The Hidden Shift In Midlife: Hormone Decline, Muscle Loss, and Healthy Aging During Menopause

All right, Dr. Nixon, I would love— I'd love to start this conversation talking about particularly midlife women. And, and you and I are both in high agreement that the experience of midlife and perimenopause and menopause is not just about hot flashes and night sweats and the symptoms themselves, that it's a huge metabolic change that actually starts long before your period stops. And in Yeah, and then we really have to look at the entire impact to a woman's body. And I've gone into a lot of detail over the years about kind of mitochondrial impact and things like that. But you have also a very similar thought process about the muscle being the healing gland, for lack of a better word, or the healing organ for metabolic changes in menopause. So let's go a little deeper in that. And what are some of the signaling things that happen? Specifically to a woman when they go through menopause?

Okay, well, let's start pre-menopause because women and men peak our hormone balance in our teens. You know, women peak theirs around 15, men usually around 18. We are a little slower than you guys, you know, but then we keep growing into our early 20s and you guys usually stop around 17 or 18. So I think one of the things that most folks don't realize is that estrogen is not a woman's primary hormone. Now, when, when women are in their late teens, they have 2 to 2.5 times more testosterone than estradiol in their bloodstream. And so that testosterone is what provides drive, ambition, self-confidence, not to mention libido and sexuality. And then by late 30s, it's already starting to decline. And by the time women hit 50 or so, when menopause usually happens, that is, they have their last period, their estradiol is down about 50%, but the estrogen won't hit the floor until about 75 years old. So you lost half your estrogen. The reason their period stops is not low estrogen, it's low progesterone, because that's down around two-thirds, 65 to 70%. But the big hit is in testosterone, which is down 80 to 85% from youthful levels. And it's that impact of testosterone on the brain that results in fatigue, depression, anxiety, ability to tolerate stress. So, you know, we, we talk about these as sex hormones and they are in our teens when we're getting ready for reproduction. But once your body is prepared to reproduce, from then on, they're primarily brain hormones. They control how we think, how we feel, how we perceive ourselves and the world around us. And as they decline, our perception of ourselves and the universe around us is altered. And usually for the worst, because all of a sudden stressors that you could tolerate easily in teens and early 20s become overwhelming. Depression or fatigue, they become your standard part of life. That you realize that 50% of all the 50-year-old women in America are on a psychotropic. It's as though too many doctors think that menopause is a Prozac deficiency.

Right.

And it's not. So my goal is to rebuild the youthful levels of all of your hormones. That was where we started way back 30 years ago when I started my first longevity clinic, was all we knew in those days was that there was a global decline in endocrine support. And that if we could move not just estrogen or testosterone, but all of your hormones back to a 25-year-old level, that the odds were you would do better. And it turned out to be true. People do do better when we move 8 different hormones all the way back to where they were in their mid-20s. And that, that has been our goal for hormone balancing for the last 30 years. In Recent years though, I have become convinced that while the hormone balancing is critically important, it didn't answer the question, why are all our hormones declining?

Mm-hmm.

And so it turns out that senescent cells, these so-called zombie cells, the living dead of our cells, are invading all of our glands. And as those senescent cells invade all of our tissue, but mostly the more active areas of our body that work turnover the quickest, then they're actually poisoning every endocrine support system in our bodies. And that is the result of, or the result of that is the drop in the hormone balancing. The unanswered question in my mind at this point is at what age do we need to intervene in removing that senescent cell load to allow our glands to recover and start making their own hormones again? So that men don't drop out their testosterone and DHEA, and women don't drop out their testosterone and DHEA. Could we keep our hormone balance at youthful levels for an extra few decades or not? Now we know that in, in the animals, in the research animals, I can treat old mice one time with senescent cell therapy and their coats will get glossy again. They'll start trying to reproduce again. They pick up their sexuality. They, their brains improve. They're able to solve their mazes faster. Their bodies are stronger. They, they run treadmills longer and faster, but rodents are tough. It's hard to kill a rat.

That's true.

We humans are relatively fragile. So my suspicion is, and I don't have the proof as yet, though I am working on it. But my suspicion is that if we want to get equivalent results in people, we're going to need to start treating them in their mid-30s to early 40s at the latest.

Yeah. Yeah. I'd like to— I'd like to take a moment to make sure, just in case my listeners have never heard of senescent cells. So senescent cells, we also talk about those as called zombie cells. So imagine you have, let's say, an ovarian cell, right? And this ovarian cell is supposed to live for a certain period of time. Now, our ovaries, our testes, stomach lining, lots of our tissues have high turnover because there's high activity, particularly the testes and the ovaries, right? So they are very subject to what's going on and they have high tissue turnover. Well, imagine you get a cell that was told, hey, you're supposed to live for like X amount of days and then it has a programmed death and it forgets and it says, screw it, I'm going to hang out. And guess what? Just like a bunch of zombies coming out of the ground and coming out of the grave and, you know, kind of like the Michael Jackson video, they start taking over the streets and all the other healthy cells go hide out and quit doing what they need to do. And so, you know, just even identifying senescent cells are relatively new, you know, and we do have that research, particularly ovarian aging tends to have a very strong time clock to the entire time clock for a woman's body. And there's, you know, there's like Boss Ovary that's trying to extend ovarian life mostly for fertility, but that would also have an impact on the act of aging when we get to midlife. So I agree, I was like, you know, the, the challenges, we know they're there, but it's like, when do you intervene and how do you identify them? Which you said you've found a way to identify through lab work. How many do you have circulating? Like, what's going on? Right. You know, because that's the, that's the holy grail, right? We know there's a problem, but how much of a problem?

Well, yeah, actually, if we look at senescent cells, this is one of God's little jokes. Okay. And I have long said that God has got a sense of humor. The, the reason that we aren't laughing is we are the joke. He has arranged things so that the human tissue that has— the only human tissue, in fact, that actually increases the number of stem cells as we age is fat. Fat for God's— why? Why fat? You know, this is like, this is a tissue that produces over 50 different destructive hormones, enzymes, peptides. That these adipokines, they cause atherosclerosis, degeneration in our joints. They damp down our immune system. They slow our brain. They cause tissues to die sooner. We don't need that. So, you know, A, we wanna get as little fat in the system as possible, but B, fat is 17 times more likely to become senescent than any other tissue in the body. And those senescent cells that build up in our fat are the ones that are actually triggering the metabolic dysfunction and causing us to become not just fatter, but diabetic, demented, cardiovascular disease, degenerative joint disease. On the other hand, muscle produces over 600 peptides, enzymes, we call them myokines, that actually help to grow new tissue and heal and repair. And so we want as much working muscle and as little excess body fat as we can practically get. The problem is that as that senescence builds up with age, we, it becomes harder and harder to make muscle and it becomes harder and harder to lose fat. And as those, those senile cells are poisoning a woman's ovaries, she actually loses her alpha estrogen receptors, which put down fat under the skin to make her smooth and curvaceous, and instead increases the number of beta estrogen cells that cause deposition of deep fat. And so she starts shifting her fat acquisition towards a male pattern, and she becomes less and less feminine and more and more masculinized. Mm-hmm. With over time. Men, on the other hand, because we are losing ours, become less and less masculine and more and more feminized with age.

Yeah. I like to call it where we're carrying the fat, right? Like, yeah. Cause when you start carrying the junk in the trunk and it kind of regressing towards the mean, we're neither truly male nor female anymore.

No, we kind of, we kind of become that neutered old person who shuffling off to the nursing home to die.

Yeah, especially the distribution. Yeah. Cause it starts to show up in the fat distribution. Like all of a sudden your waistline's gaining and men start getting, you know, fat like around their hips and thighs, which they generally don't get until—

don't forget the moobs. Yep.

The man boobs.

Yeah, sure. What we are discovering though, is that if we can remove senescent cells, we can actually shift a lot of that. Fortunately, or I guess unfortunate, I guess it depends on your point of view. My 78-year-old testicles are not likely to revert to my 18-year-old status, for which my wife is eternally grateful.

Yeah, I would say that's probably true.

The last thing she wants me is to be 18 again. However, right, I do want to function a lot better than the typical 78-year-old man. And for the last 3 years, well, for 30 years, I've been replacing all my hormones back to a 25-year-old range. And that has been good. That has helped me a lot. I wish I could show you some pictures in here of me at 50. I was round. I was soft and round. I could not have run around the block if I had to. And yet at 78, this morning I ran 3 miles before I came to work. I can bench press over 200 pounds. I've gone from a 45-inch waist to a 33-inch waist. And a lot more muscle mass at 78. 25-year-old hormone balances give you a real metabolic advantage. My wife is about 30 years my junior. She's just turned 50, but she has a 23-inch waist, solid muscle, runs like the wind, jumps rope. You, you'd swear she was in her 30s.

Yeah.

But we've never let her age. We, we started her hormone therapy when she was 30. So here she is at 50. Functioning like a much younger woman. But 3 years ago, we started treating senescent cells and lowering those loads. Okay. Now, the problem has been that we were basically treating them quasi-blindly.

Right.

Right. Because we couldn't measure them in those days. All we could do is look at how the people did, how they functioned, how they felt. And most of my patients that are getting senescent cell therapy love it. They feel better. They function better. The old man and woman aches and pains are fading away. Their skin is getting better. They're getting better muscle mass. It's easier to lose fat, though diet and activity are—

Yeah, yeah, you can't ignore that.

Absolutely critical. Energy in versus energy out, and energy out has to exceed energy in. That's just the real world. But it has— it's been a 2-year project that I've been working with a transitional laboratory group to develop a test that would let us measure accumulated senescent cell load in your immune system.

Okay, fantastic.

And the reason I picked immune system is it's the second most likely tissue to become senile. Fat is number one, 17 times baseline. Your CD8 immune cells.

Mm-hmm.

15 times more likely. So we can actually measure now the number of senile cells in your immune system that reflects roughly how much is in your heart, your lungs, your brain, your kidneys, your skin, your bones, all the other places that these things are building up. And so we're having a lot of fun with this. Yeah. And, uh, one of my, my projects now is not only working with my older patients, but with some of our younger staff members. We're actually now following theirs to see what can happen with, with hormone levels in people that we normally would not replace hormones, right? When they're 30s and 40s, we're now trying to reduce their senescent cell load to see if their endocrine glands will kick back in. And if these young men whose, whose testosterone levels are dropping and the young women whose estrogen levels are dropping to see if they go back up to more youthful levels or not.

Okay.

Don't know the results of that. Ask me in a year.

Yeah. Yeah. You just have to kind of observe it and look at it, you know, and then, but at least you've got some data there. You know, it's, you know, it's interesting. So you're looking obviously at the immune system. So obviously, is that like a fasting blood draw and you're looking at—

It's actually no. All we ask is that you don't don't attack your immune system. Don't do it after you've had a recent viral infection. Right. Don't exercise to the point of exhaustion for several days in advance. So you've got to be kind of in a steady state. So whatever you normally do is what we want you to do. Yep. And then all we have to do is draw it in a heparinized tube. Okay. Refrigerate it till we get it over to the lab. Our stability tests right now are saying we have to do the test within 72 hours. Of the blood being drawn.

Okay.

Yep. So we got to get them fairly fast. But, uh, you know, we, we get reproducible results if we can run the test, actually get them in the machines within 72 hours of the blood draw. That's interesting. That's useful information.

Yeah. You know, it's interesting because, you know, as soon as all of this information was coming out, whether it was David Sinclair talking about it, what, like a decade ago, or Others, you know, it was like all of a sudden, all these companies started flooding the market, right? With, you know, how to get rid of your zombie cells and how— and I was like, okay, cool. And I want— I'm gonna ask you some questions about that in just a second. But I'm like, of course you have no idea what the body burden is. And, and you don't know, even if you're aging, let's, let's assume as the, as the clock moves forward, that there's always gonna be an increase in senescent cells unless you're actively doing things to get rid of 'em. Cause that is part of aging in all, at least all mammals, but really all animals. With multiple cells. But then the question becomes, okay, so if now I know that, out of all the things that are out there, cuz I, you know, like I said, there's products, there's people hawking 'em online. Yeah. It's like, you know, cuz I, I looked at it and I was like, this is a wing and a pair, a prayer because I can't tell what's happening. So, and I'm a scientist, I'm a PhD, so I'm like, I need data. I need data to know.

If you don't measure, you don't know.

Yeah. And what have you found? Okay, so you're now, you've got a lab test to say they're there and they're declining based on the therapy you're doing. What are the therapies that you've found to really work clinically?

Okay. There's basically 3.

Okay.

That are available for commercial use. Okay. We started out with Dasatinib and Quercetin because that was what the Mayo Clinic used in its original studies. Yep. And I just swiped the Mayo Clinic protocol.

Yep.

Yep. Done it. I said, oh, if it's good enough for Mayo, it's good enough for me.

Yep. I mean, that's the place to start. I was there. I was like, okay, let's check it out.

So we started with, uh, you know, 100 milligrams of Dasatinib and 1,000 to 1,200 milligrams of quercetin for 3 days each week for 3 weeks. And, uh, then just see how people did because there was no way to really test effectively. The only real tests in those days was tissue biopsies. And so, you know, if I want to know what is the senescent cell load in my old heart, nobody's going to go in and biopsy my heart on, you know, just not happening, nor my brain, nor my lungs or my kidneys. I mean, come on. Yeah. But the immune system, we can check with blood, with venous blood. Hey, that's a no-brainer. That liquid biopsy is the way to go. But we started with Dasatinib. Now, in the peer-reviewed studies, they had very small groups, 7 people, 9 people, 12 people, and they were treating with Dasatinib, which is actually a cancer drug. It was approved for chronic myelogenous leukemia. And we, we know really all the side effects if you take it every day for years, but it turned out that when people only used it for 3 days each week for 3 weeks, side effect profile was very modest. And so when you look at the papers, they all say, no, side effects are transient and mild. Okay, well, I've got over 300 patients that have used it. So instead of having 7 or 8, I've got hundreds.

Mm-hmm.

I'm seeing a significant number of adverse effects with dasatinib that make it so those people can't tolerate. Blinding headaches, diarrhea, fatigue for days afterwards. I've got one person had a bizarre thing where her face turned bright red and swelled up and became— my God— tender to the touch. So I've got a fair number of folks that just do not tolerate dasatinib frequently enough to really get their levels from their 60, 70-year-old level back down to the 20-year-old where I'd Love to take them. So the next question came up, well, what about quercetin and fisetin? Quercetin was used in combination with the dasatinib, and I was really fascinated by one study in which they looked at people undergoing atrial ablation procedures for prolonged atrial fibrillation, and they ablated their, their atrium. But afterwards, a significant number of them would then rock back into atrial fibrillation.

Okay.

The procedure failed about 18 to 20% of the time. But if they prepped them with quercetin for a month or two in advance, that failure rate dropped to 4%. Hmm.

Okay.

And so Yeah. So the quercetin alone was probably reducing the senescent cell load enough to help protect them. Now, what would have happened if they used higher doses of quercetin, had used it instead of for 2 months, had used it for 6 months? You know, if we had been measuring the senescent cell load in their bodies and didn't do their ablation until the load was really low, because how low did it drop? Did it drop 10%, 20%, 40%? You know, you're doing it blindly. And the same issue with fisetin. We know that in high doses in fisetin in rodents, 100 milligrams per kilogram of body mass per day for, well, for some, some of these rats were put on it for a week at a time and then a week off and a week on and a week off. Others were done for just 2 days every 2 weeks, a variety. But the rats and mice, when you could sacrifice them and look at their organs, they saw significant drop in, in, uh, senescent cell load. But for some reason, they tried humans looking at osteoarthritis.

Okay.

Now osteoarthritis is a long-term disease process. It doesn't happen overnight. And the osteocytes, the chondrocytes, the synovial membranes, the subchondral fat pad. Each of these different tissues accumulate senile cells at different rates. And so first thing we didn't know, how susceptible were all these tissues to the, the fisetin? And B, what dose did we need and how long did we need it to drop it? Well, they took a short dose, 20 milligrams per kilogram of body mass. For 2 days every 2 weeks for 2 months. And then they said, well, we didn't see any improvement in the, in the arthritis. Well, A, it's a short dose. It, the tissues heal very slowly. You're not going to grow new bone and new cartilage in a matter of a couple of months. And so I said, what are you people setting yourselves up to fail?

100%.

Yeah.

Like there's not even good blood supply there.

Like, hello. And so I'm, I'm looking at, I'm looking at the studies that are currently underway with this and they're using the same dose, 20 milligrams per kilogram of body mass for 2 days every 2 weeks. Now they're going longer. They're going for 6 and 8 months, but I'm saying, what do you really expect? Do you really think fisetin, a polyphenol found in fruits and vegetables, is going to be more effective at clearing senescent cells than dasatinib. That's a leap of faith I'm not willing to make. So what I'm doing now, and I'm collecting the data, I'm not ready to tell you the answers yet.

Yeah. Yeah. I know you, I, as someone who pub—

yeah. All of my patients that don't tolerate the dasatinib, I'm putting them on fisetin.

Okay.

Only I'm putting on a higher dose fisetin. And I'm putting them on it for longer. Yeah. Okay. Instead of 2 days every 2 weeks, I'm putting them on it for 4 days a week, multiple weeks in a row.

Okay.

And then I'm checking their senescent cell load to see what kind of progress we made. Based on that, I can make rational changes in, do they need higher doses? Do they need longer? What is our result? So once more, I'll have more answers on that in just a few months because I got a fair number number of people that I'm, I'm doing this with now. But as I'm looking at the early results, I'm saying this is one of the two things, well, three things we're going to have to do to really extend human, not just lifespan, but healthspan.

Yeah.

I approve of Maha. Yes. Make America healthy again. I'm a doctor. What else do I want? I want healthy Americans.

It's the route. That's the problem.

Isn't getting there. And I— taking pesticides and poisons out of our food, it's a good thing. I don't know anybody to argue against that, but it's not enough. It's not enough.

Well, and that's a whole— that's a whole kind of lip service. Like, they're like, we're gonna take the colored dye out, but we just took away all responsibility for Bayer and glyphosate, and we will— we will continue to use that ad lib with no— with no recourse. Yeah, the maha, the maha thing is, yeah, that was a game. We're not getting where we need to go.

It's a start. But on the other hand, if you look at Bobby Kennedy, he's 71 years old. He's got muscles. He's got a flat, hard belly. He's got great— he's doing— someone's doing for him what I'm doing for my patients. Okay. So he isn't saying exactly what he's doing. No. But if you look at him, you know he's being treated.

100%. That's, that's not, that's not good genes and good exercise program.

It's not just exercise. No. So, you know, Bobby, come out of the closet, tell everybody what you're doing. Let's make longevity clinics the standard of care for America.

Right.

All right. That's really where we need to go.

Yeah. I mean, you know, it's, I'm going to, so I'm going to get political just for a second because it's kind of, it's without being one way or the other, but you know, there was the comment made by Dr. McEary and then, you know, Bobby Kennedy sort of jumped in earlier last week about being underbabied, right? And, you know, all these people are talking about it. Doesn't matter what you feel about it. Like, I'm like, whatever, dude. But, you know, the reality is the— what's driving it is the simple economics that our entire economic system is a Ponzi scheme running on the fact that we need young people entering the workforce that aren't sick, don't cost a lot of money, can contribute to the workforce, can contribute to insurance and all these other things. So for those of us that are getting older, that aren't biting the dust like our ancestors did at 65, you know, that the cost of managing that is you run into a math problem that becomes a problem. So that comment came from backfill the young people, right? Where the reality is, is I look at it and I go, let's undo the economic burden of the medical system by putting longevity in front of it. Yes. And actually keeping people from having the heart attack, the stroke, the osteoporosis, osteopenia that puts them in the nursing home that costs our entire industry extraordinarily. I mean, I just got through caring for my mom for almost 3 years, right? The reality is, is we need to extend healthspan, right? Because we already got lifespan there. But the problem is we cost just too damn much when we go here.

We get too sick too young and stay sick the rest of our lives.

Right.

You're singing my song.

Yeah.

I'm 78 years old. I run 3 companies. I work full-time. I'm contributing the maximum into Social Security every month while they force me to take money out of Social Security because I'm old.

Yeah, yeah, yeah. It's, it's an interest. Yeah. All of that, like, without getting heavily into politics, but that's where those weird statements come from. It's like, yes, our mathematical Ponzi scheme isn't working anymore. Japan has already felt that a decade ago, if not earlier. We have other countries— China. China's entire economic burden is the same thing. Right. They haven't answered the longevity and the healthspan problem. They're just extending life with crappy medicine.

Well, and their problem is that they got, they got old before they got rich as a society.

Right, right. So now they have old and unwell.

My wife is Chinese and I have a home there. I'm very familiar with this situation in China. Okay. You can cut this part out if you want. No, no, no. My politics are pretty simple. I believe the people who want to run their own lives stay home and do so. People who want to run other people's lives seek public office. The left wants to run my life one way. The right wants to run my life a different way. What they have in common is they all think they're better qualified to run my life than I am, and I disagree.

Leave me alone.

Let me run my life.

Yeah, I would agree with those statements, you know. Yeah, we've, yeah, our political system's just kind of a mess, you know, beyond that. But I think when we look at the medical system, you've been in this industry for 30 years, I have for 22 years, and the uphill battle that we have in getting longevity put in front of the chronic care system is all economic, right? That's the reality of it. So when people listen to this and they're like, oh my gosh, I want senescent cell testing, I wanna know how to do that and how can I understand what's doing? The reality is, is this is a, a self-fulfilling, self-motivated experience where you have to go seek out these kinds of things and jump in and address it because your insurance company is not going to cover it ever.

They are not. Now, when people ask me, why don't you accept my insurance? I tell them it's, you got it backwards. Your insurance doesn't accept what I do. Your insurance company is designed to treat diseases after you get them. I am treat the normal. But undesired changes of aging and insurance doesn't cover that. Mm-hmm. Just doesn't. So, you know, you got it backwards. Insurance doesn't cover me. It's not that I don't cover them, but I'm gonna correct one of your issues. You said I've been at this 30 years.

No, you, you've been at it longer.

Actually, this is actually my third career. I started, I was born on military bases.

Okay.

Raised on military bases. My father did 32 years in service.

Okay.

Yeah. 17, I ran off and joined the military because that's all I knew. Volunteered for lots and lots of high-risk combat situations. I picked up so many gunshot and shrapnel wounds that the Army told me I was 90% disabled and kicked me out. Wow. Medicine was actually a response to, I guess, my version of PTSD.

Okay.

I had seen far too much pain, far too much blood, far too much death. And I had killed way too many men.

Yeah.

And so when I was deciding what I wanted to do with the rest of my life, I chose medicine because I wanted to structure the rest of my life to helping people instead of killing them. The last thing I wanted was to leave this earth with a reputation as an efficient killer.

No, no, no. Yeah, no, you're right. I mean, that's what military does.

Right? Yeah. You, you kill people and break things. That's the job. And I've always tried to be good at whatever I did in this world. Then I was a country doctor for 21 years.

Okay.

Delivered babies, set broken bones, treated everything from toenail fungus to major surgeries. I was privileged to be the first human to hold new lives as they came into this world before I handed them to their mother. Yep. And I was often the only person to be with someone when they left this world, in which case I had to sit there and hold their hand. And occasionally if they were scared, crawl up on the bed and hug them while they died. Yeah. And it was 30 years ago that I made the transition to full-time longevity medicine. So third career.

Yeah, no, I totally get it. You know, but I think, um, you know, I think we all have to be sort of, particularly if you come into this arena, like most everybody that's in the longevity arena had their own, I'm going to call it just kind of jokingly a coming to Jesus moment or a moment where it's like, okay, the tool chest that I have does not work or that my friend has or my colleagues or whatever it is, I need a new tool chest. And, you know, thankfully, I guess all of us have gone through that. And so now we're in a position where we can help more, you know? So tell me, so the, it looks like you're going to probably gather your data and eventually publish, which I'm going to be very excited about reading.

I'm actually going to be presenting this at the Age Management Medical Group meeting in October.

Oh, fantastic.

Yeah. So I've been talking at the last several meetings on senescent cells and senescent cell therapies. I think the last one I gave was on senescent cells and cancer. And then this one is going to be on senescent cell testing. Yeah. So that's, uh, that's coming up in October.

That's fantastic.

Unfortunately, this test was developed in-house through Translational Lab. I can't offer it to the general public.

You knew that was my next question.

Because whenever I talk at medical meetings, every doctor in the room wants to know, when can my patients get tested? And I have to tell them, can't, because it's been approved, you know, as an experimental study for my experimental group, which definite is my my clinic. Okay. And the only way to get tested is to become a patient at my clinic, unfortunately. And I don't have clinics scattered all over the country.

Okay.

Yeah. So, Washington. So step 2 is to get this approved to let other doctors send patients. And then the final step, which will probably take 3 or 4 years, is to get so you can just offer it to the general public without medical supervision.

Right.

But it's the government. It takes time and money and I've got to go through the hoops one at a time to get there.

Totally. I totally get that. Yeah. Yeah. It's just, it's the, I mean, in, in one way it's good because it keeps things out of the market that maybe don't have real science or haven't really played out as they thought it would, like in animals or in very small population studies. But on the other side, those of us that want it now aren't happy.

70. I can't wait 30 years for the FDA to get around to this. I need it now.

No, I get it. I get it. I get it. Now you also have a book. You have a book that's available where people can read about your kind of approach to longevity and yeah, I do.

I don't— this one is a couple of years old. I had to bring out a newer one. Let me grab that. It's called Lifelong: Stronger, Faster, Leaner, Smarter, and Sexier at Any Age.

Well, I like that title. Yeah.

And you can do it on Amazon and they have a Kindle version. I keep getting told I should do an audiobook version, but I have not yet. But yeah, then the next one I want to do will be on, you know, what we've done. This is the, this would kind of stage 1 of our, of our clinic, mostly hormone balancing and so on. And now I need to redo one with Senesce cell therapy in addition to the hormone therapy. Um, I told you earlier that there's 3 ways though to lower senesce cells.

Yeah, we never got to the 3rd one. That's right.

And it's the toughest. We call it exercise. Yes. It turns out myokines produced by working muscle. Mm-hmm. Kill senescent cells. The more muscle you've got, the more frequently and vigorously and longer it's worked, the more senescent cells you kill.

Okay.

People who work out, who take up both aerobic and resistance training and push themselves to 80 to 85% of max at least 3 times a week for at least 3 months can reduce their senescent cell load by up to 40%.

That's amazing.

So without drugs, without anything fancy being done, if you're really willing to eat less and work more, if you can get lean and strong and fit and make your body work, you can kill senescent cells. Now you're not going to get rid of them all.

Mm-hmm.

But if you're 70, you might take it down to a 45 or 50-year-old level. Now I want the exercise, the muscle mass, and the senesce cell therapy because my target is the 20-year-old level.

Exactly.

Yeah. I want to move myself back. You know, I'm one of the few 78-year-olds with a 14-year-old at home.

My goodness.

Yeah. She was born when I was 65.

That's awesome.

I'm married to a woman who is 30 years my junior. Right. And, uh, you know, when she was 35 or 34, she got really baby hungry.

Yeah. Yeah.

Yeah. And if you really love a woman, you can't tell her that just because I had had my kids, she can't. Yeah.

Yeah. Yeah. So those are, those are, those are dangerous words.

I will gird up my loins and we'll do it. And so, yeah, we had a baby when I was 65 and she was 36. She is the absolute joy of my life. I love being a daddy at this point in my age. That's awesome. I just do. You know, I've got more time, I got more money. Yeah, I've got a lot more experience to share with her.

Yeah.

And I think I'm a far better daddy than I was the first time around.

Yeah. Yeah. You know, it's— yeah, the energy that you have talking about the average person is great in your 20s and 30s to have children. But the wisdom, intelligence, and emotional intelligence that you have at these ages are really where the value comes in, you know, but most of the time those aren't matches. I have a question for you. I want to swing back to the exercise because we all know— so every woman listening to this knows that I'm like, resistance training, resistance training, resistance training, and at those higher thresholds for failure, because that's where the growth happens. One of the things, like, you know, because most of the women are coming off of this crazy, I need to do cardio all the time to burn calories. We know that's not right. But there is an incredible amount of research to BDNF and mitochondrial biogenesis with cardiovascular exercise, particularly VO2 max training. And then, your NEAT exercise too. So, I think there's still a huge gap because what women want is like, "I want the thing, the one thing." I'm like, "No, no, no, sweetie. We need resistance training. We need VO2 max training. We need some NEAT activity every single day. We need some zone 2, and we need agility and jump training." That would be—

And you need to push into zone 3 periodically.

Yes, absolutely.

You need high-intensity intermittent training.

Yeah, I mean, I push 5. I'm a cyclist, I love cycling, and I'll push 5 for VO2 max. That's my thing. I'm like all out.

Yeah, I pushed my heart rate up to about 160 several times this morning during my sprints.

Yeah. But I think it's all of those things, and they don't all have to happen in a 7-day work week, you know, but you have to get them within a period of time, and it's finding ways to find that, that it's not just one thing. And I find that challenging because I'm answering those questions a lot for social media and podcasts. It really is all those things.

Let me give you Dr. Mixon's fast take on this. And I'm sorry, we're going— you said 30 minutes.

We're going a little bit longer. That's all right.

We're talking about healthy cells. You may have to cut this into a couple of podcasts. Step 1, mitochondrial function. Get enough nicotinamide Okay. Mononucleotide. Mm-hmm. NMN into your system. Get about 1,000 milligrams a day. And if you're a big guy like me at 200 pounds, get 1,500 milligrams a day in there. You may flush a bit, so start lower, maybe start at 500 or 700, but walk it up because that feeds those mitochondria and allows the, under the, the mitophagy to take place. So you replace the old worn-out mitochondria, which decreases the number of senescent cells that get formed. Okay? Because the mitochondria, bad mitochondria poison the cell. The cell becomes senescent. It now poisons more cells and the zombie chain takes off. Step number 2, you need to get your DHEA and testosterone up to more youthful levels. Because testosterone is a woman's primary sex hormone. Just, it's not estrogen, it's testosterone and it's dehydroepiandrosterone. And so you've got to provide those for your body to work. And as a side effect, you will reduce your risk of breast cancer dramatically. Glazer in, in Ohio and Donovitz in Georgia have between them over 3,500 women that have had high dose testosterone, high dose for old women, low young women's doses of testosterone over a 15-year period, and they cut their, their risk of breast cancer by 85%. And that was starting in their 30s. If we were to start them in their 30s before the breast cancer is getting started, back when that early atypia is beginning, we can probably reduce breast cancer by 95%. Okay, so let's worry less about treatment. And let's not let women get breast cancer in the first place.

Right.

So the same hormone balancing they need to make that lean, strong muscle and shift their metabolism away from fat towards muscle is also going to protect their brain. It's gonna give 'em drive, ambition, self-confidence, get rid of the depression, and in at least 30% of them, kick their libido back into high gear. Which I promise you will make your husband happier.

Yes, that's true.

And it'll give you the capacity to kick out those myokines and kill your senescent cells. Yes. So it's not just senescent cell therapy. Start with the hormone therapy. That's the base that you need to do. And now finally, the other one that we haven't touched on And it's not my research. I'm just waiting desperately for him to publish again. Is Dr. Faye out of California. He did a very small beta test on, I think it was 7 or 8 people in their 50s up to about mid to late 60s. And he put them on DHEA, zinc, metformin, and growth hormone. And he did MRI of their thymus and then measured naive thymic cells, thymocytes in their bloodstream. And after a year, he had increased the number of active naive immune cells by 20%.

That's substantial.

That's significant. And so he's got another study that's been going on for the last 18 months to 2 years with a much larger group of people, some of them up to 80 years old. Nice. And If we can really cause the thymus to reconstitute and grow and start putting out our youthful immune system again, and we couple that with hormone balancing and senescent cell ablation, 90 can be the new 50 or 60.

Right.

We could have people in their mid-90s functioning as well as people do today at 60. Yeah.

Which is huge.

That's the target we should be shooting for.

Yeah. I'll be looking forward to that study for sure. Dr. Mixon, this has been great. This has been great. Thank you. I love, I love talking. Yeah. I love talking chemistry anyway. So everybody knows, but getting deeper into the senescent cell and zombie cell kind of conversation and particularly around what, what you've seen clinically to affect it. And I can't wait till you actually publish and present your data. So that's exciting.

Should be fun.

Yeah, it should definitely be fun. And for everybody listening, thank you for listening to Menopause Mastery. Please go out and look for Dr. Mixon's book on Amazon or your favorite bookstore. It's definitely a good primer on everything you need to know. And that means you're going to have to write your other book as soon as you get ready to publish.

Or one other thing I might want to plug. I do a 4-hour doctor call-in radio show every Saturday.

Cool. Fantastic.

And we stream it live and then it is available on my website so people can download any portion of it and see it 24/7.

Fantastic. What's your website?

Lmclinic.com. That's longevitymedicalclinic.com. Okay. And there's a podcast stream live or see the old ones. And so if folks want to see more of my video stuff, there it is, lmclinic.com.

Fantastic. Well, thank you, Dr. Mixon, and thank you, everybody, for listening to Menopause Mastery. If you happen to be listening to this on your podcast platform, don't forget to leave us a 5-star review. And if you are watching this on YouTube, don't forget to subscribe and leave a comment so we can find out what you would like to learn about. And I'll be back with you next week.

Okay. Take care.