Low Testosterone: What the Research Says About Herbs, Thyroid and Lifestyle

What changed Why levels fall Traditional views Herbs Precursor hormones Thyroid Light and training Food Questions to ask

Testosterone in American men has fallen at the population level, independent of aging. The best measurement of this comes from the Massachusetts Male Aging Study, which found an age-matched decline of about 1.2% per year across cohorts measured between 1987 and 2004.¹ A 60-year-old man measured in 2003 had less testosterone than a 60-year-old man measured in 1988. Body weight and illness did not fully explain the gap.

This article covers what the research says about herbs, nutrients, precursor hormones, thyroid function, light exposure and training, and what each one has actually been tested on. Every study claim below carries a numbered footnote linking to the source list at the bottom, so you can check the original rather than take my summary of it. Hormone replacement sits outside its scope, since replacement suppresses the body's own production and reduces fertility for as long as it continues, which many men are not told before they start.

Key takeaways

• Population testosterone has declined independent of age, weight and smoking, and the cause is not established.
• The current reference range for healthy non-obese men aged 19 to 39 is 264 to 916 ng/dL, with a median near 531.
• Of the fifteen items covered here, four have randomized placebo-controlled human trials behind them. Several have only rodent data. One has documented rodent organ toxicity.
• Thyroid function has the strongest published link to male testosterone of anything in this article, and it is measurable with a standard blood panel.
• Nothing here substitutes for a workup. Low testosterone can signal pituitary, testicular or metabolic conditions that need diagnosis.

Medical disclaimer. This article is educational and is not medical advice, diagnosis or treatment. I am a certified clinical herbalist, not a physician, and I cannot diagnose or treat anyone. Persistent fatigue, low libido, mood changes or infertility warrant evaluation by a qualified healthcare provider, because they have many possible causes. Do not start, stop or change any supplement, hormone or prescription based on this article. Herbs and supplements can interact with medications and are not appropriate for everyone. Statements about dietary supplements have not been evaluated by any regulatory agency.

What actually changed

Evidence: prospective cohort study and harmonized multi-cohort reference data.

Two findings anchor this. The first is Travison and colleagues in 2007, a prospective study of randomly selected men aged 45 to 79 measured in three waves. Comparing men of the same age across waves, testosterone fell about 1.2% per year, with a confidence interval of 1.0 to 1.4%. The authors noted the decline persisted after accounting for rising body mass index, other conditions, and changes in smoking.¹

The second is Travison and colleagues again in 2017, which cross-calibrated assays across four large cohorts in the United States and Europe. Among healthy non-obese men aged 19 to 39, the harmonized range ran from 264 to 916 ng/dL, with a median of 531. That paper also found a substantial share of the variation between cohorts came from differences between laboratory assays instead of from the men themselves.²

Those two findings together undercut a comparison people make often. Measuring a lab result from today against a number remembered from decades ago produces an unreliable answer, because the measurement methods differed. What holds up is the decline documented inside standardized cohorts that used consistent measurement.

Lokeshwar and colleagues found the same pattern in younger men, analyzing national survey data from 4,045 men collected between 1999 and 2016. Mean total testosterone fell from 605 ng/dL in the 1999 to 2000 cycle to 425 ng/dL in 2011 to 2012, then 432 and 451 ng/dL in the two following cycles, with the trend significant after controlling for body mass index, activity and smoking.³ Read that with one caveat the authors themselves raise, which is that three different assay methods were used across those survey years.

Reading your own result

A reference range is built from population data, so it locates you among other men and says nothing about how you feel. A man at 320 ng/dL sits inside the current range and may feel fine, or may not. Symptoms that commonly bring men in include loss of muscle and strength, abdominal fat gain, fatigue, reduced libido, difficulty concentrating, low mood, and reduced fertility. Those symptoms overlap heavily with thyroid dysfunction, sleep apnea, iron overload, depression and chronic under-eating, so a single testosterone value tells a provider where to start looking.

What the research points to

Evidence: meta-regression, cohort and mechanistic studies. Causation is not established for any single factor.

No single cause has been demonstrated. Several lines of evidence run in parallel, and the strongest of them concerns reproductive health broadly instead of testosterone specifically.

Levine, Swan and colleagues published a meta-regression in 2017 covering 185 studies. Among Western men not selected for fertility, sperm concentration fell 52.4% and total sperm count fell 59.3% between 1973 and 2011.⁴ Their update extended the window to 2018, found a 51.6% decline across all continents, and reported that the rate of decline after 2000 was steeper than before it.⁵ Swan's book Countdown argues that endocrine-disrupting chemicals drive this pattern, particularly phthalates and compounds that interfere with fetal androgen signalling.⁶ The book is a work of popular science built on her research group's published papers, so treat the argument as her interpretation and the papers as the evidence.

Exposures with published mechanisms

Phthalates are the best-characterized of these. Animal work and human observational studies link prenatal phthalate exposure to shortened anogenital distance in male infants, an androgen-dependent measurement. PFAS compounds persist in the body and appear in drinking water, food packaging, firefighting foam and treated textiles. Reverse osmosis filtration removes them. Standard carbon pitcher filters largely do not.

For the seed oil question, the evidence is uneven. Rodent and cell work has examined how oxidized fatty acid products affect steroid synthesis in testicular tissue, though no controlled human trial has tested whether ordinary dietary intake lowers testosterone in men. The broader claim that these oils cause heart disease also remains contested, with recovered data from the Sydney Diet Heart Study⁷ and the Minnesota Coronary Experiment⁸ cutting against the mainstream position. I avoid industrially processed seed oils on grounds of oxidation and processing. The human testosterone link is not established, and I will not present it as though it were.

Alcohol has a clearer relationship. Heavy and chronic intake lowers testosterone through direct testicular effects and liver metabolism. The narrower claim that beer lowers testosterone through the hops compound 8-prenylnaringenin is weaker than it is usually presented, because concentrations in finished beer are low relative to the doses used in laboratory work.

Body fat acts through a measurable pathway. Adipose tissue expresses aromatase, which converts testosterone to estradiol, and abdominal fat correlates with lower total testosterone across large cohorts. The relationship runs in both directions, since low testosterone also promotes fat gain.

Sleep loss produces some of the fastest measurable changes of anything in this section. Leproult and Van Cauter restricted ten healthy young men to five hours of sleep a night for one week under laboratory conditions and recorded daytime testosterone falling 10 to 15%, with the lowest readings between 2 p.m. and 10 p.m.⁹

How older systems described the same pattern

Evidence: traditional frameworks and historical clinical writing. Descriptive, not experimental.

Traditional systems categorized patterns of depletion instead of measuring hormones, and those categories map onto what men with low testosterone tend to report. Treat them as a way of organizing observations, since none of them demonstrate mechanism.

Ayurveda

Ayurvedic medicine treats reproductive vitality under shukra dhatu, the last and most refined of the seven tissues, formed after all the others have been nourished. Depletion of the earlier tissues therefore shows up in reproductive function last and recovers there last. The therapeutic category aimed at this is vajikarana, which covers ashwagandha, gokshura, shilajit and kapikacchu. The framework makes a testable prediction, that reproductive complaints resolve after digestion, sleep and tissue-building have been addressed and not before.

Traditional Chinese medicine

Kidney yang deficiency describes cold extremities, low back and knee weakness, night urination, low libido and daytime exhaustion. Kidney essence, or jing, is treated as a finite inherited reserve depleted by overwork, chronic illness and excessive sexual activity. Formulas in this category use deer antler, cistanche, epimedium and morinda. The pattern description overlaps closely with hypothyroidism, and the thyroid research further down covers much of the same ground.

Weston A. Price

Price, a dentist, published Nutrition and Physical Degeneration in 1939 after surveying fourteen isolated populations.¹⁰ He documented that groups eating their traditional diets had broad dental arches, low tooth decay, well-formed nasal passages and robust facial development, while groups in the same regions eating refined flour, sugar, canned goods and processed fats did not. He also documented that many of these cultures fed specific nutrient-dense foods to couples for months before conception. Those foods were organ meats, fish eggs, seafood and dairy from rapidly growing pasture. Price attributed the effect to what he called fat-soluble activators, corresponding to vitamins A and D and to a compound he named Activator X, later identified as vitamin K2. His fieldwork is observational and its interpretation is debated, though the dietary pattern it describes is dense in exactly the vitamins and minerals steroid synthesis requires.

Broda Barnes

Barnes, a physician, argued from the 1940s onward that laboratory thyroid testing missed a large number of clinically hypothyroid patients. In Hypothyroidism: The Unsuspected Illness (1976) he described taking basal axillary temperature on waking, before rising, for ten minutes, and treating on the combination of low readings and symptoms instead of on laboratory values alone.¹¹ His position was rejected by mainstream endocrinology and remains outside it. The connection he pointed at, between thyroid function and reproductive symptoms, was later documented in the endocrinology literature, and that research appears in the thyroid section below.

Ray Peat

Peat (1936 to 2022) was a biologist who wrote extensively on steroid hormones.¹² He treated thyroid function as the frame through which everything else should be read, describing it as the rate at which cells produce energy and pointing to temperature, pulse, cholesterol and reflex speed as indicators of it. He wrote that between 1940 and 1950 the estimated share of hypothyroid Americans dropped from 30 to 40% down to 5%, and attributed that shift to the replacement of symptom-based diagnosis with laboratory testing. On his own clinical observation he stated that he never saw a person with a TSH above 2 microIU/ml who was comfortably healthy.

On the steroid hormones themselves, Peat described pregnenolone as the material the body uses to form either progesterone or DHEA. He treated DHEA as having a real ceiling, noting that excess converts to estrogen or testosterone, and gave figures of roughly 4 mg daily at age 50 against the 12 to 15 mg produced by young adults. These are his positions, reported as such.

Herbs and what has been tested

Evidence: quality varies from randomized placebo-controlled trials to rodent studies alone. Tier is labeled for each.

Each entry below gives the traditional use, what the studies found, the dose those studies used, and the design problems. Doses appear because they appear in the published protocols. They are not recommendations, and the right dose for any individual is a question for a provider who knows their history and medications.

Pine pollen No human trials

Pine pollen has been used in Chinese medicine for centuries as a food and tonic. Its modern reputation rests on the fact that pine pollen contains mammalian steroids, which Šaden-Krehula and colleagues first isolated from Scotch pine pollen in 1971.¹³

The quantities are the part that gets misreported. Tarkowská's review of animal steroid hormones in plants gives androstenedione at 0.59 micrograms per gram in Pinus sylvestris and 0.08 micrograms per gram in Pinus nigra, with testosterone present in similar trace amounts.¹⁴ Figures hundreds of times larger circulate in supplement marketing and trace back to unpublished work.

At those concentrations the arithmetic settles the question before metabolism enters into it. A daily serving measured in grams delivers steroid quantities measured in micrograms, against endogenous production measured in milligrams, and orally ingested testosterone is extensively metabolized by the liver before reaching circulation. No controlled human trial has tested pine pollen for testosterone outcomes. It remains a nutrient-dense food with a long record of traditional use, and its steroid content is not a plausible route to changing a lab value.

Tribulus terrestris fruit Mostly null

Known as gokshura in Ayurveda and used for urinary and reproductive complaints. Marketing volume for this ingredient far exceeds the evidence behind it.

Neychev and Mitev randomized 21 healthy men aged 20 to 36 to 10 or 20 mg per kilogram of body weight daily for four weeks against placebo, measuring testosterone, androstenedione and luteinizing hormone at six time points, and found no influence on androgen production.¹⁵ A 2025 systematic review in Nutrients covering ten studies and 483 participants at doses of 400 to 750 mg daily for one to three months found that eight of ten reported no significant change in androgen profile.¹⁶ The authors noted that participants in the null studies had normal androgen levels at baseline, leaving open whether men who are actually low would respond differently. Erectile function improved in three of five studies that measured it, without accompanying testosterone changes. Half the included studies scored low on methodological quality.

Shilajit One randomized controlled trial

A mineral pitch used in Ayurveda as a rasayana, or rejuvenative. Pandit and colleagues ran a randomized, double-blind, placebo-controlled trial in healthy men aged 45 to 55 using purified shilajit at 250 mg twice daily for 90 days. Total testosterone, free testosterone and DHEA-S all rose significantly against placebo, with luteinizing hormone and follicle-stimulating hormone maintained instead of suppressed, suggesting the effect was not working by shutting down the pituitary signal.¹⁷

Two features of the design limit how far the result travels. The material was a proprietary standardized extract supplied by its manufacturer, which introduces a commercial interest in the outcome, and unpurified shilajit sold as raw resin has documented heavy metal contamination. The trial result applies to purified standardized material rather than to the category as a whole.

Ashwagandha Two randomized controlled trials

An Ayurvedic adaptogen used for strength, sleep and recovery. Lopresti and colleagues ran a 16-week randomized, double-blind, placebo-controlled crossover trial in overweight men aged 40 to 70 reporting mild fatigue, using a standardized extract for eight weeks per arm. Salivary testosterone was 14.7% higher during ashwagandha than placebo, and DHEA-S was 18.0% higher. Cortisol fell 7.8% and estradiol fell 11.6%, neither significantly.¹⁸ Wankhede and colleagues separately gave 600 mg daily of a root extract to 57 men aged 18 to 50 alongside eight weeks of supervised resistance training, and found significantly greater testosterone increases than placebo.¹⁹

The Lopresti trial enrolled 57 men and completed 43, used salivary rather than serum hormones, had no washout period between arms, and reported that the hormone increases were not sustained at the 16-week mark. Self-reported fatigue and sexual wellbeing improved in both groups, including placebo, which is the usual pattern for subjective outcomes.

Fadogia agrestis Rodent only, with toxicity findings

A West African shrub used in folk medicine as a stem decoction for male vitality. It became popular through podcast and supplement marketing, and its evidence base has three parts that are rarely presented together.

Yakubu, Akanji and Oladiji published the founding study in 2005 in Asian Journal of Andrology. Male albino rats received aqueous stem extract at 18, 50 or 100 mg per kilogram daily for five days, and serum testosterone rose in a dose-dependent pattern alongside changes in sexual behavior measures.²⁰ That paper is the one cited on supplement labels.

The same research group published two follow-ups that are cited far less often. In 2008 in Journal of Ethnopharmacology, rats received the same three doses for 28 days rather than five. Testicular function indices were adversely altered at 50 and 100 mg per kilogram, and the animals recovered only at the 18 mg per kilogram dose, the amount closest to traditional preparation.²¹ In 2009 in Human and Experimental Toxicology, the group documented cellular toxicity in rat liver and kidney.²²

There are no published human trials of Fadogia agrestis, no human safety data, and no established dose. Rodent doses cannot be converted to human doses without allometric scaling, and the 2008 result indicates the window between an effect and organ damage was narrow in rats. I do not carry this herb and would not use it.

Tongkat ali Meta-analyzed, with heterogeneity

Known as Eurycoma longifolia and used across Malaysia and Indonesia as a root decoction for fatigue and male vitality. Leisegang and colleagues published a systematic review and meta-analysis in Medicina in 2022, screening nine studies and pooling five randomized controlled trials. Total testosterone rose significantly, with a standardized mean difference of 1.352 and a confidence interval of 0.565 to 2.138, and the effect was confirmed in the subgroup of men who were hypogonadal at baseline.²³

Heterogeneity between studies reached 87.27%, a high figure meaning the trials measured meaningfully different populations or preparations. The most-cited underlying study, Tambi and colleagues in 2012, gave 200 mg daily of a standardized water-soluble extract to 76 men with late-onset hypogonadism, but used a before-and-after design without a placebo arm.²⁴ Most of the trials used one of two proprietary standardized extracts, so results may not transfer to unstandardized root powder.

Of the herbs covered here, tongkat ali shows the clearest signal for working preferentially in men whose baseline androgens are already low.

Handmade in Montana

← →

Precursor hormones and organ supplements

Evidence: one large meta-analysis for DHEA. No controlled human trials for pregnenolone or glandulars in this context.

These are sold over the counter in the United States and come up often as alternatives to replacement therapy. They are hormones or hormone precursors, placing them in a different category from the herbs above.

DHEA Meta-analyzed, largely null

Corona and colleagues meta-analyzed 25 double-blind placebo-controlled randomized trials of oral DHEA in elderly men, covering 1,353 participants with a mean follow-up of 36 weeks. Fat mass fell modestly, with a standardized mean difference of negative 0.35, though that association disappeared in a multivariate model once increases in DHEA's downstream metabolites were accounted for. The review found no effect on lipid metabolism, glucose metabolism, bone health, sexual function or quality of life, and reported significant rises in serum DHEA and estradiol without a statistically significant rise in total testosterone.²⁵

Bring the estradiol finding to a provider before starting this. DHEA converts in both directions, toward androgens and toward estrogens, and the conversion ratio varies between individuals. Peat's position was that DHEA should not be taken alone for that reason, and that supporting the body's own production was preferable to supplying DHEA directly.¹²

Pregnenolone No controlled trials for this use

Pregnenolone sits upstream of both progesterone and DHEA in the steroid pathway, which forms the basis for the argument that supplying it lets the body allocate downstream products according to need. That argument is mechanistically coherent and has not been tested in randomized controlled trials for testosterone outcomes in men. Published pregnenolone trials in humans have examined cognition, mood, schizophrenia and bipolar depression rather than androgens.

Peat wrote about pregnenolone extensively and considered it the safer of the two precursors, reasoning that the enzymes converting it are regulated and so supplying the precursor corrects a deficiency without creating an excess.¹² This is his position and is not established by trial data. Pregnenolone is a hormone, it is available without prescription in the United States, and dosing it without supervision and follow-up bloodwork is not something I would suggest to anyone.

Beef organs and glandulars No human trials

Whole-animal eating has a long history and a defensible nutritional rationale. Liver, heart, kidney, pancreas and spleen are dense in vitamin A, B vitamins, copper, zinc, selenium and CoQ10, and steroid synthesis depends on several of those. Price's fieldwork documented exactly this pattern of organ consumption in the populations he studied.¹⁰ A whole-organ blend, taken as food, is a reasonable way to fill nutrient gaps if you will not eat organ meat directly.

The narrower claim that desiccated testicle, sold as orchic extract, raises testosterone has no clinical evidence behind it. No randomized trial of bovine orchic extract for testosterone outcomes has been published. Bovine testicular tissue contains only trace testosterone, and the quantity in a capsule serving amounts to a small fraction of one percent of daily endogenous production before first-pass liver metabolism reduces it further. Any benefit is more plausibly attributable to the zinc and selenium, which would only apply if you were deficient. Bovine glandulars also carry sourcing considerations around tissue identity and origin that a manufacturer should be able to answer directly.

Thyroid function

Evidence: paired clinical study with reversal of the finding on treatment. The strongest causal signal in this article.

The research here is stronger than anything above it, and a full thyroid panel is frequently absent from a low testosterone workup.

Donnelly and White studied ten men with primary hypothyroidism, measuring hormones before and after starting thyroxine replacement. Free testosterone was 161 pmol/L while they were hypothyroid and rose to 315 pmol/L on treatment, a significant change at P less than 0.001. Gonadotropin levels were not elevated, identifying the pattern as hypogonadotrophic hypogonadism, meaning the signal from the pituitary was low instead of the testes failing. Prolactin fell as free testosterone rose. The authors concluded that hypothyroidism affects gonadotropin secretion at the level of the hypothalamus and pituitary, and that low free testosterone may contribute to the symptoms men experience with low thyroid.²⁶

Ten men is a small sample, and the design compensates somewhat, because each man served as his own control and the finding reversed when the underlying condition was treated. Krassas and colleagues separately found in a prospective controlled study that hypothyroidism adversely affects human spermatogenesis.²⁷

A man with low testosterone and untreated hypothyroidism may therefore be looking at a downstream effect instead of a primary problem. A thyroid panel that includes TSH, free T4, free T3 and thyroid antibodies costs less than most supplement protocols and is a reasonable thing to request.

Levothyroxine Standard of care

Levothyroxine is synthetic T4, the storage form, which the body converts to active T3 in peripheral tissues. It is the first-line treatment for hypothyroidism, is well studied, and is what most physicians will prescribe. The Donnelly study used thyroxine replacement, so the testosterone finding above is specifically a levothyroxine finding.²⁶

The recurring complaint from patients is that TSH normalizes on levothyroxine while symptoms persist. The proposed explanation is impaired peripheral conversion of T4 to T3, which standard TSH monitoring would not detect. This remains a live disagreement in endocrinology and not a settled question.

Desiccated thyroid extract Regulatory status in flux

Desiccated thyroid extract, sold as Armour Thyroid and NP Thyroid, is porcine thyroid gland containing both T4 and T3. It predates synthetic levothyroxine by decades and is what Barnes prescribed.¹¹ Patients who report feeling better on it generally attribute that to the T3 content.

Its regulatory position changed over the past year. In August 2025 the Food and Drug Administration announced its intent to take enforcement action against manufacturers of these products on the grounds that they were never formally approved, reclassifying them as biologics requiring a Biologics License Application. In March 2026 the agency clarified that it would apply a risk-based enforcement approach while manufacturers pursue approval, and indicated further guidance on availability. Separately, and unrelated to the regulatory action, CVS Caremark removed desiccated thyroid extract from its standard formulary effective April 1, 2026, a pharmacy benefit decision affecting coverage rather than supply. No safety recall was issued at any point in this sequence, and manufacturers of both major products have stated they are continuing production while pursuing formal approval.

If you currently take one of these, stopping a thyroid medication without a plan carries more risk than any of the events above, and that is a conversation for your prescriber.

Light and training

Evidence: mechanistic animal work with limited human confirmation for light. Small uncontrolled trials for training.

Sunlight Mechanism shown in mice, correlational in humans

Parikh and colleagues published work in Cell Reports identifying a pathway from skin to brain to gonads. Ultraviolet B exposure raised sex-steroid hormone levels in mice, and conditionally knocking out p53 in skin keratinocytes abolished the effect, establishing that the skin was initiating the signal and not merely responding to it. In their human arm, patients undergoing UVB phototherapy completed questionnaires showing increased romantic passion in both sexes and increased aggressiveness in men, and those results correlated positively with testosterone levels.²⁸

The human portion is correlational and questionnaire-based, which makes it suggestive without confirming a testosterone effect. Seasonal patterns in male testosterone, with higher summer values, have been observed independently.

The vitamin D route is a separate question with a clearer answer. Lerchbaum and colleagues ran two randomized placebo-controlled trials of 20,000 IU weekly for twelve weeks, one in healthy men²⁹ and one in men with low testosterone at baseline,³⁰ and found no significant effect on total testosterone in either. A meta-analysis of eight trials found no significant effect.³¹ Vitamin D has other established roles, and supplementing it specifically to raise testosterone is not supported by trial evidence. This corrects what an earlier version of this article said.

Red light therapy Rodent only

Ahn and colleagues irradiated the testes of 30 male rats with either a 670 nm or an 808 nm diode laser at 360 J/cm² per day, delivered as 200 mW over 30 minutes, for five days. The 670 nm wavelength raised serum testosterone by day four without visible histopathological damage, while the 808 nm wavelength penetrated deeper and produced microhemorrhages in the interstitial space at that dose.³²

That dose runs far above what consumer panels deliver, and the deeper-penetrating wavelength caused tissue damage at it. No controlled human trial has tested red light applied to the testes for testosterone. The frequently cited 2016 Italian bright-light finding was presented as a conference abstract rather than published as a full paper, and it used a light box directed at the torso in men with low sexual desire, a different intervention. Peat wrote that light stimulates cellular respiration and that darkness is catabolic, though he did not address red light therapy devices in his published articles, and citing him in their support would misrepresent him.¹²

Weightlifting Well studied, commonly misread

Resistance training produces an acute testosterone spike lasting roughly 30 minutes after a session. Morton and colleagues trained 49 men and ran correlations between post-exercise hormone rises and gains in muscle and strength, finding none.³³ Mitchell and colleagues found no relationship between exercise-induced free testosterone increases and muscle fiber hypertrophy, while muscle androgen receptor content did correlate with hypertrophy.³⁴

What resistance training reliably does is build and preserve muscle, improve insulin sensitivity, lower fasting glucose and reduce fat mass, and reduced fat mass means less aromatase activity converting testosterone to estradiol. That is the pathway by which training changes hormonal status over months.

Sprints and interval training Small uncontrolled trials

Hayes and colleagues studied 22 lifelong sedentary men averaging 62 years through six weeks of conditioning exercise followed by six weeks of high-intensity interval training. Total testosterone rose about 17% overall, with roughly 10% of that occurring during the conditioning phase before the intervals began, and free testosterone rose about 4.5% after the interval training.³⁵ Herbert and colleagues found a similar free testosterone increase in 17 masters athletes using six 30-second sprints at 40% of peak power output with three minutes of recovery, nine sessions over six weeks.³⁶

Neither study had a control group, and both came from the same research group. A later systematic review by Hayes and Elliott concluded that short-term exercise training influences basal testosterone inconsistently in older men.³⁷ The larger share of the gain in the sedentary group arrived during the conditioning phase, so the initial change came from becoming active at all.

Peat's position on exercise was that lactate and not exertion was the concern, and that fatigue from overtraining likely reflected tryptophan and serotonin load from muscle protein breakdown.¹² He gave no frequency or intensity prescription.

Food first

Evidence: nutrient requirements for steroid synthesis are established. Supplementation benefits are demonstrated mainly in deficiency.

Steroid hormones are built from cholesterol, and the enzymes doing the building require zinc, magnesium, selenium, vitamin A and B vitamins. Very low fat intake reduces the substrate available for that process. Chronic caloric deficit suppresses the whole hypothalamic-pituitary-gonadal axis, which is documented in athletes of both sexes.

The foods that supply these nutrients densely are pastured egg yolks, liver and other organ meats, shellfish and small oily fish, grass-fed red meat, and full-fat dairy if it agrees with you. This overlaps almost exactly with what Price documented being fed to prospective parents in the cultures he surveyed, and that overlap is why his fieldwork appears in this article at all.¹⁰

Supplementing an individual nutrient corrects a deficiency and does little otherwise. The pattern across the micronutrient literature is that correcting a documented shortfall changes hormone measurements while adding more on top of adequate status does not.

Questions worth bringing to a provider

Evidence: not applicable. These are questions, not recommendations.

If you have been handed a low testosterone result, these are reasonable things to ask before deciding anything.

• Was the sample drawn in the morning, and has it been repeated? Testosterone varies through the day and a single value is not a diagnosis.
• Were LH and FSH measured? Those distinguish a testicular problem from a pituitary or hypothalamic one, and the answer changes what comes next.
• Has thyroid function been assessed with a full panel instead of TSH alone?
• Were prolactin, ferritin, SHBG and estradiol checked? Each can produce this picture.
• Has sleep apnea been ruled out?
• If replacement is being proposed, what happens to fertility, and what is the plan if I want children later?
• Are there reversible contributors here to address for a defined period before starting a therapy that suppresses my own production?

Fertility comes first on that list because exogenous testosterone suppresses the pituitary signal driving sperm production, and recovery after stopping is neither guaranteed nor quick. Men are frequently prescribed it without that being explained, and I would want it answered before anything else.

Sources

1. Travison TG, Araujo AB, O'Donnell AB, Kupelian V, McKinlay JB. A population-level decline in serum testosterone levels in American men. J Clin Endocrinol Metab. 2007;92(1):196-202. PubMed ↩
2. Travison TG, Vesper HW, Orwoll E, et al. Harmonized reference ranges for circulating testosterone levels in men of four cohort studies in the United States and Europe. J Clin Endocrinol Metab. 2017;102(4):1161-1173. Full text ↩
3. Lokeshwar SD, Patel P, Fantus RJ, et al. Decline in serum testosterone levels among adolescent and young adult men in the USA. Eur Urol Focus. 2021;7(4):886-889. PubMed ↩
4. Levine H, Jørgensen N, Martino-Andrade A, et al. Temporal trends in sperm count: a systematic review and meta-regression analysis. Hum Reprod Update. 2017;23(6):646-659. Full text ↩
5. Levine H, Jørgensen N, Martino-Andrade A, et al. Temporal trends in sperm count: samples collected globally in the 20th and 21st centuries. Hum Reprod Update. 2023;29(2):157-176. PubMed ↩
6. Swan SH, Colino S. Countdown. Scribner; 2021. ↩
7. Ramsden CE, Zamora D, Leelarthaepin B, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study. BMJ. 2013;346:e8707. Full text ↩
8. Ramsden CE, Zamora D, Majchrzak-Hong S, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment. BMJ. 2016;353:i1246. Full text ↩
9. Leproult R, Van Cauter E. Effect of 1 week of sleep restriction on testosterone levels in young healthy men. JAMA. 2011;305(21):2173-2174. Full text ↩
10. Price WA. Nutrition and Physical Degeneration. 1939. ↩
11. Barnes BO, Galton L. Hypothyroidism: The Unsuspected Illness. Harper & Row; 1976. ↩
12. Peat R. Articles on thyroid, hypothyroidism, exercise and the protective steroids. raypeat.com ↩
13. Šaden-Krehula M, Tajić M, Kolbah D. Testosterone, epitestosterone and androstenedione in the pollen of Scotch pine P. silvestris L. Experientia. 1971;27(1):108-109. PubMed ↩
14. Tarkowská D. Plants are capable of synthesizing animal steroid hormones. Molecules. 2019;24(14):2585. Full text ↩
15. Neychev VK, Mitev VI. The aphrodisiac herb Tribulus terrestris does not influence the androgen production in young men. J Ethnopharmacol. 2005;101(1-3):319-323. PubMed ↩
16. Vilar Neto JO, de Moraes WMAM, Pinto DV, et al. Effects of Tribulus terrestris supplementation on erectile dysfunction and testosterone levels in men: a systematic review of clinical trials. Nutrients. 2025;17(7):1275. PubMed ↩
17. Pandit S, Biswas S, Jana U, De RK, Mukhopadhyay SC, Biswas TK. Clinical evaluation of purified Shilajit on testosterone levels in healthy volunteers. Andrologia. 2016;48(5):570-575. PubMed ↩
18. Lopresti AL, Drummond PD, Smith SJ. A randomized, double-blind, placebo-controlled, crossover study examining the hormonal and vitality effects of ashwagandha in aging, overweight males. Am J Mens Health. 2019;13(2):1557988319835985. PubMed ↩
19. Wankhede S, Langade D, Joshi K, Sinha SR, Bhattacharyya S. Examining the effect of Withania somnifera supplementation on muscle strength and recovery. J Int Soc Sports Nutr. 2015;12:43. ↩
20. Yakubu MT, Akanji MA, Oladiji AT. Aphrodisiac potentials of the aqueous extract of Fadogia agrestis stem in male albino rats. Asian J Androl. 2005;7(4):399-404. PubMed ↩
21. Yakubu MT, Akanji MA, Oladiji AT. Effects of oral administration of aqueous extract of Fadogia agrestis stem on some testicular function indices of male rats. J Ethnopharmacol. 2008;115(2):288-292. PubMed ↩
22. Yakubu MT, Oladiji AT, Akanji MA. Mode of cellular toxicity of aqueous extract of Fadogia agrestis stem in male rat liver and kidney. Hum Exp Toxicol. 2009;28(8):469-478. PubMed ↩
23. Leisegang K, Finelli R, Sikka SC, Panner Selvam MK. Eurycoma longifolia improves serum total testosterone in men: a systematic review and meta-analysis of clinical trials. Medicina. 2022;58(8):1047. PubMed ↩
24. Tambi MIBM, Imran MK, Henkel RR. Standardised water-soluble extract of Eurycoma longifolia as testosterone booster for managing men with late-onset hypogonadism? Andrologia. 2012;44(Suppl 1):226-230. ↩
25. Corona G, Rastrelli G, Giagulli VA, et al. Dehydroepiandrosterone supplementation in elderly men: a meta-analysis study of placebo-controlled trials. J Clin Endocrinol Metab. 2013;98(9):3615-3626. PubMed ↩
26. Donnelly P, White C. Testicular dysfunction in men with primary hypothyroidism; reversal of hypogonadotrophic hypogonadism with replacement thyroxine. Clin Endocrinol (Oxf). 2000;52(2):197-201. PubMed ↩
27. Krassas GE, Papadopoulou F, Tziomalos K, Zeginiadou T, Pontikides N. Hypothyroidism has an adverse effect on human spermatogenesis: a prospective, controlled study. Thyroid. 2008;18(12):1255-1259. ↩
28. Parikh R, Sorek E, Parikh S, et al. Skin exposure to UVB light induces a skin-brain-gonad axis and sexual behavior. Cell Reports. 2021;36(8):109579. Full text ↩
29. Lerchbaum E, Pilz S, Trummer C, et al. Vitamin D and testosterone in healthy men: a randomized controlled trial. J Clin Endocrinol Metab. 2017;102(11):4292-4302. PubMed ↩
30. Lerchbaum E, Trummer C, Theiler-Schwetz V, et al. Effects of vitamin D supplementation on androgens in men with low testosterone levels: a randomized controlled trial. Eur J Nutr. 2019;58(8):3135-3146. PubMed ↩
31. Hosseini Marnani E, et al. The effect of vitamin D supplementation on the androgenic profile in men: a systematic review and meta-analysis of clinical trials. Andrologia. 2019;51(11):e13343. ↩
32. Ahn JC, Kim YH, Rhee CK. The effects of low level laser therapy (LLLT) on the testis in elevating serum testosterone level in rats. Biomedical Research. 2013;24(1):28-32. ↩
33. Morton RW, Oikawa SY, Wavell CG, et al. Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men. J Appl Physiol. 2016;121(1):129-138. PubMed ↩
34. Mitchell CJ, Churchward-Venne TA, Bellamy L, Parise G, Baker SK, Phillips SM. Muscular and systemic correlates of resistance training-induced muscle hypertrophy. PLoS One. 2013;8(10):e78636. Full text ↩
35. Hayes LD, Herbert P, Sculthorpe NF, Grace FM. Exercise training improves free testosterone in lifelong sedentary aging men. Endocr Connect. 2017;6(5):306-310. PubMed ↩
36. Herbert P, Hayes LD, Sculthorpe N, Grace FM. HIIT produces increases in muscle power and free testosterone in male masters athletes. Endocr Connect. 2017;6(7):430-436. ↩
37. Hayes LD, Elliott BT. Short-term exercise training inconsistently influences basal testosterone in older men: a systematic review and meta-analysis. Front Physiol. 2019;9:1878. ↩