Boost Testosterone Naturally: Mitochondria, Insulin, and Fighting Back

Summary

The Metabolic Classroom with Dr. Ben Bikman

Episode: Boost Testosterone Naturally: Mitochondria, Insulin, and Fighting Back
Date: December 7, 2025
Host: Dr. Ben Bikman (Insulin IQ)
(Ad & intro content omitted)

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Episode Overview

In this episode, Dr. Ben Bikman delves into the often-overlooked topic of "male menopause" or andropause, focusing on age-related testosterone decline in men. He unpacks the biological mechanisms behind this decline, the unique metabolic and hormonal factors involved, and, crucially, outlines lifestyle strategies to naturally support and boost testosterone levels—emphasizing that much of the process is modifiable through interventions affecting metabolism, insulin sensitivity, mitochondrial health, and more.

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Key Discussion Points & Insights

1. Defining Male Menopause (Andropause)

• Why the term matters:
  Dr. Bikman justifies using "male menopause" by drawing a useful comparison with female menopause—although not directly equivalent, men experience a parallel, gradual decline in hormone levels with age (03:02).
• Biological Basis:
  • Women’s ovaries have a finite supply of follicles (egg cells) that depletes, triggering a rapid hormonal shift at menopause.
  • Men’s Leydig cells (testosterone-producing cells in the testes) don’t run out but gradually become less efficient, leading to a slow decrease in testosterone—about 1% per year from age ~30–40, with free (active) testosterone declining even faster (04:24).

“If female menopause is like a warehouse running out of inventory, male menopause is like a factory that keeps running, but slow—less and less of the product each year. The machinery is still there, but it’s not working as well as it once did.” (05:20)

2. Hormone Decline: The Data

• Landmark studies:
  • Massachusetts Male Aging Study: Total testosterone declines ~1.6%/year, bioavailable (free) testosterone 2–3%/year (07:02).
  • By age 60, ~20% of men have clinically low testosterone; by the 70s and 80s, up to 50% (07:38).
  • Decline is gradual, often unnoticed until symptoms accumulate.

3. Why Does Testosterone Drop? Mechanisms

a. Mitochondrial Health

• Testosterone synthesis is fundamentally mitochondrial; the rate-limiting step is transporting cholesterol into the inner mitochondrial membrane.
• Proteins supporting this (STAR, TSPO) decline with age, as does mitochondrial structure.
• Promoting “mitochondrial fusion” helps restore testosterone production even in aging Leydig cells (09:40).

“When the architecture of the mitochondria is compromised or shifted, it falls apart. So does the cell’s capacity to make testosterone.” (10:32)

b. Insulin Resistance and Ceramides

• Chronically elevated insulin (from poor metabolic health) increases ceramides, which force mitochondria into a “fission” (fragmented) state—bad for testosterone synthesis (12:10).
• Insulin resistance results in Leydig cells being less responsive to brain signals—direct suppression of testosterone production, not just weaker signaling (13:06).

c. Body Fat, Aromatase, and the ‘Hypogonadal Obesity Cycle’

• Fat tissue contains aromatase, which converts testosterone to estradiol (primary estrogen).
• Increased estrogen from more fat suppresses brain signaling, which further reduces testosterone.
• This cycle, described as the “hypogonadal obesity cycle,” causes men to accumulate more fat and further depresses testosterone (19:34).

“As a man gains fat mass, the increased fat tissue means more aromatase activity, which means more testosterone gets converted to estrogen...the cycle perpetuates itself.” (19:41)

4. Recognizing Low Testosterone

• Main symptoms: reduced morning erections, decreased libido, erectile dysfunction.
• Other symptoms: fatigue, poor concentration, depression, irritability, sleep disturbances, decreased muscle mass, increased fat, bone density loss.
• Bi-directional link: low testosterone can both cause and result from metabolic dysfunction (21:37).

5. Fighting Testosterone Decline: Lifestyle Interventions

A. Weight Management

• Weight loss can boost testosterone by ~30%.
• Mechanisms: reduces fat (less aromatase activity), improves insulin sensitivity, supports Leydig cell function (22:39).

“Focus on lowering insulin as your primary mechanism for weight loss and that will yield myriad multiple benefits.” (22:59)

B. Exercise

• Resistance training is prioritized; compounds like squats, deadlifts are preferred.
• High-intensity interval training (HIIT) also beneficial.
• Don’t overtrain (can suppress testosterone via cortisol; rest matters) (23:25).

C. Cold Exposure

• Nuanced effects:
  • Cold immersion immediately after resistance training blunts the testosterone-raising effect of the workout.
  • Cold exposure before or on non-training days may boost testosterone.
  • Dr. Bikman shares his own anecdote: morning cold exposure raised his testosterone “well above 1000” (24:28).

“The key is that I keep my cold exposure separate from my resistance training sessions by at least a few hours...” (24:37)

D. Sleep

• Non-negotiable: testosterone peaks during sleep, especially REM.
• Restricting to 5 hours/night can cut testosterone by 10–15%, even in healthy young men (25:53).

E. Stress

• Chronic stress increases cortisol, which directly hampers testosterone production.
• Most relevant stressor: sleep deprivation (26:34).

F. Alcohol

• Impairs testicular function, suppresses brain-testes hormonal axis, promotes testicular shrinkage and increase in estrogen (27:09).

6. Testosterone Replacement Therapy (TRT)

• Appropriate for confirmed low testosterone with significant symptoms.
• Caution for those wanting fertility; TRT suppresses the body’s own production (27:38).

7. A Message of Empowerment

• Unlike menopause, male hormonal decline is largely modifiable through mitochondrial health, metabolism, insulin and lifestyle changes.
• Testing is encouraged; know your numbers for tracking.

“You are not powerless against this decline. Every improvement in the aspects I just mentioned has the potential to support increased testosterone production.” (28:44)

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Notable Quotes and Moments

• “It’s a metabolic vicious cycle. Insulin resistance impairs testosterone production, and low testosterone itself promotes further metabolic dysfunction.” (16:08)
• "Men need estrogen for normal, healthy function...all estradiol in men and women comes from testosterone, and it's through this process of the enzyme aromatase." (16:45)
• “Male menopause, or andropause, which is a better term, albeit an uncommon one, is real…unlike female menopause…male hormonal decline stems from decreased cellular activity. But that does mean it is potentially modifiable.” (28:53)

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Key Timestamps

• 03:02 – Introduction to “male menopause” (andropause)
• 05:20 – Warehouse vs. factory analogy for menopause/andropause
• 07:02 – Decline rates for total/free testosterone; study data
• 09:40 – Mitochondria’s role in testosterone production
• 12:10 – Elevated insulin, ceramides, mitochondrial fission
• 13:06 – Direct effect of insulin resistance on Leydig cells
• 19:34 – Hypogonadal obesity cycle explained
• 21:37 – Symptoms and impact of low testosterone
• 22:39 – Lifestyle intervention: weight loss
• 23:25 – Lifestyle intervention: exercise
• 24:28 – Lifestyle intervention: timing of cold exposure
• 25:53 – Lifestyle intervention: sleep
• 26:34 – Lifestyle intervention: stress
• 27:09 – Lifestyle intervention: alcohol
• 27:38 – TRT—benefits, cautions
• 28:44 – Encouragement: “You are not powerless against this decline.”

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Summary Takeaways

This episode leaves listeners with a clear, actionable message: testosterone decline doesn’t have to be an inevitable part of aging. By addressing metabolic health (particularly insulin sensitivity), mitochondrial function, weight management, and key lifestyle factors, men can actively influence their testosterone levels and, ultimately, their quality of life and longevity.

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“Thanks for joining me today in the Metabolic Classroom. Until next time, stay curious and stay healthy.” – Dr. Ben Bikman (29:24)

Transcript

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Welcome to the Metabolic Classroom Podcast. I'm Ben Bickman. Thanks for letting me be your guest professor for the next few minutes. Don't worry about any pop quizzes. I'm here to simply make the science of metabolism clear, practical and engaging before we get started. Just as a reminder, you can listen to both of my podcasts ad free by becoming an insider. Just go to Ben Bickman.com or click on the link at the top of the show. Notes welcome back to the Metabolic Classroom. I'm Ben Bickman, biomedical scientist and professor of cell biology. Today we're tackling a topic that affects millions of men but rarely gets the attention it deserves male menopause. Or as it's sometimes called and perhaps more accurately, andropause. Now I know what you might be thinking Male menopause? Isn't menopause something that only affects women? And you'd be, of course right to question the terminology. The word menopause literally refers to the cessation of menstruation, which obviously does not apply to men. But here's why I still find the term useful, if perhaps still a little confusing. It helps us understand that men experience their own version of hormonal decline with age, just as women do. It's the male equivalent of menopause, not the same thing, and not equal in degree, but a parallel process that does deserve some attention. Just for the sake of the men who are wanting to understand their health a little better. To really appreciate what's happening in men, let's briefly review what happens in women during menopause. This comparison will illuminate why the male experience is fundamentally different but equal in its own way. In women, menopause represents something truly remarkable from a biological standpoint, the complete exhaustion of a finite resource. Here's what I mean. When a female baby is developing in the womb, her ovaries already contain all the eggs she will ever have, somewhere between 1 to 2 million primordial follicles. By the time she reaches puberty, that number has already declined to about 300,000. This isn't because something went wrong, it's simply how the system is designed. The follicles are continuously being activated and lost through a process called atresia or just a programmed death of the follicle. The rate of follicle loss accelerates dramatically as women age. Before age 37, women lose approximately 5% of their remaining follicles each year. But after 37, that rate more than doubles to about 12% annually. This acceleration continues until typically in the late 40s or early 50s, the ovaries are essentially depleted of follicles. When this happens, estrogen production plummets by roughly 90%, because the follicles themselves are the primary source of estrogen in premenopausal women. This dramatic hormonal cliff is why menopause symptoms can be so sudden and pronounced. These are dramatic manifestations, things like hot flashes, mood changes, sleep disturbances, and more. The body is experiencing a rapid hormonal withdrawal. The male experience is quite different in origin and magnitude. Unlike ovaries, which have a finite supply of follicles. And remember, the follicle is so relevant because it's the source of all of these hormones, men's Leydig cells, that's the cells within the testes that are responsible for producing testosterone, actually persist throughout life. It's not a finite resource. Men don't run out of testosterone producing cells. Instead, these cells gradually become less capable at their job. Think of it this way. If female menopause is like a warehouse running out of inventory, male menopause is like a factory that keeps running, but slow less and less of the product each year. The machinery is still there, but it's not working as well as it once did. This gradual decline typically begins around age 30 to 40, with testosterone levels dropping approximately 1% per year. But here's what makes this particularly significant. Free testosterone, the biologically active form that's not bound to proteins in the blood, which inactivates it. It declines even faster at about 1 1/2 to 2% per year. This is partly because levels of sex hormone binding globulin, sometimes just abbreviated as shbg, tend to increase with age, grabbing more of that testosterone and make it unavailable for use. So we have this compounding effect, a reduction in testosterone production. At the same time, we have an increase in testosterone binding. So the sex hormone binding protein is locking up more of the testosterone and thus the free amount, which is, again, as I noted, the biologically active form, is greatly reduced relatively. There's a landmark study called the Massachusetts Male Aging Study, and they found that total Testosterone declined at 1.6% per year, while bioavailable, or the free Testosterone, dropped at 2 to 3% per year. Similarly, the Baltimore Longitudinal Study of Aging confirmed consistent testosterone decline across every decade from the 30s through the 80s. The clinical implications are substantial. By their 60s, approximately 20% of men have clinically low testosterone. By the 70s and 80s, that number rises to about 50%. Yet because this decline happens so gradually, unlike the more abrupt transition that women experience, many men don't realize what's happening until the effects have accumulated significantly. The mechanisms behind the decline are myriad and interesting. So I want to discuss them. Of course, as a cell biologist, I always want to look at the mechanism. So I'd mentioned this earlier. Do Leydig cells actually become less efficient? This is where the metabolic connections become particularly fascinating and where I think we can find some hope for intervention. First, let's talk about mitochondria. Testosterone synthesis is fundamentally a mitochondrial process, the rate limiting step in steroid hormone production, which is all the sex hormones. Actually, it's getting cholesterol, which is the raw material for all sex hormones, testosterone included, into the inner mitochondrial membrane, where it can be converted to a molecule called pregnenolone, which is the precursor to all steroid hormones. Now, there's a little bit of fundamental endocrinology baked into this discussion that I'm kind of assuming, you know, and that might be dangerous on my part as a teacher. The steroid hormones are their own class of hormones separate from any others, where they're all built on a steroid nucleus or a cholesterol molecule that's been modified. So all sex hormones start with cholesterol, and you have to get the cholesterol into the mitochondria. This transport depends on proteins called star, S, T, A, R, that stands for steroidogenic acute regulatory protein, and also another one called tspo, which is a translocator protein. Both of these decline with age. Research that was published in the FASEB journal just a few years ago demonstrated something interesting. They found declining tspo, that's the translocator protein, that these decline in the TSPO levels are associated with deteriorating mitochondrial structure, specifically the cristae. These are the inner foldings of the mitochondria where so much of the cell's energy production happens. You know, if you think of something like the electron transport system, all of that's located on that, on the crystal, these, the inner mitochondrial membrane. When the architecture or the structure of the mitochondria is compromised or shifted, it falls apart. So does the cell's capacity to make testosterone. But here's something that I find particularly interesting. They also showed the same study that promoting mitochondrial Fusion essentially helping the mitochondria maintain a long, connected, reticular or stringy structure. Remember, the word mitochondria is derived from the Greek word for thread, which is mitos. Mitochondria are long, stringy things woven through the cell. They found that when they could really promote a metabolic milieu of greater mitochondrial fusion, they could restore testosterone production even in older Leydig cells. Remember, the Leydig cells are the testosterone producing cells of the testes, the male gonads. This suggests that the decline is not inevitable. It's potentially reversible if we can support mitochondrial health. Indeed, this touches on some of my own work from my lab, where we've published before that ceramides, a very highly active lipid or a type of fat within the cell, can mediate forced mitochondrial fission. And we found one final point before I kind of revisit this. Chronically elevated insulin is a key signal for mitochondrial fission or ceramides production. So basically, we found increased ceramides would force the mitochondria to pull apart. That's the fission aspect of it. And when you have forced the pulling apart. This touches back on this paper from the fastib journal in 2022. If you're forcing mitochondrial to be in a fission state, you're reducing their ability to make testosterone. Now, I mentioned insulin because in my study, that same paper, we found that elevated insulin is a stimulus for ceramides. Now, there are other stimuli as well, like inflammation, but I of course want to talk about insulin because I don't talk about it enough. So by now you surely know that insulin resistance is central to virtually every chronic disease. But the connection to testosterone is both quite direct, but very often overlooked. There was a very good study published in 2005 that examined men across a spectrum of insulin sensitivity. What they found was striking. There was a strong correlation between insulin sensitivity and testosterone response to various stimuli. In other words, the more insulin resistant a man was, the less testosterone his Leydig cells could produce when they were stimulated. What makes this finding so important is that this effect bypassed the pituitary gland. So it wasn't the brain that was sending weaker signals to the testes. It was the leading cells themselves that were less capable of responding to the signals coming from the brain. This is a direct effect of insulin resistance on testosterone production at the gonad level. Now, how might this work mechanistically? In 2013, there was work that identified a key player, a protein called DAX1. Under normal circumstances, insulin helps regulate steroidogenic enzyme expression. But in insulin Resistant states. Chronically elevated insulin leads to upregulation of DAX1, which suppresses the very enzymes needed to make testosterone. It's a metabolic vicious cycle. Insulin resistance impairs testosterone production, and low testosterone itself promotes further metabolic dysfunction. And this brings us to perhaps the most insidious mechanism of all, the role of body fat in testosterone decline. Fat tissue is not just passive energy storage, as it's so often considered. Our body fat is active in both metabolism, yes, but also endocrinology. And one of its activities is particularly problematic for men's hormonal health. Adipose tissue contains an enzyme called aromatase. This enzyme is fascinating because it converts testosterone into estradiol, that's the primary female sex hormone. Now, again, just to confirm, men have estradiol. So even even though I'm calling it the primary female sex hormone, men have estradiol. And estradiol, as I have stated abundantly in the past, is the main estrogen. So even though I have been using the word estrogen throughout this, at least the beginning part of the discussion, there is no single hormone called estrogen. It's the estrogens, which is a small group of the predominant female sex hormones, and estradiol is the main one. So very often people say estrogen and they actually mean estradiol. But to put a fine point on this, all estradiol in men and women came from testosterone. And it's through this process of the enzyme aromatase. In men, approximately 85% of circulating estradiol, or I'll just say estrogen, comes from this peripheral conversion. So what I'm describing, that can happen in the fat cell that is the majority source of estradiol in men. So this is what I just said is peripheral conversion. So in other words, the main source of estradiol in men, and this is important in men's health. Men need estrogen for normal, healthy function. It's from the testes producing a lot of testosterone, and then peripheral tissues like adipose tissue converting it into estradiol or the main estrogen.

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[Ben Bickman]

Okay, so this is. There are several studies that I am relying on and you can any insiders have access to all of these in the in their in the show notes. But here's where the vicious cycle can come in. Dr. Paul Cohen, in a 1999 paper, described what he called the hypo, meaning low hypogonadal obesity cycle. And it's one of the most elegant and perhaps a little troubling examples of metabolic feedback gone wrong. It works like this as a main as a man gains fat mass, the increased fat tissue means more aromatase activity, which means more testosterone gets converted to estrogen. The rising estrogen levels then suppress the hypothalamus and pituitary, so turning off the brain signals through negative feedback, which then reduces the signal down to the testes to tell it to produce more testosterone. With less testosterone, the man accumulates even more fat, which estradiol is good at promoting. But especially he's going to accumulate more visceral fat because he's a guy which contains even more aromatase. And so the cycle perpetuates itself. The clinical data bear this out. Obese men have a prevalence of Hypogonadism ranging from 30 to 80%, depending on how obesity and low testosterone levels are defined. That can vary from study to study. There was a paper the published the paper I just actually referred to a moment ago found that obese men have elevated aromatase in their subcutaneous adipose tissue. And this was directly linked to insulin resistance. It's all connected. So how do you know if you're experiencing significant testosterone decline? The European Male Aging Study helped clarify this. And none of it will be surprising. They found that the most specific symptoms of true late onset hypogonadism are sexual. So the most obvious way to determine this is reduced morning erections Decreased libido, just general erectile dysfunction. If men had these sexual symptoms and they measured their testosterone and found it to be low, they met all the criteria for clinical hypogonadism. But testosterone affects far more than just sexual function. Men may also experience fatigue, difficulty concentrating. So even mental tasks, including just feeling good. So no surprise that depression is up. They're more irritable, they're not sleeping as well. None of these things are uncommon these days, which makes you wonder just how common this fundamental problem may be. And of course, as I noted, body composition will shift toward reduced muscle mass and increased body fat, which again creates this vicious cycle. When you have more body fat, you're converting more of that hard earned or hard produced testosterone into estrogen. At the same time, bone density can decline, increasing osteoporosis risk. And this matters more than many people realize. Approximately 20% of men over 65 who suffer from a hip fracture die within six months. The metabolic consequences are bidirectional. Research in A paper about 20 years ago found that low testosterone predicts development of metabolic syndrome in type 2 diabetes. So testosterone decline isn't just a consequence of metabolic disease, but it can also be a cause. Now here's the good news. Because so much of testosterone decline is driven by metabolic factors, lifestyle interventions can make a real difference. Let me walk through some of these key strategies that you can keep in mind if you're looking to try to reverse some of this. First of all, weight management weight loss may be the single most powerful intervention. Let me just put a plug in for my insulin IQ effort. If you feel like you need help with weight loss, that is a wonderful community structured to help you reverse weight gain. Studies show that significant weight loss can boost testosterone by approximately 30%. Why? Well, because you're addressing multiple mechanisms simultaneously. You're shrinking fat cells, so you're reducing aromatase activity and you're improving insulin sensitivity, which lowers your insulin, which itself kind of removes the brakes from the testes in their testosterone production. So focus on lowering insulin as your primary mechanism for weight loss and that will yield myriad multiple benefits. Next, exercise. You have to just resistance train. Running aerobic exercise is fine, but I strongly encourage compound movements like squats or deadlifts. Anything you can do that is getting the body to a point of fatigue in its muscles. High intensity interval training is wonderful. Don't over train. That can lower things too much, in part because of a cortisol effect. So more is not always better. Make sure you have your rest days, but do something with resistance training. Now I want to address something many of you have asked about, which is Cold plunge. The relationship between cold exposure and testosterone is nuanced and likely it's a matter of timing. The timing appears to matter enormously. Cold water immersion immediately after training may work against your testosterone gains. So resistance exercise can increase testosterone resistance exercise. Then immediate cold exposure may blunt that response. However, if you flip them cold exposure either separate from your workout or pre workout. So doing it before your workout may have a very different effect. And this is where I am relying a little more on anecdote but including my own when I started doing this so it was cold exposure either alone or workout. I personally saw my testosterone to climb well above 1000. That was just with morning exposure alone. I use a Marozka Forge ice bath and absolutely love it. I highly recommend it. I'm very biased in favor of that particular ice bath. The key is that I keep my cold exposure separate from my resistance training sessions by at least a few hours, just with my own schedule. If I had the ice bath in the same place where I do my resistance workouts, I would keep them more connected where it would be ice bath first dry off and then hit the workout. So if you're going to incorporate cold plunging, consider doing it on the non training days or before your workout rather than after.

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[Ben Bickman]

Beyond the direct hormonal effect, cold exposure can offer other benefits, like activating brown adipose tissue, which improves insulin sensitivity. And as we've discussed better insulin sensitivity supports better testosterone production. So cold exposure could be a significant player in your effort to increase testosterone. Next is sleep. That is non negotiable. Testosterone production peaks during sleep, particularly during REM cycles. Research has shown that restricting sleep to just five hours per night can reduce testosterone levels by 10 to 15% even in young, healthy men, not just old guys. And then stress is another big one, but it's also a vague one. But suffice to say, if you're able to identify known causes of stress, do everything you can to control them. Frankly, the most relevant one is going to be sleep deprivation. Sleep deprivation increases cortisol and cortisol wages war on your testes, directly, blocking your ability to produce testosterone. Finally, limit alcohol. Alcohol impairs testicular function directly and disrupts the hypothalamic pituitary axis. So that central signal coming from the brain, heavy drinking, can lead to testicular shrinkage and increased estrogen levels. So if you're drinking, bump that down as low as you can get it. Now, what about testosterone replacement therapy, or trt? For men with confirmed low testosterone and significant symptoms, TRT can be very appropriate. However, it's important to understand the trade offs. Exogenous or injected testosterone will suppress your own production. So the brain will see all that testosterone coming in and then send the signal to the testes that they're not needed. Because of that, I think a man who is trying to conceive. So if you and your wife are trying to have a baby, be very, very cautious with TRT use. If that stage of life has passed, then you can be a little more liberal with it. Let me leave you with this perspective. Male menopause, or andropause, which is a better term, albeit an uncommon one, is real. The gradual decline in testosterone with age affects millions of men and has profound implications for quality of life, metabolic health and of course, longevity. Unlike female menopause, which represents the exhaustion of a finite resource, male hormonal decline stems from decreased cellular activity. But that does mean it is potentially modifiable. The metabolic connections we've discussed today, like mitochondrial health, insulin sensitivity, body composition, and I even touched on inflammation, it really represents some several points of intervention. You are not powerless against this decline. Every improvement in the aspects I just mentioned has the potential to support increased testosterone production. But of course, if you're concerned, just get tested. It's helpful to know your numbers, if for nothing else than to know what you can track. But this is one area where the science of metabolism and the science of endocrinology intersect beautifully again. Those are two areas of profound interest for me, and this is an area where you have some real control over your health trajectory. Thanks for joining me today in the Metabolic classroom. Until next time, stay curious and stay healthy.

[Richard Jefferson]

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