How to increase testosterone naturally: 69 strategies & claims ranked by evidence

Most advice about increasing testosterone starts in the wrong place.

Lift heavy. Eat more fat. Take zinc. Stop ejaculating. Have more sex. Take cold showers. Sprint. Get more sun. Eat pomegranate. Wear cotton underwear. Ground yourself. Maybe shine red light on your balls.

Some of those ideas contain a piece of truth. Some are exaggerated. Some appear to do nothing. Others trace back to small, poorly controlled, or animal studies that eventually got repeated online as if they were settled human evidence.

But the bigger problem is the model underneath them.

Testosterone optimization is mostly about removing reasons your body is suppressing testosterone, not finding things that force it higher.

An overweight man can lose excess body fat and see testosterone rise substantially. A chronically underfed athlete can start eating enough again and restore reproductive signaling that was being suppressed by low energy availability. A man regularly sleeping four or five hours may improve his hormonal environment by fixing the sleep deprivation.

Those are not really testosterone hacks.

They are removal of interference.

Meanwhile, a healthy man with normal testosterone can take something that creates a short-lived hormonal increase and assume he has meaningfully raised his normal baseline.

He may not have.

This fits the Healthmaxxing model. Testosterone is better understood as an output of the system than as a lever you endlessly pull. Sleep, metabolic health, energy availability, physical demand, recovery, illness, medications, nutrition, environment, mating context, and circadian timing all influence the conditions under which that output is produced.

To separate those effects, I use what I call the BiohackBeast Testosterone Framework, consisting of four categories: deficiency correction, suppressor removal, true enhancement, and acute spikes.

Before asking what you can add, ask a better question:

What is interfering with normal function?

What's in this guide

• 69 testosterone strategies and claims ranked
• The BiohackBeast Testosterone Framework
• Body fat, calories, and energy availability
• Lifting, HIIT, and sprinting
• Competition and martial arts
• Sex, sexual arousal, and testosterone
• Fatherhood and paternal caregiving
• Diet, sugar, fasting, fat, protein, and cholesterol
• Supplements, herbs, and garlic
• Erectile function and libido vs testosterone
• Sunlight, red light, cold, grounding, and EMF
• Fragrance, plastics, underwear, tap water, honey, and tamarind
• Nicotine pouches and smoking
• Medical causes and testosterone-suppressing drugs

This guide goes into the studies behind the claims. If you only want the quick conclusions, use the ranking table below. If you want to know where a claim came from and whether the original research actually supports it, jump to the relevant section.

69 testosterone strategies and claims ranked by evidence

One warning before looking at the table: testosterone studies do not always measure the same thing.

Total testosterone, free testosterone, sex hormone-binding globulin (SHBG), bioavailable testosterone, dihydrotestosterone (DHT), and a temporary post-workout testosterone increase are different outcomes.

A short rise after lifting, sex, erotic stimulation, or winning a competition is not the same thing as increasing your normal resting testosterone.

The reverse is also true. A meal can temporarily lower measured testosterone for several hours without proving that the same food lowers your normal fasting baseline over months.

The BiohackBeast Testosterone Framework

Imagine two men whose morning blood tests both show a total testosterone level of 450 ng/dL.

That means each blood sample contains about 450 nanograms of total testosterone per deciliter of blood. A single test is not a perfect measure of someone's long-term baseline, but morning total testosterone is one of the standard measurements used to estimate where a man's usual testosterone level sits.

The first man is lean, sleeps well, has normal free testosterone, trains consistently, feels energetic, and has no obvious metabolic dysfunction.

The second carries substantial excess body fat, routinely sleeps five hours, drinks heavily, regularly under-eats while training, and takes a medication capable of suppressing the reproductive hormone system.

The laboratory number is identical.

The system producing it is not.

To make sense of testosterone claims, the BiohackBeast Testosterone Framework separates interventions into four categories:

• Deficiency correction: restoring something the body needs but currently lacks.
• Suppressor removal: removing something that is holding testosterone below its normal potential.
• True enhancement: raising testosterone above an already healthy, functional baseline.
• Acute spike: temporarily raising testosterone for minutes or hours without meaningfully changing the resting baseline.

This distinction matters because all four effects routinely get described online as “boosting testosterone.”

They are not the same biological outcome.

A zinc-deficient man restoring adequate zinc is correcting a deficiency.

An overweight man losing excess body fat is removing a suppressor.

A healthy man taking something that pushes his already-normal testosterone higher would be true enhancement.

A man whose testosterone rises for 45 minutes after sprinting or sex is experiencing an acute spike.

Many of the largest natural testosterone increases are not true enhancement at all. They happen because a deficiency was corrected or a suppressor was removed.

Lose excess body fat if you have it

If an overweight man wants to increase testosterone naturally, losing excess fat is one of the highest-leverage interventions available.

The relationship appears to be more than correlation.

In 2017, researchers used genetic data from 7,446 men across five European cohorts to test whether higher body mass itself contributes to lower testosterone. The analysis found evidence that genetically driven increases in body mass index caused lower serum testosterone, while the evidence for testosterone causing higher body mass was much weaker. The study was published in PLOS ONE.

Weight-loss studies point in the opposite direction. A 2013 analysis pooled studies of men losing weight through dieting or bariatric surgery. Testosterone increased after weight loss, and the increase was larger when more weight was lost. Bariatric surgery produced a much larger average testosterone increase than ordinary dietary weight loss.

This helps explain why testosterone interventions often look much more impressive in overweight, metabolically unhealthy, or low-T populations than in healthy young men.

There is more suppression available to reverse.

But lower body fat is not automatically better forever.

At some point, aggressive leanness and underfeeding create the opposite problem.

Do not get so lean or underfed that testosterone starts falling

Calorie restriction has a different effect depending on where you start.

In overweight and obese men, losing excess fat generally improves testosterone.

In lean, healthy men, aggressive calorie restriction can reduce it.

This becomes especially important when a man is training hard while eating too little.

Sports-medicine researchers use the term Relative Energy Deficiency in Sport (RED-S) to describe the wider hormonal and physiological problems that can occur when the energy left over after exercise is chronically too low.

In men, low energy availability can suppress reproductive signaling from the brain and reduce testosterone.

The practical distinction matters.

If excess body fat is suppressing testosterone, losing fat can help. If chronic underfeeding is suppressing testosterone, eating more can help.

Sleep deprivation can lower testosterone

Severe sleep loss has one of the clearer sleep-related effects on testosterone.

A widely cited 2011 study published in JAMA followed 10 healthy young men who first slept normally and were then restricted to five hours of sleep per night for one week. Their daytime testosterone levels fell by roughly 10 to 15 percent during the sleep-restricted period. The study was small, but it directly manipulated sleep rather than simply comparing good and bad sleepers.

More extreme sleep deprivation produces a clearer effect. A 2021 systematic review and meta-analysis combined 18 studies involving 252 men. Total sleep deprivation significantly lowered testosterone, with substantial declines after about 24 hours awake and again after 40 to 48 hours without sleep.

Partial sleep restriction was much less consistent. In the same meta-analysis, restricting sleep without eliminating it entirely did not produce a statistically significant overall reduction in testosterone.

That uncertainty also appears in controlled experiments. One study of healthy young men found that neither five nights of very severe sleep restriction, with less than four hours of sleep per night, nor six weeks of more modest chronic restriction, about 1.5 hours less sleep per night, meaningfully changed plasma testosterone. The researchers concluded that partial sleep restriction does not reliably suppress testosterone in healthy young men.

So the evidence does not support a simple formula where every hour of lost sleep produces a predictable drop in testosterone.

Total or near-total sleep deprivation clearly suppresses testosterone. Partial sleep restriction can lower it, as the 2011 JAMA experiment showed, but the effect is much less consistent across studies.

Does lifting increase testosterone?

Resistance training belongs near the top of almost any serious health program.

But its benefits do not depend on producing a higher resting testosterone baseline.

A 2020 analysis pooled 48 exercise studies involving 569 participants. Moderate- and high-intensity exercise reliably increased total and free testosterone immediately after exercise. The increase was short-lived and largely disappeared during the early recovery period.

Researchers have also asked a different question: what happens to testosterone measured at rest after weeks or months of regular training?

A 2021 systematic review looked at 11 randomized exercise trials involving 421 previously inactive men whose testosterone was in the normal range. The overall effect on resting total testosterone was essentially zero. Resistance training remained excellent exercise, but it was not a reliable way to move resting testosterone upward in otherwise normal men.

A physically demanding lifestyle can still improve the conditions around testosterone

This is where the indirect effect becomes more interesting.

If you lift, sprint, fight, or train hard several days per week, poor recovery becomes expensive.

Four hours of sleep shows up in the gym.

Heavy drinking shows up in the gym.

Chronically under-eating shows up in the gym.

Being exhausted all week shows up in the gym.

A physically demanding lifestyle can therefore create pressure to organize the rest of your life around adequate food, better sleep, less heavy drinking, and actual recovery.

Those are all variables that can influence whether testosterone is being unnecessarily suppressed.

Lifting itself does not reliably raise resting testosterone. But consistently training hard can give you a practical reason to protect the sleep, food intake, body composition, and recovery habits that support normal testosterone.

The reverse also applies.

If hard training is stacked on top of too little food, poor sleep, and inadequate recovery, training itself can become part of the suppressive load.

Can hard training make you better at handling stress?

Hard exercise temporarily raises cortisol. That is normal.

Cortisol is the main human glucocorticoid. Glucocorticoids are steroid hormones released by the adrenal glands that help the body respond to physical or psychological stress. Cortisol helps free up energy, maintain blood pressure, and prepare the body to deal with a challenge.

The interesting question is whether repeatedly adapting to controlled physical stress changes how strongly the body reacts to stress later.

Researchers call this the cross-stressor adaptation hypothesis.

There is real evidence behind the idea, but it is not as simple as “exercise lowers cortisol.”

In a 2007 study, researchers compared 22 elite male athletes with 22 healthy but untrained men during the Trier Social Stress Test, a laboratory challenge involving public speaking and mental arithmetic in front of evaluators. The athletes and untrained men had similar cortisol levels before the test, but the trained men produced a smaller cortisol and heart-rate response once the psychological stress began.

That is an important distinction.

The athletes did not live with lower baseline cortisol. Their bodies responded differently when a new stressor arrived.

A 2014 randomized trial provided stronger evidence. Researchers assigned 149 healthy men to endurance training, relaxation training, or a wait-list group for 12 weeks. The final analysis included 96 men. After the training period, the endurance group showed smaller cortisol and cardiovascular responses to a standardized psychological stress test.

An even more revealing 2021 experiment involved 83 healthy men.

They were assigned to treadmill exercise at 30, 50, or 70 percent of their heart-rate reserve. Forty-five minutes later, all of them completed a psychological stress test. The harder exercise produced a larger cortisol rise during the workout, yet the men in the higher-intensity condition later showed a smaller cortisol response to the psychological stressor and recovered faster afterward.

That result gets very close to the interesting idea here:

a large acute cortisol response during a physical challenge can coexist with a more controlled response to a later stressor.

But the effect is not guaranteed.

A later six-month randomized trial followed 88 previously untrained healthy adults. The exercise group became significantly fitter, but their cortisol and ACTH responses to a psychological stress test were no lower than the control group's.

ACTH is a hormone released by the pituitary gland that tells the adrenal glands to release cortisol.

There is another reason not to think of stress adaptation as simply producing less cortisol.

The EROS research compared healthy male athletes, athletes with overtraining syndrome, and non-active men. In one study of 51 men, healthy athletes produced a stronger cortisol and ACTH response to a standardized hormonal challenge than either the overtrained athletes or the inactive controls. The researchers interpreted the stronger response as part of healthy hormonal conditioning rather than evidence that the athletes were more chronically stressed.

A separate EROS analysis found that the healthy athletes also had higher testosterone than the overtrained athletes. Overtraining was associated with lower testosterone and loss of several adaptations seen in the healthy athletes.

So stress adaptation is not a farce.

What the evidence undermines is the simplistic idea that becoming fitter means permanently lowering cortisol.

A well-adapted stress system may produce a smaller response to one kind of stress, a faster recovery after another, and a strong response when a strong response is actually needed.

Where does testosterone enter the picture?

This is where the evidence becomes more indirect.

Human experiments show that sufficiently high or prolonged glucocorticoid exposure can suppress testosterone.

In one classic experiment, researchers deliberately raised cortisol in healthy men. Testosterone then fell even though luteinizing hormone did not fall to the same degree. That suggests high cortisol can interfere directly with testosterone production in the testes rather than acting only by reducing the brain's signal to make testosterone.

Laboratory research helps explain why. Glucocorticoids can act on Leydig cells, the cells in the testes that make testosterone, and interfere with the machinery those cells use to produce steroid hormones. Glucocorticoids can also interfere with reproductive signaling higher up in the brain and pituitary.

What has not been demonstrated is the entire chain:

repeated hard training → better stress adaptation → lower long-term cortisol exposure → higher resting testosterone.

No human experiment has established that full sequence.

So the goal should not be to suppress every cortisol spike.

Train hard enough to adapt, but recover well enough that acute stress stays acute instead of turning into a chronically suppressive state.

That may help protect normal testosterone production, but it should be described as a plausible protective mechanism rather than a proven way to raise baseline testosterone.

A temporary cortisol spike during lifting, sprinting, or fighting is not the same thing as chronic stress.

A cortisol spike is not the same as chronic cortisol exposure, just as a testosterone spike is not the same as high baseline testosterone.

Does HIIT increase testosterone?

High-intensity interval training produces one of the clearer short-term testosterone responses.

A 2021 systematic review and meta-analysis examined 10 controlled studies involving 213 participants, along with 50 additional before-and-after exercise comparisons involving 677 participants. Testosterone rose substantially immediately after high-intensity interval exercise. The increase largely disappeared within about 30 to 60 minutes. At later recovery points, testosterone sometimes dipped below the pre-exercise level before returning to baseline by about 24 hours.

There is also a much smaller signal that interval training may affect resting testosterone in older men.

In 2019, researchers pooled 22 exercise-training studies involving men aged 60 and older. Resistance training produced essentially no change in resting testosterone. Endurance and interval training produced small but statistically significant increases. The interval-training evidence was based on relatively few studies, so the researchers treated the finding cautiously.

Does sprinting increase testosterone?

Sprinting can produce a real short-term testosterone response.

In a 2013 study, 14 healthy, physically active young men performed ten 30-second all-out cycling bouts with 90 seconds of recovery between sprints. Total testosterone, free testosterone, and DHT were all significantly higher five minutes after the workout. By 60 minutes after exercise, all three had returned to baseline.

The harder question is whether repeated sprint training raises resting testosterone over months.

One six-month study divided 12 adolescent boys into a sprint-training group and a control group. After training, the boys who sprinted produced a larger total-testosterone response when they performed a six-second sprint test. But bioavailable testosterone did not significantly increase, the study included only six boys per group, and the participants were adolescents rather than adult men.

No large adult trial has shown that regular sprint training creates a substantial long-term increase in resting testosterone.

Competition and martial arts can change testosterone, but the response depends on context

Testosterone responds not only to physical exertion but also to anticipation, competition, and outcome.

Testosterone can rise before a fight even starts

A 1999 study followed 20 male judo competitors before actual competition. Testosterone and cortisol both increased before the matches began. Because nobody had won or lost yet, the result suggests that anticipation of a meaningful competitive challenge can alter hormone levels before the contest itself.

Actual fighting does not reliably produce a large testosterone surge

A review of striking combat-sport research found a surprisingly inconsistent testosterone response. Across the studies that measured it, testosterone showed only a modest average increase after combat, and the combined result was not statistically convincing. Cortisol rose much more consistently.

Individual experiments show why the average is messy.

A 2013 randomized crossover study tested 10 national- or international-level karate athletes, six men and four women. Each athlete completed three minutes of kumite, meaning free sparring against another fighter, and on another day performed kata, a choreographed sequence of karate techniques.

Testosterone increased after both conditions, from a baseline of about 6.7 nmol/L to 9.1 after kumite and 7.9 after kata. The testosterone difference between kumite and kata was not statistically significant, although epinephrine rose much more during actual sparring.

So the simple claim that actual sparring raises testosterone while choreographed kata does not is not what the experiment showed.

A much larger study of 100 male professional K-1 kickboxers produced an even less intuitive result. Fighters were assigned either to an actual competitive fight or to a simulated fight using a punchbag.

After the real fight, average testosterone moved slightly downward from about 13.7 to 12.4 nmol/L, a change that was not statistically significant. Cortisol rose sharply from about 313 to 570 nmol/L. The punchbag group showed a small, non-significant testosterone increase instead.

Actual combat therefore produced a powerful stress response without producing a reliable testosterone surge.

A separate study followed 20 MMA fighters at four points around real competition: 24 hours before the fight, one hour before it, immediately afterward, and 24 hours later. Average testosterone fell from about 18.0 nmol/L at the first measurement to 13.0 one hour before the fight and 9.5 immediately afterward. It partially recovered to about 14.7 nmol/L the following day. So in this real-world sample, testosterone was already substantially lower before the fighters entered the cage and had not fully returned to the earlier value 24 hours afterward.

The study cannot tell us exactly why. It did not isolate dehydration, calorie restriction, weight cutting, sleep, psychological stress, or the fight itself as separate variables. That ambiguity matters.

The winner effect

A 2017 analysis pooled more than 60 competitive testosterone effects involving over 2,500 participants. Winners experienced a slightly larger testosterone response than losers on average. The effect was modest and varied substantially between different kinds of competition.

Winning therefore appears capable of changing testosterone acutely, while testosterone itself can also influence competitive and social behavior. 

There is no good evidence that accumulating wins progressively raises your normal resting testosterone. 

Weight cutting can suppress testosterone through fight day

A combat-sport weight cut is not necessarily one event.

Fighters may gradually reduce body fat over several weeks of fight camp, then use much more aggressive manipulation of calories, carbohydrates, fluids, and sodium during the final days before weigh-in.

In professional MMA, boxing, and kickboxing, the official weigh-in may occur roughly a day before competition. Athletes can then eat, drink, and restore some of the body mass they lost. A 2025 combat-sports position statement describes this distinction between longer-term weight descent and rapid weight loss, including aggressive fluid manipulation during the final 24 to 48 hours before weigh-in.

The important question is whether refeeding and rehydrating after weigh-in also restore testosterone before the fight.

We do not have clean evidence showing that testosterone reliably returns to its previous baseline during that recovery window.

The MMA study above is useful precisely because it measured fighters close to competition. Testosterone was about 27 percent lower one hour before the fight than it had been 24 hours earlier. That shows that a meaningful testosterone decline can still be present on fight day despite whatever eating and rehydration occurred during the preceding hours.

But it does not prove that weight cutting alone caused the decline. Real fight preparation combines several things at once, including energy restriction, dehydration, disturbed sleep, psychological stress, and sometimes very large changes in body mass.

Separate wrestler data strengthen the weight-cutting case. In elite wrestlers undergoing rapid weight loss, greater plasma osmolality, a marker of dehydration, was significantly associated with lower total testosterone and higher stress hormones. The more dehydrated the wrestlers were, the lower their testosterone tended to be.

So there are probably two different time scales worth separating.

• Acute weight cutting: dehydration and short-term calorie restriction can lower testosterone around competition, and available data show that the decline can still be present close to fight time.
• Chronic fight-camp stress: weeks of energy restriction, hard training, poor recovery, repeated weight cycling, and overtraining may create a broader suppressive environment that cannot necessarily be reversed by one large post-weigh-in meal.

The exact recovery timeline is not well established. It would therefore be too strong to claim either that every weight cut lowers fight-night testosterone or that a night of rehydration automatically restores it.

Does sex increase testosterone?

Sexual cues can produce another short-term testosterone response.

Erotic visual stimulation

In a 1985 experiment, researchers measured salivary testosterone in 20 healthy young men while they watched different kinds of films.

One condition involved erotic material. The comparison conditions included emotionally neutral footage and aggressive, nonsexual material.

Testosterone increased after the erotic film, beginning roughly 15 minutes after exposure and rising by about 35 percent during the experiment. The neutral and aggressive films did not produce the same increase, suggesting the hormonal response was more specifically related to sexual stimulation rather than simply emotional arousal.

But the effect is not universal.

One controlled study followed eight men for several hours while they viewed erotic material. The men became clearly sexually aroused, but testosterone and the other measured hormones did not significantly change. Sexual arousal can therefore increase testosterone without doing so reliably in every experiment.

Simply talking to an attractive woman is different

A later speed-dating experiment followed 79 participants through romantic speed-dating interactions and a same-sex comparison condition. Women's testosterone increased during romantic speed dating, while men's did not. Cortisol showed stronger relationships with romantic attraction than testosterone did in the men.

So the evidence does not support the broader claim that simply talking to an attractive woman reliably causes a male testosterone spike.

Masturbation and ejaculation

A small study of seven men aged 32 to 41 measured serum testosterone from before erection through ejaculation. Average testosterone increased from about 5.86 ng/mL before erection to about 7.01 ng/mL around ejaculation, then returned toward baseline within roughly ten minutes. The sample was extremely small, and the experiment measured a minutes-scale response rather than a long-term change.

That is a temporary testosterone spike, not a baseline increase.

Partnered sexual activity

A naturalistic study measured salivary testosterone in 44 men attending a U.S. sex club.

Testosterone increased by about 36 percent overall.

The difference between behavior groups was much larger. Men who actively participated in sexual activity showed an average increase of about 72 percent, compared with only about 11 percent among men who watched. The study suggests active partnered sexual behavior can produce a substantially larger acute testosterone response than passive observation.

The measurement was still taken around the sexual event.

No good evidence shows that simply having more sex every week progressively raises resting testosterone.

Fatherhood and paternal caregiving can lower testosterone

The transition to fatherhood is associated with lower testosterone

A large longitudinal study from the Philippines gives us unusually strong evidence because researchers measured the same men before and after major life changes.

The study followed 624 men for about 4.5 years.

Men who had higher testosterone at the beginning were more likely to become partnered fathers later.

After becoming partnered fathers, however, those same men showed much larger declines in testosterone than men who remained single and childless.

Median waking testosterone fell about 26 percent.

Evening testosterone fell about 34 percent. Because testosterone had been measured before fatherhood, the study could show both directions: higher-T men were more likely to become fathers, and testosterone then fell after the transition.

That does not prove that the mere biological fact of having a child automatically switches testosterone downward.

Becoming a father also changes behavior. Sleep may change. Pair-bonding may change. Time spent competing for mates may change. Daily contact with a child and caregiving may increase.

The first study measured the overall transition into partnered fatherhood. It could not isolate which part of that transition caused the testosterone decline.

Active childcare appears to contribute further

Follow-up research helps narrow the picture.

Among fathers, men doing at least three hours of childcare per day had lower testosterone than fathers doing relatively little childcare.

Researchers also followed changes within the same fathers. Men who increased the amount of childcare they performed experienced additional declines in testosterone. That makes active caregiving more than a random detail. The amount of hands-on childcare itself was associated with how low testosterone became.

So the evidence supports two related findings:

• Transitioning into fatherhood is associated with a substantial testosterone decline.
• Among fathers, doing more active childcare is associated with still lower testosterone.

We cannot say that caregiving explains the entire fatherhood effect.

But the data make it very plausible that the daily behavioral shift toward caring for a dependent child is part of the biology being measured.

A crying infant can move testosterone in either direction

A 2012 experiment placed 55 men in a simulated infant-care situation and exposed them to baby crying.

What happened to testosterone depended on what the men were able to do.

When a man could respond in a nurturing way and successfully calm the simulated infant, testosterone tended to fall.

When the crying continued and he could not resolve the situation, testosterone could rise instead. The researchers concluded that the testosterone response depended on the interaction between infant distress and successful caregiving.

So simply being physically near a toddler has not been shown to suppress testosterone.

The stronger finding is that the transition to fatherhood and greater active caregiving are both associated with lower baseline T.

Researchers often interpret the pattern through a mating-effort versus parenting-effort framework. Higher testosterone may favor competition and mate seeking, while lower testosterone after fatherhood may be compatible with greater paternal investment.

Diet matters most clearly at the extremes

Very-low-fat diets

A 2021 systematic review combined six controlled diet studies involving 206 men and compared lower-fat diets with higher-fat diets.

The lower-fat diets produced modest reductions in total testosterone, free testosterone, and DHT. The evidence base was small, with only six eligible intervention studies, so this should not be treated as proof that a precise dietary-fat percentage maximizes testosterone.

Saturated fat, polyunsaturated fat, and seed oils

Before looking at the studies, the terms need to be clear.

Saturated fat is common in foods such as butter, cheese, fatty meat, and coconut fat.

Polyunsaturated fat includes both omega-6 and omega-3 fats. Many seed oils are rich in omega-6 polyunsaturated fat, while fatty fish contains large amounts of omega-3 polyunsaturated fat.

Monounsaturated fat is another type of unsaturated fat and is especially abundant in olive oil and avocados.

These categories describe the chemical structure of the fat. They do not mean that every food within one category has the same biological effect.

A common online claim is that saturated fat raises testosterone while polyunsaturated “seed oils” lower it.

There is some real evidence behind the broader idea that dietary fat can affect testosterone. But the evidence does not cleanly show that seed oils themselves are the problem.

A 1984 controlled experiment put 30 healthy men on a different diet for six weeks. Their normal diet provided about 40 percent of calories from fat and relied heavily on animal fat. The experimental diet provided only about 25 percent of calories from fat and contained much more polyunsaturated fat relative to saturated fat. Testosterone fell from about 22.7 to 19.3 nmol/L, a decline of roughly 15 percent. Free testosterone fell as well, and the changes reversed after the dietary intervention ended.

That sounds like strong evidence against polyunsaturated fat until you look at what the researchers actually changed.

They changed two major things at the same time: the men ate much less total fat, and the fat they did eat became much more unsaturated.

So the experiment cannot tell us whether testosterone fell because total fat dropped from 40 to 25 percent of calories, because the type of fat changed, or because both happened together.

The study supports the idea that a lower-fat, more highly unsaturated diet can reduce testosterone. It does not isolate seed oils as the cause.

A much larger 2023 study looked at 2,546 middle-aged Finnish men.

At first, men eating more polyunsaturated fat appeared to have lower total and free testosterone. But after researchers accounted for differences such as age, body composition, total calorie intake, smoking, alcohol use, and other lifestyle factors, the relationship disappeared.

In plain English, the men who ate more polyunsaturated fat were also different in other ways that could affect testosterone.

Once the researchers statistically accounted for those differences, eating more polyunsaturated fat by itself no longer predicted lower testosterone.

That does not prove polyunsaturated fat has zero effect.

It does make the claim that polyunsaturated fat independently lowers resting testosterone much weaker.

A large fatty meal can temporarily lower testosterone

Short-term feeding experiments add another piece to the puzzle.

A 2019 pilot study involved nine overweight or obese fertile men. The researchers gave them different meals on different testing days and measured their hormones every hour for five hours.

A meal containing about 52 grams of polyunsaturated fat lowered testosterone by about 3.2 nmol/L after one hour, and the suppression remained measurable several hours later. But a meal containing roughly the same amount of monounsaturated fat produced a similar testosterone decline.

That matters because monounsaturated fat is the main type of fat in olive oil.

If both types of unsaturated fat temporarily lower testosterone after a large dose, the effect does not look unique to seed oils.

An older controlled experiment in healthy men found another version of the same pattern.

After a high-fat meal, both total and free testosterone fell. After a low-fat meal containing carbohydrate and protein, they did not. Luteinizing hormone, or LH, stayed roughly the same.

LH is the signal released by the pituitary gland that tells the testes to make testosterone.

If testosterone falls because the brain suddenly stops telling the testes to produce it, we would normally expect LH to fall too.

That did not happen.

So the temporary testosterone decline probably was not caused simply by the pituitary turning down its LH signal. Something farther downstream changed, such as testosterone production in the testes, how testosterone moved through the blood, or how quickly it was cleared.

The study does not tell us exactly which of those explanations is correct.

Another study found that a 1,300-calorie meal containing 86 percent of its calories from fat reduced total testosterone about 22 percent and free testosterone about 23 percent one hour later. The decrease lasted for hours, but the men's fasting testosterone did not fall after eight weeks of eating a higher-fat diet.

The implication is very different from “fat lowers testosterone.” A large fatty meal can temporarily lower the testosterone measured in your blood for several hours. That does not mean the same diet lowers your normal fasting baseline over weeks or months.

What about canola oil specifically?

There is no convincing human trial showing that canola oil specifically lowers resting testosterone.

The claim comes largely from animal research.

In a 2010 experiment, researchers fed canola oil or soybean oil to a special strain of rats bred to develop severe high blood pressure and strokes. Testosterone in both the blood and testes was significantly lower in the canola-oil group. That is a real finding, and it makes a possible hormonal effect of canola oil worth investigating.

But these were not ordinary healthy rats, much less healthy men. They were stroke-prone spontaneously hypertensive rats, a genetically selected disease model with abnormal cardiovascular physiology.

And even the rat literature does not point in one direction.

A 2018 experiment used 30 ordinary Sprague-Dawley rats and fed them either a control diet, hazelnut oil, or canola oil for 16 weeks. This time, the rats receiving canola oil had higher luteinizing hormone and testosterone than the control rats.

So one rat experiment found lower testosterone with canola oil, while another found higher testosterone.

That alone should make us cautious about declaring canola oil a human testosterone suppressor.

Why doesn't a positive rat study prove something will happen in humans?

Animal studies are useful. A positive rat experiment can show that an effect is biologically possible and give researchers a reason to test it in people.

So “it only happened in rats” does not mean the finding should be ignored.

It means the finding should be labeled plausible, not proven.

Humans and rats share a large amount of biology, but sharing genes does not mean every substance produces the same hormonal response. Rats can absorb and break down chemicals differently. The dose relative to body size can be very different. Their diets, gut bacteria, reproductive systems, and hormone feedback loops differ. Researchers also frequently use rats that have been castrated, poisoned, overtrained, made diabetic, or genetically bred to develop a disease.

Those experiments are excellent for answering questions such as “could this pathway exist?”

They are much worse at answering “will eating this food raise or lower testosterone in a healthy man?”

Tribulus shows how animal evidence can fail to translate

Tribulus terrestris gives us a good testosterone-specific example.

Animal experiments have produced very convincing-looking results. In one study, tribulus dramatically increased testosterone in overtrained rats. Other animal experiments have reported increases in testosterone, sexual behavior, or androgen signaling.

Then researchers gave tribulus to humans.

In a randomized study of 21 healthy men aged 20 to 36, participants received either tribulus or placebo for four weeks. Neither tested dose produced a significant increase in testosterone, luteinizing hormone, or androstenedione.

That does not mean animal studies are worthless.

It shows the correct sequence:

animal result → plausible human hypothesis → human experiment → either confirmation or failure to replicate.

Canola oil is still near the beginning of that chain.

There is also an important distinction between different polyunsaturated fats.

DHA, one of the main omega-3 fats in fish oil, is also a polyunsaturated fat. In a randomized trial of overweight and obese men, DHA-rich fish oil increased total testosterone compared with a corn-oil control. So even within the broad category of “polyunsaturated fat,” different fatty acids can produce different effects.

Verdict: dietary fat can influence testosterone, and very-low-fat diets may modestly lower it. Large fatty meals can also cause temporary testosterone drops. But there is not solid human evidence that canola oil or seed oils specifically lower resting testosterone.

Dietary cholesterol

Cholesterol is used to make steroid hormones, including testosterone.

That biological fact is often turned into the claim that eating more cholesterol automatically causes the testes to make more testosterone.

No strong modern human trial has isolated dietary cholesterol and shown that increasing it reliably raises testosterone in adequately nourished men.

Does intermittent fasting increase testosterone?

Intermittent fasting is another case where the answer depends on the population.

A review of human fasting studies found that several trials using time-restricted eating in lean, physically active men reported lower total or free testosterone, including 16:8 protocols combined with resistance training. The same review found a different pattern in men with obesity, where fasting-induced weight loss was generally neutral for reproductive hormones rather than suppressive.

More extreme fasting appears more suppressive. Human fasting research has reported substantial temporary testosterone reductions during multi-day complete fasts. Those experiments are metabolically very different from simply skipping breakfast or using a modest daily eating window.

Fasting can still be useful for appetite control, calorie management, or fat loss.

It is not a universal testosterone booster.

Does sugar lower testosterone?

This claim contains a real effect, but the timing changes the conclusion.

Eating glucose can temporarily lower testosterone. That does not automatically mean a high-sugar diet chronically lowers your resting testosterone.

A glucose load can drop testosterone by about 25 percent for several hours

A widely cited 2013 study followed 74 men aged 19 to 74 through a standard oral glucose tolerance test.

After an overnight fast, each man drank 75 grams of glucose. Researchers measured testosterone before the drink and again 30, 60, 90, and 120 minutes afterward.

The men included people with normal glucose control, impaired glucose tolerance, and newly diagnosed type 2 diabetes.

Average testosterone fell by about 25 percent. Two hours after the glucose drink, testosterone was still significantly below the fasting starting level. Among 66 men whose testosterone started in the normal range, 10 temporarily dropped below about 280 ng/dL, a level that could look clinically low if the blood test were interpreted without knowing the man had just consumed glucose.

That is a surprisingly large short-term effect.

But several other hormones did not move with it.

SHBG stands for sex hormone-binding globulin. It is a protein made mainly by the liver that carries much of the testosterone circulating in the blood. When SHBG changes, total testosterone can change even when the amount of freely available testosterone behaves differently.

SHBG remained essentially unchanged in this experiment.

Luteinizing hormone, or LH, also did not significantly fall. LH is the pituitary signal that tells the testes to make testosterone.

Cortisol did not explain the change either.

Because testosterone fell without a matching fall in LH or SHBG, the researchers suspected that at least part of the acute effect occurred farther downstream, possibly at testosterone production itself rather than simply because the brain stopped signaling the testes.

A normal mixed meal can produce the same effect

This is where the simple claim that “sugar tanks testosterone” starts to break down.

A 2018 study tested 60 men aged 23 to 97 who had normal testosterone and no diabetes or prediabetes. Researchers compared a 75-gram glucose drink with an ordinary mixed meal containing protein, carbohydrate, and fat.

Testosterone fell after both.

The average lowest point was about 100 ng/dL below baseline after glucose and about 123 ng/dL below baseline after the mixed meal. About 11 percent of the men temporarily fell below 300 ng/dL after glucose, while about 56 percent fell below 300 ng/dL after the mixed meal.

That is important.

If an ordinary mixed meal can lower measured testosterone as much as or more than pure glucose, the acute effect is not unique to table sugar or sugary drinks.

Eating itself can temporarily change the testosterone concentration measured in the blood.

This is one reason testosterone testing is better interpreted under standardized conditions rather than comparing a fasting morning test with one drawn after a large meal.

How does glucose cause the drop?

The mechanism is not completely settled.

The 2013 experiment found little change in LH, pointing toward a possible effect farther downstream at the testes.

But another study of 57 men produced a somewhat different result.

Researchers repeatedly sampled LH and testosterone after glucose ingestion and found that glucose reduced the pulsatile release of LH as well as the non-pulsatile secretion of testosterone. In that experiment, a greater fall in LH closely tracked a greater fall in testosterone.

So different experiments point to more than one possible pathway. In some men or under some conditions, the brain-to-testis LH signal may fall. In others, testosterone can fall without much change in LH.

What is well established is the result: glucose and substantial meals can temporarily lower measured testosterone for several hours. Exactly why that happens is less certain.

Does fructose uniquely tank testosterone?

No convincing evidence supports that claim.

A controlled crossover trial directly compared glucose and fructose supplementation and measured SHBG, total testosterone, and free testosterone. Researchers found no clinically meaningful difference between glucose and fructose for those hormone outcomes.

That does not make unlimited fructose metabolically harmless.

It does mean there is not good evidence that fructose has some unique testosterone-suppressing effect compared with glucose.

What about eating lots of sugar for years?

This is a separate question, and the evidence becomes much weaker.

A 2018 analysis looked at sugar-sweetened beverage intake and testosterone in young U.S. men.

Men in the highest intake group consumed at least about 442 calories per day from sugary drinks. They had roughly 2.3 times the odds of having low testosterone compared with men in the lowest intake group. Being overweight was also independently associated with low testosterone and produced an even larger increase in risk.

That gives us an association between heavy sugary-drink consumption and low testosterone.

It does not show that sugar itself was the direct cause.

Men drinking large amounts of sugar are also more likely to consume excess calories, gain body fat, become insulin resistant, develop fatty liver, and experience other metabolic changes that can lower testosterone.

That makes it difficult to separate:

sugar itself → lower testosterone

from:

high sugar intake → calorie excess / fat gain / insulin resistance → lower testosterone.

Weight loss appears to matter more than simply cutting carbohydrates

A 52-week randomized trial followed 118 overweight or obese men during weight loss and compared a higher-protein diet with a higher-carbohydrate diet.

Testosterone and SHBG increased as the men lost weight in both diet groups. There was no meaningful testosterone advantage from the lower-carbohydrate approach.

That fits the broader weight-loss literature.

If someone drinks huge amounts of soda, removing it may help testosterone indirectly because it makes losing excess fat and improving metabolic health easier.

But that is different from proving that removing sugar has a direct testosterone-boosting effect while calories, body fat, and metabolic health remain unchanged.

No convincing trial has isolated that experiment.

Could repeated post-meal testosterone drops matter over time?

It is possible to imagine a hypothesis where repeatedly producing large testosterone dips throughout the day somehow changes long-term hormone physiology.

But that experiment has not been done.

No study has shown that repeatedly causing the normal post-meal testosterone decline eventually lowers fasting baseline testosterone.

So that remains speculation.

Verdict: glucose and substantial meals can temporarily lower testosterone by roughly 20 to 25 percent for one to several hours. That acute effect is well supported. Evidence that dietary sugar independently lowers long-term fasting testosterone is much weaker and heavily mixed with obesity and insulin resistance.

Protein is good. Extremely high protein intake is a separate question

The evidence does not show that an ordinary high-protein diet lowers testosterone.

A 2022 systematic review and meta-analysis examined 27 controlled diet studies involving 309 healthy adult men. The important finding was not simply that “more protein lowers testosterone.” The result changed depending on how extreme the diet became.

Moderate protein intake, roughly 1.25 to 1.9 grams per kilogram of body weight per day, did not consistently lower resting testosterone. Even higher intakes between roughly 1.9 and 3.4 g/kg per day did not show the same clear suppressive effect.

The concerning signal appeared at the extreme end, particularly in low-carbohydrate diets where protein supplied at least about 35 percent of total calories.

In that very-high-protein subgroup, resting total testosterone was lower by about 5.23 nmol/L on average. That is roughly 150 ng/dL, which would be a meaningful difference if the effect is real.

But that number should not be applied to anyone who simply eats a lot of protein.

A follow-up analysis found that the concerning signal was concentrated above roughly 3.4 grams of protein per kilogram of body weight per day. Below that level, higher protein intake was not consistently associated with lower testosterone.

To put 3.4 g/kg into perspective, a 180-pound man would need to eat roughly 278 grams of protein per day to reach that level. A 200-pound man would need roughly 308 grams per day.

That is far beyond what most people mean when they say they eat a high-protein diet.

There is another complication. The diets producing the strongest testosterone drop were also very low in carbohydrates. That makes it difficult to say whether the problem was extreme protein itself, severe carbohydrate restriction, or the combination.

The useful conclusion is not “high protein lowers testosterone.” Normal bodybuilding-style high-protein intake appears fine. The possible problem begins at unusually extreme intakes, especially when very high protein is paired with very low carbohydrate intake.

Zinc can restore testosterone when zinc intake is genuinely inadequate

Zinc is one of the clearest examples of a deficiency-correction effect being marketed as a universal testosterone boost.

A classic human experiment found that restricting zinc in young men lowered testosterone, while supplementing zinc-deficient older men for several months substantially increased their testosterone. A later review combining eight human studies with a much larger animal literature reached the same general conclusion: zinc deficiency can impair testosterone production, while correcting deficiency can restore it. The dramatic improvements are mainly seen when low zinc is part of the problem.

In men who already get enough zinc, taking additional zinc has not reliably pushed testosterone higher.

The first move should generally be adequate dietary intake rather than automatically taking a high-dose supplement.

Good food sources include oysters and other shellfish, beef and other meats, dairy, eggs, and some seeds and legumes.

If diet is inadequate or deficiency is confirmed, supplementation may be useful.

Why can too much zinc cause a copper problem?

High supplemental zinc can interfere with the intestine's ability to absorb copper. The National Institutes of Health notes that doses of 50 mg of zinc per day or more, taken for weeks, can inhibit copper absorption. The adult tolerable upper intake level for zinc is 40 mg per day from all sources unless a higher dose is being used under medical supervision.

Copper deficiency can cause problems such as anemia and neurological dysfunction.

This copper warning is mainly about the safety of chronic zinc megadosing. It is not evidence that copper itself is a proven testosterone booster.

Vitamin D, magnesium, boron, and iron

Vitamin D

Men with higher vitamin D levels often have higher testosterone in observational studies.

That creates an obvious question: does giving vitamin D actually raise testosterone?

One of the better tests came in 2017. Researchers randomized 100 men with insufficient vitamin D to vitamin D supplementation or placebo for 12 weeks. Vitamin D status improved, but testosterone did not significantly increase compared with placebo.

A 2019 systematic review and meta-analysis of randomized trials reached a similar conclusion, finding no significant overall increase in total testosterone or SHBG from vitamin D supplementation. That helps explain why the observational association has not translated cleanly into a supplementation effect.

So low vitamin D and low testosterone can occur together without vitamin D deficiency necessarily being the cause of the low testosterone.

Correct a deficiency when one exists, but do not assume testosterone will rise as a result.

Magnesium

Magnesium appears frequently in testosterone supplements, especially products called ZMA, a combination of zinc, magnesium, and vitamin B6.

In an eight-week double-blind study, 42 resistance-trained men were randomly given either ZMA or placebo while following a standardized lifting program. ZMA produced no significant advantage in testosterone, another anabolic hormone called IGF-1, strength, body composition, or training performance.

That does not prove magnesium status is irrelevant.

It shows that adding zinc and magnesium to already trained, adequately nourished men did not produce the testosterone effect commonly advertised for the supplement.

Boron

The boron story largely rests on two very small human experiments that disagree with each other.

In 2011, eight healthy men took boron daily for one week. Their average free testosterone increased from about 11.8 to 15.2 pg/mL. The study was extremely small and did not follow a full parallel placebo group through the seven-day intervention.

An earlier controlled study tested boron for seven weeks in 19 male bodybuilders. Boron increased blood boron levels but produced no significant advantage in total testosterone, free testosterone, muscle gain, or strength compared with placebo.

That is why the evidence is weak.

The positive result comes from eight men studied for only one week, while the longer placebo-controlled trial failed to reproduce a testosterone benefit.

Iron

Iron can create problems at both extremes.

Iron deficiency can impair reproductive function, although the human evidence that iron supplementation directly restores serum testosterone is less developed than the zinc literature.

Severe iron overload can clearly suppress reproductive hormones.

In conditions such as hereditary hemochromatosis, excess iron can accumulate in the pituitary gland and damage the cells that release luteinizing hormone, the signal that tells the testes to produce testosterone. That can produce low luteinizing hormone and low testosterone.

Iron is therefore another nutrient where correcting deficiency may help, while blindly taking more can eventually create the opposite problem.

Which supplements actually increase testosterone?

Ashwagandha

Ashwagandha survives evidence review better than most herbs marketed for testosterone.

In a randomized placebo-controlled crossover study of overweight men aged 40 to 70, eight weeks of ashwagandha produced about a 15 percent greater testosterone increase than placebo. The study also found an increase in DHEA-S, another steroid hormone produced mainly by the adrenal glands.

Other trials and pooled analyses have pointed in the same general direction.

The important qualifier is the population.

Positive studies often involve men who are older, stressed, overweight, infertile, fatigued, or starting with lower testosterone.

That does not establish the same effect in an already healthy young man with normal testosterone.

Tongkat ali

Tongkat ali has a more credible human evidence base than most testosterone herbs.

A 2022 systematic review pooled clinical studies of tongkat ali and found an overall increase in total testosterone. The effect appeared stronger in men with lower testosterone or diagnosed testosterone deficiency than in already healthy and trained men.

Again, starting point appears to matter.

Fenugreek

Fenugreek has enough human trials that researchers can now pool the results.

A 2026 systematic review examined 13 randomized trials in adult men, with six contributing usable data to the pooled total-testosterone analysis. Total testosterone increased slightly on average, but free testosterone did not show the same reliable effect. The reviewers rated the overall certainty of the evidence as very low.

That means fenugreek may have a small effect, but the current evidence is much weaker than typical supplement marketing suggests.

Shilajit

Shilajit has one genuinely interesting human testosterone trial.

A double-blind placebo-controlled study tested purified shilajit in 75 healthy men aged 45 to 55.

After 90 days, the shilajit group showed roughly a 19 to 20 percent increase in total testosterone, with increases in free testosterone and DHEA-S as well. Because the men were healthy rather than specifically testosterone-deficient, this is one of the more interesting possible examples of true enhancement rather than simple deficiency correction.

But there are two reasons not to treat the result as settled.

First, the men were all between 45 and 55. Comparable placebo-controlled evidence has not established that healthy men in their 20s or 30s get the same effect.

Second, this result still rests largely on one positive trial.

Independent replication means a different research team repeats a similar experiment in another group of people and gets a similar result. That matters because even a well-designed randomized trial can occasionally produce an unusually positive result because of chance, the particular people recruited, the exact supplement used, or other details unique to that experiment.

If several unrelated research groups reproduce the result, those explanations become much less likely.

Verdict: the shilajit result is legitimate and interesting. What is missing is confirmation that the effect repeats in other trials and extends beyond healthy middle-aged men.

Royal jelly

Royal jelly also has more human testosterone evidence than its reputation as a fringe supplement might suggest.

One placebo-controlled study divided 20 healthy sedentary men aged 21 to 23 into two groups. Ten men received 1,000 mg of royal jelly per day and ten received placebo.

After 15 days, testosterone significantly increased in the royal-jelly group while it did not in the placebo group. That is a legitimate positive human experiment, but only ten men actually received royal jelly.

Calling that study small does not mean the result should be dismissed.

There is no magic number of participants that suddenly makes a study trustworthy. The number needed depends on how large the effect is, how much testosterone naturally varies between people, and how precisely the study is designed.

But with only ten treated men, one or two unusually strong responders can have a large effect on the group average. A small study therefore gives us a useful signal, but less confidence about how large the effect really is or how reliably it would appear in other men.

The longer trial adds weight to the signal.

A Japanese double-blind study randomized 61 healthy adults aged 42 to 83 to either 3,000 mg of liquid royal jelly per day or placebo for six months. Testosterone increased modestly in the royal-jelly group compared with placebo. The researchers proposed that royal jelly may have increased conversion of DHEA-S into testosterone rather than directly stimulating the testes.

So we now have two placebo-controlled human trials pointing in the same direction: one very small trial in young men and one longer trial in older adults.

That is more interesting than a single tiny study.

It is still a thin evidence base compared with an intervention that has been tested across hundreds or thousands of people by several unrelated research groups.

The right conclusion is not “royal jelly works” or “the study is too small, ignore it.” It is: royal jelly has a real positive human signal that deserves larger independent trials.

Animal studies more consistently show royal jelly restoring testosterone after diabetes, oxidative damage, chemotherapy, or other testicular injury.

That restoration effect is not the same thing as showing royal jelly pushes testosterone above normal in healthy men.

Is raw royal jelly better?

No human study has directly compared fresh raw royal jelly with freeze-dried or standardized royal jelly for testosterone.

Does garlic increase testosterone?

Garlic is another example where an internet testosterone claim traces back to a very specific animal experiment.

The famous garlic + high-protein testosterone study was done in rats

In 2001, Japanese researchers fed rats diets containing either 10, 25, or 40 percent casein protein, with or without garlic powder, for 28 days.

The garlic dose was about 0.8 grams per 100 grams of diet.

In the higher-protein groups, adding garlic increased testosterone measured inside the testes and lowered corticosterone, the main stress hormone measured in rats. The effect was most apparent when garlic was combined with the higher-protein diets.

The researchers then performed a second experiment to explore why.

Instead of feeding garlic normally, they injected rats with diallyl disulfide, one of garlic's sulfur compounds, directly into a vein.

Plasma luteinizing hormone, or LH, increased in a dose-dependent manner.

LH is the pituitary signal that tells Leydig cells in the testes to produce testosterone.

That experiment produced the popular proposed pathway:

garlic sulfur compounds → more LH signaling → more testicular testosterone.

But there are two big translation problems.

First, the testosterone experiment was done in rats eating unusually high-casein diets.

Second, the LH experiment involved injecting an isolated garlic compound into a vein. That is very different from chopping garlic into dinner and digesting it through the gut.

Extremely high garlic doses produced the opposite result in rats

Some rat experiments used enormous amounts of raw garlic and found that testosterone actually fell while LH increased. In other words, the pituitary was sending a stronger signal telling the testes to make testosterone, but the testes were producing less.

That does not create a serious concern that eating normal amounts of garlic with food lowers testosterone.

The doses were far beyond ordinary culinary intake.

The reason the finding matters is narrower: even in animals, garlic does not always push testosterone upward. The result changes with the dose, the preparation, and the condition of the animal.

So the animal evidence supports “garlic can interact with testosterone biology,” not “the more garlic you eat, the higher your testosterone goes.”

Garlic looks more convincing when testosterone has already been suppressed

Other animal studies have tested garlic after obesity, oxidative damage, or chemical injury has already impaired reproductive function.

In those situations, garlic or garlic-derived compounds have sometimes restored LH, testosterone, or testicular function toward normal. That looks more like protection or suppressor removal than true enhancement above an already healthy baseline.

A sulfur compound found in aged garlic, called S-allyl cysteine, has also increased testosterone in healthy mice and in testis-derived cells. But the mouse experiment used an injected dose rather than ordinary oral garlic consumption.

What happens in men?

This is where the evidence becomes surprisingly thin.

No robust, independently replicated randomized trial has shown that eating garlic or taking an ordinary garlic supplement meaningfully raises testosterone in healthy men.

One tiny pilot study gave aged garlic extract to six healthy sedentary men for 10 days and measured testosterone alongside inflammatory and stress markers. The reported findings focused on changes in inflammatory proteins rather than demonstrating a convincing testosterone increase.

There are scattered claims from small or commercially sponsored human studies, but the current human evidence is nowhere near strong enough to reproduce the confident “garlic boosts testosterone” claim made from the rat literature.

Verdict: garlic has a real animal and mechanistic testosterone signal, including possible effects on LH and Leydig-cell steroid production. But the famous garlic + protein claim comes from rats, and no robust human trial has shown that ordinary garlic raises resting testosterone in healthy men.

Pomegranate: where did the famous 24% testosterone claim come from?

Pomegranate is frequently listed as a natural testosterone booster.

The famous percentage comes from surprisingly weak evidence.

In 2012, researchers presented a conference abstract involving 60 healthy men and women who drank roughly 200 to 250 mL of pomegranate juice per day for two weeks.

Men's salivary testosterone increased from about 242 to 298 pg/mL, roughly a 23 to 24 percent rise. But the experiment had no placebo beverage, was not randomized, and was published as a conference abstract rather than a full journal paper.

The distinction between saliva and blood measurements matters too.

The study did not demonstrate a 24 percent increase in serum total testosterone.

Better-controlled pomegranate studies do not reproduce the famous result

In a 2020 double-blind crossover experiment, nine elite male weightlifters consumed either pomegranate juice or placebo around an Olympic-style weightlifting session. Pomegranate did not produce a testosterone increase over placebo. Plasma testosterone was actually slightly lower shortly after exercise in the pomegranate condition.

A separate randomized phase II trial tested pomegranate extract in men with prostate cancer whose PSA was rising after treatment. Serum testosterone did not significantly change with pomegranate extract.

Those populations and protocols are not perfect tests of ordinary juice in healthy men. But importantly, better-controlled experiments have not reproduced anything resembling the famous 24 percent salivary-testosterone increase from the uncontrolled 2012 abstract.

Pomegranate has better evidence for circulation

A randomized double-blind crossover trial followed 61 men with mild-to-moderate erectile dysfunction through pomegranate-juice and placebo periods. Erectile-function scores showed a favorable trend with pomegranate, but the study did not establish a testosterone increase.

Pomegranate may influence vascular function without increasing testosterone.

The cocoa + pomegranate extract study is genuinely interesting

There is one result here that should not be brushed aside.

A randomized, double-blind, placebo-controlled study tested a standardized extract made from pomegranate rind and cocoa seed in 120 healthy men aged 21 to 35. The men received placebo, 200 mg of the combined extract, or 400 mg per day for 56 days.

Free testosterone increased significantly compared with placebo at both tested doses. At the higher 400 mg dose, total testosterone and luteinizing hormone, or LH, also increased. So this absolutely was a positive controlled human testosterone trial.

The part that was not tested in humans was which ingredient caused the effect.

Every man receiving the active treatment received both pomegranate and cocoa together.

There was no pomegranate-only group.

There was no cocoa-only group.

So the human trial tells us:

pomegranate-rind extract + cocoa-seed extract together raised testosterone under these study conditions.

It does not tell us:

• whether pomegranate alone would have produced the same increase,
• whether cocoa alone would have produced the same increase, or
• whether combining them truly produces a larger effect than either ingredient alone in humans.

But the combination was not chosen blindly.

The developers had already tested the ingredients separately in cells

Before the human trial, the developers of the formulation tested pomegranate-rind and cocoa-seed extracts in testosterone-producing mouse Leydig cells.

Those experiments were reported in the patent for the formulation rather than in an independent human trial.

In one example, a pomegranate-rind extract increased testosterone production in the cells by about 7.1 percent. A cocoa-seed extract increased it by about 3.85 percent.

If the two effects simply added together, the expected increase would have been about 10.95 percent.

Instead, a 4:1 mixture of the two extracts produced about a 25.74 percent increase in the cell assay. The developers reported similar greater-than-additive effects across several other pomegranate-to-cocoa ratios.

That suggests the ingredients may interact synergistically, meaning the combination produced a larger effect in those cells than researchers would expect by simply adding the two individual effects together.

They also reported that the mixture inhibited aromatase, the enzyme that converts testosterone into estradiol, more strongly than would be expected from the individual extracts alone.

This makes the positive human result more interesting because there is at least a proposed biological reason for combining the ingredients.

But the two experiments answer different questions.

The human trial showed that the combination works.

The cell experiments suggest why the combination might work.

What remains untested in humans is whether the two extracts truly work synergistically or whether one ingredient is doing most of the work.

The next useful human experiment would compare pomegranate extract alone, cocoa extract alone, the combination, and placebo.

Verdict: ordinary pomegranate juice has weak testosterone evidence. A concentrated pomegranate-rind + cocoa-seed extract increased testosterone in a controlled human trial of 120 healthy young men. Cell experiments suggest the ingredients may work synergistically, but human research has not yet separated their individual contributions.

Dark chocolate and cocoa

The cocoa-pomegranate result also changes how we should think about cocoa.

To be clear, the combination was tested successfully in humans.

What has not been tested in humans is cocoa extract by itself using the same protocol.

The positive trial used a concentrated cocoa-seed extract combined with pomegranate-rind extract, not a chocolate bar.

That distinction matters because a normal serving of chocolate contains a very different mixture and dose of compounds.

A typical 30 to 40 gram serving of dark chocolate contains roughly 50 to 65 mg of magnesium, much less than the doses usually used when researchers directly study magnesium supplementation.

Cocoa flavanols can also improve blood-vessel function and nitric oxide signaling, but no controlled human experiment has shown that eating ordinary cocoa or dark chocolate raises testosterone.

So there are two separate conclusions:

Ordinary dark chocolate: no convincing direct evidence that eating it raises testosterone.

Concentrated cocoa-seed + pomegranate-rind extract: a positive human trial showed that the combination raised testosterone.

We simply cannot credit cocoa alone with the result because the human study never gave cocoa alone to one group.

Erectile function, libido, and testosterone are not the same thing

Testosterone discussions frequently mix together four different outcomes:

• testosterone
• libido
• erection quality
• fertility

They interact, but they are not interchangeable.

An intervention can improve erections without increasing testosterone. It can increase sexual desire without increasing testosterone. It can improve sperm quality without increasing testosterone.

Watermelon

Watermelon frequently appears on testosterone lists because it contains the amino acid L-citrulline.

Your body can convert citrulline into arginine, which supports nitric oxide production.

That gives watermelon a plausible circulation story.

It does not create direct testosterone evidence.

No convincing controlled human experiment has shown that eating whole watermelon meaningfully raises total or free testosterone.

L-citrulline can improve erections without increasing testosterone

In penile tissue, nitric oxide relaxes smooth muscle and allows more blood to enter the erectile tissue.

That can improve erection quality without requiring testosterone to change.

A 2011 placebo-controlled crossover study tested 1.5 grams of L-citrulline per day in 24 men with mild erectile dysfunction.

Only 2 of 24 men reached a normal erection-hardness score during placebo treatment.

During citrulline treatment, 12 of 24 did. Monthly intercourse frequency also increased from about 1.4 to 2.3 times per month. The researchers did not measure testosterone.

The better-supported pathway is:

citrulline → more arginine availability → more nitric oxide signaling in blood vessels → improved penile blood flow

not:

citrulline → higher nitric oxide → higher testosterone.

Nitric oxide in blood vessels and nitric oxide inside the testes are different

This distinction can sound confusing until we look at where nitric oxide is actually being made.

Nitric oxide is not one giant pool circulating through the body.

Cells make it locally using enzymes called nitric oxide synthases.

In penile blood vessels, nitric oxide produced around the vessel wall relaxes smooth muscle and helps blood flow into the penis.

The testes have their own nitric oxide-producing system.

Human testicular research has found nitric oxide synthase inside Leydig cells, Sertoli cells, and some of the blood-vessel cells within the testes. That means testicular tissue can make nitric oxide locally rather than needing it to arrive from the nose, a supplement, or another distant part of the body.

The amount matters too.

Normal local nitric oxide signaling appears to have useful jobs in testicular blood flow, sperm biology, and cell communication. But excessive nitric oxide production, especially during inflammation or oxidative stress, can become damaging. So nitric oxide is not simply “good” or “bad” for male reproductive function.

Laboratory experiments using Leydig cells have found that sufficiently strong nitric oxide signaling can inhibit both baseline and LH-stimulated testosterone production. Other experiments have found a similar inhibitory effect on Leydig-cell steroid production.

This does not mean you should avoid citrulline, exercise, vegetables, nasal breathing, or other things that support nitric oxide in blood vessels.

There is no evidence that improving vascular nitric oxide through those routes somehow floods the testes with enough nitric oxide to suppress testosterone.

And there is no evidence-based biohack where you would want to deliberately increase nitric oxide inside the testes either.

The useful distinction is location: nitric oxide improving penile blood flow and nitric oxide being produced locally around testosterone-making cells are different biological events.

Ginseng can improve erections without reliably raising testosterone

Ginseng provides an unusually clean example because researchers have measured both sexual function and hormones.

A review of six randomized human trials included 512 male participants between ages 18 and 79 and examined Panax ginseng, the species often called Asian ginseng. Korean red ginseng is a prepared form of Panax ginseng rather than a completely different plant.

Five of the six trials found no significant testosterone increase. Only one reported a modest positive testosterone result.

The erectile-function evidence is better.

One systematic review pooled six randomized trials involving 349 men and found red ginseng performed better than placebo for erectile dysfunction. Later reviews have judged the average benefit modest, but the signal is more consistent than the testosterone evidence.

A Korean clinical trial makes the distinction particularly clear. Men taking red ginseng improved erectile-function scores and sexual desire, while measured reproductive hormones did not significantly differ between groups. Sexual function improved without evidence that testosterone caused the improvement.

Better erections. More reported desire. No demonstrated testosterone increase.

Maca can increase libido without increasing testosterone

Maca makes the same point from the sexual-desire side.

In a 12-week double-blind placebo-controlled study of healthy men, sexual desire improved after maca supplementation while testosterone and estradiol remained unchanged. The researchers concluded that the libido effect was not explained by changes in circulating reproductive hormones.

Higher libido is not proof of higher testosterone.

Tribulus is one of the clearest testosterone failures

Tribulus terrestris has been studied often enough that we do not need to rely on its traditional reputation.

A 2014 systematic review examined the available human studies and concluded that tribulus did not reliably increase testosterone. The authors specifically noted that commercial claims had moved beyond the evidence.

Tribulus may influence erectile function through other pathways.

That still does not make it a testosterone booster.

D-aspartic acid is a classic hype cycle

D-aspartic acid became popular after an early study reported a roughly 42 percent testosterone increase in untrained men.

Later studies tested resistance-trained men, the population most likely to buy it.

The result changed.

One controlled study involving 20 resistance-trained men found no meaningful effect on testosterone or other reproductive hormones after 28 days.

A second study tested 24 trained men using either 3 grams or 6 grams per day. Three grams produced no significant testosterone increase, while 6 grams significantly reduced both total and free testosterone.

The pattern is familiar:

promising first result → huge marketing claim → weak replication.

Fadogia agrestis: no human efficacy trial and unresolved safety

Fadogia became popular almost entirely from animal research and online promotion.

No credible published human clinical trial has demonstrated that it raises testosterone.

Safety comes up because the same animal literature that generated interest in Fadogia also produced warning signals.

In a 28-day rat experiment, animals were given 18, 50, or 100 mg of Fadogia agrestis extract per kilogram of body weight each day. Researchers found changes in several markers of testicular function and concluded that the extract produced adverse effects on the testes, particularly at the higher doses.

A separate rat experiment using the same dose range found biochemical signs suggesting damage to cell membranes in the liver and kidneys. The animals did not die or show obvious severe illness, but the laboratory findings raised toxicity concerns.

That does not prove that a normal commercial dose of Fadogia is unsafe in humans.

Rat doses do not translate directly to human supplements, and we do not have a proper human safety trial showing what actually happens in people.

But that is precisely the problem.

We have no convincing human evidence that it works, no established safe human dose, and animal research that gives us reasons not to assume it is harmless.

Verdict: skip it until human efficacy and safety are actually established.

Creatine improves performance without reliably raising testosterone

Creatine is not primarily a testosterone supplement.

It still gets pulled into testosterone discussions because it reliably improves strength and high-intensity exercise performance, which makes people wonder whether some of the effect comes from androgens.

A major review of the controlled creatine literature found that creatine does not reliably increase resting total testosterone or free testosterone. The review also discusses an isolated DHT finding that helped fuel interest in a possible androgen effect, but the broader literature has not consistently reproduced a meaningful hormonal increase.

Creatine does not need a testosterone mechanism to work.

It improves the muscle's ability to rapidly regenerate ATP during repeated high-intensity effort.

Verdict: excellent performance supplement, not a reliable testosterone booster.

No-fap does not keep testosterone elevated

The famous abstinence claim comes from a small study of 28 men.

Researchers repeatedly measured serum testosterone while the men abstained from ejaculation.

On day seven, testosterone reached about 145.7 percent of the starting level. After that peak, testosterone returned toward baseline even though abstinence continued.

The study therefore supports a temporary day-seven change.

It does not show that continued abstinence produces chronically elevated testosterone.

Does sunlight increase testosterone?

A 1939 paper is repeatedly cited online to claim that exposing the chest or genitals to ultraviolet light dramatically raises testosterone.

The original experiment looks very different from the modern claim.

It included only five male psychiatric inpatients and used a mercury-quartz ultraviolet lamp rather than ordinary sunlight. The researchers exposed different areas of the body and measured urinary androgen metabolites.

The study did not actually measure testosterone

The key measurement was urinary androsterone.

Androsterone is a weak androgen formed downstream as stronger androgens such as testosterone, DHT, and androstenedione are metabolized. The body eventually excretes much of it in urine. Urinary androsterone can therefore provide information about androgen metabolism, but it is not the same measurement as serum total testosterone or free testosterone.

That distinction is important because more androsterone in urine could reflect more androgen production, but it could also reflect changes in how existing hormones are converted, broken down, or excreted.

It does not tell us directly that circulating testosterone increased.

And androsterone itself is downstream in the pathway. The 1939 experiment does not show that increased androsterone somehow stimulated the pituitary or caused testosterone to rise.

What the 1939 UV experiment actually found

In the tiny sample, chest irradiation increased urinary androsterone from roughly 70 to 155 international units per liter. Genital irradiation produced larger increases, while comparable irradiation of the back did not produce the same result. The experiment was never replicated with modern serum testosterone measurements.

So the widely repeated claim that UV light caused a “200% testosterone increase” changes both the hormone that was measured and the strength of the evidence.

Modern human evidence is much less dramatic

A 2020 pilot experiment exposed older men to ultraviolet light before resistance exercise and directly measured blood hormones. The additional ultraviolet exposure did not significantly increase serum testosterone compared with resistance exercise alone.

A 2021 Cell Reports study found a more interesting biological pathway. Researchers showed in mice that ultraviolet-B exposure to the skin could activate reproductive signaling through a skin-to-brain pathway. The human portion found associations between sunlight exposure, season, circulating sex hormones, and romantic behavior, but it was not a controlled human trial showing that a particular UV dose raises testosterone.

Sunlight clearly matters to circadian and general physiology.

A validated sunlight testosterone protocol does not exist.

Red light on the testes: animal evidence, no human testosterone trial

The idea of shining red light directly on the testes did not come from nowhere.

It did, however, make a large jump from animal experiment to consumer protocol.

As of 2026, no published peer-reviewed human study has directly exposed men's testes to red or near-infrared light and demonstrated an increase in serum testosterone.

The rat experiment behind the claim

A 2013 experiment divided 30 male Sprague-Dawley rats into groups receiving either 670 nm red light, 808 nm near-infrared light, or no light treatment. The testes were exposed for 30 minutes per day over five days. The 670 nm group showed an increase in serum testosterone by the fourth day, while the 808 nm wavelength did not produce the same clear testosterone increase.

That is a legitimate animal signal.

It is still one short rat experiment using direct testicular laser exposure.

Wavelength and dose may matter for safety too

Separate animal research raises caution about simply assuming deeper-penetrating near-infrared light is harmless to reproductive tissue.

In a 2016 experiment using ram testes, researchers exposed testicular tissue to 808 nm light. The exposure increased oxidative stress and damaged sperm membrane integrity and motility.

That does not prove that an ordinary consumer red-light panel will damage a man's testes. The species, dose, treatment geometry, and tissue penetration are different.

It does show why “red light” should not be treated as one interchangeable intervention. A wavelength and dose that produces one result in a rat cannot automatically be translated into a human protocol using another wavelength, power density, exposure time, and device.

Verdict: direct testicular red light is biologically plausible enough to study, but there is still no controlled human evidence that it raises testosterone and no validated human dose for doing so.

Do cold showers or cold plunges increase testosterone?

A 1991 Japanese experiment is frequently brought up in discussions about cold exposure and testosterone.

The actual protocol is important.

Researchers studied 32 healthy 19-year-old men.

The cold stimulus was not an ice bath.

Participants placed a wrist in 4°C water for one minute, removed it for two minutes, then immersed it again for another minute.

The researchers also tested 20 minutes of cycling at a fixed workload. Exercise increased testosterone by about 20.8 percent, while the cold-water stimulus itself decreased testosterone by about 10 percent even though luteinizing hormone increased.

That mismatch is interesting.

Luteinizing hormone is the pituitary signal that tells the testes to produce testosterone.

The upstream signal increased, while the downstream testosterone response moved in the opposite direction.

Newer cold-exposure research is mixed, but it still does not establish a chronic testosterone boost. For example, a four-day cold-shower experiment found essentially no change in salivary testosterone, while several post-exercise cold-water and whole-body cryotherapy studies have reported either suppression or no effect.

No convincing evidence shows that ordinary cold exposure chronically raises resting testosterone.

Cold can still make someone feel energized, alert, or intensely stimulated because it activates the sympathetic nervous system.

That feeling does not show that testosterone increased.

Sauna, heat, and testicular cooling

Heat appears to affect sperm production much more readily than it affects testosterone production.

A 2013 study gives us a useful example because researchers measured both fertility-related changes and reproductive hormones in the same men.

Researchers followed 10 healthy men with normal semen parameters through three months of Finnish sauna use. The men used an 80 to 90°C sauna for 15 minutes twice per week. Over the three months, sperm concentration and motility worsened. Researchers also found changes in sperm mitochondrial function and chromatin packaging, which are measures related to how well sperm function and how their genetic material is organized.

But testosterone did not fall.

LH and FSH also remained stable. LH is the pituitary signal that tells testosterone-producing Leydig cells to make testosterone, while FSH helps regulate sperm production.

This tells us something important about how the testes respond to heat.

The testes perform at least two major reproductive jobs. Leydig cells make testosterone. A separate system inside the seminiferous tubules produces sperm.

Those two systems do not have the same sensitivity to heat.

Sperm production depends on the testes remaining cooler than core body temperature, which is one reason the testes sit outside the body. Repeated heat exposure can disturb the environment needed for normal sperm development even while the testosterone-producing machinery continues functioning normally.

That appears to be what happened in the sauna study.

The sauna exposure was enough to impair sperm production, but not enough to meaningfully suppress testosterone production or the hormonal signals controlling it.

The sperm changes also reversed after the men stopped the sauna protocol, suggesting the heat exposure temporarily disrupted sperm production rather than permanently damaging it.

So when someone says that sauna “heats the testes,” two very different questions have to be separated:

• Does the heat affect fertility and sperm? Human evidence says it can.
• Does the same heat lower testosterone? This study found no meaningful reduction.

It also gives us no evidence that sauna raises testosterone.

The practical conclusion is that testicular heat is a more credible fertility concern than a testosterone concern. Heat can impair sperm even while testosterone remains normal.

Testicular cooling is a separate claim

The inverse idea is that because heat can damage sperm, deliberately cooling the testes might improve testosterone.

Those are not the same conclusion.

No published human randomized trial has shown that putting ice packs on normal testes or using a dedicated testicular-cooling device raises serum testosterone.

Bryan Johnson has publicly described using ice packs around the groin during sauna sessions and tracking his own fertility markers. His self-experiment suggested that cooling may have helped protect sperm-related measurements from the heat exposure.

That is interesting, but it is an n=1 self-experiment, not a peer-reviewed clinical trial, and the outcome was fertility rather than a demonstrated testosterone increase.

Protecting sperm from heat is not the same thing as raising testosterone.

Does mouth taping increase testosterone?

This claim is a useful example of individually true facts being connected into a stronger conclusion than the evidence supports.

Nasal breathing really does increase nasal nitric oxide

A classic physiology experiment directly compared nitric oxide during nasal and oral breathing. Nasal-derived exhaled nitric oxide averaged roughly 141 nl/min/m² compared with about 68 during mouth breathing. Most of that nitric oxide came from the upper airway and paranasal sinuses.

So this part of the argument is real:

nasal breathing → more nitric oxide in the nasal airway.

The problem is what happens next.

Nasal nitric oxide has not been shown to travel to the testes and raise testosterone

Nitric oxide is a short-lived signaling molecule. Measuring more of it in air coming from the nose does not demonstrate that enough of that nitric oxide enters the bloodstream, survives transport through the body, reaches testicular tissue, and increases testosterone production.

No human experiment has demonstrated that chain.

And the testicular nitric oxide literature actually makes the simplistic “more nitric oxide equals more testosterone” idea harder to defend.

The testes make their own nitric oxide

Nitric oxide inside the testes is largely produced inside the testicular tissue itself.

Cells use enzymes called nitric oxide synthases to manufacture it.

Human tissue studies have found nitric oxide synthase in Leydig cells, which make testosterone, as well as Sertoli cells and some of the blood-vessel cells inside the testes. So local testicular nitric oxide is part of the testes' own signaling system.

That local system has useful roles in normal reproductive biology.

But nitric oxide can become excessive, particularly during inflammation and oxidative stress. A review of reproductive research describes nitric oxide as a molecule with both normal physiological roles and potentially damaging effects when production becomes excessive. The effect depends on where it is produced, how much is produced, and what cells are exposed.

Laboratory experiments using Leydig cells have found that sufficiently strong nitric oxide signaling can suppress testosterone synthesis. Nitric oxide donors inhibited both baseline and luteinizing-hormone-stimulated testosterone production in these cell models.

A separate experiment similarly found that nitric oxide inhibited Leydig-cell steroid production. Again, this was a local testicular effect.

This does not mean that you should try to lower nitric oxide throughout your body.

It does not mean citrulline is bad for testosterone.

It does not mean nasal breathing is bad for testosterone.

And there is no known lifestyle behavior where a healthy man needs to intentionally avoid “stimulating nitric oxide inside the testes.”

The relevant concern would be abnormal local conditions such as inflammation or oxidative stress that cause testicular nitric oxide signaling to become excessive, not ordinary healthy nitric oxide production elsewhere in the body.

Nasal nitric oxide, vascular nitric oxide, and nitric oxide produced locally around Leydig cells are not interchangeable pools flowing around the body doing the same job.

Different tissue, different concentration, different effect.

So neither of these chains is currently justified:

nasal breathing → more NO → more testosterone

or

nasal breathing → more NO → less testosterone.

Neither has been demonstrated in humans.

The more plausible mouth-taping pathway is sleep

A 2022 pilot study tested mouth taping in 20 habitual mouth-breathers with mild obstructive sleep apnea.

The average apnea-hypopnea index, which counts breathing interruptions per hour of sleep, fell from 8.3 to 4.7 events per hour. Snoring also improved. That is an interesting result, but it applies to a small and highly selected group.

A 2025 systematic review looked at 10 mouth-taping studies involving 213 people.

Only a minority showed clear improvements in breathing or oxygen-related outcomes, and the reviewers raised concerns about taping in people with nasal obstruction. The evidence does not justify treating mouth tape as a universal sleep treatment.

No mouth-taping trial has demonstrated an increase in testosterone.

The reasonable hypothesis is narrower:

If mouth taping improves nighttime breathing and sleep in someone who is actually a good candidate for it, that could remove one source of poor recovery that might otherwise contribute to hormonal suppression.

That is different from claiming mouth tape directly raises testosterone through nitric oxide.

For a dedicated breakdown of this question, see Does Mouth Tape Increase Testosterone?

Grounding has weak stress and sleep evidence, not testosterone evidence

Grounding is easy to dismiss because the marketing often runs far ahead of the research.

There is still a small amount of human data worth examining.

In 2004, researchers had 12 people with sleep problems, pain, and stress sleep on grounded conductive mattress pads for eight weeks.

Salivary cortisol was sampled repeatedly across the day.

The researchers reported that cortisol rhythms shifted toward a more typical morning-high and nighttime-low pattern, while participants also reported better sleep and less stress. The experiment was tiny and was not blinded or placebo-controlled.

What would a proper placebo have looked like?

Ideally, some participants would sleep on a grounded pad while others slept on an identical-looking pad that was secretly not electrically connected to ground.

Neither the participants nor the researchers evaluating the results would know who had the real setup until the experiment ended.

Without that comparison, expectations can influence subjective outcomes such as sleep quality and stress.

The broader grounding literature is also concentrated among a small number of researchers, some with commercial ties to grounding products, and independent replication is limited.

Most importantly here, grounding studies have not demonstrated an increase in testosterone.

Even if future research confirms a meaningful effect on sleep or cortisol rhythm, researchers would still need to show that the change actually alters testosterone.

For a deeper look at the grounding evidence, see Grounding Mat for Sleep: What the Evidence Shows.

Can phones, Wi-Fi, or 5G lower testosterone?

There is enough evidence here to take the question seriously, but “RF exposure” needs to be defined before the studies make sense.

RF-EMF means radiofrequency electromagnetic fields, the non-ionizing radio waves used by technologies such as mobile phones, Wi-Fi routers, and cellular base stations.

Exposure is not one uniform thing.

A transmitting phone held directly against the body creates a concentrated, local exposure close to that device. A Wi-Fi router across a room produces a different exposure pattern. A cellular base station farther away is different again. Animal experiments sometimes place a phone or radiofrequency antenna very close to a cage for hours per day.

Frequency, distance, signal strength, exposure time, and which body part is closest to the source can all change how much radiofrequency energy reaches a tissue.

That is why a study involving a phone beside an animal cage cannot automatically tell us what a distant cell tower does to a man.

Why a testicular effect is biologically plausible

The testes are unusually sensitive organs.

Sperm-producing cells divide rapidly, and testicular cells have high energy demands. That makes the tissue vulnerable to oxidative stress, which occurs when reactive molecules overwhelm the body's ability to control them.

Testosterone-producing Leydig cells can also be damaged if oxidative stress becomes severe enough.

A 2021 systematic review examined 19 animal and human studies of radiofrequency exposure from mobile-phone and Wi-Fi-type signals. Twelve of the 14 animal mobile-phone studies reported lower testosterone after exposure. Several also found oxidative stress, damage to Leydig cells, or increased death of those cells.

That is enough to make the testosterone hypothesis biologically plausible.

But the animal experiments were extremely different from one another. Some exposed animals for 30 minutes per day, others for hours, and one for as much as 24 hours per day. Frequencies, signal strength, distance from the antenna, animal species, and exposure systems also varied.

So the animal literature tells us that RF-EMF can affect testicular biology under some experimental conditions. It does not tell us that ordinary human phone or Wi-Fi exposure produces the same dose or the same testosterone effect.

Human testosterone studies conflict

One of the cleaner controlled human studies followed 20 healthy men exposed to a 900 MHz mobile-phone signal for two hours per day, five days per week, for four weeks.

Researchers repeatedly sampled hormones across the day and night rather than relying on one testosterone measurement. The normal testosterone rhythm did not significantly change during the four weeks of exposure.

That is evidence against a large testosterone effect from that particular exposure protocol.

A 2012 study pointed in the opposite direction. Researchers followed people with longer-term exposure to radiofrequency signals from mobile phones and nearby cellular base stations and reported progressively lower testosterone with longer exposure. The study also reported changes in several other hormones.

The problem is that this was not an experiment where researchers randomly assigned one group to years of RF exposure and another group to none.

The people with longer exposure were simply observed over time.

That makes it much harder to know what caused the hormonal difference. People with different amounts of phone or base-station exposure can also differ in occupation, age, sleep, stress, lifestyle, and many other variables. The actual absorbed RF dose is also harder to measure from years of ordinary life than it is during a controlled laboratory exposure.

So the 2012 result is a real human signal worth investigating, but it cannot by itself prove that the radiofrequency exposure caused the lower testosterone.

What does the fertility research show?

A major 2024 systematic review examined nine human studies of RF-EMF and male fertility. Seven involved the general public and two involved occupational exposures such as radar or microwave work. Most of the general-public studies estimated exposure from things such as hours of mobile-phone use, and relatively few carefully measured where the phone was carried relative to the testes.

The reviewers rated most of the evidence as very uncertain.

That phrase deserves an explanation.

The studies were difficult to combine because they were often testing different things. One might compare hours of daily phone use. Another might examine whether a phone was carried near the body. Others involved occupational radar or microwave exposure. Some measured sperm count, others sperm movement or shape. The study populations and methods also differed.

Researchers call that heterogeneity. It simply means the studies are different enough that averaging them together can become misleading.

Exposure measurement was another major problem. Asking someone how many hours they use a phone does not tell researchers exactly how much RF energy reached the testes. Signal strength, phone position, network conditions, distance, and behavior all change the dose.

That is why the 2024 reviewers could not confidently conclude that ordinary mobile-phone exposure harms human fertility.

If RF-EMF affects sperm, shouldn't testosterone fall too?

Not necessarily.

Fertility and testosterone are connected, but they are produced by different systems inside the testes.

Leydig cells make testosterone.

Sperm develop inside the seminiferous tubules with support from Sertoli cells.

An exposure can damage sperm production without meaningfully changing testosterone. The sauna experiment above is a perfect human example: sperm quality worsened while testosterone stayed stable.

So evidence of a fertility effect does not prove a testosterone effect.

But it does make a broader testicular effect more plausible.

If RF-EMF produces enough oxidative stress to affect sperm-producing tissue, it is reasonable to ask whether a sufficiently large exposure could also affect Leydig cells. Animal experiments suggest that it can under some conditions.

The missing piece is convincing human evidence showing that realistic everyday exposure damages Leydig cells enough to lower resting testosterone.

What about 5G specifically?

5G is still a form of radiofrequency electromagnetic exposure, so the broader biological questions do apply.

But most direct human testosterone studies used older mobile-phone technologies, often around 900 MHz.

Different generations of wireless technology can use different frequencies, signal patterns, and exposure conditions. Evidence from an older 900 MHz phone therefore cannot simply be treated as a direct 5G experiment.

No convincing human trial has demonstrated that realistic 5G exposure lowers serum testosterone.

Verdict: RF-EMF is a plausible but unproven testosterone suppressor. Animal studies provide a real mechanism involving oxidative stress and possible Leydig-cell damage, and some human observational data point toward lower testosterone. Controlled human evidence is limited and inconsistent, and the actual dose matters enormously.

Does perfume or fragrance lower testosterone?

There are two separate questions hiding inside this claim.

First: does wearing perfume or cologne actually increase your exposure to chemicals used in fragrance products?

Second: do those particular chemicals lower testosterone?

The answer to the first question is much clearer than the answer to the second.

Cologne and perfume clearly increase exposure to one fragrance-associated phthalate

One chemical historically used in fragrances is diethyl phthalate, or DEP.

DEP can help dissolve fragrance ingredients and make scent last longer.

Once DEP enters the body, it is rapidly broken down into monoethyl phthalate, or MEP. Researchers can measure MEP in urine as a marker of recent DEP exposure.

A 2005 study examined 406 men and asked about their use of products such as cologne, aftershave, lotions, deodorants, and hair products during the previous 48 hours.

Men who had used cologne had median urinary MEP concentrations around 265 ng/mL, compared with about 108 ng/mL among men who had not used cologne. After researchers adjusted for factors such as age, body mass index, smoking, and race, cologne users still had about 2.6 times as much MEP in their urine.

A later study followed 400 men who supplied more than 1,000 urine samples across multiple visits. Using cologne or perfume was associated with about an 83 percent higher urinary MEP concentration.

So this part is not vague:

using fragranced personal-care products can measurably increase DEP exposure inside the body.

But DEP is not the phthalate with the clearest testosterone evidence

This is where the argument usually jumps too far.

Phthalates are a large family of chemicals.

DEP is one phthalate.

DEHP, DINP, and DBP are different phthalates used for different purposes, often in plastics and other materials rather than mainly as fragrance ingredients.

Those different chemicals should not be treated as interchangeable.

A large U.S. study measured 13 phthalate metabolites and testosterone in 2,208 people from the general population.

Researchers found several associations between phthalates and lower testosterone, but the pattern depended heavily on age and which phthalate was measured. In adult men, the clearest inverse findings appeared in men aged 40 to 60 and involved metabolites related to DEHP and dibutyl phthalate, not a broad consistent testosterone reduction from the fragrance-associated DEP metabolite MEP.

A second study examined 881 healthy Danish men and measured 14 phthalate metabolites along with testosterone, free testosterone, LH, FSH, SHBG, and semen quality.

Men with a higher proportion of the DEHP metabolite MEHP had lower total testosterone, lower free testosterone, and a lower ratio of testosterone to LH. Men with greater exposure to a DINP-related marker also had a lower free androgen index. The researchers interpreted the pattern as possible impairment of testosterone production or reproductive-hormone feedback.

Those findings are genuinely concerning.

But notice what happened.

The evidence that perfume raises DEP exposure is strong.

The more concerning adult testosterone findings involve several other phthalates.

We do not yet have the missing bridge:

wear perfume → DEP exposure rises → testosterone falls.

No controlled human study has demonstrated that full sequence.

Why can't we just assume all phthalates behave the same?

Because they are different chemicals.

They enter the body from different sources, are processed differently, reach different concentrations, and can interact with hormone biology in different ways.

Saying “DEHP may suppress testosterone, therefore DEP in perfume must do the same thing” would be like saying two medications must have the same effect because both belong to the same broad drug family.

The family relationship gives us a reason to investigate.

It does not establish the result.

Parabens add another possible concern, but still do not prove a perfume effect

Parabens are another group of chemicals used as preservatives in some cosmetics and personal-care products.

A study of 315 men attending an infertility clinic found that higher urinary levels of several parabens were associated with lower testosterone and poorer sperm measures. That provides another reason to study personal-care-product exposure more carefully.

But again, the researchers measured chemicals in urine and hormones in blood.

They did not assign men to wear a particular perfume and then show that the perfume lowered testosterone.

And a urinary paraben measurement does not tell us whether the exposure came from perfume, lotion, deodorant, food, medication, or another source.

Verdict: perfume and cologne can clearly increase exposure to fragrance-associated chemicals such as DEP. Some phthalates and parabens have concerning human testosterone data. But the strongest testosterone findings involve chemicals other than the main fragrance-associated DEP marker, and no human study has shown that wearing perfume lowers testosterone or that quitting perfume raises it. Reducing fragrance is therefore a reasonable exposure precaution, not a proven testosterone intervention.

Phthalates have a more credible testosterone signal than perfume itself

Once we separate perfume from the larger phthalate question, the evidence becomes more interesting.

A 2009 study examined 425 men attending a U.S. fertility clinic and measured chemicals in their urine alongside reproductive hormones in their blood.

The researchers focused partly on MEHP, a breakdown product the body produces after exposure to the plasticizer DEHP.

Higher MEHP was associated with lower testosterone even after researchers adjusted for age, body mass index, smoking, season, and time of day. An increase in MEHP from the lower to the higher part of the population's exposure range was associated with about a 3.7 percent decrease in testosterone.

That makes DEHP exposure a plausible testosterone suppressor in humans.

But it still does not prove that DEHP caused the testosterone difference.

The researchers did not randomly assign men to receive high or low phthalate exposure. They measured what was already present in the men's bodies and compared it with their hormones.

Other unmeasured differences could therefore contribute to the result, and all 425 participants were recruited through a fertility clinic rather than from a random sample of healthy men.

Human testicular tissue strengthens the biological case

Researchers have also exposed adult human testicular tissue directly to DEHP and its metabolite MEHP outside the body.

Testosterone production fell. The researchers reported inhibitory effects at concentrations in the same general range as measured human exposures, providing direct evidence that at least some phthalates can interfere with steroid production in human testicular tissue.

That is not the same as proving that everyday DEHP exposure lowers a man's blood testosterone.

But combining a human association with a direct effect in human testicular tissue makes the hypothesis considerably more credible than a claim supported only by rat experiments.

Verdict: some phthalates, especially DEHP-related exposure, are plausible testosterone suppressors. What is still missing is a controlled human intervention showing that lowering phthalate exposure raises testosterone.

BPA and broader plastic exposure: a different chemical with mixed testosterone evidence

BPA is not a phthalate.

BPA is a bisphenol, a different family of chemicals.

It often gets discussed alongside phthalates because both can be associated with plastics and both can interact with hormone biology.

But grouping them together does not mean they produce the same effects.

The InCHIANTI study examined 715 Italian adults aged 20 to 74 and used 24-hour urinary BPA measurements rather than a single spot urine sample. Among men, higher BPA excretion was associated with a small increase in serum testosterone, not a decrease.

This was a cross-sectional study.

That simply means exposure and testosterone were measured during the same general period, giving researchers a snapshot rather than showing what changed first over months or years.

Because of that, the study cannot tell us whether BPA caused testosterone to increase, whether hormone biology affected BPA metabolism, or whether another factor influenced both.

The result matters because it shows why “plastic lowers testosterone” is too broad.

Different plastic-associated chemicals can behave differently, and the adult human evidence is not one uniform story.

Plastic exposure can be reduced quickly

Human intervention experiments have shown that measured exposure can change very quickly.

In a 2011 intervention, five families avoided canned and packaged foods for three days and instead ate fresh foods prepared with limited plastic contact. Average urinary BPA fell by about 66 percent, while metabolites of the phthalate DEHP fell by roughly 53 to 56 percent.

That is strong evidence that behavior can materially change exposure.

The researchers did not measure whether testosterone increased afterward.

This is the missing experiment:

reduce plastic-associated chemical exposure → confirm exposure fell → remeasure testosterone.

Verdict: reducing unnecessary plastic exposure is a reasonable precaution, but BPA specifically has inconsistent adult testosterone evidence and no intervention has shown that lowering BPA exposure raises testosterone.

Cotton vs polyester underwear: the bizarre experiment behind the claim

This claim traces largely to experiments by Egyptian researcher Ahmed Shafik in the early 1990s.

In a 1992 human experiment published in Contraception, 14 men aged 32 to 47 wore a specially constructed polyester scrotal sling day and night for 12 months. All 14 eventually became azoospermic, meaning no sperm were detected in their semen, after an average of about 140 days.

After the sling was removed, sperm production eventually returned, taking an average of roughly 157 days.

Testicular volume also fell during the intervention and later recovered.

That sounds dramatic.

The testosterone result is the critical part:

Serum reproductive hormones did not significantly change.

So even the strange original experiment does not show polyester lowering testosterone.

There are also major limitations.

• Only 14 men participated.
• The intervention was a special scrotal sling worn continuously, not ordinary underwear worn during the day.
• The sling altered the physical position of the testes.
• The experiment has not been independently reproduced with comparable methodology in more than three decades.

The original experiment was an unusual fertility finding, not evidence that polyester underwear suppresses testosterone.

Is tap water meaningfully estrogenic?

Trace hormones and other endocrine-active chemicals really can be detected in wastewater, rivers, and sometimes finished drinking water.

The crucial question is not whether a laboratory instrument can detect them.

The crucial question is whether the dose reaching a person is large enough to alter human hormones.

What about birth-control hormones in tap water?

This version of the claim usually focuses on 17α-ethinylestradiol, or EE2, a potent synthetic estrogen used in many combined birth-control pills.

EE2 absolutely can suppress male reproductive hormones at a high enough dose.

Controlled human dosing studies have given EE2 directly to men as tablets. Doses around 15 micrograms per day have been sufficient to suppress luteinizing hormone and testosterone in normal men. At higher doses, the effects become clearer.

Another experiment gave healthy men 30 micrograms of EE2 per day for five days. LH and testosterone initially fell, while sex hormone-binding globulin, or SHBG, rose dramatically.

So the basic biological claim is real:

enough synthetic estrogen can disrupt male testosterone regulation.

The question is whether drinking water provides anything close to that dose.

The dose in treated drinking water is dramatically smaller

A large U.S. investigation screened drinking water serving more than 28 million people across 19 utilities for pharmaceuticals and endocrine-active chemicals.

EE2 was usually not detected. When it was quantified in finished or distribution water, reported concentrations were around 1.0 to 1.4 nanograms per liter, close to the detection limits of the testing methods. Other surveys and models generally estimate even lower typical concentrations.

The difference between a nanogram and a microgram is enormous.

One microgram equals 1,000 nanograms.

The lowest human dose above was about:

15 micrograms per day = 15,000 nanograms per day.

If a man drank two liters of water containing a relatively high EE2 concentration of 5 nanograms per liter, he would ingest about:

10 nanograms per day.

That is still roughly 1,500 times lower than the 15,000-nanogram dose that has altered male reproductive hormones in controlled human research.

And 5 ng/L is already above what is normally found in finished U.S. drinking water.

Using a modeled typical concentration around 0.003 ng/L, drinking two liters would provide only about 0.006 nanograms of EE2 per day. That is about 2.5 million times lower than 15 micrograms.

Those comparisons are not perfect toxicology experiments. Long-term low-dose exposure is not automatically identical to a short-term pharmaceutical-dose study.

But the dose gap is so large that the claim that ordinary U.S. tap water provides birth-control-level estrogen exposure becomes very difficult to defend.

No human study identified in the literature reviewed here has shown that measured EE2 exposure from ordinary drinking water lowers testosterone, LH, free testosterone, or SHBG in adult men.

Birth-control estrogen can suppress testosterone. The evidence does not show that the tiny amount reaching ordinary U.S. tap water does.

Why do estrogen-contaminated rivers affect fish?

This is where much of the alarm originally came from.

Estrogenic wastewater effects in aquatic wildlife are absolutely real.

A classic 2001 experiment exposed juvenile roach for 150 days to different concentrations of treated sewage water released from wastewater plants. That released water is technically called effluent. The fish developed dose-dependent feminization of their reproductive ducts, with the strongest effects occurring in fish continuously living in the highest concentrations.

That does not contradict the drinking-water dose comparison.

Fish live in the contaminated water 24 hours per day. Their gills, skin, and reproductive systems are continuously exposed to it.

A human drinks a few liters of treated water, absorbs only the chemicals present in that volume, and is much larger than a fish.

A concentration capable of affecting an aquatic animal living continuously inside the water therefore does not automatically represent a meaningful human drinking-water dose.

The fish research proves that environmental estrogen contamination can matter.

It does not show that ordinary municipal tap water delivers enough estrogen to lower male testosterone.

Fluoride is a more interesting testosterone question

Unlike the broad “estrogen in tap water” claim, fluoride has actually been measured against testosterone in several human populations.

Some of those results are concerning.

A U.S. analysis using 2013 to 2016 NHANES data included 3,392 children and adolescents aged 6 to 19. Participants in the highest third of plasma-fluoride exposure had testosterone levels about 21.7 percent lower than those in the lowest third. Among adolescent boys specifically, the highest-exposure group had about 21 percent lower testosterone.

That is a strong association.

It is still not proof that fluoride caused the lower testosterone.

The reason is the study design.

Researchers did not assign one group to high fluoride and another group to low fluoride and then watch testosterone change. They measured fluoride exposure and hormones in the same population at roughly the same point in time.

That leaves open the possibility that another factor affected both measurements. Diet, kidney function, socioeconomic conditions, other environmental exposures, or differences between the groups could potentially contribute.

So the NHANES result is meaningful evidence supporting the fluoride-testosterone hypothesis. “Not proof” does not mean “not evidence.” It means the study cannot isolate fluoride as the cause by itself.

High-exposure adult studies also produce a concerning signal

One Chinese study compared residents who had lived for more than five years in an area where drinking water contained about 3.89 mg/L of fluoride with residents of an area containing less than 1 mg/L. Men in the high-fluoride area had significantly lower testosterone and higher luteinizing hormone.

That combination is especially interesting.

Higher LH means the brain and pituitary were sending a stronger signal telling the testes to make testosterone, yet testosterone was still lower. That is compatible with the possibility that high fluoride exposure was interfering farther downstream, potentially at the testes themselves.

A 2016 study of male farmers aged 18 to 55 in Chinese villages also compared men with higher and lower fluoride exposure. Men with higher urinary fluoride had significantly lower testosterone, with the association appearing strongest among the younger adult groups.

So there is more than one human dataset pointing toward lower testosterone at greater fluoride exposure.

But another adult study found the opposite

A 2013 study from China compared adult men from three types of villages: a high-fluoride area, an area where a defluoridation project had reduced exposure, and a lower-fluoride control area.

The result did not fit the simple “more fluoride equals lower testosterone” model.

Average testosterone was about 4.83 ng/mL in the high-fluoride group compared with 3.69 ng/mL in the control group. The high-fluoride men therefore had higher measured total testosterone, even though they also had substantially lower SHBG.

That directly conflicts with the other adult studies.

Why could different studies disagree?

All of these were observational population studies rather than randomized experiments. They used different villages, different ways of defining fluoride exposure, different age distributions, and different groups of men. Testosterone and SHBG also vary with body composition, metabolic health, age, liver function, time of blood collection, and other factors.

When several observational studies point in opposite directions, it usually means the real relationship is either more complicated than a simple dose-response rule or the studies have not yet controlled enough variables to isolate the effect.

There is a plausible testicular mechanism at high enough exposure

Laboratory researchers have exposed testosterone-producing Leydig cells directly to sodium fluoride.

In a 2018 cell experiment, sodium fluoride reduced testosterone production in a dose-dependent manner and altered the expression of several proteins needed for steroid synthesis. That gives the fluoride-testosterone hypothesis a real mechanistic basis.

Combined with the NHANES association and several high-exposure adult studies, this makes excessive fluoride a plausible testosterone suppressor.

High fluoride exposure is not the same thing as ordinary U.S. fluoridation

This distinction is important.

One of the concerning Chinese studies involved drinking water containing about 3.89 mg/L of fluoride.

The target used for community water fluoridation in the United States is about 0.7 mg/L.

So the Chinese high-exposure level was more than five times the U.S. fluoridation target.

Areas with endemic fluorosis are places where people are naturally exposed to enough fluoride over long periods to produce visible dental fluorosis or, at still higher chronic exposure, skeletal problems. Those are not the same exposure conditions as a municipal system intentionally targeting around 0.7 mg/L.

A toxic effect at roughly 4 mg/L also does not prove that the same effect occurs at 0.7 mg/L.

Biological effects do not always scale in a straight line where one-fifth of the dose produces exactly one-fifth of the effect.

At the same time, lower-dose effects cannot simply be ruled out because higher doses are more clearly concerning. They have to be tested.

Verdict: excessive fluoride exposure is a plausible testosterone suppressor with supportive human and laboratory evidence. It is also biologically plausible that lower chronic exposure could matter, but ordinary U.S. fluoridation around 0.7 mg/L has not been shown to meaningfully suppress testosterone. That lower-dose question remains unresolved rather than proven safe or proven harmful by the testosterone studies above.

Honey has an interesting animal testosterone signal

A 2019 scientific review examined the research connecting honey with male reproductive hormones. The authors identified several possible mechanisms, including greater LH signaling, antioxidant protection of testosterone-producing Leydig cells, and changes in proteins involved in steroid-hormone production.

The important limitation is that this evidence was predominantly from animal experiments.

No controlled human testosterone trial demonstrated that eating honey raises LH or testosterone in healthy men.

So honey is not biologically random here.

Verdict: plausible from animal and mechanistic evidence, but unproven in humans.

Tamarind has a different evidence story

Tamarind's most interesting human evidence is not a testosterone trial.

It is a fluoride-excretion trial.

Indian researchers studied 18 boys living in a high-fluoride environment and added about 10 grams of tamarind per day to their diet for 18 days.

Average urinary fluoride excretion increased from roughly 3.5 to 4.8 mg per day. The researchers proposed tamarind as a possible dietary tool for increasing fluoride elimination in populations with excessive exposure.

A later human study found additional fluoride mobilization when tamarind was combined with defluoridated water. So tamarind increasing fluoride excretion is not merely an internet claim.

Tamarind also has animal reproductive evidence

A mouse experiment tested tamarind-seed extract in males eating a high-fat diet. Tamarind altered expression of genes involved in testicular steroid production and produced a tendency toward higher LH, but serum testosterone did not significantly increase.

Another animal experiment went further under very different conditions.

A 2020 conference report described 70 rats exposed to sodium fluoride to create reproductive dysfunction. Tamarind fruit-pulp extract increased LH and testosterone in the fluoride-damaged animals. That makes a restorative effect biologically plausible when reproductive function has first been impaired by excessive fluoride.

Again, these were rats with experimentally induced fluoride toxicity, not healthy men.

Verdict: tamarind can increase fluoride excretion in humans and has animal reproductive evidence, but no human experiment has shown that tamarind itself raises testosterone.

Does taking honey and tamarind before bed raise testosterone?

Combining two biologically interesting foods does not automatically prove that the combination works.

There is a possible chain:

excess fluoride exposure → impaired reproductive signaling → tamarind increases fluoride elimination → reproductive function potentially recovers.

Honey adds separate animal evidence involving LH signaling and Leydig-cell protection.

That creates an interesting hypothesis.

But no human experiment has completed the chain.

Researchers have not taken men with excessive fluoride exposure and suppressed testosterone, given them tamarind, confirmed that fluoride burden fell, and then shown that LH and testosterone recovered.

No human trial has tested honey and tamarind together for testosterone.

No human trial has shown that taking the combination before bed is better than taking it in the morning or at any other time.

And no human experiment has demonstrated:

honey + tamarind → increased pituitary LH → increased testicular testosterone.

Verdict: plausible hypothesis, untested protocol. Honey and tamarind each have their own pieces of relevant evidence, but the combined bedtime testosterone protocol has never been tested in humans.

Soy does not lower male testosterone

The human evidence here is unusually consistent.

A 2021 analysis pooled 41 clinical studies involving 1,753 men and examined soy protein and isoflavone intake against total testosterone, free testosterone, estradiol, and estrone. The researchers found no significant effect on any of those male reproductive hormones.

The analysis updated an earlier meta-analysis that had reached the same conclusion.

Avoid soy if you have another reason to avoid it.

Raising testosterone is not a well-supported one.

Coffee and caffeine: a plausible indirect suppressor, but not a proven one

The caffeine story is more complicated than either “coffee tanks testosterone” or “coffee has no hormonal effect.”

Caffeine can acutely raise cortisol.

In a controlled crossover study involving 96 adults, repeated caffeine doses increased cortisol. Regular caffeine users developed partial tolerance, but the cortisol response was not completely eliminated. So caffeine really can increase a hormone that is capable of interacting with testosterone production.

And sufficiently high cortisol can suppress testosterone.

In a human experiment, researchers increased cortisol through induced hypoglycemia and through hydrocortisone administration. Testosterone fell rapidly even though LH did not change much, suggesting at least part of the suppression occurred directly at the testes. That makes the caffeine-cortisol-testosterone pathway biologically plausible.

But plausibility is not the same thing as showing that ordinary coffee consumption lowers resting testosterone.

A double-blind crossover experiment tested caffeine in 24 professional rugby players before resistance exercise. Each athlete completed exercise after 0, 200, 400, and 800 mg caffeine conditions. Caffeine increased the normal exercise-related testosterone response in a dose-dependent fashion, with the highest dose producing about a 21 percent larger testosterone response than exercise alone.

Cortisol also rose much more strongly at the highest dose, by roughly 52 percent.

So testosterone and cortisol increased at the same time.

That directly contradicts a simplistic model where any caffeine-induced cortisol increase must immediately reduce testosterone.

No controlled human trial has shown that quitting coffee reliably raises resting testosterone.

Caffeine can raise cortisol, and sufficiently elevated cortisol can suppress testosterone. That makes a negative effect plausible, particularly with high intake, chronic stress, or sleep disruption. But human studies have not shown that ordinary caffeine use reliably lowers resting testosterone.

Caffeine can still matter indirectly

If late or excessive caffeine delays sleep, reduces sleep quality, or allows someone to repeatedly compensate for exhaustion instead of recovering, reducing intake could improve the conditions that support normal testosterone production.

Circadian timing and testosterone

Testosterone follows a daily rhythm, but that rhythm is tied to sleep and wake timing more closely than the phrase “morning testosterone” sometimes implies.

A 2005 experiment studied seven healthy young men during normal nighttime sleep and during experimentally displaced daytime sleep while measuring testosterone repeatedly across 24 hours. Testosterone rose during sleep and declined during waking regardless of whether the men slept from 11 PM to 7 AM or from 7 AM to 3 PM.

The daytime-sleep condition is what makes the result interesting.

If testosterone's rise were controlled mainly by the clock saying “it is morning,” shifting sleep into the daytime should have broken the pattern.

Instead, testosterone rose while the men slept even when that sleep happened during the day, then declined while they were awake.

That suggests the sleep period itself is a major driver of the daily testosterone rise, while the body's internal circadian clock appears to play a smaller additional role.

A later study of 73 male police officers working different numbers of consecutive night shifts found that the timing of the testosterone rhythm moved with the sleep-wake schedule. A morning blood draw can therefore look very different in a night worker than in someone who sleeps on a conventional schedule.

A 2022 randomized simulated-shift-work experiment gives an even cleaner test. Fourteen healthy adults were assigned to three days of either simulated night work or day work, followed by intensive 24-hour blood sampling under controlled conditions. Night-shift exposure altered the timing of several biological rhythms but did not significantly lower the mean 24-hour testosterone concentration.

So circadian disruption does not appear to act like a simple testosterone off-switch.

Real-world night work can still be a problem because it commonly comes with shorter sleep, fragmented sleep, nighttime light exposure, irregular eating, and poorer recovery.

The cleaner conclusion is that circadian misalignment changes when testosterone rises and falls, while chronic sleep loss associated with shift work is a more convincing pathway to lower testosterone than circadian timing alone.

Do nicotine pouches affect testosterone?

Nicotine pouches deserve their own entry because they are not cigarettes and they are not traditional smokeless tobacco.

A tobacco-free nicotine pouch such as Zyn contains nicotine without tobacco leaf.

Snus is different. Snus is moist oral tobacco placed under the lip. It delivers nicotine through the mouth in a way that resembles a nicotine pouch, but it also contains tobacco and other tobacco-derived compounds that a tobacco-free pouch does not.

That makes snus useful as indirect evidence about oral nicotine exposure, but it is not a perfect stand-in for Zyn or other nicotine pouches.

Direct nicotine-pouch testosterone research is surprisingly absent

A 2025 comprehensive review of oral nicotine-pouch research examined the available chemical, laboratory, survey, and human clinical evidence. The human research focused largely on nicotine delivery, withdrawal, acute physiological effects, product use, and toxicant exposure rather than testosterone or the male reproductive hormone system.

No controlled human trial identified in the literature reviewed here directly tested tobacco-free nicotine pouches and repeatedly measured total testosterone, free testosterone, LH, FSH, SHBG, and estradiol.

That means a claim such as “Zyn lowers testosterone” or “Zyn raises testosterone” is currently much stronger than the direct evidence allows.

Snus gives us indirect evidence because it delivers nicotine orally

One of the best human comparisons comes from Swedish snus.

A 2022 study examined 613 men from the general population. Researchers measured semen, reproductive hormones, and urinary cotinine, the major nicotine metabolite. Of the 613 men, 109 used snus.

After adjusting for smoking and other factors, snus users had about 14 percent higher testosterone than non-users. At the same time, they had about 24 percent lower total sperm counts. Higher urinary cotinine was also associated with higher testosterone and estradiol.

That result is fascinating for two reasons.

First, it shows that using an oral nicotine-containing tobacco product is not automatically associated with lower measured testosterone.

Second, the same men had worse sperm counts.

Higher testosterone and better fertility were clearly not the same outcome.

But because snus contains tobacco, the study cannot tell us whether nicotine itself, another tobacco compound, or some difference between snus users and non-users explains the testosterone result.

Could nicotine or cotinine explain the higher testosterone seen in smokers?

Possibly, but that remains a hypothesis.

A 2016 meta-analysis pooled 22 studies involving 13,317 men and found higher testosterone among smokers. The authors noted that cotinine can inhibit testosterone breakdown and specifically proposed testing nicotine replacement and e-cigarettes to see whether nicotine-related products produce a similar effect.

That offers a possible explanation other than “cigarette smoke makes the testes produce more testosterone.”

If testosterone is broken down more slowly, the concentration measured in blood could rise even without the testes producing substantially more testosterone.

But that mechanism has not been cleanly demonstrated for modern tobacco-free nicotine pouches.

Verdict: we do not currently know whether tobacco-free nicotine pouches meaningfully raise or lower resting testosterone. Snus and smoking studies suggest nicotine or cotinine could partly contribute to higher measured testosterone, but direct pouch-specific hormonal trials are missing.

Smoking shows why a higher testosterone number is not automatically better

One of the stranger findings in this literature is that smokers often have higher measured testosterone.

A 2016 systematic review and meta-analysis pooled 22 studies involving 13,317 men. Current smokers had significantly higher average total testosterone than nonsmokers.

A large population study from Tromsø, Norway, examined 3,427 men and found a similar pattern. Current smokers had roughly 15 percent higher total testosterone and 13 percent higher free testosterone than men who had never smoked.

These are associations, not proof that intentionally starting smoking will causally raise testosterone by those percentages.

And even if smoking did raise measured testosterone in some men, it would still be a terrible optimization strategy.

Smoking dramatically increases cardiovascular disease, cancer, respiratory disease, and mortality risk.

Finasteride can raise testosterone while lowering DHT

Finasteride creates a useful example of why two androgen measurements can move in opposite directions.

Your body normally uses an enzyme called 5-alpha-reductase to convert some testosterone into another androgen called dihydrotestosterone, or DHT.

DHT is made from testosterone, but it is not simply “extra testosterone.” It is a separate, more potent androgen in several tissues and plays an important role in areas such as the prostate, skin, and hair follicles.

Finasteride blocks the enzyme that performs that conversion.

So less testosterone gets turned into DHT.

As a result, DHT falls while some of the testosterone that otherwise would have been converted remains circulating as testosterone.

A four-year clinical trial of 3,040 men with enlarged prostates compared finasteride with placebo. Researchers repeatedly measured testosterone in a randomly selected subgroup of 301 men. Finasteride produced a modest but significant increase in serum testosterone compared with placebo, with the largest increases occurring in men who started with lower testosterone.

At the same time, the drug's intended biological effect is to sharply reduce DHT.

So the result is:

more testosterone left in the blood, but much less of it being converted into DHT.

That is not the same thing as globally increasing androgen activity throughout the body.

A testosterone number can therefore rise while an important downstream androgen signal falls.

Heavy alcohol can suppress testosterone

Alcohol's hormonal effect depends heavily on whether we are talking about one drinking episode or repeated exposure over time.

A 2024 meta-analysis gives us a surprisingly clear separation between the two.

Researchers pooled 21 studies containing 30 comparisons and more than 10,000 men. Four studies examined acute alcohol exposure, meaning alcohol taken during a single experimental occasion. Seventeen examined chronic exposure, meaning alcohol consumed repeatedly over days, weeks, or much longer. Acute alcohol exposure did not significantly lower testosterone. Chronic alcohol exposure did.

Among the chronic studies, men exposed to alcohol had lower total testosterone and lower free testosterone than controls.

In the researchers' detailed analysis, total testosterone in healthy men with chronic alcohol exposure was lower by roughly 4.9 nmol/L on average compared with abstainers. That is approximately 140 ng/dL. The effect was not seen after a single acute alcohol dose.

What did “chronic” actually mean?

It was not one uniform dose.

The studies ranged from controlled experiments where volunteers consumed alcohol repeatedly for several weeks to observational studies of men's normal long-term drinking habits.

For example, one controlled trial gave men four units of beer per day for three weeks. Other studies examined men consuming more than 12 drinks per week, while some older studies involved extremely heavy intake exceeding 150 grams of alcohol per day.

That huge range is important.

It means the meta-analysis supports the idea that repeated alcohol exposure can suppress testosterone, but it cannot give us one exact number of drinks where the effect suddenly begins.

Why would chronic drinking be different from one night of drinking?

One exposure is brief.

Chronic drinking repeatedly exposes the reproductive system and liver to alcohol and its metabolic effects.

The exact testosterone mechanism is still being worked out, but experimental research suggests alcohol can interfere at several points: signaling from the brain and pituitary, testosterone production inside the testes, and liver processes that control how sex hormones are transported and metabolized. The meta-analysis also found higher estradiol and lower SHBG alongside the lower testosterone in chronically exposed men.

So there is direct human evidence behind the statement that chronic exposure is the bigger testosterone concern.

Why do different alcohol studies produce different numbers?

A separate 2023 meta-analysis pooled 17 testosterone studies involving 13,373 men and also found lower testosterone among drinkers overall. But the results varied dramatically from one study to another.

The studies did not all define drinking the same way.

Some included moderate drinkers. Others focused on heavy drinkers or people with alcohol-use problems. Some measured recent drinking while others measured long-term habits. Testosterone was also measured using different laboratory methods and in different populations.

When research studies differ that much in who they study and how they measure the exposure, their exact testosterone estimates will naturally differ too.

That is why the evidence can support a chronic suppressive effect without supporting a precise rule such as “X drinks per week lowers testosterone by exactly Y percent.”

What counts as “heavy” drinking?

There is no validated testosterone-specific cutoff.

For general public-health purposes, the U.S. National Institute on Alcohol Abuse and Alcoholism defines heavy drinking for men as five or more drinks on any single day or 15 or more drinks per week.

That is useful for orientation, but it was not designed as a testosterone threshold.

For example, two drinks every night equals 14 drinks per week, which sits just below that particular weekly definition.

That does not mean 14 drinks are hormonally harmless and 15 suddenly suppress testosterone.

The hormone research simply is not precise enough to draw that line.

Verdict: a single drinking episode does not reliably lower testosterone, while repeated chronic alcohol exposure is associated with lower total and free testosterone. The risk appears more credible as intake becomes heavier and more sustained, but there is no proven testosterone-specific drink threshold.

Cannabis and testosterone: the human evidence is mixed

The old story was simple: marijuana lowers testosterone.

The modern human evidence is much more mixed.

A famous 1974 report studied 20 young men who had used marijuana at least four days per week for at least six months and reported substantially lower plasma testosterone than in controls. That study helped establish the long-running belief that chronic cannabis use suppresses testosterone.

Later research did not consistently reproduce it.

A 2017 analysis of 1,577 U.S. men from NHANES found no significant testosterone difference between men who had ever used marijuana and men who had never used it. More recent use was actually associated with somewhat higher testosterone.

A separate 2020 analysis also reported slightly higher testosterone among regular THC users, with a nonlinear relationship between exposure and hormone levels. That still does not establish cannabis as a testosterone booster.

Why not?

Because these were observational comparisons.

Researchers did not randomly assign men to use THC for several months and then show that their testosterone rose relative to placebo.

Cannabis users can differ from non-users in age, body composition, alcohol use, physical activity, sleep, sexual behavior, medications, and other factors that can also influence testosterone.

The relationship was also not a clean pattern where more THC consistently produced more testosterone.

A convincing booster claim would be much stronger if controlled trials repeatedly showed that giving cannabis to men caused their resting testosterone to rise.

We do not have that evidence.

Researchers have even exposed adult human testicular tissue directly to THC and CBD outside the body. In that experiment, cannabinoid exposure did not produce a clear reduction in testosterone secretion from human Leydig cells.

So the testosterone story remains genuinely uncertain.

Verdict: cannabis is neither a reliable testosterone suppressor nor a demonstrated testosterone booster based on current human evidence.

The studies above answer a testosterone question. They should not be treated as proof that cannabis has no effect on every other reproductive endpoint, such as sperm or fertility, which are separate outcomes and require their own evidence.

Underlying medical problems can matter more than any supplement

If repeated testing shows genuinely low testosterone, medical causes can matter much more than whether you eat pomegranate or take fenugreek.

Hypothyroidism

Low thyroid function can disturb reproductive hormone signaling and alter SHBG, which changes how much testosterone is available in circulation.

Clinical studies of men with hypothyroidism show that testosterone abnormalities can improve when thyroid function is treated and normalized.

Hyperprolactinemia

Excess prolactin can suppress gonadotropin-releasing hormone in the brain.

That reduces luteinizing hormone, which then reduces the signal sent to the testes to make testosterone.

When the underlying prolactin problem is successfully treated, testosterone can recover.

Obstructive sleep apnea

Sleep apnea deserves consideration when testosterone is low, particularly in men with obesity or severe symptoms.

A pooled analysis of 18 studies involving 1,823 men found lower testosterone in men with obstructive sleep apnea, with the largest difference in severe disease. The association persisted after researchers adjusted for age and body mass index.

But treating apnea with continuous positive airway pressure, or CPAP, does not reliably raise testosterone on its own.

A meta-analysis combining randomized and observational treatment studies found no significant average testosterone increase after CPAP. That suggests obesity, metabolic dysfunction, and other shared factors explain part of the sleep-apnea/testosterone relationship.

Insulin resistance and type 2 diabetes

Insulin resistance, obesity, and lower testosterone frequently cluster together.

Weight-loss studies repeatedly show that improving the metabolic state can restore testosterone in many affected men.

If repeated morning tests show low testosterone, especially alongside symptoms like depression or other mental-health changes, it makes more sense to investigate the reason than to cycle through increasingly obscure supplements.

Some drugs can suppress testosterone more strongly than natural interventions can raise it

Anabolic steroids and exogenous testosterone

Anabolic-androgenic steroids suppress the body's own testosterone production through negative feedback.

In plain English, the brain detects the external androgen signal and reduces the hormones that normally tell the testes to make testosterone.

A 2019 clinical review found that men using anabolic steroids for shorter periods often recover hormone production over the following months. Longer and heavier exposure is less predictable, and some men remain testosterone-deficient for years after stopping.

Medically prescribed testosterone involves a different clinical decision, but external testosterone still suppresses endogenous production while it is being used.

Chronic opioids

Opioids are another strong suppressor of male reproductive signaling.

A 2025 meta-analysis covering more than 3,000 chronic opioid users found biochemical testosterone deficiency in roughly 63 percent of men. Long-acting opioids were associated with particularly high rates.

Opioids act partly by suppressing the brain signals that normally stimulate the testes.

Testosterone can recover after opioid cessation, but prescribed opioids should not be stopped abruptly without medical guidance.

Systemic glucocorticoids

Long-term systemic steroids such as prednisone can also lower testosterone.

In one classic study, 14 of 16 men receiving long-term systemic glucocorticoids had reduced testosterone. Their average level was around 211 ng/dL compared with about 449 ng/dL in matched controls. Higher glucocorticoid exposure was associated with greater suppression.

Inhaled corticosteroids generally appear much less suppressive than systemic treatment.

Do not abruptly stop prescribed glucocorticoids. Sudden withdrawal can be dangerous.

Statins

Statins appear to have a much smaller hormonal effect.

A 2024 systematic review found a modest reduction in total testosterone among statin users, while free testosterone did not show the same clear decline. The average change generally was not large enough to cause clinical testosterone deficiency by itself.

Why chasing the testosterone number can fool you

The evidence above repeatedly separates testosterone from the outcomes people assume it represents.

• Smoking can be associated with higher measured testosterone while damaging long-term health.
• Snus can be associated with higher testosterone while sperm counts are lower.
• Finasteride can raise serum testosterone while lowering DHT.
• Lifting can create a temporary testosterone increase without raising resting baseline T.
• Sex can produce a large short-term increase without evidence of a higher chronic baseline.
• Fatherhood and caregiving can lower testosterone while supporting paternal behavior.
• A glucose drink or ordinary meal can temporarily push testosterone down without proving a lower long-term fasting baseline.
• Maca can increase libido without increasing testosterone.
• Ginseng can improve erections and desire while reproductive hormones remain unchanged.
• Citrulline can improve erection hardness without increasing testosterone.
• Pomegranate may affect vascular function without a reliable serum-T increase.
• Cold can make you feel intensely stimulated while testosterone stays flat or falls.
• Polyester dramatically changed sperm production in one strange experiment without changing reproductive hormones.
• Tamarind can increase fluoride excretion without any human evidence yet showing that testosterone rises.

So whenever a testosterone claim sounds impressive, ask what researchers actually measured.

Was it total testosterone?

Free testosterone?

A short-lived post-exercise spike?

A temporary post-meal drop?

Sexual desire?

Erection quality?

Sperm quality?

Cortisol?

A urinary metabolite?

An animal testis?

A real biological effect somewhere in the chain does not prove the final testosterone claim.

The Healthmaxxing testosterone hierarchy

The BiohackBeast Testosterone Framework also gives us a practical order of operations.

Step 1: Remove major suppressors

• Lose excess body fat if you are overweight.
• Stop chronically underfeeding yourself if you are lean and training hard.
• Avoid extreme weight cutting.
• Avoid severe chronic sleep deprivation.
• Reduce chronic heavy alcohol use.
• Do not stack excessive training on inadequate food and recovery.
• Improve metabolic health if excess calorie and sugar intake are contributing to obesity or insulin resistance.
• Understand whether a medication or drug may be suppressing testosterone.
• Investigate genuine metabolic or endocrine disease when testosterone is repeatedly low.

Step 2: Correct actual deficiencies

If your diet is deficient in zinc, iron, vitamin D, or another essential nutrient, correct the deficiency.

Food should usually be the first place to solve an ordinary dietary shortfall.

Supplementation becomes more useful when diet cannot reasonably correct the problem or a deficiency is documented.

The mistake is assuming that because deficiency lowers testosterone, taking extra amounts above adequacy must continue pushing testosterone higher.

Step 3: Live physically enough that recovery matters

Lift.

Sprint.

Do intervals.

Practice martial arts.

Compete.

Use your body hard enough that poor sleep, heavy drinking, under-eating, and inadequate recovery have consequences you can immediately feel.

A demanding physical life does not guarantee a higher baseline testosterone level.

But it can create a powerful reason to maintain the sleep, food intake, body composition, and recovery habits that prevent testosterone from being unnecessarily suppressed.

There may also be a stress-adaptation benefit. Exercise can change how the body responds to later stress, although the research does not show that this reliably raises resting testosterone.

The goal is not to eliminate acute stress. It is to recover well enough that acute stress does not become chronic physiological strain.

Step 4: Experiment with marginal boosters only after the obvious problems are handled

If the foundation is stable and you still want to experiment, a small number of interventions have human evidence worth taking seriously:

• Ashwagandha: repeated positive human signal, especially in stressed, older, overweight, or lower-T populations.
• Tongkat ali: promising, particularly when baseline testosterone is low.
• Fenugreek: possible small effect, but low certainty.
• Shilajit: one interesting controlled human trial in healthy middle-aged men that needs replication.
• Royal jelly: two small positive controlled human trials that need larger independent studies.
• Pomegranate-rind + cocoa-seed extract: one randomized, double-blind, placebo-controlled trial in 120 healthy young men found increases in free testosterone, with total testosterone and LH also increasing at the higher dose. The result is promising, but it applies to the specific combined extract and still needs independent replication.

Garlic sits below that group because its testosterone case is still mainly animal and mechanistic.

Honey and tamarind sit lower still. Honey has animal evidence related to LH and Leydig-cell function. Tamarind has human evidence for increasing fluoride excretion and animal reproductive evidence. But neither has a convincing human testosterone trial.

The honey + tamarind bedtime protocol is another step beyond that evidence because the combination and the timing have never been tested for testosterone in humans.

So they are interesting hypotheses, not members of the same evidence tier as interventions that have actually raised testosterone in controlled human trials.

Bottom line

Healthmaxxing treats testosterone as an output rather than the first lever to pull.

The BiohackBeast Testosterone Framework separates what gets casually called “boosting testosterone” into four very different things: correcting a deficiency, removing a suppressor, truly enhancing an already-functional system, or creating a temporary hormonal spike.

That distinction changes how most testosterone advice looks.

Testosterone optimization is mostly about removing reasons your body is suppressing testosterone, not finding things that force it higher.

An overweight man may need to lose fat.

An underfed athlete may need to eat more.

A severely sleep-deprived man may need to sleep.

A deficient man may need to restore what is missing.

A man with normal testosterone, adequate nutrition, good metabolic health, and good recovery may simply have much less room to move his baseline naturally.

Once you understand that, the question changes from:

What can I take to boost testosterone?

to:

What is preventing my body from producing the testosterone it should?

That is usually where the useful answer begins.

Note: Testosterone varies with time of day, illness, calorie intake, meals, sleep, medications, and testing conditions. A single low result does not establish testosterone deficiency. Persistently low testosterone or significant symptoms should be evaluated by a qualified clinician, and prescribed medications should not be stopped solely to change a hormone number.