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129: Boost Testosterone Naturally - Mitochondria, Insulin, and Fighting Back with Dr. Ben Bikman — Transcript

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0:00Men, yes, you have a menopause, too.
0:03[music] Men don't have the sudden
0:04hormonal crash women get in menopause,
0:07but we do experience a steady
0:09testosterone decline starting around age
0:12[music] 30. And the biggest cause isn't
0:14age, it's metabolism. Testosterone is
0:17made inside your mitochondria. When they
0:20weaken, testosterone drops. Insulin
0:23resistance makes this worse by blocking
0:25the enzymes your testes need to produce
0:28it. and extra body fat. It converts
0:31testosterone into estrogen, which
0:33[music] drives even more fat gain, a
0:35vicious cycle. The good news, you can
0:38influence this by losing excess [music]
0:40fat, improving insulin sensitivity,
0:43lifting weights, sleeping well, managing
0:45[music] stress, and keeping alcohol in
0:48check. If you're concerned about
0:50testosterone, get tested. [music]
0:51But remember, most of this decline is
0:54metabolic, which means you can change
0:56it. This is lecture 129 of the metabolic
0:59[music] classroom.
1:02Looking to improve your own metabolic
1:03health? Visit insuliniq.com
1:05for courses, coaching, consultations,
1:08and dive deep into the science behind
1:10metabolic health. Become an insider at
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1:18live stream Q&A access, and more. Hey
1:21everyone, before we get started today, I
1:23want to tell you about something brand
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1:28Bickman's digital mind. It's an AI
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1:32questions about the science behind
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1:37using nearly 3 million of my own words
1:40from my lectures, published research, my
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1:46private Q&A sessions. You can chat with
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2:01whether or not you'd like to have
2:03unlimited access by becoming an insider.
2:06You can find it right now on my website,
2:08and there's a direct link below at the
2:10top of the show notes.
2:14Welcome back to the metabolic classroom.
2:16I'm Ben Bickman, biomedical scientist
2:18and professor of cell biology. Today,
2:20we're tackling a topic that affects
2:22millions of men, but rarely gets the
2:24attention it deserves. Male menopause,
2:28or as it's sometimes called, and perhaps
2:30more accurately, andropause. Now, I know
2:34what you might be thinking. Male
2:36menopause. Isn't menopause something
2:38that only affects women? And you'd be,
2:40of course, right to question the
2:41terminology. The word menopause
2:44literally refers to the sessation of
2:46menstruation, which obviously does not
2:49apply to men. But here's why I still
2:52find the term useful, if perhaps still a
2:55little confusing. It helps us understand
2:57that men experience their own version of
2:59hormonal decline with age, just as women
3:02do. It's the male equivalent of
3:05menopause. Not the same thing and not
3:08equal in degree, but a parallel process
3:10that does deserve some attention. Just
3:13for the sake of the men who are wanting
3:15to understand their health a little
3:16better. To really appreciate what's
3:18happening in men, let's briefly review
3:21what happens in women during menopause.
3:24This comparison will illuminate why the
3:27male experience is fundamentally
3:29different but equal in its own way. In
3:33women, menopause represents something
3:35truly remarkable from a biological
3:37standpoint, the complete exhaustion of a
3:40finite resource. Here's what I mean.
3:43When a female baby is developing in the
3:45womb, her ovaries already contain all
3:47the eggs she will ever have. Somewhere
3:50between 1 to 2 million primordial
3:52follicles.
3:54By the time she reaches puberty, that
3:56number has already declined to about
3:58300,000.
3:59This isn't because something went wrong.
4:01It's simply how the system is designed.
4:04The follicles are continuously being
4:06activated and lost through a process
4:09called atreia or just a programmed death
4:12of the follicle. The rate of follicle
4:15loss accelerates dramatically as women
4:17age. Before age 37, women lose
4:21approximately 5% of their remaining
4:23follicles each year. But after 37, that
4:26rate more than doubles to about 12%
4:29annually. This acceleration continues
4:32until typically in the late 40s or early
4:3550s, the ovaries are essentially
4:37depleted of follicles. When this
4:40happens, estrogen production plummets by
4:43roughly 90% because the follicles
4:46themselves are the primary source of
4:48estrogen in premenopausal women. This
4:51dramatic hormonal cliff is why menopause
4:54symptoms can be so sudden and pr and
4:57pronounced. These are dramatic
4:59manifestations. Things like hot flashes,
5:02mood changes, sleep disturbances, and
5:04more. The body is experiencing a rapid
5:07hormonal withdrawal.
5:10The male experience is quite different
5:12in origin and magnitude. Unlike ovaries,
5:15which have a finite supply of follicles,
5:17and remember the follicle is so relevant
5:20because it's the source of all of these
5:22hormones. Men's leading cells, that's
5:25the cells within the testes that are
5:27responsible for producing testosterone,
5:30actually persist throughout life. It's
5:31not a finite resource. Men don't run out
5:35of testosterone producing cells.
5:37Instead, these cells gradually become
5:40less capable at their job. Think of it
5:43this way. If female menopause is like a
5:46warehouse running out of inventory, male
5:49menopause is like a factory that keeps
5:51running but slowly produces less and
5:54less of the product each year. The
5:57machinery is still there, but it's not
5:59working as well as it once did. This
6:02gradual decline typically begins around
6:05age 30 to 40 with testosterone levels
6:08dropping approximately 1% per year. But
6:11here's what makes this particularly
6:14significant. Free testosterone, the
6:16biologically active form that's not
6:18bound to proteins in the blood, which
6:21inactivates it, it declines even faster
6:24at about 1 and a half to 2% per year.
6:27This is partly because levels of sex
6:30hormone binding globbulin, sometimes
6:32just abbreviated as SHBG,
6:36tend to increase with age, grabbing more
6:38of that testosterone and we're making it
6:40and make it unavailable for use. So we
6:44have this compounding effect, a
6:46reduction in testosterone production. At
6:49the same time, we have an increase in
6:51testosterone binding. So this sex
6:54hormone binding protein is locking up
6:56more of the testosterone and thus the
6:59free amount which is again as I noted
7:01the biologically active form is greatly
7:04reduced relatively.
7:06There's a landmark study called the
7:08Massachusetts male aging study and they
7:11found that total testosterone declined
7:13at 1.6% per year while bioavailable or
7:17the free testosterone dropped at 2 to
7:19three uh percent per year. Similarly,
7:22the Baltimore Longitudinal Study of
7:25Aging confirmed consistent testosterone
7:27decline across every decade from the 30s
7:30through the 80s. The clinical
7:33implications are substantial. By their
7:3660s, approximately 20% of men have
7:38clinically low testosterone. By the 70s
7:42and 80s, that number rises to about 50%.
7:45Yet, because this decline happens so
7:48gradually, unlike the more abrupt
7:50transition that women experience, many
7:52men don't realize what's happening until
7:54the effects have accumulated
7:56significantly.
7:58The mechanisms behind the decline are
8:01myriad and interesting. So, I want to
8:03discuss them. Of course, as a cell
8:05biologist, I always want to look at the
8:06mechanism.
8:08So, I'd mentioned this earlier. Do lead
8:10egg cells actually become less
8:12efficient? This is where the metabolic
8:14connections become particularly
8:15fascinating and where I think we can
8:17find some hope for intervention. First,
8:20let's talk about mitochondria.
8:23Testosterone synthesis is fundamentally
8:25a mitochondrial process. the rate
8:28limiting step in steroid hormone
8:30production which is all the sex
8:32hormones. It actually it's getting
8:34cholesterol which is the raw material
8:36for all sex hormones testosterone
8:38included into the inner mitochondrial
8:42membrane where it can be converted to a
8:44molecule called pregnnenolone which is
8:46the precursor to all steroid hormones.
8:49Now, there's a little bit of fundamental
8:51endocrinology baked into this discussion
8:53that I'm kind of assuming, you know, and
8:55that might be dangerous on my part as a
8:57teacher. The steroid hormones are their
9:00own class of hormones separate from any
9:02others where they're all built on a
9:05steroid nucleus or a cholesterol
9:07molecule that's been modified. So, all
9:09sex hormones start with cholesterol and
9:13you have to get the cholesterol into the
9:15mitochondria. This transport depends on
9:18proteins called star s that stands for
9:22steroidogenic acute regulatory protein
9:26and also another one called tspo which
9:29is a transllocator protein. Both of
9:31these decline with age. Research that
9:34was published in the fast journal just a
9:36few years ago demonstrated something
9:38interesting. They found declining tspo
9:41that's the transllocator protein that
9:43these a decline in the tspo levels are
9:46associated with deteriorating
9:48mitochondrial structure specifically the
9:51christe these are the inner foldings of
9:54the mitochondria where so much of the
9:56cell's energy production happens you
9:57know if you think of something like the
9:59electron transport system all of that's
10:01located on that on the christa these the
10:03inner mitochondrial membrane when the
10:06architecture or the structure of the
10:07mitochondria
10:09is is compromised or shifted, it falls
10:12apart, so does the cell's capacity to
10:14make testosterone.
10:16But here's something that I find
10:18particularly interesting. They also
10:21showed the same study that promoting
10:22mitochondrial fusion, essentially
10:25helping the mitochondria maintain a long
10:28connected reticular or stringy
10:31structure. Remember the word
10:32mitochondria is derived from the Greek
10:34word for thread which is mitos.
10:37Mitochondria are long stringy things
10:40woven through the cell. They found that
10:43when they could really promote a
10:45metabolic millu of greater mitochondrial
10:47fusion, they could restore testosterone
10:50production even in older lead cells.
10:52Remember the lead cells are the
10:54testosterone producing cells of the
10:57testes, the male gonads. This suggests
11:00that the decline is not inevitable. It's
11:03potentially reversible if we can support
11:05mitochondrial health. Indeed, this
11:08touches on some of my own work from my
11:10lab where we've published before that
11:13ceramides, a very highly active lipid or
11:16a type of fat within the cell, can
11:18mediate forced mitochondrial fision.
11:23And and we found one final point before
11:25I kind of revisit this. chronically
11:27elevated insulin is a key signal for uh
11:30mitochondrial fision or ceramides
11:32production. So basically we found
11:35increased um ceramides would force the
11:38mitochondria to pull apart. That's the
11:40fision aspect of it. And when you have
11:43forced the pulling apart, this touches
11:45back on this paper from the fast journal
11:47in 2022. If you're forcing mitochondrial
11:50to be in a fision state, you're reducing
11:53their ability to make testosterone.
11:56Now I mentioned insulin because in my
11:59study that same paper we found that
12:00elevated insulin is a stimulus for
12:03ceramides. Now there are other stimuli
12:05as well like inflammation but I of
12:08course want to talk about insulin
12:10because I don't talk about it enough. So
12:12by now you surely know that insulin
12:14resistance is central to virtually every
12:16chronic disease. But the connection to
12:18testosterone
12:20is both quite direct but very often
12:23overlooked.
12:24There was a very good study published in
12:262005 that examined men across a spectrum
12:29of insulin sensitivity. What they found
12:31was striking. There was a strong
12:34correlation between insulin sensitivity
12:36and testosterone response to various
12:39stimuli. In other words, the more
12:41insulin resistant a man was, the less
12:43testosterone his leading cells could
12:46produce when they were stimulated.
12:49What makes this finding so important is
12:51that this effect bypassed the pituitary
12:54gland. So it wasn't the brain that was
12:58sending weaker signals to the testes. It
13:00was the leading cells themselves that
13:02were less capable of responding to the
13:05signals coming from the brain. This is a
13:07direct effect of insulin resistance on
13:09testosterone production at the gonad
13:12level. Now how might this work
13:14mechanistically?
13:16In 2013, there was work that identified
13:19a key player, a protein called DAX 1.
13:23Under normal circumstances, insulin
13:25helps regulate steroidogenic enzyme
13:28expression. But in insulin resistant
13:30states, chronically elevated insulin
13:32leads to upregulation of DAX 1, which
13:36suppresses the very enzymes needed to
13:39make testosterone. It's a metabolic
13:41vicious cycle. Insulin resistance
13:44impairs testosterone production and low
13:47testosterone itself promotes further
13:50metabolic dysfunction.
13:52And this brings us to perhaps the most
13:54insidious mechanism of all, the role of
13:58body fat in testosterone decline. Fat
14:01tissue is not just passive energy
14:03storage as it's so often considered. Our
14:07body fat is active in both metabolism,
14:09yes, but also endocrinology. And one of
14:12its activities is particularly
14:14problematic for men's hormonal health.
14:19Atapost tissue contains an enzyme called
14:21aromatase.
14:23This enzyme is fascinating because it
14:26converts testosterone into estradiol.
14:29That's the primary female sex hormone.
14:31Now again just to confirm men have
14:33estradiol. So even um even though I'm
14:36calling it the primary female sex
14:38hormone, men have estradiol and
14:40estradiol as I have stated abundantly in
14:43the past is the main estrogen.
14:46So even though I have been using the
14:48word estrogen throughout this at least
14:50the beginning part of the discussion,
14:52there is no single hormone called
14:54estrogen. It's the estrogens which is a
14:57small group of the predominant female
15:00sex hormones and estradiol is the main
15:02one. So very often people say estrogen
15:04and they actually mean estradiol.
15:07But to put a fine point on this, all
15:10estradiol in men and women came from
15:13testosterone.
15:16And it's through this process of the
15:18enzyme aromatase. In men approximately
15:2185% of circulating estradiol or I'll
15:25just say estrogen comes from this um
15:28peripheral conversion. So what I'm
15:29describing that can happen in the fat
15:31cell that is the majority source of
15:34estradiol in men. So this is what I just
15:37said is peripheral conversion. So in
15:40other words the main source of estradiol
15:43in men and this is important in men's
15:45health. Men need estrogen for normal
15:48healthy function.
15:50It it's from the test the testes
15:53producing a lot of testosterone and then
15:55peripheral tissues like atapost tissue
15:58converting it into estradiol or the main
16:01estrogen.
16:03Okay. So this is there are several
16:06studies that I am relying on and you can
16:09any insiders have access to all of these
16:11in the in their in the show notes. But
16:14here's where the vicious cycle can come
16:16in. Dr. Paul Cohen in a 1999 paper um
16:21described what he called the hypo
16:23meaning low hypogonatal
16:26obesity cycle and it's one of the most
16:28elegant and perhaps a little troubling
16:31examples of metabolic feedback gone
16:33wrong. It works like this. As a man as a
16:36man gains fat mass, the increased fat
16:40tissue means more aromatase activity
16:43which means more testosterone gets
16:46converted to estrogen. The rising
16:49estrogen levels then suppress the
16:51hypothalamus and pituitary. So turning
16:53off the brain signals through negative
16:55feedback which then reduces the signal
16:58down to the testes to tell it to produce
17:00more testosterone. with less
17:02testosterone, the man accumulates even
17:05more fat, which estradiol is good at
17:07promoting. Um, but especially he's going
17:10to accumulate more visceral fat because
17:12he's a guy, which contains even more
17:14aromatase. And so the cycle perpetuates
17:17itself. The clinical data bear this out.
17:21Obese men have a prevalence of
17:23hypogonadism
17:24ranging from 30 to 80% depending on how
17:27obesity and low testosterone levels are
17:29defined. that can vary from study to
17:31study.
17:33There was a paper the published the
17:34paper I just actually referred to a
17:37moment ago um found that obese men have
17:39elevated aromatase in their subcutaneous
17:42atapost tissue and this was directly
17:45linked to insulin resistance. It's all
17:47connected.
17:49So how do you know if you're
17:50experiencing significant testosterone
17:52decline? The European male aging study
17:55helped clarify this and none of it will
17:57be surprising. They found that the most
17:59specific symptoms of true late onset
18:02hypogonatism are sexual. So the most
18:04obvious way to determine this is reduced
18:07morning erections, decreased libido, and
18:10just general erectile dysfunction. If
18:12men had these sexual symptoms and they
18:15measured their testosterone and found it
18:16to be low, they met all the criteria for
18:19clinical hypogonetism.
18:21But testosterone affects far more than
18:23just sexual function. Men may also
18:26experience fatigue. uh difficulty
18:28concentrating, so even mental tasks,
18:31including just feeling good. So, no
18:33surprise that depression is up, they're
18:35more irritable, they're not sleeping as
18:37well. None of these things are uncommon
18:39these days, which makes you wonder just
18:41how common this fundamental problem may
18:43be. And of course, as I noted, body
18:46composition will shift toward reduced
18:48muscle mass and increased body fat,
18:51which again creates this vicious cycle.
18:53When you have more body fat, you're
18:55converting more of that hardearned or
18:57hard produced testosterone into
18:59estrogen. At the same time, bone density
19:03can decline, increasing osteoporosis
19:05risk. And this matters more than many
19:07people realize. Approximately 20% of men
19:10over 65 who suffer from a hip fracture
19:13die within six months.
19:16The metabolic consequences are
19:18birectional. research in a paper about
19:2020 years ago found that low testosterone
19:23predicts development of metabolic
19:25syndrome in type 2 diabetes. So
19:27testosterone decline isn't just a
19:29consequence of metabolic disease, but it
19:31can also be a cause. Now, here's the
19:34good news. Because so much of
19:36testosterone decline is driven by
19:38metabolic factors, lifestyle
19:40interventions can make a real
19:42difference. Let me walk through some of
19:45these key strategies that you can keep
19:46in mind if you're looking to try to
19:49reverse some of this. First of all,
19:51weight management. Weight loss may be
19:52the single most powerful intervention.
19:54Let me just put a plug in for my Insulin
19:56IQ effort. If you feel like you need
19:58help with weight loss, that is a
20:00wonderful community structure to help
20:02you reverse weight gain. Studies show
20:05that significant weight loss can boost
20:07testosterone by approximately 30%.
20:10Why? Well, because you're addressing
20:12multiple mechanisms simultaneously.
20:15You're shrinking fat cells, so you're
20:16reducing aromatase activity and you're
20:18improving insulin sensitivity, which
20:20lowers your insulin, which itself kind
20:23of removes the breaks from the testes in
20:26their testosterone production. So, focus
20:29on lowering insulin as your primary
20:31mechanism for weight loss, and that will
20:33yield myriad multiple benefits.
20:37Next, exercise. Um, you have to just
20:40resistance train. Running, aerobic
20:43exercise is fine, but I strongly
20:45encourage compound movements like squats
20:47or deadlifts. Anything you can do that
20:49is getting the body to a point of
20:51fatigue in its muscles. High-intensity
20:53interval training is wonderful. Um,
20:56don't overtrain. That can lower things
20:58too much in part because of a cortisol
21:00effect. So, more is not always better.
21:02Make sure you have your rest days, but
21:04do something with resistance training.
21:07Now, I want to address something many of
21:08you have asked about, which is cold
21:10plunge. The relationship between cold
21:12exposure and testosterone is nuanced,
21:15and likely it's a matter of timing.
21:18The timing appears to matter enormously.
21:21Cold water immersion immediately after
21:24training may work against your
21:26testosterone gains. So, resistance
21:29exercise can increase testosterone.
21:31Resistance exercise, then immediate cold
21:33exposure may blunt that response.
21:36However, if you flip them, um, cold
21:38exposure either separate from your
21:40workout or preworkout, so doing it
21:43before your workout may have a very
21:45different effect. And this is where I am
21:48relying a little more on anecdote, but
21:49including my own when I started doing
21:52this. So, it was cold exposure either
21:54alone or workout. I personally saw my
21:57testosterone to climb well above 1,000.
22:01Um, that was just with morning exposure
22:03alone. I use a Marroska Forge. ice bath
22:06and absolutely love it. I highly
22:08recommend it. I'm I'm very biased in
22:10favor of their of that particular ice
22:12bath. The key is that I keep my cold
22:15exposure separate from my resistance
22:17training sessions by at least a few
22:19hours just with my own schedule. If I
22:21had the ice bath in the same place where
22:23I do my resistance workouts, I would
22:26keep them more connected where it would
22:27be ice bath first, dry off, and then hit
22:30the workout. So, if you're going to
22:32incorporate cold um plunging, consider
22:34doing it on the non-training days or
22:36before your workout rather than after.
22:39Beyond the direct hormonal effect, cold
22:42exposure can offer other benefits like
22:45activating brown atapost tissue, which
22:47improves insulin sensitivity. And as
22:49we've discussed, better insulin
22:51sensitivity supports better testosterone
22:54production. So, cold exposure could be a
22:55significant player in your effort to
22:58increase testosterone. Next is sleep.
23:01That is non-negotiable. Testosterone
23:04production peaks during sleep,
23:06particularly during REM cycles. Research
23:08has shown that restricting sleep to just
23:10five hours per night can reduce
23:12testosterone levels by 10 to 15% even in
23:15young healthy men, not just old guys.
23:18And then stress is another big one,
23:20which but it's also a vague one, but
23:22suffice to say, if you're able to
23:24identify known causes of stress, do
23:27everything you can to control them.
23:29Frankly, the most relevant one is going
23:31to be sleep deprivation. Sleep
23:33deprivation increases cortisol and
23:35cortisol wages war on your testes
23:39um directly blocking your ability to
23:41produce testosterone.
23:43Finally, limit alcohol. Alcohol impairs
23:47testicular function directly and
23:49disrupts the hypothalamic pituitary
23:51axis. So that central signal coming from
23:54the brain. Heavy drinking can lead to
23:56testicular shrinkage and increased
23:59estrogen levels. So, if you're drinking
24:02to bump that down as low as you can get
24:04it. Now, what about testosterone
24:06replacement therapy or TRT? For men with
24:10confirmed low testosterone and
24:12significant symptoms, TRT can be very
24:14appropriate. However, it's important to
24:16understand the tradeoffs. Exogenous or
24:19injected testosterone will suppress your
24:22own production. So your the brain will
24:25see all that testosterone coming in and
24:27then send the signal to the testes that
24:29they're not needed. Because of that, I
24:31think a man who is trying to conceive,
24:34so if you and your wife are trying to
24:36have a baby, um be very very cautious
24:39with TRT use. If that stage of life has
24:42passed, then you can be a little more
24:43liberal with it. Let me leave you with
24:47this perspective. Male menopause or
24:49andropause, which is a better term,
24:51albeit an uncommon one, is real. The
24:54gradual decline in testosterone with
24:56age, affects millions of men and has
24:58profound implications for quality of
25:00life, metabolic health, and of course,
25:02longevity. Unlike female menopause,
25:05which represents the exhaustion of a
25:06finite resource, male hormonal decline
25:09stems from decreased cellular activity.
25:12But that does mean it is potentially
25:14modifiable. the metabolic connections
25:17we've discussed today like mitochondrial
25:19health, insulin sensitivity, body
25:21composition, and I even touched on
25:23inflammation. It really represents some
25:26uh several points of intervention. You
25:28are not powerless against this decline.
25:30Every improvement in the aspects I just
25:33mentioned has the potential to support
25:35increased testosterone production. But
25:37of course, if you're concerned, just get
25:39tested. It's helpful to know your
25:41numbers if for nothing else than to know
25:43what you can track. uh but this is one
25:46area where the science of metabolism and
25:49the science of endocrinology intersect
25:51beautifully. Again, those are two areas
25:53of profound interest for me and this is
25:55an area where you have some real control
25:57over your health trajectory.
26:00Thanks for joining me today in the
26:01metabolic classroom. Until next time,
26:04stay curious and stay healthy.
26:08[music]
26:12Looking to improve your own metabolic
26:14health? Visit insuliniq.com
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26:33more.

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This page contains the full transcript of 129: Boost Testosterone Naturally - Mitochondria, Insulin, and Fighting Back with Dr. Ben Bikman by Ben Bikman, generated from the public captions YouTube serves with the video. The transcript has 3,858 words across 648 segments, with the original timestamps preserved so you can click any line to jump to that moment in the embedded player.

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