Study Reveals You Need LESS Sleep Than You Think | Ben Greenfield

In this episode of the Boundless Life Podcast, how to increase fertility for males and females, how much sleep is too much or too little, and a minimalist approach to increasing VO2 max. Well, howdy, howdy, ho. Welcome to today's show. I'm sporting my blue light concentrating glasses. These are the opposite of blue light blockers. I don't remember what they're officially called, but basically, they concentrate blue light rather than blocking blue light. They're made by a company called Ra Optics. And, they're kind of relevant to the first thing that I wanted to share with you on today's show. That was a headline that I saw entitled Long-Term Melatonin Use Linked to 90% Higher Heart Failure Risk. Wow. So, the summary of this headline was that people with chronic insomnia who used melatonin long-term had a roughly 90% higher risk of developing heart failure over 5 years according to a pretty large study. So, what did they actually look into here? So, this was presented at the American Heart Association's Scientific Sessions. As you know, melatonin is a hormone naturally made by our pineal gland. And it helps control sleep-wake cycles or your circadian rhythmicity. So, levels of that hormone typically rise when it gets dark and then fall during daylight. That's why the glasses I'm wearing are relevant because if I would have, although I didn't, if I would have taken melatonin last night and I would have woken up groggy, one of the best ways to get rid of that grogginess is to engage the eyes with blue light. And you can do that with screens, you can do that with blue light producing devices like seasonal affective disorder boxes, or you could do it with wearing glasses that concentrate blue light. But that's a little bit of an aside. What they actually did in this study was they looked at melatonin supplements. This is just synthetic melatonin. It's chemically identical to the hormone that's produced in your body. It's commonly used as a sleep aid for insomnia. I use melatonin in pretty high doses for jet lag, which is a reason why I looked at this study because I am concerned about my heart and my mortality. So the researchers divided participants according to their documented melatonin use, right? This wasn't some kind of a study where they put one group of people in one room and one group of people in another and did some controlled sleep-worn study where they gave one group melatonin and one group didn't get it. They instead looked at recorded melatonin use long-term via electronic medical records and then a non-melatonin group. Okay. What they found was that among adults with insomnia, people with documented long-term melatonin use, 12 months or more, had about a 90% higher chance of developing heart failure during the following 5 years compared with non-melatonin users. That 90%, of course, does not mean that in the, whatever, non-melatonin group, 1 out of 10 people died, and the melatonin group, 9 out of 10 people died. That is a relative risk score, not an absolute risk score. So, it was still significant, however. Heart failure occurred in 4.6% of the melatonin use group compared with 2.7% of the non-melatonin group. People in the melatonin group were almost 3.5 times more likely to be hospitalized for heart failure compared to the non-melatonin group. And that, when we engage it with absolute risk, again, is pretty big, but even relative risk is sizable. That means hospitalization rates in the melatonin group were 19%, and then they were 6.6% in the non-melatonin group. So what do I think about this? Well, in my opinion, there are a few things to consider here. First of all, this is a conference abstract. This is not a paper. It hasn't gone through peer review yet. And I think the biggest thing that you need to know about is the exposure and the way that they tracked it is a huge issue. The melatonin cohort required at least one melatonin prescription, yes, I said prescription, plus 365 exposure days. And control groups had no melatonin exposure. Now, when I say prescription, that's important. If you live in the U.S. or you're listening and you're an American or you live in America, Then you can go buy melatonin at CVS or Walgreens or Amazon. However, in countries like the UK, melatonin is prescription only. That means that a clinician has decided that your insomnia is so bad that you need a prescription for melatonin. Now, if your insomnia severity is so high that the doctor is writing you a prescription for medication for it, might that not indicate that that level of insomnia could be predisposing you to cardiac events or increased risk of mortality, melatonin use aside. Let me think of an example. So this would be like me saying, well, statin use increases your risk of dying, right? And then we were to say, well, it appears that people who are put on statins have increased risk of dying from a heart attack. Well, maybe the very fact in the first place that your doctor thought your heart condition was severe enough or your lipid abnormality was severe enough to put you on a statin already puts you into a higher mortality risk group, right? They also did not look at dose. They didn't break out people using 0.3 versus 300 milligrams. They didn't look at the formulation, which we know based on other podcasts I've done widely varies. Although, of course, for prescription melatonin, that's a little bit less of an issue. They didn't look at timing, right? Were they taking it at 9:00 PM? Were they taking it at 2:00 AM? And, I've also done a podcast with Dr. John Lieurance on high-dose melatonin. I'll link to all of this if you go to BenGreenfieldLife.com/506. But long story short is this is not a nail in the coffin for melatonin. I have seen enough data on the beneficial effects of melatonin. And again, I'll link to these in the shownotes. And therefore, I continue to use melatonin. I don't use it every day. I'm not convinced. I haven't seen the mechanism. That convinces me that there is a negative feedback loop, meaning if you take it, do you downregulate receptor sensitivity or downregulate your own melatonin production? But nonetheless, since I don't need to take it every night, I don't take it every night. However, if I am traveling across more than 3 time zones, I will take a high dose of melatonin for the first 1 to 2 nights upon reaching my final destination. And, by high dose, I actually get melatonin in the form of a supplement called SandMan, From Dr. John Lieurance in Sarasota, Florida. He has, don't laugh, a suppository, but fear not, also an oral and a liquid version. And that is very high-dose melatonin. And for example, I'm flying to London for the Health Optimization Summit, shout-out to the Health Optimization Summit, on Tuesday, tomorrow. And when I get to my hotel, when evening has arrived, about 30 to 60 minutes prior to bed, I'll take 300 to 1,000 milligrams of melatonin. Why such a range? Typically, it will depend on how much sleep I've gotten on the plane, how early I need to get up the next morning, et cetera. But that's my range and it works like gangbusters. I'm not a doctor. Do not take this as medical advice, but extremely well for jet lag. You're groggy in the morning, yes, from that dose of melatonin. But again, concentrate blue light. I will probably bring these glasses with me. And you get rid of the grogginess pretty quick. Well, I know we just jumped right in. By the way, for those of you who might be new to the podcast, this is one of those episodes where it's just me. I'm not interviewing anyone. I get into listener Q&A sometimes. I get into different news flashes that have come up. Today's mostly just news flashes. And yeah, that's what the show is. And all the shownotes are juicy. Today, they're going to be at BenGreenfieldLife.com/506. All right. So, VO2 max. This is interesting. A lot of people have heard of the classic way that folks like, oh, wonderful public health and public science educators like Dr. Andrew Huberman and Dr. Rhonda Patrick will recommend to increase VO2 max. Perhaps one of the most common recommendations is a Norwegian 4x4 protocol, a Norwegian 4x4 protocol. So, this typically takes about 35 to 40 minutes. You warm up for 5 to 10 minutes aerobically, then you do 4 minutes at maximum sustainable pace. I used to coach people through these workouts when I was a personal trainer, and I worked with a lot of triathletes and cyclists and marathoners who wanted to increase VO2 max, even though we now know that it's wonderful for just general population as a longevity tool. And so, 4 by 4 minutes, maximum sustainable pace for 4 minutes, but that's not balls to the wall, pardon the expression. Meaning, if I put you on a cycle ergometer or a bike for 4 minutes, then you begin by pedaling at 90 RPM, you would still want to be at around 90 RPM by the end of that 4 minutes. If you're at 85 or 80 or 75, I know that that is over and above what would technically be the 85 to 95% that you want to be at. If you're slowing down and slowing down, that means you're pushing too hard. Too hard. So, it's hard breathing, but it's challenging, however sustainable, for the full 4 minutes. And then, you do active recovery. The active recovery is usually around a 1-to-1 work-to-rest ratio. So, if you go for 4 minutes, you recover for 4 minutes. And, you do that 4 times through, right? 4 by 4, 4 minutes on, 4 minutes off. Some people will say 3 minutes off. It's not that important in the scheme of things for 4 times through. So, why am I telling you about this general tactic to increase VO2 max? Well, there was a recent study I was reading in the Scandinavian Journal of Medicine and Science in Sports. And, what they looked at was sprint interval training, AKA SIT, as a time-efficient method for improving VO2 max. So, rather than doing the 4x4 Norwegian protocol, typically this is just 4 up to a maximum of 6 30-second All-out sprints, which sounds like it could actually go by a little bit faster than a 4x4 protocol. We're still talking about a 20 to 25-minute workout. And, what they looked at was a whole bunch of different studies in which they used all-out cycling or sprint intervals for increasing VO2 max. And, they did find that there was a significant effect on VO2 max. It's not as big as what you get from a 4x4 protocol, but It's good to know that if you wanted to maintain VO2 max, you could do so with these quick 30-second sprints. So, this backs up what other studies have looked into when it comes to sprint intervals. Now, what you need to know is that they typically involve pretty short recovery periods. So, a 30-second sprint would involve 15 seconds of rest. Other studies have looked at a 40-second sprint with 20 seconds of rest. They go from anywhere from as few as 4 sprints to up to 13 sprints in a row. Just imagine, 13 reps of 30 seconds hard, 15 seconds easy. That's very hard. It's more difficult than, say, a classic Tabata set, which is 20 seconds hard, 10 seconds easy, 8 times through. Now, most of these short interval studies have shown a small increase in VO2 max, but a much smaller change than the classic 4x4 protocol. The 4x4 protocol typically has resulted in, depending on the study, anywhere from an 8 to 10% increase in VO2 max, which is pretty significant. These other studies have shown an increase, but it doesn't come near what the 4x4 does. So, that's good to know. Alright. So, in addition to sprint interval training and this 4x4 VO2 max, what else could you do to increase VO2 max? Well, now we get into some of the things that go beyond exercise. For example, Heat acclimation. There was one study in 2010 where they took a bunch of trained cyclists and they had them train in hot conditions. This would be very similar to going somewhere like Phoenix in the summer and doing 10 days of cycle training there. Well, they found maximum cardiac output increased significantly. Plasma volume, total amount of blood that you're pumping around or the oxygen you're carrying to cells, that resulted in a VO2 max increase of 8% in the hot condition. Wow. Now, if you step back and look at this, VO2 max is a combination of how much air you can move in and out of your lungs, the ability of blood to be delivered to tissue, and then the ability of your mitochondria to use oxygen to produce ATP. So it would make sense that training in the heat would increase a couple of those parameters, right? Cardiac output and plasma volume. So heat acclimation is another tool that you could use to increase VO2 max. No studies have actually been done with people just sitting in a dry sauna. But mechanistically, you could potentially see an increase in cardiac output and plasma volume if you were sitting in there for, let's say, greater than 200 degrees Fahrenheit for more than 15 minutes, for example. Exercising, doing hot yoga, things like that may also increase it. But again, no direct studies. Correcting iron deficiency. This may be one other way to increase VO2 max. So, if you have low hemoglobin mass, if you have low ferritin, If you have low iron, oxygen-carrying capacity is going to be a limiter to your VO2 max. This is something that would be more of an issue in, say, plant-based eaters, vegans, vegetarians, et cetera. Nothing against you if you don't like to eat animals, they are just a better source of heme-rich iron. And if you're eating things like organ meats, the copper that's also necessary as a cofactor for that iron, as I get into in great detail in the podcast that I did with Morley Robbins. So correcting iron issues, copper issues, hemoglobin issues, ferritin issues, that also could be a way to increase VO2 max. Training at altitude or doing some type of hypoxic training. This could involve what's called IHHT, intermittent hyperoxic-hypoxic training, where you're breathing large amounts of oxygen, then typically using a switch on an oxygen concentrator to lower the amounts of oxygen that you're breathing So, you're kind of going back and forth from high altitude to low altitude, which logistically for most people who live at anywhere below 6,000 feet is easier than going up into the mountains to train. If you're a serious athlete, you would actually go to a place like Mexico City or Boulder and actually do training sessions there. And anywhere from a 3% to 4% increase in VO2 max via erythropoiesis, right? That's the formation of new red blood cells. is something that has been observed in studies in people who go from sea level to training at altitude. And there are, of course, like I mentioned, biohacks like intermittent hyperoxic-hypoxic training. I have a machine that does this. It's called the LiveO2. There's a few others out there. The Cellgym is one other that I've seen get decent reviews for this. But the idea is even if you're unable to go to the mountains to train, by putting yourself into a state of oxygen starvation or hypoxia, And then blasting yourself with oxygen, you could actually achieve that. And, if you want to get into the subtle details in the studies in athletes where they've looked at altitude training for VO2 max, typically the athletes are living high and training low. So, that would be living at greater than 6,000 feet, sleeping at greater than 6,000 feet, maybe your meals are there, but then you go down low to train because If you're training low, you're able to push harder, but then you're also getting some of the red blood cell benefits of living high. Obviously, that's a lot of logistics. However, if you're a pro athlete, it's certainly something that might be up your alley. Can strength training increase VO2 max? Not really. Not really any great studies. Can elevation training masks do it? Not really. Can respiratory muscle training do it, like breathing into those power lungs, et cetera? There hasn't really been a significant increase in VO2 max observed with any of these tools. That's not to say that they're not good, right? If I wear a training mask, I'm still training my inspiratory-expiratory muscles. These are the ones that look like Bane from Batman. If I'm breathing in and out of a resisted breath training device, as I describe in my book Boundless, I'm also training the diaphragm, inspiratory-expiratory muscles, massaging organs, improving lymph flow. Potentially improving breath and physiology mechanics, a level that doesn't necessarily increase VO2 max but is still beneficial. But, as far as increasing VO2 max, summary is Norwegian 4x4 protocol is going to be your best bet. Short sprints with short recovery periods is going to be your next best bet. And then, you've got heat training and living at altitude or training in a state of hypoxia and then correcting any iron deficiency, hemoglobin, or ferritin issues. And, those would be some of the— Some of the best ways to increase it. So let's move along. All right, this next one, I think somebody sent it to me on X. It's pretty interesting. It's a sleep chart of biological aging clocks in middle and late life. This one's interesting. I'll get into it. This is all human data. It's no mice, no worms, no fruit flies, no yeast, no Petri dishes. They took about half a million. That's a lot. Half a million UK Biobank participants. Wow. These folks range from mid-30s to mid-80s. And then they asked one question in this study, how does sleep duration track with biological age across the whole body? Not just the brain, not just cognitive function, not just executive function, not just reaction time, a lot of the things that are commonly looked at when it comes to sleep studies. Instead, they actually looked at 23 different aging clocks spanning 17 organ systems and tissues built from 3 different aging clock measurements. They looked at MRI, brain, heart, liver, pancreas, spleen, adipose tissue, and kidney. They looked at what's called plasma proteomics. These are aging clocks related to blood measurements. And then, they looked at plasma metabolomics, very similar, different measurement. We aren't going to get into the details of each of those measurements. I've done podcasts on biological aging clocks. I'm more interested in filling you in on what the data actually found. Basically, what we're looking at here is a U-shaped curve, a U-shaped curve. What that means is both short sleep, meaning sleeping less than 6 hours, and long sleep, sleeping more than 8 hours, were both associated with accelerated aging in organs. Now, in a second, I'll get into this, but it differed in terms of what organ systems are affected if you're short on sleep Versus which are affected if you're long on sleep. The best effects in terms of the largest or the slowest rate of aging of all organ clocks landed between 6.4 and 7.8 hours of sleep, a little bit less than you might have expected because you'll hear some people say sleep 7 to 8 hours, right? 6.4 to 7.8 hours is less than 7 to 8 hours. But nonetheless, that's going to depend quite a bit on your activity levels, right? Some pro athletes need to sleep 9 to 10 hours. But for most people, and this is a pretty big study, it basically comes out to sleeping too little not being good for you and sleeping too much not being good for you. Okay. So what did they actually find? If you're sleeping under 6 hours, they showed that most of the organs have accelerated aging, blood pressure increases significantly, Diabetes risk, right? Blood sugar management climbs, 50% higher risk of dying during the study period. And then, if you're sleeping more than 8 hours, meaning maybe you're hitting the snooze button too many times, maybe you're just so tired or have some type of autoimmune issue or something that's leaving you in bed for too long, aging showed up more in brain tissue and in fat tissue. Those are the 2 main tissues that are affected by sleeping too long. Interesting. 40% higher mortality risk, right? So, less than short sleeping. So, if you're going to choose one, stay in bed longer. And, a lot of these folks would typically have some type of condition also, like I referred to just a second ago, that might be leaving them in bed longer, injury, immobility, frailty, et cetera, right? So, if you could bank on either side of 6.4 to 7.8 hours, getting closer to the 7.8 hours, no surprises here, Still seems beneficial. But the long story short is that if you can hit 6.4 to 7.8 hours, pretty good. It appears that 6.4 to 7.8 hours of sleep is going to be the range to shoot for, and you should err more towards that 7.8 hours if you can. Now, I personally short sleep. I sleep anywhere from 6 to 7 hours per night, so I'm less than the range here, but I also tuck away for anywhere from 30 to 45 minutes in the afternoon. For a siesta, typically a post-lunch siesta. So, I'm kind of combating that short sleep. And, the advantage of that from a productivity standpoint is I'm able to get more work done earlier in the morning when my phone isn't blowing up and people don't expect me to be on Slack, et cetera. So, alright. So, now I'm going to get to what I know a lot of folks have been asking me about. People seem to want more babies. I would say the top 2 questions I get these days when I'm doing webinars and guest podcasts, et cetera, is how do you keep hair from graying or falling out? And how do you have more babies? So maybe it spans both young to aging populations, right? First you get worried about having kids, then you get worried about losing your hair. So I'm going to give you my big picture overview. This is going to be bullet point by bullet point. I could probably spend an hour on each of these, but let's go over the basics when it comes to first male fertility, Then, we'll move on to female fertility. So, male fertility. Number 1, avoid heating your testicles. I just saw my son. He was in his bedroom. He was working on his laptop. His laptop was in his lap and he had the anti-radiation pad that I got for him on Amazon sitting in his lap protecting his gonads, his sperm, my future grandkids from getting fried. Hot tubs, saunas, laptops, seat warmers, All of these can affect spermatogenesis for the same reason both of my sons have this ball cooling underwear that they can wear in the sauna that has little ice packs that you can put into it. I'm talking about my children's balls too much right now. So spermatogenesis, basically the generation of new sperm, as the name implies, that only works a few degrees below core body temperature. That's why a male's testes sits outside the body in the ball sack. So human studies that go back decades show that raising your scrotal temperature by even 1 to 2 degrees Celsius measurably drops sperm count and motility. And that effect does reverse once the heat exposure drops, but it's typically around a 60 to 90-day sperm production cycle. So if you're trying to conceive, that means you're stopping regular use of a sauna or hot tub unless you have some type of a ball cooling strategy in place 60 to 90 days before you want to conceive. So, that's a big one. The next one is timing intercourse around ovulation. The sperm will survive about 3 to 5 days in a female's reproductive tract. Maybe there's a few that are hardier than that, the David Goggins of sperm, but most are 3 to 5 days. But, the egg is only fertilizable for about 24 hours. So, one of the strategies that you can use is you can abstain 2 to 3 days before she ovulates to let sperm concentration that you're producing build And then, have intercourse as much as possible on the day before and the day of ovulation. That's because every time a male ejaculates, sperm count will drop. So, you're trying to bank your sperm up as much as possible to hit that ovulation window. So, the next one, smoking, alcohol, cannabis, all of those should be avoided. Nicotine and cannabis increase reactive oxygen species not only in the brain, especially in high doses and with cannabis, especially when THC is present, But also in the testes, in seminal fluid. The sperm are pretty vulnerable to oxidative damage. And there was, for example, a systematic review in 2019 in the Journal of Urology that found that cannabis use resulted in lower sperm concentration and altered sperm morphology in humans. Alcohol can also have a similar effect as can higher-dose nicotine. Like, if you're going above 5 milligrams of nicotine per day, And you want to conceive, I know I'm asking to stop a lot, but I'd actually stop weed, stop alcohol, and stop nicotine. All 3 of those are not going to help you much when it comes to fertility. The next is exercise. This one's pretty straightforward. Cardiovascular training, aerobic training, resistance training, they all increase mitochondrial density and mitochondrial function. And sperm motility is basically often related to mitochondrial health because the mitochondria in the sperm actually generate the ATP that powers the little swimming tail of the sperm. Regular exercise is not only going to increase mitochondrial health, but also long-term lower oxidative stress, which you just learned can affect spermatogenesis, and increase sleep quality and insulin sensitivity. And both of those can indirectly affect testosterone and sperm parameters. So pretty broad mechanistic support for exercise. The next, as I just referred to, is sleep. So, the pulse of luteinizing hormone that drives testosterone production, that happens primarily during sleep. Testosterone concentration inside your testes, that's what's needed for spermatogenesis, it's a lot higher than in the blood. So, sleep restriction shows measurable drops in testosterone in men after just 1 week of sleeping around 5 hours a night. Poor sleep is also going to elevate cortisol. And the way that that's going to affect spermatogenesis is that's going to suppress What's called gonadotropin-releasing hormone, GnRH, release at the hypothalamic level. That will basically cause upstream downregulation of testosterone production and spermatogenesis. And this obviously is something that's important, not just if you're trying to conceive, but if you're trying to build muscle, lift weights, recover faster, et cetera. So sleep's a biggie. Avoid commercial lubricants in any type of sex lube. So most water, And silicone-based lubricants, those have an osmolality and a pH that differs from both her cervical mucus and from semen. And that can reduce sperm motility within just a few minutes of contact. So, there are, for example, some fantastic coconut oil-based lubricants. That's primarily what my wife and I use. We are not currently trying to conceive, but they're also fantastic. They're low in any type of toxins and typically the pH of those Especially if you look at the label and look at the acid-alkaline balance. And sometimes a quick Google can fill you in on whether or not something is actually friendly or not to conception when it comes to the lubricant that you're choosing. Most of the coconut oil ones that I've looked into have a pH that's appropriate for conception. So, yay for coconut oil. L-carnitine would be another one. People often ask me about supplements and I'm going to give you basically 5 or 6 rather, that work pretty well. One is L-carnitine that helps shuttle fatty acids into the mitochondria. So it's going to assist with beta oxidation. And the sperm concentration of carnitine is going to correlate with sperm motility. And that's been shown in human studies. So that's at a dose of around 1 to 3 grams per day for around 30 days to raise L-carnitine levels and sperm concentration of carnitine. The next one would be coenzyme Q10. All right, that's part of the mitochondrial electron transport chain. It's going to function as an antioxidant. It will protect the sperm membrane from the same oxidative stress that smoking and cannabis causes. That is not an excuse to smoke cigarettes and weed and then take CoQ10, but anywhere from 100 to 400 milligrams per day of CoQ10 taken with a fat-containing meal, which will increase absorption, can increase sperm concentration and motility. And that's been looked into. In infertile men who do that for around 3 months in that range of 100 to 400 milligrams a day of CoQ10. And remember, it's fat-soluble. Preferably, you take it with a fat-containing meal. Speaking of fats, the next one is omega-3 fatty acids. So, around 1 to 3 grams per day of EPA/DHA. Sperm membranes are very rich in polyunsaturated fatty acids. So, that makes them very flexible for swimming where they need to swim. It also makes them more vulnerable to oxidative damage. Higher omega-3 intake correlates with better sperm morphology and motility, and this has been shown in human studies. Not as much as the literature behind CoQ10, but popping a couple of fish oil capsules that are clean, that are not rancid, that have been protected from heat and light appears to be a pretty good idea when it comes to conception. The next is zinc. Zinc is a cofactor for enzymes involved in testosterone synthesis, but also sperm maturation. Zinc deficiency is a reproducible cause, pun intended there, of low sperm count in human studies. And there are a few studies going back as far as the '80s that have shown a zinc-testosterone-sperm link. And deficiency of zinc is pretty common. So that's another one to look into. Levels are going to vary depending on the type of zinc that you use, but Adding zinc into your stack is a good idea. And then, there's a couple of herbal adaptogen type of remedies that may help. Tongkat Ali is one. It may lower sex hormone-binding globulin, which would free up more testosterone to be biologically active. There's a handful of very small randomized controlled trials that show a slight increase in free testosterone via that drop in sex hormone-binding globulin. I would admit the evidence is thin on this one, but if you have high SHBG, Try taking Tongkat Ali at around 400 milligrams a day and see what it does, you know, with a pre and post test around four to eight weeks between, and it may actually lower SHBG in you. It's also fantastic for overall libido, and I mean, seems to give you good energy pre-workout as well. So it's not going to be something that that's a total waste of time and money. Shilajit is another one. Shilajit is a mineral. It's very dark black. A lot of people don't like the way it tastes for a while. I haven't had them in a while, but a company called Organifi was making shilajit. gummies that were pretty good. But it has very good antioxidant properties, very good mineral-chelating properties. And there was a human trial in which they gave people 100 milligrams of shilajit 2 times a day for 90 days. These are 28 infertile men, and they did find increases in sperm count and motility. There was another separate randomized controlled trial that noted a 20 to 25% increase in total and free testosterone in healthy men who were taking a little bit higher dose, around 250 milligrams of shilajit. Okay. So, that would be another one to look into. And then finally, if a guy is on testosterone replacement therapy or is hypogonadal and wants to increase testosterone without impairing fertility, right? Because paradoxically, if you get testosterone levels too high or more specifically if you're taking exogenous testosterone replacement therapy, which is going to shut down LH and FSH, which will affect spermatogenesis, You want to do things to limit the damage there. So, if you're on testosterone replacement therapy, typically a lot of doctors will recommend that you take HCG or Clomid, clomiphene, sometimes enclomiphene, and occasionally Kisspeptin. That's a peptide that may upregulate LH and FSH. These are all things to talk with your doctor about. Basically, what HCG does is it mimics luteinizing hormone. So, it keeps intratesticular testosterone high enough to sustain spermatogenesis in in men who are on TAT because exogenous testosterone, again, shuts down that LH signal. Clomiphene works differently. It blocks what's called estrogen receptor feedback at the hypothalamus, and that will raise FSH and LH output. And, the only issue with enclomiphene is in some people, they feel like it affects libido if estrogen is not balanced properly. And then, kisspeptin would indirectly increase LH and FSH. HCG is probably the one that has the most evidence behind it, but I highly suggest you work with a physician on any type of protocol behind that. Currently, the people I work with because I'm on exogenous testosterone therapy is Dr. Rosensweet at Brighte Medical, B-R-I-T-E Medical. And, he does a good job with both my wife and I. So, I'll link to his stuff in the shownotes if you go to BenGreenfieldLife.com/HCG. Okay. 5:06. For women, it's a little bit simpler. Women, step 1, send your husband this podcast. Step 2, ovulation tracking. So, let's just jump right in. You can use a Whoop for this. I believe the Oura is doing body temperature tracking now. My wife uses a Whoop. Your basal body temperature is going to rise about half a degree Fahrenheit after ovulation. Because progesterone is very thermogenic. So, what these ovulation kits do is they give you about a 24 to 36-hour window before the egg releases. The egg is viable, as I mentioned earlier, for about 24 hours. So, that narrows down the fertility window. And, using a temperature tracking tool, an ovulation kit, many of these apps that are out there now for tracking ovulation, that's a huge tool in your toolbox because you know The egg is going to be pretty available right around then. That's a no-brainer for women is to time the ovulation. The next one would be to, very similar to men, avoid smoking and cannabis and excess alcohol. The oxidative stress mechanism is the same one that damages sperm, but eggs are arguably even more vulnerable because you as a woman are born with a lifetime supply and you can't regenerate damaged eggs. So cannabis use is probably the one that's been most associated with disrupted ovulatory function in human studies. Smoking is also one that's been a highly replicated risk factor for reducing what's called ovarian reserve, and even in some cases causing earlier onset of menopause. So smoking in general is just bad news bears for both men and women who want to have kids. I don't know how people used to make babies back in the days of Mad Men and chain-smoking cigarettes. Exercise, same thing as men. The same mitochondrial health logic that we had for sperm applies to egg quality. Since eggs heavily depend on mitochondrial function, the egg has to supply all the energy for the first several days of embryo development before the embryo's own genome activates. So, women move, strength train, aerobic training, same recommendations as for men. Similar to sleep, the same luteinizing hormone, follicle stimulating hormone pulsatility that Sleep protects in men, also governs the menstrual cycle in women. So, sleep disruption can blunt the LH surge that is going to trigger ovulation. So, chronic sleep restriction, chronic stress, that's something that is correlated with higher rates of menstrual irregularity. The question is, was it the sleep? Was it the stress? Was it the cortisol? The more you can control all 3, the better. Then, there's a few interesting ones for women. Acupuncture. There is some research including work out of Harvard Medical School that shows that acupuncture can affect chemical signaling regulating FSH and cortisol and also outcomes like uterine and ovarian blood flow. So, acupuncture, I'm always surprised I've come across. I've seen a doctor just literally get rid of my son's allergies overnight. I have been put into a dead sleep during acupuncture. I've seen plenty of anecdotes and some trials on acupuncture. I don't have an acupuncturist who I regularly see just for the general reason that I haven't logistically been able to pull it off. But, if I were trying to conceive, if I were a woman, it's certainly one that I would look into. Very similar to men, CoQ10 for women in the range of 100 to 400 milligrams a day. Again, because oocytes or eggs have unusually high mitochondrial density and there are, again, human RCTs in women just like men in this case undergoing IVF, who showed that CoQ10 supplementation for a couple of months before egg retrieval improved egg quality and embryo quality parameters. And then also for women, about 3 other compounds to consider. Inositol, inositol, I-N-O-S-I-T-O-L, around anywhere from 1 to 5 grams per day. That's involved in FSH signaling, follicle stimulating hormone signaling. inside the ovarian follicle. That one has some pretty decent RCT evidence, multiple double-blind trials in women undergoing IVF, and they had fewer immature and degenerated oocytes and more high-quality embryos when taking inositol. Omega-3 fatty acids, same membrane fluidity and anti-inflammatory logic as in men, but also in women, omega-3s are the precursor to prostaglandins. And those are involved in ovulation and uterine receptivity. So, higher omega-3 intake gives better odds of conception. That's both men and women. And then, very similar to men, shilajit, right? Same fulvic acid antioxidant mechanism as in men. And so, there's not a lot of studies or human RCT data that I could find on women taking shilajit. But mechanistically, I mean, if it's already around and your guy's taking it, It seems like it's something that could potentially help out a little bit with fertility just based on its antioxidant function. So, a lot there, I realize. You could replay that. You could go visit the shownotes, check out the transcript. But, if you were to just start into those things, you would definitely increase the chances of having a baby, making a little human. So, that being said, that is all the time that I have for today. I hope this has been helpful. 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