← The Dr. Gabrielle Lyon Show
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Here's the paradox I want to address with you today. The molecular pathway that the longevity world wants you to suppress is the same pathway that builds and protects muscle. We know that muscle is the single and strongest, most modifiable predictor of whether you stay independent or frail. The protein scare is a case study in how biology can outrun real evidence. Protein does raise IGF1, but here's the lever everyone's pulling on the wrong end. In a body with insulin resistance, chronic high insulin from too much refined Carbohydrates means bioavailable. IGF1 runs high all the time, not because of protein, because of the insulin. The biggest driver of your IGF1 is your growth hormone, set by your genes, your age, your sleep, your and your body composition. The longevity message asks the people most likely to die of muscle loss to eat less of the only thing that defends them. So what is actually killing people at scale isn't a slightly busy growth pathway. It's frailty. It's the slow, silent, entirely preventable loss of the muscle you were told to stop feeding. So here is the plan. The longevity world has convinced a generation of women that protein is shortening their lives. The science says they've got it backwards. And the people most hurt by the message are the ones in perimenopause who need protein the most. Now here's a quick disclaimer. I am not your physician and this episode is for educational purposes only, not medical advice. And if you have kidney disease or any other illness, please talk to your healthcare provider. I have to address something head on because I keep hearing it from you. It's all over the comments and frankly, it's creating real torment. The fear is this dietary protein will shorten your life. That every chicken breast, every egg steak is aging you, Feeding cancer, switching on the machinery of your own decline. This idea didn't come out of nowhere. It was actually popularized by scientists in the longevity world. Guys like Valter Longo, whose lab has produced some of the most cited work on this, David Sinclair and the broader anti aging movement. And it lands hardest on one specific the woman in perimenopause. Because let's face it, she's already watching her body change, anxious about aging, being told to fear foods that built her. And she's hitting all of this at the time. Her estrogen is a bit more erratic. Maybe her muscle is also walking out the door. Here's the paradox I want to address with you today. The molecular pathway that the longevity world wants you to suppress is the same pathway that builds and protects muscle. We know that muscle is the single and strongest, most modifiable predictor of whether you stay independent or frail. And today I'm going to do something rare. I'm going to give you the strongest version of the protein. Shortens your life argument to. To the best of my ability. Then I'm gonna walk you through what the evidence shows when you refuse to drop the inconvenient parts. And by the end, you're gonna understand this well enough that nobody on the Internet can scare you with words again. You get to decide. Segment 1 what MTOR actually is. Let's define the villain. In every story there's a villain. Because almost all fear comes from people throwing this word around like a curse word. Mtor. MTOR stands for mechanistic target of rapamycin. It's an enzyme that sits at the center of one of the most important decisions your cells make. Do I grow right now or do I conserve and repair? MTOR switches on when fuel, especially the amino acid leucine is available. When insulin and growth factors are up. And when your muscle is under load, for example, training. When it's on, the cells build. It quiets down when you're fasted calorie restricted or low on protein. Then the cells shift into a cleanup mode like autophagy, your cellular recycling program. Now, here is the distinction what I have seen that every viral video gets wrong. Mtor isn't one thing. It runs as two separate complexes. MTOR1 is the build complex. It drives muscle protein synthesis. This is the one that the longevity crowd is afraid of. And then there's MTOR2, which handles glucose and insulin signaling. And here's the catch. Nobody mentions rapamycin, the drug this whole pathway is named after the drug behind nearly every MTOR inhibition extends life headline. It doesn't cleanly hit only one bild complex. And here's the catch. No one mentions rapamycin, the drug this whole pathway is named after. The drug behind nearly MTOR inhibition extends life headline doesn't cleanly hit only the built complex. With chronic use, it suppresses MTOR C2. And that gives you glucose intolerance, insulin resistance, and potentially a weakened immune system. So the next time someone says just suppress mtor for longevity, the honest question is the following. Which complex, in which tissue, at which age, and at what dose? Because mtor isn't a light switch you flip on and off. It's on and in every cell there's a dimmer dial. And that does completely different things in your muscle versus your liver at 30, at 80 after a workout or when you're fasted. Treating it as if it's one villain to be silenced is not sophisticated. It's do I dare say, biologically illiterate. Now hold that thought. And this is going to carry us through the whole episode. Segment 2 the high protein Deception and this is the RDA deception. What High Protein actually Means now, before we get into the evidence on either side, we need to fix a definitional problem that has corrupted this entire debate because of the words high protein and low protein don't mean what you think they mean. The RDA is not a recommendation. It is a minimum to prevent deficiency. The RDA is set at 0.8 grams per kilogram that was derived from short term nitrogen balance studies, experiments measuring whether the body is losing more nitrogen than it takes in, which is a marker of net protein loss, albeit not a marker of health, but protein loss. The true physiological minimum, the bare minimum amount needed to maintain nitrogen balance in a healthy young adult male. And that said it, just to round it up, 0.6 grams per kilogram a day, the RDA adds a safety margin on top of that to cover 97.5% of the healthy population. It was never designed to define optimal intake for muscle function, disease prevention or longevity. It was designed to answer one question how little protein can a person eat without measurably wasting away? Friends, this is a very different question from how much protein should a person eat for optimal health? So the RDA sits just above the danger zone. It is a floor, not a target. And here is where the the definitional problem poisons the debate. The Levine 2014 study this is probably one of the most cited papers in the protein shortens lifespan camp classified high protein as greater than 20% of the total calories. But the acceptable macronutrient distribution range for protein set by the National Academies is the following 10 to 35% of total energy. So Levine's high protein falls squarely in the middle of the accepted range. And at the 2025 Dietary Guideline Changes for Americans, they just moved the recommended protein intake to 1.2 to 1.6 grams per kilogram, roughly 16 to 21% of calories. Which means what the longevity literature has been calling dangerously high is now what the US government calls recommended. The Falconi 2025 reanalysis of the Levene paper is the closest thing to a direct rebuttal that we've seen. This study, co authored by Stu Phillips, one of the most prominent protein researchers in the world and a handful of other experts went back to the exact same data set that Levine used with a larger sample size. For example, Levene used around 7,000 and this study used around 16,000 people and took a longer follow up and more rigorous intake methodology. What did they find? It found no association between animal protein or plant protein and all cause mortality in any age group, including the 50 to 65 cohort. IGF1 showed no link to mortality at any age. Animal protein was mildly protective for cancer mortality. Again, let this land for a moment. This the intake that one camp says accelerates aging and causes cancer is the intake that the latest Federal Dietary Guidelines, the Prodage Study Group, the European Society for Clinical Nutrition and Metabolism and the Asian Working Group for Sarcopenia all now recommend. Especially for older adults. The actual protein landscape looks like the following 0.8 grams per kilogram a day. This is the RDA, a deficiency prevention floor derived from 1940s era methodology essentially unchanged for over 70 years to now. 1.2 to 1.6 grams per kilogram. The new dietary Guidelines and the range recommended during active weight loss, which is closer to 1.6 grams per kilogram which is approximately twice the RDA, the level supported by the Protein Summit 2.0 consensus for optimal muscle and body composition. Now the one important exception here as we talk is adults with advanced chronic kidney disease. Specifically if your GFR is below 30 who are not on dialysis, you guys need to talk to your doctor and again, this is a medical decision with your provider. The bottom line for this debate is the next time someone tells you high protein intake is associated with increased mortality, ask them what they mean by high. Because in most of these studies high means the intake that every major expert consensus group now recommends. The protein longevity debate has been fought on a battle where the definitions were rigged from the the start. What do I mean by these definitions were rigged from the start? Well, what is high protein versus what is low protein? There is a ton of confusion which is why I laid out those numbers. High protein is not 1.2 to 1.6 g per kg. That would be a moderate amount of protein simply by definition because if the RDA is set at the minimum and you double that, that's moderate, that's not high protein definitions become important because that is how we are judging the information. Segment 3 Now I'm going to argue the case against protein the other side and I'm going to argue it to the best of my ability because if I can't state the opposition, then there's no way for Me to have earned a right to disagree. Number one, the animal data is genuinely impressive when it comes to mtor. Rapamycin, the drug that we talked about earlier, is the most reproducible drug we have for extending lifespan in mice. In the gold standard program run across multiple labs specifically to kill off junk findings, it extended medium lifespan somewhere around this is impressive. 15 to 25%. That's real. It's been replicated, which is really important. And when you restrict protein or even just the amino acid methionine, which is a model of say a vegan diet in rodents, you trigger a hormone called FGF21 and you see metabolic benefits and longer life. The coherent biology. Less protein, less growth signaling, longer life. Okay, that's number one. Number two, the study everyone quotes the Levine paper in Cell Metabolism 2014. And note Valter Longo is the senior author on this paper. In adults aged 50 to 65. There's that word again. High protein intake was tied to roughly 75% jump in overall mortality and a several fold jump in cancer death. And the Signal tracked with IGF1, the major growth hormone you make in response to protein number three. The logic is intuitive. MTOR and IGF1 promote growth. In an adult, the cells dividing most aggressively are often the ones at risk of turning cancerous. So stop lowering the growth pedal three times a day. Lower your cancer risk. Slow aging, that's the case. I want you to feel its weight. Not because it's not nothing. Real scientists believe it and now we're going to stress test it because honesty cuts both ways and this is where things kind of start, start coming apart. Segment 4 Rodent data is not human data and unfortunately I've spent a lot of time with rodents. Here's the thing most people wave off in a single sentence. Well, mice aren't people. This is really important. Ad libitum fed laboratory mice are essentially metabolic disease models and this is critical and it is underappreciated and a confounder in the entire MTOR protein restriction longevity literature. The MTOR activation pattern is completely different in this group of quote obese mice. This is a key mechanistic point for the podcast. In ad libitum fed mice, MTOR C1 is essentially activated around the clock because the animals never stop eating. A 2024 Cell Report study demonstrated that the observed differences in MTOR activity between the ad libitum and and calorie restricted mice were entirely dependent on when relative to feeding the measurements were taken. This is not some fundamental biological shift. Mice die of different things than you do. The mouth strains in those landmark longevity studies die mostly of lymphomas and connective tissue tumors. They don't get atherosclerosis, they don't get Alzheimer's. And here's the part that should stop you, because it stopped me. A major 2013 analysis found that rapamycin barely touched most actual markers of aging in those mice. The lifespan extension was largely explained by suppressing the specific cancers that kill lab mice. So the precise, honest version of rapamycin extends lifespan is rapamycin can block the tumors that kill a particular mouse. Whether that does anything for the human disease landscape, heart disease dementia is genuinely unknown. Here's the argument that does hold. Even genetically diverse lab mice still die overwhelmingly of cancer. And that 2013 analysis found rapamycin lifespans benefit is largely about suppressing those tumors, not broadly slowing aging. And every one of these mice, diverse or not, lives the same artificial life, caged, never foraging, fed unlimited chow. And in rodent studies, MTOR is turned on 24 hours a day by constant feeding. Because that's what rodents do in humans. Last time I checked, there is more of an on, off switch, more of one. You eat. MTOR activates, you stop eating, it quiets down. You cannot model the benefits of dialing down growth in an animal that never stops eating and does nothing all day and then prescribe it to humans whose actual problem is the opposite. Not enough muscle, not enough movement and not enough protein. There is, to date, to my knowledge, 00 human longevity data. There is no completed human trials showing that suppressing MTOR extends lifespan or health span or muscle span. The strongest human result is a six week study showing a better flu vaccine response in older adults. A large trial of an MTOR inhibiting drug in over 1,000 older adults designed to reduce respiratory illness failed. So when I say rodent data isn't human data, I'm not waving it off. I'm just telling you to make the leap from a short lived, caged, hairy animal raised in a lab that is sedentary to a load bearing human who needs to be strong at 80 is one of the largest unexamined leaps in all of nutrition science. From my perspective, the MTOR longevity story is a beautiful plausible hypothesis. Anyone selling it to you as a settled fact is running ahead of the evidence. Segment 5 the IGF 1 cancer story is smaller than you've been told. This is the heart of it, so stay with me. The whole protein scare leans on one chain. Protein rises IGF1, IGF1 causes cancer let's look at the chain, link by link, because it does not hold the weight, no pun intended. They're hanging onto. First, the effect sizes are tiny. Yes, there is a real association between IGF 1 and a few cancers, but size is everything, so I've been told. In the UK Biobank, nearly 400,000 people, a meaningful rise in IGF1 nudged cancer risk up by roughly 3 to 11%, depending on the cancer. Now put that in perspective. Smoking raises lung cancer risk by 1 to 2000%. Obesity 50 to 100%. We are comparing a speed bump to a cliff and calling them both dangerous. Driving number two. IGF1 protects against some cancers. In that same data, higher IGF1 was associated with lower risk of lung, ovarian and liver cancer, and liver dramatically. So that is not how a real life cancer fuel behaves. Real life is messier than the slogan. Third, the age paradox breaks the logic. IGF1 peaks in puberty and falls your whole adult life by 70, you're running at maybe half of your young adult levels. But cancer risk climbs as you age, exactly as IGF1 is dropping. If IGF1 were really the engine of cancer, those two curves should rise together. They run in opposite directions. Fourth, and this is the one that should change how you feel walking out of here. The relationship with death is U shaped. When researchers pooled the data, both low and high IGF1 raised mortality. The safest place was to be in the middle. And the people with the lowest IGF one had a nearly 40% higher risk of dying than the people in the middle. Think about what that means to you. If you aggressively crush your IGF1 by slashing protein, which is exactly the advice the longevity crowd gives, which again, I don't even know if that's gonna work. You don't reach some safe zero, you can fall off the other side of the mountain into the low IGF1 danger zone, which is every bit as deadly. Now the confounders. Because this is where the causal chain truly snaps. Calories, not protein, are what most people think they're cutting. And calories barely move. IGF1, the most rigorous human trial cut calories by 25%. For two full years, IGF1 didn't budge. When researchers pooled the trials, the effect of calorie restriction on IGF1 was essentially zero. You only move IGF1 by starving, cutting intake by half, which no one can live on, at least not for long. Protein does raise IGF1, but here's the lever everyone's pulling on the wrong end. Total IGF1 isn't the same as free active IGF1. Insulin is what frees it up. When you eat carbohydrate insulin rises. It knocks down the binding protein that keeps IGF1 leashed and free. Active IGF1 then goes up even when total IGF1 hasn't changed. In a body with insulin resistance, chronic high insulin from too much refined Carbohydrates means bioavailable IGF 1 runs high all the time, not because of protein, because of the insulin. So picture the advice. Eat less protein to lower your IGF one while ignoring the hyperinsulinemia that drives the active fraction, that's grabbing the wrong lever entirely. And when researchers use the one method that's designed to cut through confounding, which is Mendelian randomization, which uses your genes as the natural experiment, the story flips outright. Genetically higher protein intake tracked with lower colorectal cancer risk, while higher carbohydrate intake tracked with higher risk. The German Nutrition Society did a full umbrella review and concluded total protein intake is not associated with breast, prostate, colorectal, ovarian or or pancreatic cancer. The honest summary the biggest driver of your IGF1 is your growth hormone, set by your genes, your age, your sleep and your body composition, not by whether you're eating 1 gram or 1.6 grams of protein per kilogram. The protein to cancer chain is far weaker than confident voices online would ever admit. Segment 6 what saves you and what harms you? So let's talk about what the strong human data on actual death is. Let's start with the headline that they bury. A massive analysis. 32 studies, over 700,000 people found that higher total protein intake was associated with lower death from all causes. Not higher, lower. That's the largest body of human evidence we have. And it points the opposite direction from the scarcity, from scaring people to eat protein. Now the real body count, which I have seen all too much of sarcopenia, that's age related loss of muscle and strength. And it roughly doubles your risk of death when it shows up alongside frailty. Mortality is three and a half times higher. Low grip strength, slow walking speed, can't rise from a chair. They aren't quaint, small, quiet signs of aging. They're among the best predictors of death we have. And this is where I need to bring it back to the woman I opened with. Because perimenopause and menopause ride along with muscle and bone loss, estrogen falls, anabolic resistance worsens many of you have been there. It gets harder to build. It's kind of like at the exact moment she's being told to be afraid of food, and specifically foods that build it. This is tragically disguised as health advice and quite frankly, it's just a really important topic. These are issues that ride along with aging. And the official numbers are set for the wrong goal. The RDA, 0.8 grams per kilogram was set to prevent deficiencies, not to keep you strong and active. The international expert consensus for older adults, the protage group recommends at least 1:1 to 1.2 kg of protein or higher with an illness. The aging body has anabolic resistance. It needs a louder protein signal to build muscle, not a quieter one. The longevity message asks the people most likely to die of muscle loss to eat less of the only thing that defends them. Now let's fix the food fears, because most of them don't survive a controlled trial. Here we go. For example, red meat is worse than white meat. Not true. In head to head feeding trials, the gold standard, when you match the saturated fat and compare lean, unprocessed red and white meat directly, the cholesterol numbers come out awash, indistinguishable. Okay, another one. TMAO from red meat clogs your arteries. This one has fatal flaws and it's super annoying. The single biggest meat dietary driver of TMAO in your blood is not steak, it is fish. Shellfish and fish raise it far more than red meat does because fish carry TMAO preformed in their flesh. If TMAO were really the artery villain, fish would be killing us dead. All dead. Decades of data show the opposite. What about this one? Plant protein is just better protein says no one ever. When the data says plant protein is protective, likely what they're really capturing is everything that travels with plants. The fiber, the polyphenols, the unsaturated fats. Fiber alone is tied to roughly 23% lower risk of death in over a million people. And that's a bigger signal than plant protein itself. Eat more plants. Absolutely. For the whole package, but don't eat more plants because you think it's a better source of protein. Plant protein beats animal protein. And this one is not what controlled trials show. So I mean, we need a villain here. We need one, right? I'm going to throw it out there. Maybe it's processing. And to what extent that we process our red meats, is it drastically more dangerous? I don't know. But we all need a villain. So here it is. Process red meats segment 7 the honest verdict here's what the evidence supports when you refuse to drop the inconvenient findings. Six things I'll start with the villain. Number one Processing meat may not be good for you. Not protein friends, not animal protein, not saturated fat by itself. But perhaps the nitrites and the preservatives in processed meat maybe they carry a consistent signal for harm, though the certainty of that evidence is rated low to very low by the grade system and that is the gold standard. And the absolute risk increases are modest. The IR classified processed meat is a Group 1 carcinogen, the same category as smoking. But come on. That classification reflects the strength of evidence that some risk exists, not the size of the risk. Smoking raises lung cancer by 1 to 2000%. Processed meat raises colorectal cancer risk by about 17% per 50 grams a day. Maybe same category, wildly different magnitude. So may not be good for you is the honest framing. Not red meat that is processed will kill you. Number two, unprocessed red meat and white meat are basically equivalent for heart disease risk in controlled trials. The scary observational signal for unprocessed red meat is small, shaky, and mostly reflects the junk food lifestyle it tends to travel with. A 2022 burden of proof study in Nature Medicine found weak evidence of association between unprocessed red meat and colorectal cancer, breast cancer, type 2 diabetes and ischemic heart disease, and no evidence of association with stroke. The plant advantage is real, friends, but it's the food matrix. It's the fiber and the phytonutrients doing the work, not some superiority of of the protein itself. Eat your plants for the whole package, not because animal protein is poison. Number four, the IGF1 cancer story is far weaker than advertised. The effect sizes are tiny, the relationship with death is U shaped, so crushing IGF1 is its own danger. The age paradox undercuts the logic and calories and carbohydrates confound the protein signal in ways that people fail to mention. Number five and this is the correction I want to make directly. You've heard that protein is harmful before the age of 65 and only safe thereafter. That comes from one single observational study built on one day's worth of food recall. A 2025 reanalysis of that very same data set, bigger sample, longer follow up, better methods, found no association between protein and death in any age group, including the 50 to 65 crowd. IGF1 showed no link to mortality at any age and animal protein was actually mildly protective against cancer, death. There is no good basis for restricting protein by age. There is strong consensus that older adults need more. Number six, MTOR is not your enemy. The healthy pattern is pulsing it. Switch it on with training and protein. Let it settle down between meals. And here is the contradiction to catch. The influencers telling you to suppress MTOR are usually also telling you to exercise. Exercise is one of the most powerful MTOR activators there is. They're giving you advice that fights itself. So in closing, what are you going to do Monday morning? The protein seeds scare is a case study in how beautiful biology can outrun real evidence. The MTOR story is elegant, yes it is. It might even be right in broad strokes. But beautiful biology in a three year old mouse is not a treatment plan for a living human. And it is certainly not a reason for a woman in perimenopause to be afraid of her own dinner. So what is actually killing people at scale isn't a slightly busy growth pathway. It's frailty. It's the slow, silent, entirely preventable loss of the muscle you were told to stop feeding. So here is the plan. You're going to eat for adequate protein. For most women, that means landing roughly closer to a gram per pound of your target body weight. Don't flinch, just get after it, front load it, don't skip it. At breakfast, build your plate around minimally processed foods like fish and eggs and poultry and quality meat. And pile on plants for the fiber and the nutrients hit your leucine threshold each meal, the muscle gets the signal. And then lift heavy things for the rest of your life to give that growth signal a reason to exist. So for that healthy woman lying awake wondering if her protein is aging her, looking at the ceiling, having nightmares, it almost certainly isn't. Be deeply skeptical of anyone who solved aging with a single molecule found in a lab mouse. And be even more skeptical of anyone who wants you to be afraid of your own strength. Eat for the body. You want to be living at 90. Go out there, get strong and I'll say see you next week.