menopausal hormone therapy, because if there are a lot of other reasons to do so, then I'm perfectly willing to do it, even if I don't think that I'm like specifically targeting this four weight loss in particular, because it may make the rest of the person's life easier.

[SPEAKER_00]: It may make it easier for them to adhere to the dietary changes we're recommending, or the exercise habits, or [SPEAKER_00]: just might make their life less unnecessary suffering, which is all great. [SPEAKER_00]: But again, if they have nothing else at all that I can pin on it, then I'm probably kind of trying to redirect and say, look, we have way more effective options.

[SPEAKER_00]: If we're looking to try something outside of just kind of quote unquote lifestyle alone, for weight management, there are far more effective options that I would be way more confident would get you to where you want to be in a shorter time period than menopausal hormone therapy. [SPEAKER_01]: Yeah, I mean, this is the same way that I think about GLP ones, for example, right, is that they're mostly a behavior change sort of instrument or tool and that they help people who use them to do the things that they likely set out to do multiple times and they're like before and have yet to be successful and so to the extent that menopausal hormonal therapy addresses.

[SPEAKER_01]: any of these underlying drivers of the behaviors that happen, associated with the Parameda Pulse Transition, whether it's compromised sleep, and subsequently that effect on appetite, or willingness to participate in exercise, things of that nature, then yeah, we would predict a pretty, pretty good response from a weight management standpoint.

[SPEAKER_01]: However, if those things aren't really happening and you, you know, as you're almost asking a patient for a reason to describe a little therapy, not exactly. [SPEAKER_01]: Not because you're gatekeeping, because it's likely to be safe. [SPEAKER_01]: But to the extent it's going to benefit them is directly proportional to are they experiencing symptoms.

[SPEAKER_01]: We know are are well treated well managed by these things versus something else. [SPEAKER_01]: And so yeah, if a person had that, it would make, I would predict. [SPEAKER_01]: Very good response. [SPEAKER_01]: But if not, it's like, well, let's use a better tool because we have some of those if it's purely about the way change.

[SPEAKER_01]: Is that kind of square with what you're saying. [SPEAKER_01]: It's all agree. [SPEAKER_01]: Yep. [SPEAKER_02]: Let's talk about a concern that a lot of my patients bring to their clinic visits. [SPEAKER_02]: Women often come in feeling frustrated because they are eating the same, they're maintaining roughly similar activity levels, but still struggling with their body composition.

[SPEAKER_02]: They feel like something has changed, despite their best efforts. [SPEAKER_02]: Because these changes seem to accelerate around menopause, it's completely natural to want to blame the hormones. [SPEAKER_02]: But the best evidence that we have shows it's not that simple of a story. [SPEAKER_02]: When researchers have followed women over long periods of time during the menopausal transition, we actually don't find rapid accelerations in muscle loss during perimenopause, especially in those women who remain physically active.

[SPEAKER_02]: The weight gain curve is actually steeper before perimenopause begins, which already suggests that those most dramatic hormone shifts that come along with menopause aren't the main culprit here. [SPEAKER_02]: Now what menopause does do is shift the location where the fat distribution ends up so more towards the waistline and the belly as compared to the hips and thighs [SPEAKER_02]: And there's lots of theories as to why this happens, but the truth is that we are not 100% sure yet.

[SPEAKER_02]: The question of metabolism frequently comes up in this conversation. [SPEAKER_02]: And metabolic rate is actually a target that's been rigorously measured, but declines in metabolic rate that are specific to menopause or hormone status haven't been found. [SPEAKER_02]: There are some age-related declines that tend to appear at around age 60 on average, but menopause itself doesn't seem to accelerate these changes.

[SPEAKER_02]: So what can MHT do for body composition? [SPEAKER_02]: Unfortunately, a lot less than we'd hope, at least directly. [SPEAKER_02]: It doesn't directly increase fat loss or fat redistribution. [SPEAKER_02]: What it definitely does do however is treat symptoms like hot flashes and night sweats.

[SPEAKER_02]: And when this leads to improved sleep, energy and motivation, improved lifestyle habits tend to follow as well. [SPEAKER_02]: And these are important downstream effects, even if in direct. [SPEAKER_02]: On the topic of testosterone, we don't have strong evidence to prescribe it to perimenopausal women for body composition.

[SPEAKER_02]: There's actually paradoxical data from this one study that would suggest that higher levels of bio-available testosterone during menopausal timeframe may contribute to central bad accumulation. [SPEAKER_02]: And so this is not a tool that I reach for in this case. [SPEAKER_02]: Ultimately, the changes that women in the stage of life experience are real, but they are not inevitable and they are not insurmountable, treating your symptoms, protecting your sleep, and supporting physical activity often will make the most meaningful difference.

[SPEAKER_01]: All right, well that's the body composition story when we come back from the break. [SPEAKER_01]: I'm going to talk about what happens to cardiovascular disease risk. [SPEAKER_01]: All right, we're back here on the barbell medicine podcast and in the first section, we talked about body composition, metabolism, things that happen around the peri-minopausal transition, but now I want to talk about this sort of cardiometabolic shift.

[SPEAKER_01]: So body composition is half of the story. [SPEAKER_01]: The other half is what's happening to person's cardiovascular health, the lipid panel, blood pressure, insulin sensitivity, all the things that drive cardiovascular disease over the long run. [SPEAKER_01]: And there's one specific change here that's clearly driven by menopause, which is anchored to the final menstrual period, not just background aging.

[SPEAKER_01]: So in 2009, Matthews and colleagues published a study in the Journal of American College of Cardiology, where they ran annual lipid panels on just over a thousand women in the swans study that we talked about earlier. [SPEAKER_01]: They use a statistical method that lets the rate of change in low density lipoprotein LDL.

[SPEAKER_01]: These are the sort of proteins that carry around cholesterol in your body. [SPEAKER_01]: And so this statistical method lets you detect the rate of change in LDL at a specific time point. [SPEAKER_01]: And they set that point at each women's own final menstrual period, which let them separate the slow drift of aging from the sharper change that happens around menopause itself.

[SPEAKER_01]: In the two years, around the last menstrual period, LDL cholesterol rose by about five milligrams per deciliter per year and apolipoprotein B, those levels rose by about three milligrams per deciliter per year. [SPEAKER_01]: If you don't recall what apolipoprotein B or apob is, this is the kind of detectable protein that's attached to what we think causes [SPEAKER_01]: If you were unclear if you were at risk for heart disease based on your standard lipid panel, an apolipoprotein B test would be more instructive because it captures all of your athergenic load, or at least most of it.

[SPEAKER_01]: So in any case, across this perimenopausal window, low density lipoprotein LDL went up by about 10 points, and apolipoprotein B or apobi rose by about 6 points beyond what aging alone would have done. [SPEAKER_01]: And the rise is concentrated in [SPEAKER_01]: Now, Waser conference, as we mentioned earlier, does tend to increase across this window, but it's too crude of a measurement to separate the visceral fat redistribution from general midlife weight gain.

[SPEAKER_01]: That's why they had to rely on CT data, which is ultimately impractical for most folks. [SPEAKER_01]: The American Heart Association sells, put it the same way, in their scientific statement on midlife women. [SPEAKER_01]: The menopausal transition is a window of accelerated, atherogenic lipid changes, but the magnitude is modest.

[SPEAKER_01]: So that's the picture on lipids. [SPEAKER_01]: Next question is whether the rest of the cardiometabolic profile follows the same pattern, or whether something different is going on with insulin sensitivity and metabolic syndrome risk. [SPEAKER_01]: So in 2008, Janssen, again, looked at the swan data and looked for the rates of metabolic syndrome.

[SPEAKER_01]: The cluster of high-wacer conference, worsening lipid panels, high blood pressure, and high blood sugar that often traveled together. [SPEAKER_01]: Now, women in late perimenopause or early post-menopause had about 45 to 60% higher odds of developing these issues compared to pre-menopausal women of the same age, those who hadn't gone through their final menstrual period.

[SPEAKER_01]: But when the analysis adjust for the visceral fat redistribution, we just covered most of that effect disappears. [SPEAKER_01]: The hormonal change kicks the visceral fat redistribution into gear, and the visceral fat is what's actually causing the metabolic problems. [SPEAKER_01]: Actually think if they would have measured liver fat directly, perhaps that would have been even more predictable, but harder to measure that on some level.

[SPEAKER_01]: In any case, the hormone change is upstream, and the fat is what's doing the damage. [SPEAKER_01]: Austin, is this something that you talk about with patients when you're kind of, you know, because you are such a good clinician and so thorough and also very, very deeply into sort of cardi metabolic health?

[SPEAKER_01]: Is this something you bring up as like an add-on at a visit like, and by the way, we need to measure your lipid panel because of these changes that we predict. [SPEAKER_01]: Is that something you talk about? [SPEAKER_00]: I don't necessarily directly tie it into as soon as we have determined that the person has crossed, quote unquote, to the menopausal transition, then suddenly we need to do this because we have probably been doing it all along already.

[SPEAKER_00]: The situation where I tend to emphasize kind of the cardiometabolic risk assessment much more. [SPEAKER_00]: and just the overall degree of risk is when menopause is either early, meaning before age 45, or when the person is frankly having premature ovarian insufficiency or premature ovarian failure before 40, because those are much more substantial, long-term cardiovascular risks having it that early.

[SPEAKER_00]: And, or, if the woman has had prior history of significant obstetric complications, so that means they have preeclampsia with one of their pregnancies, or certain things like that, because all of those factors are things that are generally predictive of much higher, longer-term cardiovascular risk and the higher the risk.

[SPEAKER_00]: is for the person. [SPEAKER_00]: That's usually when we treat them more aggressively. [SPEAKER_00]: By the time we've gotten to quote unquote natural menopausal transition, if they're going through that about the expected timeframe, we're monitoring all these things anyway, and I'm not necessarily rigidly tying them to menopause.

[SPEAKER_00]: There's already enough kind of catastrophizing messaging out there around what menopause does to you. [SPEAKER_00]: And it's just, I'm looking out for your health and all the things that we need to be thinking about as we transition into the, you know, through, through midlife is, you know, your general health, your body composition, your physical activity, your bone density, your, yeah, and cardiovascular metabolic function and things like that.

[SPEAKER_00]: So that's generally the way I approach it. [SPEAKER_00]: I emphasize it much more explicitly when it is a much, much higher risk situation. [SPEAKER_00]: Otherwise, it's just I think a good part of a routine primary care. [SPEAKER_01]: All right, so that's a deal on insulin sensitivity, some lipid changes, but what about blood pressure?

[SPEAKER_01]: Now blood pressure does tend to rise across midlife in women, also in men. [SPEAKER_01]: But it's similarly tracks aging in body composition more than menopause itself. [SPEAKER_01]: So if you take an otherwise healthy 45-year-old, if you took everything menopause does to her lipids and blood pressure and run it through a 10-year heart disease risk calculator, it moves her absolute risk of having an unwanted cardiovascular event.

[SPEAKER_01]: By about one to three percentage points, that's a real effect over time, especially when it stacks on whatever trajectory she was already on in the United States, generally is not very good. [SPEAKER_01]: A woman whose LDL was already creeping up before her final menstrual period is much more likely to cross the sort of treatment threshold during this window than a woman who started at quote optimal levels.

[SPEAKER_01]: The clinical implication here isn't that menopause flips her into a high risk category overnight. [SPEAKER_01]: It's just that the transition is the right moment for a full cardiovascular risk assessment because the lifestyle interventions that address these changes return the most when they started early before the risk accumulates.

[SPEAKER_01]: We think that the risk is proportional to not only how high these risk factors are, but for how long they're elevated for. [SPEAKER_01]: Now, you alluded to a specific case premature menopause, especially before the age of 40. [SPEAKER_01]: Well, this is formally recognized as a cardiovascular risk enhancing factor, and it does get treated differently.

[SPEAKER_01]: For natural menopause in the typical 45 to 55 range, [SPEAKER_01]: The cardiovascular changes are real as the American Heart Association's scientific statement makes clear. [SPEAKER_01]: But they're not categorized in the way in risk calculators. [SPEAKER_01]: So to be clear, natural menopause does affect cardiovascular risk.

[SPEAKER_01]: The reason premature ovarian insufficiency gets categorized separately is that the magnitude and the clinical implications are different, and we'll come back to that later in this episode. [SPEAKER_01]: So Austin, the patient, she's 51, her final menstrual period was last year, and her lipid panel shows that her LDL's 145, first 125, two years ago, her apolipoprotein B is elevated.

[SPEAKER_01]: Her menopause coach told her that this is an estrogen crisis and she needs menopausal hormonal therapy to fix her lipids. [SPEAKER_01]: What does that conversation do? [SPEAKER_00]: Yeah, this is a, I think the audience is maybe picking up on a common theme of the, the menopause coach catastrophizing menopause and saying that the hormones are going to fix everything.

[SPEAKER_00]: This comes up both in lipids, this comes up with bone density, this comes up with a lot of things. [SPEAKER_00]: And as we've alluded to, both between the last episode and already here, there are certain symptoms where we can feel very, very confident that estrogen therapy is very likely to have a substantial impact arguably, a bigger impact than any other treatment that we have available.

[SPEAKER_00]: The prime examples of that are the vasomotor symptoms, right? [SPEAKER_00]: Very, very likely, or the genital urinary syndrome, delivering local vaginal estrogen. [SPEAKER_00]: Very, very likely to deliver better effects on that particular symptom than anything else that we have available.

[SPEAKER_00]: This does not extend to every potential manifestation of the Manipausal Transition. [SPEAKER_00]: When it comes to lipid changes, for example, using Manipausal hormone therapy for that purpose, [SPEAKER_00]: less effective than directly addressing that risk factor when it comes to bone density.

[SPEAKER_00]: Let's say somebody has already established postmenopausal osteoporosis using estrogen therapy at that stage less effective than directly treating the osteopor... doesn't mean that the hormone therapy may have no role at all, but I think we need to put these things in their proper context and recognize the magnitude of benefit that is likely to be gained by by using them depending on the situation that we're in.

[SPEAKER_00]: And so, this woman, again, just like the one who was concerned about her weight gain earlier, this woman may have some other reasons to use menopause or hormone therapy. [SPEAKER_00]: She may have the ways of motor symptoms. [SPEAKER_00]: She may have some of the other justifications that may make it more strongly justifiable.

[SPEAKER_00]: But just if she has, again, no other symptoms whatsoever, no other concerns whatsoever. [SPEAKER_00]: Just to modest, I would say, increase in her blood lipids from an LDL cholesterol of 125 to 145. [SPEAKER_00]: That itself, I would not expect to be directly and substantially reverse to very low risk levels by offering her an estrogen patch, for example.

[SPEAKER_00]: There are still many other aspects of the conversation. [SPEAKER_00]: I'm going to talk about all the things that we hammered on in our cholesterol, article series, and podcast series talking about the dietary habits, making some smart substitutions, the physical activity, thinking about insulin resistance, family history, doing a risk assessment, and trying to determine does this need directed medical treatments for the lipids in particular?

[SPEAKER_00]: Or is there some other secondary cause, for example, did this woman develop hypothyroidism? [SPEAKER_00]: That's another reason that people's lipids can go up. [SPEAKER_00]: Has she had her TSH check? [SPEAKER_00]: That can also make you feel tired. [SPEAKER_00]: And again, this is a good example of why, if you are, for example, a quote unquote menopause coach and, you know, default shades to people who identify as that.

[SPEAKER_00]: But. [SPEAKER_00]: If that is the extent of your expertise and your tendency is to view everything through the lens of menopause and hormone therapy, you are going to miss a lot of things because again, thyroid dysfunction can look similar. [SPEAKER_00]: Sleep apnea can look similar. [SPEAKER_00]: Anemia, iron deficiency can look similar.

[SPEAKER_00]: Chronic infections can look similar. [SPEAKER_00]: Autoimmune diseases can look similar. [SPEAKER_00]: You have to have some degree of experience and expertise in recognizing thinking about differentiating all of these [SPEAKER_00]: So that you don't lead people down the wrong path of cranking a hormone dose is higher and higher and higher.

[SPEAKER_00]: Meanwhile, you're giving them the wrong hormone and they need it thyroid hormone replacement or they need it an iron infusion or they needed something else entirely. [SPEAKER_01]: We, this is not unique to the menopause space, though. [SPEAKER_01]: I mean, you think about the testosterone.

[SPEAKER_01]: That's why the man is fear and so. [SPEAKER_01]: And if everything looks like testosterone deficiency to you, you're going to miss a lot of stuff. [SPEAKER_01]: And so, [SPEAKER_01]: And the results are predictable. [SPEAKER_01]: Every man needs these tests, and it's all about testosterone and estrogen, or whatever, I'm like, could you use a CBC to see if they're anemic?

[SPEAKER_00]: Yeah, this is why, this is why generalists are good, in fact, that's my hot take. [SPEAKER_01]: Yeah, wow, wow, really, really, really killing it. [SPEAKER_01]: All right, so that's the story on Cardi Metabolic Health. [SPEAKER_01]: Now we get to bone where the clinical picture and the underlying data have been out of sync for longer than just about any other area of women's health.

[SPEAKER_01]: What women have been told to do and what the data say they should do are diametrically opposed. [SPEAKER_01]: We're going to start out with the swan bone sub-study. [SPEAKER_01]: So this is from the same research group at UCLA Greendale. [SPEAKER_01]: They published another swan analysis in 2012 this time on bone in just under 2,000 women followed across their final menstrual period with regular dexoscans.

[SPEAKER_01]: Yes, this dex rate technology not only tells you body composition indirectly, it also and perhaps more accurate degree tells you bone mineral density. [SPEAKER_01]: The pattern of bone loss across menopause isn't a straight line. [SPEAKER_01]: It's a slow in the years leading up to the transition.

[SPEAKER_01]: It picks up as a woman enters perimenopause. [SPEAKER_01]: It peaks in the year or two around the final menstrual period and then slows back down within a few years afterwards. [SPEAKER_01]: Peak annual loss at the Lumbar spine was about 1.8% per year. [SPEAKER_01]: At the femoral neck in the leg, about 1 to 1.2%.

[SPEAKER_01]: The cumulative loss across the five-year transmenopause window was about 10.6% at the Lumbar spine and about 9% at the femoral neck. [SPEAKER_01]: The distal radius in the arm shows the same pattern but at a smaller magnitude. [SPEAKER_01]: Now, the problem here is that Dexa misses most of these sort of fragility fractures that women will have.

[SPEAKER_01]: Most fragility fractures in postmenopausal women don't happen to women who have officially crossed the line into osteoporosis on a Dexa scan. [SPEAKER_01]: They happen to women whose bone densities in the osteopenia range or even in the normal range. [SPEAKER_01]: The classic study here is from series in 2001, where 82% of women showing up with fractures had bone density that wouldn't have qualified them for an osteoporosis diagnosis.

[SPEAKER_01]: Their T score, which is the standardized score decks that gives you, was better than the cutoff, which is again, when people report studies. [SPEAKER_01]: on Dexa, improving bone mineral density, you know, Dexa measured improvement in bone mineral density. [SPEAKER_01]: That's only half of the story.

[SPEAKER_01]: You also have to look, well, did they fall lesser more? [SPEAKER_01]: Did they have more or less fractures? [SPEAKER_01]: Because that's what you really care about. [SPEAKER_01]: The score is nice to have, but it's, you know, on some some levels, it's just a surrogate number. [SPEAKER_01]: You want the actual clinical, the hard clinical outcomes.

[SPEAKER_01]: All right, so enter the lift more study from 2018. [SPEAKER_01]: For decades, postmanopausal women with low bone mineral density were told to avoid heavy lifting. [SPEAKER_01]: There was actually a 1995. [SPEAKER_01]: Recommendation say look if you got osteoporosis or osteopenia do not load the spine because it's going to be risk of fracture and that for generations of women Had put them in a bad place the thought here was that fragile bones plus heavy loading equals vertebral compression fractures Again, this is from eight the ACS M the American College of Sports Medicine.

[SPEAKER_01]: They should have known better, but you know, it is what it is [SPEAKER_01]: Now, Belinda Beck's group at Griffith University, I believe it's in Australia, ran the trial in direct opposition to this. [SPEAKER_01]: So this is the lift more trial. [SPEAKER_01]: It included 101 postmenopausal women with low bone mass and they randomize them to either do high intensity progressive resistance training, plus impact training, which if you've listened to a few of our podcast episodes before, you'll know that this is from when they were doing jumping pull-ups and they landed from those with straight legs.

[SPEAKER_01]: So they either did that or a low intensity home exercise program. [SPEAKER_01]: The intervention was eight months of supervised training twice a week, about 30 minutes per session, and they did five reps for five sets at 80 to 85 percent of the one red max on barbell exercises like dead lifts, overhead presses, back and back squats, plus the jumping chin ups.

[SPEAKER_01]: Now before any of the lifters at home, you know, cry out. [SPEAKER_01]: They did five reps at 85 percent of the one red max, no way. [SPEAKER_01]: Maybe it was a training max. [SPEAKER_01]: These people were also new to exercise so that it is possible. [SPEAKER_01]: They can do that. [SPEAKER_01]: Let's just say that it was heavy, okay?

[SPEAKER_01]: Now, across 2,613 supervised sessions, the published total injury rate was one mild lower back strain that fully resolved. [SPEAKER_01]: The person didn't miss any sessions. [SPEAKER_01]: The intervention was safe in a population that the field had spent decades telling to avoid the exercise.

[SPEAKER_01]: Now, awesome, before we get to the results on what happened to bone mineral density, let's take the same patient that you would have seen 10 years ago, maybe even longer. [SPEAKER_01]: She's 65. [SPEAKER_01]: She has osteopenia, and she's been told for 15 years by her family doctor to avoid heavy lifting and stick to walking and Pilates.

[SPEAKER_01]: What would your priors have been? [SPEAKER_01]: What would you predict the Lumbar spine bone mineral density change in eight months of supervised heavy lifting? [SPEAKER_00]: Yeah, I mean, I think that there's the traditional perspective on this that that is something that at best you might be able to slow the decline a bit, but unlikely to have a substantial effect.

[SPEAKER_00]: And then there's the side of things that we recognize based on our kind of experience working with people who train and seeing just how adaptable people can be and that might lead us to a little bit more favorable of a of a prediction, but I think the overall you know view in the medical community.

[SPEAKER_00]: would have been that this is going to have a somewhat modest, even negligible effect just based on, you know, the their level of knowledge and experience of what this sort of thing can do to, you know, somebody's body. [SPEAKER_00]: Yeah, yeah, I agree. [SPEAKER_01]: Perhaps even harmful.

[SPEAKER_01]: You're predicted a higher injury rate and you say, well, that's interesting, but like, not that while you got away with it, it's still probably didn't do much. [SPEAKER_00]: Yeah, maybe predicted the try would have been halted early because everyone, you know, dissolved under the park. [SPEAKER_00]: That's right.

[SPEAKER_01]: Well, here's what the lift more study found. [SPEAKER_01]: Lumbar, spine, bone mineral density rose 2.9% in the lifting group. [SPEAKER_01]: And it fell 1.2% in the control group. [SPEAKER_01]: Femoral neck bone mineral density held steady in lifting group, walk controls, lost almost 2% this is an 8 months.

[SPEAKER_01]: Again, it's this is in postmenopausal women with an average age of 65, with bone mineral density well below normal, doing deadlifts at 85% of their one rep max twice a week for eight months, and they gained bone while the controls lost bone. [SPEAKER_01]: So lift more trial establish that heavy progressive resistance training is not only safe in individuals with osteopeenia and osteoporotic osteoporosis rather in postmenopausal women, but it also showed that it produces measurable bone mineral density gains in this population [SPEAKER_01]: Still, this trial did not address fractures and thus you can't really say that, well, heavy lifting prevents fractures.

[SPEAKER_01]: We might predict due to our biases that that would happen, but that trial to date has not been done. [SPEAKER_01]: So the bone mineral density finding is reliable and seems to be rather large, but the fracture sort of inference from there is another leap that we just need to have studied.

[SPEAKER_01]: There's another study that repeated a similar type of setup. [SPEAKER_01]: This is how a Germany is called E-Fops, which stands for Urlingin, fitness, and osteoporosis prevention study. [SPEAKER_01]: I'm certainly butchering the name of that city. [SPEAKER_01]: So sorry to all of our listeners who are near there.

[SPEAKER_01]: This is the longest controlled trial in the space. [SPEAKER_01]: 16 years of follow-up in early postmenopalza women. [SPEAKER_01]: They were doing multi-component exercise, which is a fancy way of saying they were doing a bunch of things. [SPEAKER_01]: This included resistance training, and they compare that to controls who mostly didn't exercise.

[SPEAKER_01]: The results showed, preserved, lumbar spine bone mineral density in the exercise group, and roughly 4.5% loss in controls. [SPEAKER_01]: There were no major adverse events attributed to the exercise intervention across 16 years. [SPEAKER_01]: Now, since Pilates is trending, I want to talk about it, in the MedEx op trial, the same group that ran the lift more a study, compared their heavy resistance training program against a Pilates base program called buff bones.

[SPEAKER_01]: And this was in 115 postmenopalzo women with low bone mass. [SPEAKER_01]: Across eight months, the heavy lifting group gained 1.9% in lumbar spine bone mineral density, the Pilates group gained essentially nothing, 0.1% which is well within the error bars of the test. [SPEAKER_01]: And in the subgroup of women who are not on bone mineral density medications, so medications you can take to actually increase bone mineral density.

[SPEAKER_01]: Pilates actually lost a bit of lumbar spine bone mineral density. [SPEAKER_01]: And whereas the lifting group gained the same 1.9%. [SPEAKER_01]: The heavy lifting group also did better on functional measures. [SPEAKER_01]: So back extension, back extensor, strength, leg strength, and the five times sit to stand test that we sometimes use to screen for sarcopenia.

[SPEAKER_01]: Both programs were equally well tolerated, but the heavy lifting just worked much better. [SPEAKER_01]: So I keep coming back to the same thing I've been saying about Pilates for years. [SPEAKER_01]: It is fine as a physical activity, and if you like it, I love it. [SPEAKER_01]: but it is not adequate for building bone and muscle and strength.

[SPEAKER_01]: And I think that people who have a pretty balanced view of this would agree. [SPEAKER_01]: It is interesting to me when I get pushback saying that I don't know what Pilates is or Pilates does X, Y, and Z, and to that I say, show me. [SPEAKER_01]: I'm open to the fact or the idea that Pilates would be sufficient to meet the current muscle strengthening guidelines, resistance training guidelines, but to date.

[SPEAKER_01]: Every time that it's been investigated, it has fallen short. [SPEAKER_01]: Austin, is that kind of your take on Pilates or we can send it to yoga or tai chi or water aerobics? [SPEAKER_01]: I don't know, what do you think about all that? [SPEAKER_00]: I would not classify all of those things in the same bucket.

[SPEAKER_00]: It's certainly water aerobics is one that, while again, a great activity for a lot of people, social environment, you know, might feel good in various ways is definitely the one that I would say is the outlier here in terms of like, actually, essentially no skeletal stimulus is being delivered here and we need to have something else as a form of true load bearing.

[SPEAKER_00]: For the others, I don't have extremely strong opinions for [SPEAKER_00]: or what I'll call like the undifferentiated trainee. [SPEAKER_00]: Somebody who has been insufficiently active and is choosing among their menu of options of how they're going to enter the physical space. [SPEAKER_00]: If their way of introduction is going to be Pilates and I feel like that might be the way that they get bit by some bug and then we came build from there.

[SPEAKER_00]: Again, going from nothing to doing something is likely to have some measurable benefit but is unlikely to have very, very large effect sizes on some of these things that we care about more that there are probably better ways to achieve the goal. [SPEAKER_00]: I think there's the perspective of use the best tool for the goal outcome, but then there's also the more like real-world pragmatic approach of like, well, if the person is unwilling or unable to engage with that best tool, is there a slightly less best tool that they might engage with to start out with and kind of build from there?

[SPEAKER_00]: As far as like specific outcomes, I have honestly outsourced many of my opinions on Pilates to you because you choose to fight those battles more than I do And so I'll I'll take your word for for for many of those things, but honestly like I just had this same conversation this morning with another patient and yesterday Who are in these low-bond density type situations and so these topics do come up pretty regularly in practice and so that's kind of how I lay it out is and I'm also getting a read on the person in the conversation of [SPEAKER_00]: And like when we've talked about quote unquote maximizers and minimizers before somebody who's highly motivated to do everything they can to use the best tool for the job, it gets an easy sell to say we need to do some like true, you know, skeletal load bearing, somebody who's much more of a minimizer and I'm like struggling to get them to do much of anything that I might see what entry point can I find to get them at least started and then maybe we can build from there as they build some confidence, some self-efficacy, even they might start to enjoy it depending on the setting.

[SPEAKER_01]: Yeah. [SPEAKER_01]: No, I'm with you, especially like this goes back to how we kind of prescribe exercise, generally speaking to people that's undifferentiated people who are kind of new to it. [SPEAKER_01]: Whatever, whatever, turns your crank. [SPEAKER_01]: I'm here for it. [SPEAKER_01]: Later, though, I am going to try to push you to not only meet the current physical activity guidelines, but to exceed them.

[SPEAKER_01]: And so the main thing first is like, yes, you're making this part of your lifestyle, you're excited, you're having fun, you're bought in, and then I need to kind of push you potentially towards doing something. [SPEAKER_01]: This is the same way I feel about people who get bit by the powerlifting book.

[SPEAKER_01]: Like, great, we are aligned. [SPEAKER_01]: For whatever reason, we're all degenerates. [SPEAKER_01]: We like powerlifting, but now I got to push you to do some conditioning. [SPEAKER_01]: You know, or the endurance athlete, I'm so impressed by you, but we got to do some look. [SPEAKER_01]: Like so it's not unique to Pilates.

[SPEAKER_01]: The Oreo go or whatever else. [SPEAKER_01]: The whole point is this is like, I don't think that they should be represented as like, this is enough. [SPEAKER_01]: But that again, that's not unique to Pilates. [SPEAKER_01]: There's no single exercise modality that is enough. [SPEAKER_01]: It can't stop CrossFit.

[SPEAKER_01]: Anyway, all right, we've we've we've beaten this this horse a few times. [SPEAKER_01]: All right, we'll look, increasing bone mineral density is one thing, but to reduce fractures, we also have to reduce falls. [SPEAKER_01]: Now, there is a Cochrane review done in 2019 that pulled 108 trials in over 23,000 community dwelling older adults.

[SPEAKER_01]: Exercise reduced the rate of falls by about 23%. [SPEAKER_01]: The strongest signals were from programs that combined balance training with progressive resistance training. [SPEAKER_01]: Now, the balance training is, as you like to say, heterogenous. [SPEAKER_01]: People, there's not a single protocol, which is why none of our programs include the specific balance component, and further the majority of our programs what we recommend have that intrinsically baked into it.

[SPEAKER_01]: There are free standing exercises that do challenge your balance. [SPEAKER_01]: And we feel like that adequately addresses this balance component while also building, not only bone, but also muscle and muscular strength. [SPEAKER_01]: So, Austin, the patient, she's 64, she's post-menopausal.

[SPEAKER_01]: She had a dexus scan last year that showed that her T score was negative 1.4 at the Lumbar spine and negative 1.6 at the femoral neck. [SPEAKER_01]: Her primary care doc told her to avoid heavy lifting. [SPEAKER_01]: She's asking, hey, should I be deadlifting? [SPEAKER_01]: Walk me through that conversation.

[SPEAKER_01]: Assuming this actually happens in practice. [SPEAKER_00]: I just had this conversation about three hours ago today and I had another conversation of the same type yesterday morning as well with a few different patients. [SPEAKER_00]: So pretty common, near daily sort of experience for me at this point.

[SPEAKER_00]: These T-scores are not in terribly alarming territory. [SPEAKER_00]: Obviously, this is more in the osteopeenia range rather than immediately meeting criteria on their own for osteoporosis. [SPEAKER_00]: Now, if the person had a history of fragility fractures, that would automatically upgrade them to that osteoporosis.

[SPEAKER_00]: category, despite the, despite the T scores. [SPEAKER_00]: But the conversation starts out by just getting a sense of, you know, the person's understanding of their condition, and then also, what might they be willing to do? [SPEAKER_00]: They might be coming in with tons of fear and apprehension about deadlifting right off the bat.

[SPEAKER_00]: And a lot of times, you know, in the conversation that I had earlier today, I actually don't tend to use the word deadlifting with people who are not already in the lifting space that often. [SPEAKER_00]: We've talked about before and so that was how I actually started the conversation earlier today.

[SPEAKER_00]: Can you pick something up? [SPEAKER_00]: It's like maybe a little bit challenging for you something like that and she's like, oh, yeah, I can totally do that. [SPEAKER_00]: So that was how I framed that that conversation now. [SPEAKER_00]: I don't think that you know the way the question is framed [SPEAKER_00]: think everyone has to do this.

[SPEAKER_00]: There are a variety of ways to deliver an axial load through the skeleton, particularly through the axial spine, through the pelvis, through the hips, things like that. [SPEAKER_00]: So for the individual that I spoke with earlier today, you know, I asked if she was able to do essentially chair sit to stance one of my favorite introductory exercises as folks get get older.

[SPEAKER_00]: Was she able to do them, you know, unassisted without using her hands, was she able to do them while holding a load even in front of her and she was able to do all of these things. [SPEAKER_00]: So then we started talking about, you know, how we might introduce an even heavier load, potentially across the back, she had access to a barbell and in the home, whether a straight bar or a safety squat bar, whatever something like that, and then whether she wanted to do it as a free standing squat or whether she wanted to do as a box squat as something that's like a little bit more accessible and may have a little bit of less apprehension at the bottom of the movement, but can still deliver a challenging stimulus.

[SPEAKER_00]: So that was one example and then just picking something up the heavy off the ground. [SPEAKER_00]: If her preference had been to start out with maybe more machine-based training and we wanted to do that, I would similarly be able to pivot that way and think about things that could deliver some sort of axial stimulus through the lower extremities, through the hips, through the pelvis, a little bit harder in that situation to deliver something through the spine when it's not necessarily freestanding, but there are some creative things that we've done before.

[SPEAKER_00]: I don't kind of my opically focus on like, okay, the deadlift is the cure for the sort of thing. [SPEAKER_00]: It is an option if you're interested in willing to do it. [SPEAKER_00]: And I don't have apprehensions about prescribing them if the patient's interested in doing them based on the T-score minus 1.4, that doesn't really concern me.

[SPEAKER_00]: I'm more concerned about is the person training regularly, is the dose appropriate, and then do they have comfort in guiding this on their own, or they would they benefit from some additional supervision? [SPEAKER_01]: I think this is just where our bedside manner just differs, you know, because I would just send her the video of John Paul Sigmerson, deadlifting 1,000 and 3, we're at the top of his lock out.

[SPEAKER_01]: He says, there's no reason to be alive if you can't do deadlift. [SPEAKER_00]: And I think that that data catering to slightly different populations, it seems. [SPEAKER_01]: Yeah, yes, also like to population. [SPEAKER_01]: All right, so that's the story on metabolism, cardiometabolic health, and bone, next up is cognition, because this is a big concern that women raise.

[SPEAKER_01]: Brain fog, for example, is the second most common complaint that patients bring up across the menopausal transition, outside of vasomotor symptoms, the hot flashes, and the night sweats. [SPEAKER_01]: Now, patients often describe it as word-finding difficulties, trouble-holding multiple tasks in working memory, and the feeling that thoughts arrive more slowly.

[SPEAKER_01]: Across the public literature, roughly half to two-thirds of Perry Metapausalone report cognitive complaints, depending on the group and the test being used. [SPEAKER_01]: The complaint is real, but the harder question is whether the subjective experience maps to objectively measurable declines in cognitive function.

[SPEAKER_01]: So again, we go back to the Swan study and they have a cognition sub-study that followed approximately 2,300 women in the Swan cohort with serial neuropsychological testing. [SPEAKER_01]: This test included verbal episodic memory, processing speed, working memory, and more. [SPEAKER_01]: During late menopause, women's processing speed dropped a bit more than you'd expect from aging alone.

[SPEAKER_01]: The size of the drop was small to moderate, memory took a similar hit, but even smaller than that. [SPEAKER_01]: And once women got into early postmenopause, their trajectory went back to the normal age-related pace. [SPEAKER_01]: So during the transition, didn't turn into a permanent deficit.

[SPEAKER_01]: Women got back on their sort of regular aging curve once they were through the menopause transition. [SPEAKER_01]: Those two caveats here. [SPEAKER_01]: First, this is a population level finding. [SPEAKER_01]: Individual women have variable trajectories at baseline. [SPEAKER_01]: Some recover fully, some don't.

[SPEAKER_01]: Second, the swan cognition substudy was observational, and it's not an RCT, right? [SPEAKER_01]: It's not randomized control trial where we have definitive sort of proof. [SPEAKER_01]: But one of the major contributors to this sort of cognitive complaint is poor sleep. [SPEAKER_01]: Specifically, sleep disturbance is one of the most disabling perimenopausal symptoms, and underpins much [SPEAKER_01]: of what gets described as, quote, brain fog.

[SPEAKER_01]: Now, two things happen to sleep across the sort of perimenopausal transition. [SPEAKER_01]: First, vasomotor symptoms fragment sleep, particularly in the second half of the night, when core body temperature rises, and the awakening threshold gets lower. [SPEAKER_01]: Second, sleep architecture itself shifts in a way that's partially independent of these vasomotor symptoms.

[SPEAKER_01]: Multiple studies have shown reductions in slow wave sleep. [SPEAKER_01]: This is the deepest, most restorative phase of sleep. [SPEAKER_01]: More frequent awakeenines also have occurred, and longer sleep onset or sleep latency across this perimenopausal transition. [SPEAKER_01]: Sleep lab data shows modest reductions in sleep efficiency in late Perry and early post-menopausal individuals compared to when people are premenopausal.

[SPEAKER_01]: So overall, a meaningful portion of perimenopausal cognitive complaints comes through sleep, rather than estrogen acting directly on the brain, which means that the treatment is should be directed at the sleep, not necessarily the brain. [SPEAKER_01]: So if you treat the vasomotor symptoms, whether with MHT, so menopausal hormonal therapy, and eligible women, or with non hormonal options, like we covered on a last episode, [SPEAKER_01]: like vasylinotent or peroxotene or cognitive behavioral therapy for insomnia, you can improve sleep and you indirectly improve daytime cognitive function.

[SPEAKER_01]: That's an indirect cognitive benefit by a sleep, not a direct effect of menopausal hormonal therapy or estrogen on the brain. [SPEAKER_01]: So Austin, imagine this, a 49 year old woman comes in with brain fog, night sweats, and broken sleep. [SPEAKER_01]: She's anxious that her cognition is going.

[SPEAKER_01]: Her menopause coach told her that menopausal hormonal therapy will fix all of it. [SPEAKER_01]: Walk me through how you talk to this patient. [SPEAKER_00]: Yeah, right at the outset, I think it's worth recognizing that this is going to be a longer term kind of clinical relationship. [SPEAKER_00]: Meaning I don't think it's reasonable to expect that we're going to, just [SPEAKER_00]: one and done like nail everything and fix it all in a single visit.

[SPEAKER_00]: And I think from that perspective, there's a couple ways that you could go about this. [SPEAKER_00]: My thought would be, you know, to whatever extent the brain fog, quote unquote, may or may not be related to the hormonal changes, I am much more confident that the night sweats and secondary to that, the broken sleep are likely to improve if she's otherwise appropriate to receive hormonal therapy.

[SPEAKER_00]: And so maybe I just kind of pick my battles here and say, look, I'm very confident that we can help the night sweats the sleep by instituting some menopausal hormone therapy. [SPEAKER_00]: If it's appropriate for you, and then we can see how you do once you're sleeping better, and maybe the brain fog just like lifts at that point.

[SPEAKER_00]: That's one way to go about this. [SPEAKER_00]: At the same time, though, we do need to be vigilant for other things that could be contributing so that we don't kind of kick the can down the road too far. [SPEAKER_00]: And a perfect example, literally a visit that I had with a patient a couple of hours ago, a different woman earlier today, so you can see how often I'm having these conversations with folks.

[SPEAKER_00]: This was woman who was, you know, in her mid 40s, had an IUD, so she was not having menstrual periods, so there's not really a sense of, you know, where she's at in her menopausal transition. [SPEAKER_00]: With that said, she had been experiencing some fatigue and some brain fog. [SPEAKER_00]: She brought this up.

[SPEAKER_00]: Somebody started her on menopausal hormone therapy. [SPEAKER_00]: She is not exactly clear on whether it's helping or not. [SPEAKER_00]: She does not feel confidently that it's helping. [SPEAKER_00]: And I don't really know where she's at in the menopausal sort of transition. [SPEAKER_00]: Meanwhile, she has obesity.

[SPEAKER_00]: She snores. [SPEAKER_00]: She's had witnessed apnea's at night. [SPEAKER_00]: She's extremely high risk for having obstructive sleep apnea. [SPEAKER_00]: And so now I'm wondering, you know, [SPEAKER_00]: Has this been untreated, obstructive sleep apnea all the time, leading to non-restorted sleep, leading to cognitive functions, mood changes, all the other things that we know go sleep apnea during the day, and the menopausal hormone therapy is treating nothing, because it has not led to a meaningful benefit for her.

[SPEAKER_00]: And I don't even know whether she's even perimenopausal, because she's not having any, you know, menstrual peers or any other, novaise of motor symptoms, no hot flashes, no night sweats, right? [SPEAKER_00]: So what do we end up doing? [SPEAKER_00]: We're pausing the hormonal therapy. [SPEAKER_00]: see how she feels, see if she develops any of those parry menopausal or menopausal symptoms, and then you're going to do a sleep study and see if nearly a hundred percent certain she's going to have obstructive sleep apnea that will get treated, and then we'll see if we get things kind of on the right track.

[SPEAKER_00]: So this happens regularly. [SPEAKER_00]: So to the scenario in this question, I would be not only very willing to treat the night sweats, if that is a predominant symptom and concern that this patient has, but [SPEAKER_00]: also thinking about what are the other things that can lead to this ultimate manifestation that is often described as brain fog for someone.

[SPEAKER_00]: Do they have any of these other things that the less specific sort of syndromes that we talk about so often, the sleep apnea, the thyroid, the anemia, the iron deficiency, all these other sorts of things and checking off all those boxes along with this rather than framing it as this is 100% exclusively estrogen deficiency and getting you back on estrogen is going to immediately take away all these things because it happens all the time that that doesn't actually end up panning [SPEAKER_00]: but not always.

[SPEAKER_01]: The menopausee is going to be upset with you for telling big truths here in the menopause space. [SPEAKER_00]: Go seek care from whoever you'd like. [SPEAKER_00]: That is okay. [SPEAKER_01]: All right, so that's the story on sleep. [SPEAKER_01]: Let's talk about depression, because period menopause is a sort of vulnerability window for new onset depression and for recurrence and women with prior major depressive disorder history.

[SPEAKER_01]: So, one of the, uh, a couple of the classic studies here are the Harvard study of moods and cycles and also the swan mental health study plus some others. [SPEAKER_01]: They all converge to roughly the same point. [SPEAKER_01]: There's a two to four fold increase in the odds of new onset major depression in late Perry menopause compared to premenopause.

[SPEAKER_01]: This sort of window of vulnerability tracks the hormonal instability of late Perry menopause, not really the steady state situation that we see in post menopause. [SPEAKER_01]: But the nuance about timing matters. [SPEAKER_01]: A 47-year-old presenting with new anxiety, irritability, and or broken sleep deserves a differential that certainly includes perimenopausal depression.

[SPEAKER_01]: The clinical pattern of an SSRI prescription with no further work up, though, misses a potentially big part of the picture. [SPEAKER_01]: S-S-R-I's and other treatments for depression can work for these perimenopausal mood symptoms. [SPEAKER_01]: So does MHT in symptomatic women? [SPEAKER_01]: So does the combination?

[SPEAKER_01]: The right answer depends on the patient and their symptom profile. [SPEAKER_01]: So new onset depression itself produces subjective cognitive complaints and measurable executive function decreases. [SPEAKER_01]: A patient describing brain fog plus new, low mood plus sleep fragmentation has three different issues that need a comprehensive workup like Dr. Baraki alluded to.

[SPEAKER_01]: The other concern that comes up in this window is dementia. [SPEAKER_01]: And that is a bit of a different question to my mind. [SPEAKER_01]: Dementia and postmenopausal women is dominated by aging, vascular risk factors, education status, cardiovascular fitness, sleep quality depression, and hearing loss.

[SPEAKER_01]: Now, the Lancet Commission on Dementia Prevention identifies 12 modifiable risk factors. [SPEAKER_01]: menopause isn't on that list. [SPEAKER_01]: Now, that may be something that changes, but to date has not been on there. [SPEAKER_01]: The wrinkle here is that premature ovarian insufficiency, so that happens under the age of 40, particularly when it's surgically induced, is recognized as a modest risk risk factor for cognitive decline and dementia.

[SPEAKER_01]: It's one of the indications for a systemic estrogen replacement until the average age of natural menopause, but that's a different population [SPEAKER_00]: And, and one of the really important things about premature ovarian insufficiency that you mentioned when it's happening at that age below 40 you do not put those patients on menopausal hormone therapy you put them on high dose because you are trying to give them the same high level of a hormonal exposure that they would have had until that age of natural menopause and then at that age if you want to transition them to lower dose menopausal hormone therapy that would be perfectly appropriate it would be a mistake.

[SPEAKER_00]: to take somebody who's either naturally or surgically induced menopause of age 38 and put them on menopausal hormone therapy that would be an error and under treating them. [SPEAKER_01]: Yeah. [SPEAKER_01]: But I think the broader question here that women want answered is whether menopausal hormone therapy started around their actual menopause transition will protect their brain.

[SPEAKER_01]: Now, there are three major trials here that anchor that conversation. [SPEAKER_01]: The first one is Wims, the Women's Health Initiative Memory Study. [SPEAKER_01]: This is published in the early 2000s. [SPEAKER_01]: About 4,500 women aged 65 and older were randomized to one of three groups.

[SPEAKER_01]: One group got Premorin, that's an estrogen, and Provera, that's a progesterone, so they got both together. [SPEAKER_01]: The second group got Premorin alone at third group got Placibo. [SPEAKER_01]: In the combined estrogen plus progesterone arm, the risk of developing probable dementia was roughly double that of Placibo.

[SPEAKER_01]: Now, that sounds alarming, but when you translate that into absolute numbers, it works out to about an extra 23 cases of dementia per 10,000 women per year. [SPEAKER_01]: It's real, but not necessarily the catastrophe that the doubled risk suggests. [SPEAKER_01]: And here's where the study design kind of matters the most.

[SPEAKER_01]: The women in the women's study were 65 and older. [SPEAKER_01]: The trial did not test the question that patients in the late 40s and early 50s really [SPEAKER_01]: So the second study here is called Keeps Cog, the cognitive arm of the Kronos Early Estrogen Prevention Study, this was published in 2015.

[SPEAKER_01]: This one did look at the younger window. [SPEAKER_01]: Almost 700 women aged 42 to 58 within three years of their final menstrual period were randomized to get Premorin, again, that's estrogen, transdermal, estrogen, or a placebo for four years. [SPEAKER_01]: The primary cognitive input was null, no difference.

[SPEAKER_01]: Neither MHT had neither of the MHT regiments had a significant effect on cognitive function in this younger population. [SPEAKER_01]: Moode, which was a secondary endpoint, did show some benefit in the Premoran arm that's an oral estrogen. [SPEAKER_01]: But the implication here is that whatever MHT does for symptomatic women in this age range when it does anything comes through mood and sleep, not from a direct effect on the brain.

[SPEAKER_01]: And the third trial is the elite trial, which stands for Early Versus Late Intervention trial with Esther Dial. [SPEAKER_01]: This was published in 2016. [SPEAKER_01]: Elite was designed to test the timing hypothesis directly. [SPEAKER_01]: Over 600 women were randomized to one of two groups, women within six years of menopause, the early stark group, and women 10 or more years out from menopause, the late stark group.

[SPEAKER_01]: Both groups got either oral, estradiol, or placebo, with vaginal progesterone added for women who still had their uterus. [SPEAKER_01]: The primary outcome was actually corroded artery thickness, a marker of cardiovascular disease, not cognition, but cognition was tracked as a secondary outcome, and there was no clinically significant effect in either the early start or the late start group.

[SPEAKER_01]: taken together what these three trials tell us is pretty straightforward. [SPEAKER_01]: In younger women starting MHT closer to menopause, neither benefit nor harm to cognition was detected. [SPEAKER_01]: The trials weren't powered to rule out smaller effects, so we can't definitively say that MHT does nothing, but we can say it doesn't really prevent dementia, at least not with a robust signal that many in the space are maybe claiming.

[SPEAKER_01]: So Austin, imagine this, patients 49, she's perimenopausal. [SPEAKER_01]: She has new, word-finding difficulties and trouble with her working memory. [SPEAKER_01]: She's got broken sleep with night sweats and some new irritability. [SPEAKER_01]: She's afraid she's developing early dementia.

[SPEAKER_01]: Her menopause coach told her this is hormonal and systemic menopausal hormonal therapy, MHT will fix it. [SPEAKER_01]: How does that conversation go? [SPEAKER_00]: Well, I got to be honest that the way you initiated that question, my hospital medicine brain, John and that said 49 year old with new word finding difficulty and I'm calling a code stroke on this on this patient.

[SPEAKER_00]: So I got to rewind and get back to the outpatient clinic and that this is probably a more chronic sort of sort of presentation that this patient has. [SPEAKER_00]: similar to our prior conversations where, you know, the night sweats again being the most specific symptom that I can potentially modify and treat and there may be some additional downstream benefits of that on sleep quality on, you know, how she functions during the day.

[SPEAKER_00]: I think that contextualizing this based on the data that you have described so far, I kind of want to summarize my thoughts and general take on this whole area of cognition and the dementia [SPEAKER_00]: that you pointed out was able to show us that among late starters of hormonal therapy, so in the older demographic who were already 65 and older, initiating hormone therapy, at that age, does not prevent the development of dementia.

[SPEAKER_00]: I think that we can say that with reasonable confidence. [SPEAKER_00]: You're right that there's remained the caveat of starting earlier. [SPEAKER_00]: The second study started earlier and did not find a substantial benefit over the four-year follow-up period and I think that that caveat is worth noting, right?

[SPEAKER_00]: So, you know, dementia is a very chronic sort of condition and so is that the same as saying that it wouldn't have any detectable impact over a 20-year time for that remains possible. [SPEAKER_00]: But the interesting thing here is if you look at the conversation in like the menopause space, they will say with a great deal of confidence that hormonal therapy when started early has a massive effect on lowering the risk of cognitive deterioration in that way.

[SPEAKER_00]: I would love for that to be the case, yet we do not have strong evidence supporting that at this particular time. [SPEAKER_00]: So again, while I remain open to these possibilities, at this point, we don't have the direct evidence to really show us that that is likely to have such a huge impact.

[SPEAKER_00]: And to kind of compare this to one of the conversations we had last time, this stands in stark contrast to several other, as you pointed out, like a modifiable risk factors for dementia that don't get nearly the attention that this does. [SPEAKER_00]: So there's all this [SPEAKER_00]: Hormon therapy for dementia prevention, which lacks a great deal of evidence, while we're not seeing all of this around, you know, the same degree of emphasis on cardi metabolic health improvements for vascular risk factors on alcohol reduction on, you know, hearing loss as you mentioned there's even evidence on like the shingles vaccine.

[SPEAKER_00]: has direct evidence on lowering the risk of dementia and there is not this if you were primarily concerned with a certain degree of benefit on lowering the risk of dementia, there would be many other things that you should be emphasizing at least as much if not more based on the magnitude of evidence that we have available.

[SPEAKER_00]: Could you imagine where it's at? [SPEAKER_01]: Could you imagine a Stacey Sims podcast that was like, you should get your singles vaccine. [SPEAKER_00]: I think that would be the end of her popularity in that one. [SPEAKER_01]: I've repost. [SPEAKER_00]: Yeah, so it's really interesting because if purely we're looking on just like comparative effect sizes, I would love for there to be evidence showing it.

[SPEAKER_00]: I'd be happy to recommend it for that purpose. [SPEAKER_00]: I don't have that. [SPEAKER_00]: right now. [SPEAKER_00]: And so I'm happy to treat for very well-established indications. [SPEAKER_00]: I'm even happy to, again, color outside the lines and treat a little bit for off-label indications, as long as it's safe with a plan for monitoring and to say, hey, is this helping?

[SPEAKER_00]: Great. [SPEAKER_00]: Is it not helping? [SPEAKER_00]: Okay, maybe we may be we bail on this plan. [SPEAKER_00]: Maybe we try something different. [SPEAKER_00]: So that's usually the way I would go about it. [SPEAKER_00]: But if somebody has no other concerns, no other complaints, and they just have weren't finding difficulty.

[SPEAKER_00]: Oh my gosh, the differential diagram. [SPEAKER_00]: Like, again, I'm thinking of like, this person could [SPEAKER_00]: And if it's like, oh, you just need estrogen. [SPEAKER_00]: It's like, hmm, maybe not the right move when I think about the whole scope of differential diagnosis for, you know, new ones that neurological dysfunction, that could be a mystery case of itself.

[SPEAKER_00]: And I could go down a much longer list than, oh, this is likely a perimenopausal manifestation. [SPEAKER_01]: Yeah, yeah. [SPEAKER_01]: If all you have is a hammer, everything looks like a nail. [SPEAKER_01]: Exactly. [SPEAKER_01]: Need some more tools. [SPEAKER_01]: Yeah. [SPEAKER_02]: Brain Fong is an extremely common concern, and unfortunately, one of the most dismissed, subjective cognitive concerns do correlate with objective cognitive testing.

[SPEAKER_02]: Also correlates with things like mood, anxiety, and vasomotor symptoms like hot flashes and night sweats. [SPEAKER_02]: now does MHT help? [SPEAKER_02]: We think so, but probably in an indirect way. [SPEAKER_02]: The thought is that estrogen may help protect the brain, but only if it started soon after menopause when we believe that the brain is still responsive to it.

[SPEAKER_02]: This has been termed at the timing hypothesis. [SPEAKER_02]: by waiting years or decades that window of benefit may have closed. [SPEAKER_02]: The WIMS trial tested MHT in women with an average age of 71 and found no cognitive benefit. [SPEAKER_02]: was it too late we wonder? [SPEAKER_02]: So researchers designed additional studies to answer this question.

[SPEAKER_02]: The elite trial compared early versus late initiators of hormone therapy and found no differences in cognitive outcomes when they followed them after two and a half and five years. [SPEAKER_02]: The keeps trial, who enrolled women aged 42 to 58, [SPEAKER_02]: Even post-talk analysis of the WHO showed a similar finding.

[SPEAKER_02]: So what we're left with is a bit of a mixed bag, including a growing list of underwhelming clinical trial results. [SPEAKER_02]: Now what we can confidently offer is effective treatment for Bayesian motor symptoms, like hot flashes and night sweats, when those resolve sleep improves and cognitive symptoms tend to follow.

[SPEAKER_02]: There's also evidence that vasomotor symptoms affect cognition through pathways other than through sleep disruption alone. [SPEAKER_02]: So cognitive improvement may be a secondary benefit, but it isn't something that we can confidently promise as a primary outcome. [SPEAKER_02]: Lastly, it's important to consider all of the other conditions that can impact cognition and not only focus on menopause just because that's the stage that a woman may be in her life.

[SPEAKER_02]: Conditions like anemia, thyroid disorders, sleep apnea, or evidence to prescribe just to name a few examples. [SPEAKER_01]: All right, well, we've covered body composition, covered lipids, bone, and now the brain. [SPEAKER_01]: Each of those is something that women are told to worry about, and each has a real, but bounded, menopause-specific signal, but none of them are what's actually going to kill a post-menopause woman, or even the biggest predictor of how the next 30 years will go.

[SPEAKER_01]: Let's talk about what does. [SPEAKER_01]: Using the U.S. National Center for Health Statistics data on causes of death in women aged 45 to 64, cancer is a leading single cause. [SPEAKER_01]: In women aged 65 to 74, cancer remains the leading cause with heart disease at close second. [SPEAKER_01]: From 75 onward, heart disease is number one, stroke, lower respiratory disease, Alzheimer's disease, diabetes, and accidents round out the top causes.

[SPEAKER_01]: The UK data is similar, but with one difference, dementia and Alzheimer's disease become the most common cause of death in UK women in 2011, it's held that position since. [SPEAKER_01]: Part of that is coding, just medical coding, but part is real, whether deaths in advanced dementia get coded to dementia or downstream condition like pneumonia is very well and depends on the provider.

[SPEAKER_01]: Still, osteoporosis as an underlying cause of death is below 1% in every age sort of group. [SPEAKER_01]: Hip fracture related deaths are predominantly coded to circulatory or respiratory complications most often. [SPEAKER_01]: So, let's talk about the largest modifiable predictors of all-cage mortality, and that comes down to fitness.

[SPEAKER_01]: Fitness is the combination of a few different physical capacities, and two of them carry most of the mortality signal. [SPEAKER_01]: The first is cardiovascular fitness, sometimes called aerobic fitness or CRF. [SPEAKER_01]: That's the body's ability to deliver oxygen to working muscles during a sustained or prolonged effort.

[SPEAKER_01]: That's the thing you're testing when you run vicar take like a graded exercise test. [SPEAKER_01]: The second is muscular fitness, which itself is split into strength, the maximum amount of force that you can produce, and power the ability to produce force quickly. [SPEAKER_01]: Both components carry independent mortality signals in the data, and the size of those signals is rather large.

[SPEAKER_01]: So let's start off by talking about cardiovascular fitness. [SPEAKER_01]: So we go back to a study we've talked about a few times on this podcast by Man Sager and colleagues out of the Cleveland Clinic. [SPEAKER_01]: They published a large retrospective cohort in JAMA in 2018 over a hundred thousand patients undergoing treadmill exercise testing at the Cleveland Clinic from 1991 to 2014.

[SPEAKER_01]: Now, these individuals were followed for an average of eight years, and if you compare those with the top level of fitness compared to those with the bottom level of fitness, the people in the top group had roughly 80% lower all cause mortality. [SPEAKER_01]: That's a headline number. [SPEAKER_01]: But two important things to note before we sort of run with this 80% number.

[SPEAKER_01]: First, this is observational data. [SPEAKER_01]: The people in the study were patients referred for clinical exercise testing at the Cleveland Clinic, not a general sample of adults, so there's some selection bias there. [SPEAKER_01]: Second, the 80% figure comes from comparing the very top of the fitness distribution to the very bottom.

[SPEAKER_01]: The effect between adjacent groups is much smaller. [SPEAKER_01]: So a better comparison, perhaps, comes from a 2009 meta-analysis by Kodama, which pulled 33 studies [SPEAKER_01]: Fitness, and that analysis was measured in Met's or metabolic equivalence, which is just a standardized way to express how hard an activity is more specifically how much energy it uses while you're doing it.

[SPEAKER_01]: One Met is the energy that you burn at rest, walking at a normal pace is about three Met's and it costs you three times as much energy jogging is around seven costs you seven times as much energy as sitting at rest. [SPEAKER_01]: For every one met increase in somebody's measured fitness, all cause mortality dropped by about 13%.

[SPEAKER_01]: So the lever here for cardiovascular fitness is real and it's meaningful at any starting point, but the 80% stat kind of overstates it. [SPEAKER_01]: Even with those caveats, the fitness lover exceeds traditional cardiovascular risk factors in the same Cleveland Clinic cohort, including established coronary artery disease.

[SPEAKER_01]: Mainly because low fitness has this predictive power in the short term. [SPEAKER_01]: Whereas established coronary artery disease is more of a long-term risk factor. [SPEAKER_01]: In older adults, the death rate in the lowest fitness group was about four times the death rate in the highest fitness group with most of the benefits landing as you move from the lowest level of fitness to the second lowest.

[SPEAKER_01]: So basically doing anything and to get you out of that lowest group is going to have the biggest benefit. [SPEAKER_01]: So that's a story on Cardi respiratory fitness, but when it comes to muscular strength, the muscular power resistance training adds a partially independent signal. [SPEAKER_01]: The first studies from Mama 22 in 2022 in the British Journal Sports Medicine, they pulled 16 studies together on resistance training and mortality.

[SPEAKER_01]: People who did regular resistance training had about a 15% lower all-cosm mortality rate than people who didn't. [SPEAKER_01]: Cardiovascular mortality looked similar. [SPEAKER_01]: When resistance training was combined with aerobic training, the reduction was about 40%. [SPEAKER_01]: The two interventions are partially additive.

[SPEAKER_01]: Then there's a question of what to actually measure on the muscle side, because strength and power are two different things. [SPEAKER_01]: Strength is how much force you can produce maximally, also sometimes called low velocity strength, and power is how fast or how quickly you can produce that force, also sometimes called high velocity strength.

[SPEAKER_01]: A 2025 paper from the Clinton-Mex cohort in Brazil compared the two head-to-head as mortality predictors. [SPEAKER_01]: In about 3,900 adults aged 46 to 75, who were followed for a median of about 11 years when comparing the lowest group on relative muscle power to the highest, the people in the lowest group had a roughly sixfold higher risk of dying during the follow-up.

[SPEAKER_01]: and grip strength, the standard measure of muscle strength in this kind of study was a much weaker predictor in the same people. [SPEAKER_01]: So power, the ability to produce force quickly, looks like the more useful power measurement for mortality purposes, not raw strength. [SPEAKER_01]: Now, if you haven't read this study, I thought it was pretty ingenious how they actually tested muscle power.

[SPEAKER_01]: It wasn't just how fast they could do hand grip strength. [SPEAKER_01]: That would be kind of a goofy way, I think, to compare these things. [SPEAKER_01]: It was pulling up on like a weight stack. [SPEAKER_01]: Just like imagine like you're starting a lawnmower with both arms and yet rip a weight stack up to do so that's how they did it.

[SPEAKER_01]: I was like, oh, it's just like a high pole like a, you know, it's just like a similar to the high poles or something like that. [SPEAKER_01]: Yeah, pretty interesting. [SPEAKER_01]: So no hatecoms towards grip strength. [SPEAKER_01]: Well, maybe some hatecoms. [SPEAKER_01]: Because grip strength still carries a useful signal.

[SPEAKER_01]: And what you've probably heard about is, particularly if you listen to a T is podcast, the belabored this point, the pure study. [SPEAKER_01]: About 140,000 adults across 17 countries found that every, for every five kilogram, decreasing grip strength, there was a 17% higher all cause mortality.

[SPEAKER_01]: Now, you laid this out very eloquently before. [SPEAKER_01]: Grip strength is this sort of integrated high quality readout of not just total muscle mass, but how well it functions, the neuromuscular function, and how everything is integrated together in order to work in a coordinated manner, which is why it predicts mortality so reliably in untrained populations kind of reflects the work of everything involved in that sort of system from brain to your fingertips.

[SPEAKER_01]: but it's also why the test isn't so good at self. [SPEAKER_01]: When you train the grip directly, you can increase grip strength, but it has no correlation to improve mortality. [SPEAKER_01]: And similarly, there's a strong genetic component to a grip strength, as well as a strong mass component to grip strength.

[SPEAKER_01]: So how bigger people generally carry more lean body mass, whether that's [SPEAKER_01]: an individual with obesity or an individual without. [SPEAKER_01]: And so there's a sort of paradox here where just, you know, absolute grip strength numbers can be misleading, which is why we're not big fans of like grip strength testing.

[SPEAKER_01]: I don't think that you've ever handed a patient, a grip strength, dynamometer. [SPEAKER_00]: No, zero times. [SPEAKER_00]: I've subjectively assessed grip strength, but that's again more often when I'm doing a stroke evaluation. [SPEAKER_00]: I'm trying to see if there's one arm is weaker than the other acutely, but even that is not ideal.

[SPEAKER_01]: Yeah, we did a whole episode on this, so if you want the deeper dive, check that out, it's linked in the description below. [SPEAKER_01]: So to my mind, the biggest modifiable lever against the leading causes of death in postmenopausal women is fitness, both the aerobic side and the muscular side, cardiovascular fitness and muscle power, each carry independent mortality signals and the two are additive in some ways synergistic when you do both.

[SPEAKER_01]: The largest absolute benefit on the A-Robic side comes from moving out of the bottom of the fitness distribution, so low levels of cartitous torque fitness to the second lowest level. [SPEAKER_01]: So going from sedentary to even modestly active is where most of the gain is. [SPEAKER_01]: On the muscle side, the data points towards not only being able to produce a lot of force, which is strength, but also being able to do so quickly, which is power.

[SPEAKER_01]: Now, the training that builds both of those things is not unique to menopause. [SPEAKER_01]: It's just engaging in progressive resistance training [SPEAKER_01]: Now, the menopause content space, the menopause influencer space often has the priorities reversed. [SPEAKER_01]: Heavy resistance training only, often with conditioning work framed as cortisol elevating that you should avoid it.

[SPEAKER_01]: But the actual data is quite clear here. [SPEAKER_01]: You should do both. [SPEAKER_01]: Because the two together carry the largest combined mortality benefit of any modifiable intervention available. [SPEAKER_01]: So Austin, the patient, she's 58. [SPEAKER_01]: She's postmenopausal. [SPEAKER_01]: She has been insufficiently active for the last 20 years.

[SPEAKER_01]: She's otherwise healthy. [SPEAKER_01]: She has read enough to know that she should exercise like most people, but she's overwhelmed by conflicting advice. [SPEAKER_01]: What does that conversation look like? [SPEAKER_00]: Yeah, gosh, I feel like I just need to get patients permission to start recording my visits every day because I just had another conversation like this earlier today.

[SPEAKER_00]: It is interesting to recognize that she has read enough to know that she should exercise, because she has that background information she's coming in. [SPEAKER_00]: I'm already staging her in like the kind of stages of change, behavior, behavior change sort of model. [SPEAKER_00]: She's coming in already, you know, curious.

[SPEAKER_00]: interested asking questions. [SPEAKER_00]: That already gets my foot further in the door than it might with many other patients who are either. [SPEAKER_00]: They might be aware that it's good for you, but otherwise uninterested. [SPEAKER_00]: She is at least interested, yet she feels overwhelmed.

[SPEAKER_00]: And so that's where having some professional guidance, some reassurance, helping her kind of dismiss with things that aren't worth being worried about, getting her maybe off of TikTok or social media algorithmic media that is going to [SPEAKER_00]: You know, exacerbate this problem and giving her a set of like really, really quite basic straightforward advice that can start to take her out of that like bottom quartile into the next one up in a relatively short time frame not that difficult to do.

[SPEAKER_00]: And so my first question is going to be whether she has any prior experience with physical activity in general. [SPEAKER_00]: Any sports experience, any group class fitness things, does she have any kind of social circle, anybody else that does this or anyone else who would be willing to do it with her to see?

[SPEAKER_00]: What levers can I pull to improve, you know, initiation and then adherence to this over time? [SPEAKER_00]: getting a sense of what her knowledge base is now and kind of tying that into what she might be willing to do. [SPEAKER_00]: So some form of a, you know, aerobic conditioning, whether starting out with walking and progressing to, you know, jog walks or progressing to stationary biking or some form of, you know, aerobic fitness based on her current abilities.

[SPEAKER_00]: her limitations if she has any like orthopedic or otherwise considerations that we need to think about. [SPEAKER_00]: And what does she willing to do? [SPEAKER_00]: What does she has acts? [SPEAKER_00]: What does she have access to doing? [SPEAKER_00]: And then finding a way to set the volume and the intensity of that aerobic activity.

[SPEAKER_00]: The intensity we tend to set most often in folks like this. [SPEAKER_00]: with something as simple as a talk test, we want to get you to a point where you can, you know, talk, but not sing. [SPEAKER_00]: Maybe speak in a couple word sentences, but not be able to sing fluently. [SPEAKER_00]: If you can, you know, be able to belt out a whole verse of a song.

[SPEAKER_00]: It's still probably a bit too easy. [SPEAKER_00]: That's a reasonable way to do it. [SPEAKER_00]: If that doesn't resonate, then maybe introduce them to just a subjective effort scale and push in them to the right degree of effort. [SPEAKER_00]: That would be the way we do that. [SPEAKER_00]: And then starting out with a very low volume.

[SPEAKER_00]: You know, maybe two sessions a week, something like that at a moderate amount of duration, say 15 minutes, 20 minutes, and then working that up with our current physical activity guidelines in mind with a defined timeline of how long it should ideally take us to get there. [SPEAKER_00]: That would be the way on the aerobic side of things.

[SPEAKER_00]: As far as strength training goes, I'll go back to my traditional sit-to-stance as the place where I start, assess what is the person's current level of muscular strength and power by having them try to stand up again as quickly as they can, because that can introduce a little bit of velocity to it and then see can they do that loaded, especially if they can stand up already without the use of their hands, and then from there that can be my launching point to explore what forms of loaded resistance training is this person able and willing to do.

[SPEAKER_00]: are they going to have access and be interested in going to a gym is going to be a home-based program if so what sort of loads do they have available to them and how can those be progressed over time? [SPEAKER_00]: If ultimately all I can negotiate is basically for somebody to do some loaded sit-to-stands and some pick-ups at home twice a week that can be loaded to a level that's again kind of hard.

[SPEAKER_00]: I'm okay with that as a starting point and then again a couple sessions a week. [SPEAKER_00]: of moderate intensity, erobic activity to where they can talk, but not sing. [SPEAKER_00]: I'm also okay with that as a starting point. [SPEAKER_00]: That will be life-changing for this person, and then we can kind of progress it over time based on their abilities based on the interests based on their motivation, things like that.

[SPEAKER_01]: Yeah. [SPEAKER_01]: Yeah. [SPEAKER_01]: I think when people hear that, they're like, I don't sound like much, especially if you listen to this and you're a coach or you've been training for a long time and so you think about your own current like training load or whatever, you're like, that doesn't sound like much.

[SPEAKER_01]: And yeah, that's the point. [SPEAKER_01]: This person has not been, you know, gradually doing this for decade upon decade, which is unfortunate, but, you know, while the best time would have been to start 20 years ago, the second best time is to start today. [SPEAKER_01]: I think the disconnect is, though, when you start talking about optimal, right?

[SPEAKER_01]: And you're like, well, look, if we're trying to optimize all of the potential outcomes from exercise, the amount of exercise that we would really want to get you to work up to is probably more than you can do, not because like, you're a bad person or something sort of more hang up. [SPEAKER_01]: It's like, dude, you don't have enough time.

[SPEAKER_01]: You mean you're not a professional athlete, you can't dedicate your life just to being in an awesome shape. [SPEAKER_01]: Unfortunately, that's the case for most people, you know? [SPEAKER_00]: And that's where the algorithmic media can really become a problem because people either see like amazing feats, which may be natural, maybe chemically enhanced, or the messaging on it is really centered around optimizing and optimize our culture and maximizing, which is fine for somebody who really has the time resources and [SPEAKER_00]: and motivation to do that, but that's not most folks, and so that could be overwhelming and why people can end up feeling like they have conflicting messaging and why women are worried about, oh, if I exercise too hard, it's gonna be give me cortisol belly and other not-sense like this, which is just not a thing.

[SPEAKER_01]: No, I have no concern about somebody training to the point where cortisol becomes a dominant hormone, and now we've suddenly induced exercise related cushions for anything. [SPEAKER_01]: Yeah, not a thing, not a thing. [SPEAKER_01]: All right, we'll look. [SPEAKER_01]: There's one more thing worth covering before we wrap up.

[SPEAKER_01]: Now, most of what gets marketed to midlife women as a menopause crisis is better explained by 20 years of declining physical activity. [SPEAKER_01]: Now, in researchers put accelerometers on people instead of asking them how active they were. [SPEAKER_01]: Less than 5% of US adults, over the age of 40, hit the recommended 150 minutes per week of moderate to vigorous activity.

[SPEAKER_01]: For women specifically, those age 40 to 49, only 3.4% hit this level of conditioning each week. [SPEAKER_01]: For those 50 to 59, it's about 2.7%. [SPEAKER_01]: Sedentary time average more than seven hours per day. [SPEAKER_01]: Now, when you compare this to the 42% of women who self-report that they are doing this much conditioning, you see where part of the problem lies.

[SPEAKER_01]: This is not unique to women, men do the same thing. [SPEAKER_01]: Now consider that only about 15% of women, self-report that they're lifting weights. [SPEAKER_01]: How big of a problem do you think? [SPEAKER_01]: So this lack of exercise has predictable consequences. [SPEAKER_01]: In the 2005 Baltimore longitudinal study of aging, 375 women were followed with serial measurements of their VO2 max over a meeting of eight years.

[SPEAKER_01]: VO2 max is just a way to measure your cardiovascular fitness. [SPEAKER_01]: So they found that a aerobic capacity does not decline in a straight line. [SPEAKER_01]: Rather, the rate gets faster each decade after 30. [SPEAKER_01]: In your 40s, women lose about eight to 10 percent of their aerobic capacity per decade.

[SPEAKER_01]: In your 50s, that climbs to 10 to 14 percent. [SPEAKER_01]: The menopause specific piece is worth about 1% per decade, whereas most of the drop is aging plus the activity decline that we just talked about. [SPEAKER_01]: For lean mass in 2000, Janssen measured whole body muscle mass using MRI, which is very, very accurate in 468 women.

[SPEAKER_01]: Scale little muscle mass holds relatively steady until about age 50, then declines about 0.7% per year after that. [SPEAKER_01]: Strength declines about three times faster. [SPEAKER_01]: The piece that the swan data can attribute to menopause itself is about 200 grams of lean mass loss across the transition.

[SPEAKER_01]: Now, compare lifelong trained postmenopausal women against women of the same age who haven't been exercising. [SPEAKER_01]: The catch is, this kind of comparison comes from selected populations. [SPEAKER_01]: Master's athletes and people enrolled in long-term studies of exercise, so certainly some survivor bias and selection bias.

[SPEAKER_01]: lifelong exercises tend to be healthier to begin with, more consistent with their exercise habits, and more likely stick around for follow-up. [SPEAKER_01]: So while these comparisons tell us what's biologically possible, they don't tell us what an average insufficiently active woman starting fresh at age 55 is able to achieve.

[SPEAKER_01]: Now, with that caveat in mind, let's talk about aerobic capacity. [SPEAKER_01]: For aerobic capacity, the Pollock Studies followed Masters in Durans running women over 20 years. [SPEAKER_01]: Trained women in their 60s had VO2 max levels of 45 to 55. [SPEAKER_01]: Verse age matched sedentary controls at levels of 22 to 28.

[SPEAKER_01]: That's roughly a two-fold difference, and the trained 60 year olds in the sample had aerobic capacities that would put them in the fit range for women decades younger. [SPEAKER_01]: Right, if you look at the average VO2 max for women in their 30s, it's not even that high. [SPEAKER_01]: It's lower.

[SPEAKER_03]: Okay. [SPEAKER_01]: For bone that eFops study we talked about earlier, at 16 years, showed that Lumbar spine bone mineral density dropped 4.5% in controls, burst 1.2% in the exercise group over 16 years. [SPEAKER_01]: It's not a gain, but a meaningful preservation over 16 years. [SPEAKER_01]: And, oh, by the way, their resistance training component was not very intense.

[SPEAKER_01]: First strength, a 2024 longitudinal analysis of competitive power lifters showed something even more striking. [SPEAKER_01]: The general population loses about 1% of their strength per year after middle age, but in this study, women over 59 who kept training and competing gained a 2.5% to 5% per year.

[SPEAKER_01]: That's the opposite direction of what's supposed to happen. [SPEAKER_01]: So a trained 60 year old looks more like an untrained woman 15 years her junior across the measurements the matter. [SPEAKER_01]: She isn't reversing aging as father time is undefeated, and the biology that takes muscle and aerobic capacity away over time keeps doing what it does.

[SPEAKER_01]: But a meaningful amount of what gets lost between age 30 and 60 is recoverable, and the data shows how much. [SPEAKER_01]: So Austin, the woman listening to this is probably somewhere in this window. [SPEAKER_01]: Maybe she's 48 and she's just starting to notice changes. [SPEAKER_01]: Maybe she's 58 and she hasn't been exercising for 20 years.

[SPEAKER_01]: Maybe she's 65 with a dexa scan showing osteopenia and a primary care doc who told her not to lift heavy. [SPEAKER_01]: Pull the threads together. [SPEAKER_01]: What is the actual plan for any of them? [SPEAKER_00]: Yeah, not a fan of the advice from the primary care. [SPEAKER_00]: So I think that initially seeking out some better guidance and expertise in this space would be worthwhile, whether the person has symptoms that are concerning to them.

[SPEAKER_00]: And I don't even qualify them as perimenopausal symptoms because I'm going to say that they're going to be a wide variety of potentially specific and non-specific symptoms. [SPEAKER_00]: Like seek out some qualified expertise and guidance to help you work through it in a comprehensive way.

[SPEAKER_00]: I think that that's been [SPEAKER_00]: One of the two consistent themes throughout this episode is that there are symptoms that you may experience some are more suggestive of the perimenopausal menopausal transition that can be very effectively treated with say things like menopausal hormone therapy or non-hormonal options there are also other symptoms that are maybe less suggestive.

[SPEAKER_00]: and that those deserve their own, you know, broad evaluation to make sure that nothing is being missed, that can be treated more effectively in an alternative way. [SPEAKER_00]: That's the first, I think, key theme is seeking competent expertise to explore the full breadth of these things that you may be experiencing.

[SPEAKER_00]: The other is this most powerful lever that you have pointed out and hammered on in the latter segment of this episode, the most powerful lever being fitness in general, which we break down into our cardiovascular respiratory component, which the prescription of which does not need to be terribly complex.

[SPEAKER_00]: It's more a question of [SPEAKER_00]: It's a sufficient volume where you're meeting certain targets on the on the talk test is fantastic and then the strength training component which can involve some both general strength or low velocity strength can involve if you like some power training can be something fun can be something explosive if you like can involve something like pickle ball if you if you love that something that a lot of folks are are picking up these days that has numerous benefits both physical social outside lots of other things.

[SPEAKER_00]: And so I think that leaning into these two aspects is a great strategy for improving your mid-life and later life health. [SPEAKER_00]: Targeting the biological components through medical evaluation and treatment when needed. [SPEAKER_00]: Psychosocial factors, as well as protecting your longevity, your physical function, your muscles and your bones, by meeting these kind of physical activity guidelines that we've been hammering on for, you know, as you said, better part of two decades at this point.

[SPEAKER_00]: They have not. [SPEAKER_00]: change that much over that period of time, it's more the uptake that we need to keep working on improving. [SPEAKER_00]: So strength training likely to be safe for the person in this demographic who's listening, cardiovascular respiratory activity, there's likely to be some modality that we can find.

[SPEAKER_00]: And then to the extent you're experiencing debilitating frustrating symptoms, if you're making progress or not making progress with your clinician. [SPEAKER_00]: Again, seeking out other opinions specifically with expertise in this space can be worthwhile for you. [SPEAKER_01]: Yeah. [SPEAKER_01]: Yeah.

[SPEAKER_01]: Well said. [SPEAKER_01]: And I think, you know, it's a recurring theme when we talk about exercise and dietary pattern change. [SPEAKER_01]: There are very few situations that actually require, I don't want to say necessarily specialized knowledge, but a specialized approach. [SPEAKER_01]: it's mostly the same.

[SPEAKER_01]: And when you talk about individualizing it to the person, meeting them where they're at, highlighting their preferences, their resources, what do they want to do, what's their motivation to stand the other? [SPEAKER_01]: That's universal. [SPEAKER_01]: And so I hesitate to kind of come up with a menopause specific program, unless it were to sort of be taken up better.

[SPEAKER_01]: Right, if it is branded as such, and I'm very clear that, look, while this is not specific to menopause, [SPEAKER_01]: I wrote Jen and now you're going to get some real training. [SPEAKER_01]: That's probably to the extent I could do it and feel good about myself and sleep at night. [SPEAKER_01]: But I do have to say that one of my recurring issues when investigating various topics in the space is that there is not only just so much misinformation, but it's almost like siloed in a way.

[SPEAKER_01]: It was like, no, no, you need this specific fund of knowledge in the specific person. [SPEAKER_01]: that does not seem to be well supported by evidence. [SPEAKER_01]: If there was, then you know, let's develop a new medical specialty, you know, which I know has been discussed, but I think that's mostly because OBGYNs are kind of, there's a broad base of things that they have to address.

[SPEAKER_01]: And so yeah, that might change. [SPEAKER_01]: But anyway, Austin is anything you want to add for the woman listening to this, who's somewhere in this window. [SPEAKER_00]: I think this is probably, you know, to the extent that you are interested in detailed information on this, these episodes can potentially be quite dense.

[SPEAKER_00]: Might need some multiple listens if you are in need of additional opinions or expertise. [SPEAKER_00]: Again, we are available and happy to help by way of consultations either the other doctor Barack here or myself. [SPEAKER_00]: We do this every day with folks. [SPEAKER_00]: So yeah, happy to help.

[SPEAKER_01]: a few things to take away from today. [SPEAKER_01]: First, body composition. [SPEAKER_01]: The menopause transition adds about 1.5 kilograms of fat and takes about 200 grams of lean mass over a time period of about three to four years. [SPEAKER_01]: That is real and the menopause specific piece is where the fat goes.

[SPEAKER_01]: This rule fact goes up and fat that doesn't get stored as subcutaneous or under the skin ends up in places it shouldn't be, which we call ectopic fat. [SPEAKER_01]: First is a liver and the visceral compartment that's around the organs inside your abdomen and then in the muscle potentially.

[SPEAKER_01]: The other 8 to 13 kilograms though that's associated with midlife weight gain, let's mostly aging and habits that predate the transition and outlast it. [SPEAKER_01]: Second, party metabolic. [SPEAKER_01]: LDL and apolipoprotein B or apobi rise in a narrow window around the final menstrual period, and that part is really menopause.

[SPEAKER_01]: The rest of the picture, though, blood pressure, insulin resistance, metabolic syndrome risk, well that tracks with the visceral fat redistribution and aging more than the hormonal change. [SPEAKER_01]: The hormons are upstream, the fat is what's doing the damage, and exercise can play a big role here.

[SPEAKER_01]: third is bone. [SPEAKER_01]: The biggest deposit window or opportunity window to build bone mass is in the teenage years through the late 20s when peak bone mass is laid down. [SPEAKER_01]: After 30, it's mostly about preservation. [SPEAKER_01]: Bone loss accelerates sharply around the final menstrual period, with most women losing about 10% of lumbar spine bone mineral density across this window.

[SPEAKER_01]: The bone that you build by 30 is kind of what you have to draw down from. [SPEAKER_01]: Now for women with low bone mass when they hit menopause, resistance training is still the standard recommendation. [SPEAKER_01]: You gotta do. [SPEAKER_01]: The 2018 Lyftmore study established that heavy training is safe and effective in postmenopausal women with low bone mass.

[SPEAKER_01]: But for women with the established osteoporosis with prior fragility fractures, pharmacotherapy enters the picture. [SPEAKER_01]: There are many different medications that can be helpful, including MHT, especially as an option for younger postmenopausal [SPEAKER_01]: 4th cognition. [SPEAKER_01]: Brain fog is real in this phase, but it's mostly recoverable.

[SPEAKER_01]: It generally is the result of poor sleep, mood changes, and vasomotor symptoms, especially those that keep people up at night, or disrupt sleep, more than estrogen alone acting directly on the brain. [SPEAKER_01]: Menopausal hormonal therapy does not prevent dementia based on any evidence that we have, but treating the sleep and particularly hot flashes that disrupt sleep can help cognition indirectly.

[SPEAKER_01]: The fifth takeaway is about mortality. [SPEAKER_01]: Cardiovascular fitness and muscle power are the two biggest modifiable mortality levers that we have, and they stack. [SPEAKER_01]: The menopause content space mostly has this backwards. [SPEAKER_01]: Heavy lifting only with conditioning treated like it'll spike your cortisol and ruin you.

[SPEAKER_01]: The data says to do both, and the biggest single gain is going from doing nothing to doing something. [SPEAKER_01]: And finally, Metapausal hormonal therapy or MHT. [SPEAKER_01]: It is certainly the right answer for hot flashes for the genital urinary symptoms and for some bone protection in eligible women, but it's not really the answer for body composition, cardiovascular disease prevention, cognition, or mortality.

[SPEAKER_01]: Now next week, we get into the actual prescription, what the training and nutrition and other lifestyle changes actually look like for a woman who's in this window, how they should start, how they should progress, and what to do when life gets in the way. [SPEAKER_01]: I'm Dr. Jordan Fagan-Mom, that's Dr. Austin Baraki and Dr. Lorraine Baraki.

[SPEAKER_01]: This has been the part of Madison podcast. [SPEAKER_01]: Thanks for listening.

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