Andropause (Male Hormonal Aging)

Andropause (Male Hormonal Aging)

Overview and Nomenclature

Late-onset hypogonadism (formerly called the andropause) is a clinical and biochemical syndrome associated with advancing age, characterized by typical signs and symptoms and a deficiency in serum testosterone levels. This syndrome carries many names, including male menopause or climacterium, andropause, and partial androgen deficiency of the ageing male (PADAM); late-onset hypogonadism (LOH) describes it best and is therefore generally preferred.

The word "andropause" derives from the Greek "andras" (human male) and "pause" (a cessation). In 1946, Werner published a landmark paper in JAMA entitled "The male climacteric," characterizing the syndrome by nervousness, reduced potency, decreased libido, irritability, fatigue, depression, memory problems, sleep disturbances, and hot flushes.

The existence of the so-called "andropause" is an irrefutable fact, although the terms "SLOH" (symptomatic late-onset hypogonadism) or "symptomatic ADAM" (androgen deficiency of the aging male) are more accurate. The term "andropause" is, in most cases, inappropriate, except when the gonads cease functioning entirely. In contrast to menopause, which is a universal, well-characterized, timed process associated with absolute gonadal failure, andropause is characterized by insidious onset and slow progression.

Testosterone deficiency (TD), also known as male hypogonadism, is a complex syndrome encompassing physical, biochemical, and social aspects that increasingly affects the aging population. There is ongoing debate whether testosterone decline leading to hypogonadism is directly and primarily related to age-specific processes or whether it is the subsequent result of accumulating comorbidities throughout a lifetime.

Epidemiology

Andropause or late-onset hypogonadism is a common disorder that increases in prevalence with advancing age. The changes in average serum testosterone levels with aging mean that the proportion of men fulfilling a biochemically defined diagnosis of hypogonadism increases with aging. Twenty percent of men aged over 60 have total testosterone levels below the normal range, and the figure rises to 50% in those aged over 80.

Although suppressed serum testosterone is common in ageing men, only a small proportion of them develop the genuine syndrome of low testosterone associated with diffuse sexual symptoms (e.g., erectile dysfunction), physical symptoms (e.g., loss of vigor and frailty), and psychological symptoms (e.g., depression). Some men present with symptoms but have normal testosterone levels, while others with low testosterone levels have no symptoms. The reasons for this phenomenon are currently unknown.

A systematic review of 40 studies found that the prevalence of low testosterone ranged between 2% and 77% across studies, and threshold testosterone levels used as reference standards varied substantially. The same review concluded that there is a weak correlation between signs, symptoms, and testosterone levels, and there is considerable uncertainty about what threshold testosterone levels should be considered low for aging men, making it difficult to extrapolate methods of diagnosing pathologic hypogonadism in younger men to clinical decisions regarding age-related testosterone decline in aging men.

Physiology: What Happens in the Aging Male Body

Testosterone Production and Decline

Andropause results from a gradual drop in testosterone; a steady decline in testosterone levels of about 1% per year can occur and is well documented in both men and women. More precisely, in men aged 40–70 years, total serum testosterone decreases at a rate of approximately 0.4% annually, while free testosterone shows a more pronounced decline of 1.3% per year. In men, serum testosterone levels decrease with age by 2–3% annually, a decline associated with specific symptoms of late-onset hypogonadism (LOH) syndrome, whose various clinical signs and symptoms include decreased libido and sexual desire, muscle weakness, increased visceral fat, obesity, osteoporosis, deterioration of insulin resistance, and dyslipidemia.

The mechanism of age-related decreases in serum testosterone levels has been the subject of investigation. Metabolic clearance declines with age, but this effect is less pronounced than a reduction in testosterone production, so the overall effect is to reduce serum testosterone levels.

The Hypothalamic-Pituitary-Gonadal (HPG) Axis

According to the Endocrine Society, male hypogonadism is a syndrome that results from the inability of the testis to produce physiological levels of testosterone and spermatozoa, caused by disruption of the hypothalamic-pituitary-gonadal (HPG) axis. The arcuate nucleus in the medial basal region of the hypothalamus is under negative control of testosterone and its metabolites; it secretes gonadotropin-releasing hormone (GnRH), sensing lower levels of testosterone. GnRH acts on the pituitary to secrete luteinizing hormone (LH), which acts on Leydig cells of the testis to produce testosterone.

Age-related testosterone decline involves complex disruptions throughout the HPG axis that extend beyond simple testicular dysfunction. Age-related hypogonadism reflects a combination of primary testicular failure and secondary hypothalamic-pituitary axis dysfunction, highlighting the multifactorial mechanisms underlying acquired androgen deficiency in aging men.

In males over 35 years old, aging leads to alterations in the HPG axis, primarily manifesting as decreased GnRH secretion and reduced Leydig cell (LC) responsiveness to LH stimulation. Early biomathematical models predicted a 33–50% decline in GnRH secretion in males from ages 20 to 80 years. A 2020 clinical study that evaluated 40 healthy men aged 19–73 years found that increasing age led to decreased GnRH outflow, while pituitary responsiveness to GnRH remained normal.

The underlying pathophysiology involves disruptions of the HPG axis, affecting both central and peripheral mechanisms. At the testicular level, microenvironmental alterations include Leydig cell decline, oxidative stress, inflammatory upregulation, and mitochondrial dysfunction, all of which contribute to reduced steroidogenic capacity.

Sex Hormone-Binding Globulin (SHBG)

Serum total testosterone concentration represents the sum of unbound and protein-bound testosterone in circulation. Most of the circulating testosterone is bound to SHBG and to albumin; only 0.5–3% of circulating testosterone is unbound or "free." SHBG levels tend to rise with age, further reducing the bioavailable fraction of testosterone beyond the absolute decline in total testosterone. The figures concerning free testosterone are even higher than those for total testosterone, as would be expected in view of the concurrent decrease in SHBG levels.

The Hypogonadism Subtypes

The decrease of testosterone in LOH is often marginal, and hypogonadism can be either due to primary testicular failure (low T, high LH) or secondary to a hypothalamic-pituitary failure (low T, low or inappropriately normal LH). The latter form is more common and is usually associated with overweight/obesity or chronic diseases such as type 2 diabetes mellitus, the metabolic syndrome, and cardiovascular and chronic obstructive pulmonary disease.

Crucially, aging per se does not precipitate hypogonadism; rather, age-associated comorbidities catalyze the emergence of functional hypogonadism.

Other Hormonal Changes

Other hormones — including dehydroepiandrosterone (DHEA), growth hormone, thyroxine, and melatonin — also decrease with age. Such multi-hormone alterations are closely inter-related and may influence "andropause-related" symptoms. Beyond its crucial roles in male sexual function and reproduction, testosterone influences mood, cognition, metabolism, and immune function.

Clinical Presentation and Body Systems Involved

Sexual Symptoms

Late-onset hypogonadism is characterized by measurably low testosterone levels and clinical symptoms mostly of a sexual nature, including decreased desire for mating, fewer spontaneous erections, and erectile dysfunction. Prominent among the diagnostic symptoms are sexual symptoms such as loss of libido, absence of morning penile erection, and erectile dysfunction; these must be accompanied by demonstration of low testosterone levels.

Physical and Musculoskeletal Symptoms

In their late 40s and early 50s, some men may experience depression, loss of libido, and erectile dysfunction. Other symptoms include irritability, loss of muscle mass and reduced ability to exercise, weight gain, lack of energy, difficulty sleeping, and poor concentration.

Sarcopenia — a decrease in muscle strength, muscle mass, and walking speed — is an important pathophysiological factor associated with frailty in older adults. Testosterone directly interacts with the androgen receptor expressed in myonuclei and satellite cells, and is also indirectly associated with muscle metabolism through various cytokines and molecules. Declining testosterone levels that accompany aging may also be a contributing factor to increased and redistributed fat mass and to decreased fat-free mass. This decline in muscle mass translates to decreased muscle strength, which in turn leads to functional limitations, including balance problems, higher fall risk, chronic conditions such as obstructive sleep apnea, depression, obesity, type 2 diabetes mellitus, and decreased quality of life.

Metabolic and Cardiovascular Involvement

Hypogonadism commonly manifests through disturbances of mood and cognition (including depression, fatigue, and mental decline), sexual dysfunction (diminished libido and impaired erectile capacity), disproportionate visceral adiposity, sarcopenia, osteopenia or osteoporosis, and anemia. These cumulative impairments markedly degrade quality of life.

Age-related testosterone decline significantly affects metabolism, cardiovascular health, bone density, muscle mass, and psychological well-being in aging men.

Diagnostic Complexity

Questionnaires such as the Aging Male Symptom (AMS) Score and ADAM are not recommended for the sole diagnosis of hypogonadism because of low specificity (30% and 39%, respectively). Serum testosterone levels vary significantly as a result of circadian and circannual rhythms, episodic secretion, and measurement variations. In the presence of symptoms, a serum sample for total testosterone determination should be obtained between 0700 and 1100 h.

Contributing and Associated Factors

Comorbid Chronic Disease

Risk factors for LOH may include chronic illnesses including diabetes mellitus, chronic obstructive lung disease, inflammatory arthritic disease, renal disease, HIV-related disease, obesity, metabolic syndrome, and hemochromatosis. Chronic comorbidities that have commonly been associated with testosterone deficiency include hypertension, cardiovascular disease, diabetes mellitus, obesity, metabolic syndrome, chronic kidney disease, and tobacco use.

Obesity and Adipose Aromatization

Adiposity plays a particularly important mechanistic role. Excess visceral adipose tissue elevates levels of the enzyme aromatase, which converts testosterone into estradiol, thereby reducing circulating androgens. Serum testosterone levels in obese males were lower than those in age-matched non-obese males, and lifestyle modification-induced weight reduction — combining aerobic exercise training and dietary modification — has been shown to increase serum testosterone levels in overweight and obese men.

Sleep Disruption

Sleep architecture is intimately linked to testosterone secretion, which peaks during sleep. Abrupt shifts of the sleep period induce a profound disruption in the daily cortisol rhythm, while sleep deprivation and/or reduced sleep quality result in a modest but functionally important activation of the HPA axis. HPA hyperactivity is clearly associated with metabolic, cognitive, and psychiatric disorders and could be involved in the well-documented associations between sleep disturbances and the risk of obesity, diabetes, and cognitive dysfunction.

Psychological Stress and the HPA Axis

Chronic psychological stress elevates cortisol through HPA axis activation. Cortisol and testosterone have a well-documented reciprocal relationship; elevated glucocorticoids suppress GnRH pulsatility and Leydig cell steroidogenesis. Ashwagandha researchers have proposed that stress-induced elevations in cortisol and prolactin reduce testosterone levels by directly lowering GnRH and LH concentrations. This mechanism highlights the interplay between the stress response and the HPG axis in age-related hormonal decline.

Physical Inactivity and Sedentary Behavior

Physical activity among older adults can reduce inflammation and oxidative stress through multiple mechanisms, including the reduced formation of reactive oxygen species (ROS) and the accelerated production of DNA-repairing enzymes and antioxidant proteins. However, there is conflicting evidence on the effect of physical activity on hormone levels, depending on the kind and duration of activity, which can increase the levels of DHEA and testosterone, but there is no clear consensus evidence.

Dietary Patterns

In recent decades, dietary compounds have demonstrated the ability to modulate testosterone levels in the body. Clinical studies have identified variations in testosterone levels among individuals with distinct dietary patterns.

Nutrients and Micronutrients: Traditional Use and Scientific Evidence

Zinc

Traditional/Historical Context: Zinc-rich foods — including oysters, red meat, seeds, and legumes — have long been associated in various folk traditions with male virility and reproductive capacity, though this association predates any formal understanding of endocrinology.

Scientific Evidence: Zinc deficiency is prevalent throughout the world, including the USA. Severe and moderate deficiency of zinc is associated with hypogonadism in men. The pivotal study by Prasad et al. (1996), published in the journal Nutrition, studied the relationship between cellular zinc concentrations and serum testosterone cross-sectionally in 40 normal men aged 20 to 80 years. In four normal young men, marginal zinc deficiency induced by dietary restriction was induced experimentally. The study also measured serum testosterone in nine elderly men (mean age 64 ± 9 years) who were marginally zinc-deficient before and after 3–6 months of supplementation with oral zinc gluconate. Dietary zinc restriction caused testosterone levels to fall substantially in young men; the same study showed that zinc supplementation in elderly men with marginal deficiency raised average testosterone from 8.3 nmol/L to 16.0 nmol/L over 24 weeks. The study was small, and more research would need to confirm how much testosterone levels are impacted by zinc levels.

Albeit medicinal doses of zinc may increase total testosterone and improve sperm count, the current body of evidence does not suggest broad recommendations regarding the use of zinc for all types of hypogonadism. Micronutrient optimization, particularly zinc and vitamin D, proves essential for maintaining steroidogenic enzyme function.

Evidence strength: Zinc's role in testosterone maintenance is best established in men who are actually zinc-deficient. Evidence for benefit in zinc-replete men is weak. The primary human data originates from small, older studies; broader RCT replication in aging men specifically is lacking.

Vitamin D

Traditional/Historical Context: Vitamin D is not an herb or traditional supplement per se, but its importance was historically linked to sunlight exposure in pre-industrial lifestyles, when outdoor labor ensured adequate synthesis. Reduced sunlight exposure with aging and indoor lifestyles is a recognized contributor to insufficiency in older populations.

Scientific Evidence: Observational studies suggest an association between higher testosterone and serum vitamin D concentrations. Conversely, most randomized clinical trials that investigated the effect of vitamin D administration on testosterone levels have failed to detect any significant effect.

An early RCT by Pilz et al. (2011), published in Hormone and Metabolic Research, found that healthy overweight men undergoing a weight reduction program who participated in a randomized controlled trial were analyzed for testosterone levels. The study included 165 participants; those receiving 3,332 IU vitamin D daily for 1 year showed a suggestion of increased testosterone compared to placebo. However, a subsequent, rigorously designed RCT (the Graz Vitamin D and TT-RCT) found no significant vitamin D effect on androgen levels including total testosterone, free testosterone, and FAI in a cohort of middle-aged healthy men with low baseline serum testosterone levels.

These findings suggest that vitamin D treatment has no clinically relevant effect on testosterone levels in men. Future studies should only be performed in truly vitamin D-deficient subjects with levels below 25 or 30 nmol/L and in men with low testosterone levels, to evaluate any vitamin D effects on testosterone.

Mechanistically, vitamin D exhibits essential roles in the testis and prostate; otherwise, there is no apparent evidence to support the use of vitamin D supplementation to increase testosterone in vitamin D-replete men.

Evidence strength: Mixed. Observational data shows correlations; interventional RCT data largely does not support a causal effect on testosterone except potentially in men with frank vitamin D deficiency (<25–30 nmol/L). Overall evidence is insufficient to support supplementation as a testosterone-raising strategy in the absence of confirmed deficiency.

Herbs and Botanical Ingredients: Traditional Use and Scientific Evidence

Ashwagandha (Withania somnifera)

Traditional Use: In Ayurveda, ashwagandha is a popular plant for promoting youthful energy, longevity, and overall well-being. It is classified as a rasayana (rejuvenating tonic) and an adaptogen in Ayurvedic medicine, used traditionally in India and parts of the Middle East to combat fatigue, stress, and sexual debility. The root is the primary part used, typically as a powdered preparation mixed with milk or ghee. Withania somnifera (L.) Dunal, also known as "Indian Ginseng," "Winter Cherry," or "Ashgandh," is widely used and is distributed in India, Sri Lanka, the Middle East, China, Africa, and warm areas of Europe and Australia.

Scientific Evidence: A systematic review identified ashwagandha as one of the most effective herbal extracts for increasing testosterone concentrations in men. The proposed primary mechanism involves HPA axis modulation: according to detailed analysis of human and animal studies, ashwagandha prevents the reduction of testosterone levels induced by stress by moderating cortisol and prolactin, leading directly to increased GnRH and LH concentrations.

A pilot RCT on oligospermic males, published in Evidence-Based Complementary and Alternative Medicine, used a full-spectrum root extract at 675 mg/d in three doses for 90 days; results showed a 167% increase in sperm count, a 53% increase in semen volume, and a 57% increase in sperm motility on day 90 from baseline.

A 2022 RCT published in Health Science Reports enrolled 50 adult male participants with lower sexual desire in an 8-week, randomized, double-blind, placebo-controlled study. Participants receiving 300 mg of ashwagandha root extract twice daily showed statistically significant increases in total DISF-M sexual functioning scores (mean difference −9.8, p < 0.0001) and in serum testosterone levels (p < 0.0001) compared to placebo.

A separate extract (KSM-66) study in the systematic review by Smith et al. found that 46 infertile men supplementing with 675 mg/d of KSM-66® experienced a significant 17.3% increase in testosterone concentrations after 90 days compared with a 3.8% increase in the placebo group (P < 0.01). However, a study using a different extract (Shoden®) found that in 19 male participants (mean age 41 years), daily intake of 240 mg of ashwagandha extract was associated with no statistically significant difference in testosterone concentrations compared with the placebo group after 60 days of treatment.

These findings suggest ashwagandha's stress-relieving effects may occur via its moderating effect on the hypothalamus-pituitary-adrenal axis. However, further investigation utilizing larger sample sizes, diverse clinical and cultural populations, and varying treatment dosages is needed to substantiate these findings.

Evidence strength: Moderate, but heterogeneous. Several small-to-medium RCTs in specific populations (infertile or stressed men, men with low libido) show positive effects on testosterone and sexual function. Evidence is limited by varying extract types, small sample sizes, and short durations. Effect size is inconsistent across extracts. More robust, large-scale RCTs in aging men specifically are needed.

Eurycoma longifolia (Tongkat Ali / Long Jack)

Traditional Use: The majority of human supplementation trials have been conducted on specific hot-water-extracts of Eurycoma longifolia, which is the traditional Malaysian preparation produced using a patented extraction process to isolate and concentrate the bioactive compounds. Tongkat Ali has been used for centuries across traditional medicine systems of Southeast Asia — particularly Malaysia, Indonesia, and Thailand — as a general tonic and aphrodisiac. The root decoction was traditionally consumed for treating lethargy, low libido, and general fatigue.

Scientific Evidence: A 2022 systematic review and meta-analysis (PMC9415500) searched PubMed, Scopus, Web of Science, Cochrane, Ovid/Embase, and Google Scholar, identifying a total of nine studies in the systematic review; five RCTs were included in the meta-analysis. A significant improvement in total testosterone levels after Eurycoma longifolia treatment was mostly reported in both healthy volunteers and hypogonadal men.

A 6-month, randomized, double-blind, placebo-controlled, four-arm clinical trial in androgen-deficient aging males found that Eurycoma longifolia increased testosterone levels in almost 50% of study participants and that testosterone level was correlated with function in domains of men's sexual health. The proposed mechanisms include stimulation of LH release by the pituitary leading to greater testosterone production by Leydig cells; eurypeptides enhancing steroidogenic enzyme activity (CYP450c17) to increase DHEA and testosterone production; and quassinoids (eurycomanone) acting by inhibiting aromatase and diminishing conversion of testosterone to estradiol.

Tongkat ali, used for centuries in traditional medicine systems of Southeast Asia for treating lethargy, low libido, depression, and fatigue, appears to have significant potential for restoring hormone balance (cortisol/testosterone ratio) and improving psychological mood state in humans exposed to various modern stressors, including aging, dieting, and exercise stress.

Evidence strength: Moderate. The systematic review and meta-analysis supports a positive effect on total testosterone. However, many studies used patented extracts, sample sizes are small, and methodological quality is variable. Most studies are of short duration. Moderate evidence supports the use of long jack (Eurycoma longifolia) to increase total testosterone relative to less-studied botanicals, but replication in larger, independent RCTs is needed.

Fenugreek (Trigonella foenum-graecum)

Traditional Use: Fenugreek has a long history of use in Ayurvedic and Unani medicine, as well as in traditional North African and Middle Eastern traditions, where seeds are used as a food spice, a galactagogue in women, and a general tonic in men. Traditional preparations include seed powders, decoctions, and seed soaks.

Scientific Evidence: A 2024 double-blind RCT published in PLOS ONE enrolled 95 men aged 40–80 years in a 12-week intervention taking placebo, 600 mg, 1200 mg, or 1800 mg of fenugreek extract (Trigozim®) daily. Samples were collected at weeks 0, 2, 6, and 12, and participants also answered questionnaires on libido. Results showed that plasma total testosterone and free testosterone index increased after any dose of Trigozim® versus baseline (13.0% and 16.3% respectively), but did not reach statistical significance versus placebo in all measures. Saliva testosterone concentration increased after any dose versus baseline (31.1%) and versus placebo (37.2%, p = 0.042).

Moderate evidence supports the use of fenugreek to increase total testosterone levels, based on published RCTs. The proposed mechanism involves inhibition of 5-alpha-reductase and aromatase enzymes by furostanol saponins (particularly protodioscin), which would reduce testosterone conversion to dihydrotestosterone (DHT) and estradiol respectively, thereby raising circulating free testosterone.

Evidence strength: Moderate-preliminary. Several small-to-medium RCTs show some positive signals on testosterone measures, but effect sizes are modest, studies differ in extracts and populations, and the clinical significance of observed changes remains to be established in larger trials in aging men.

Tribulus terrestris

Traditional Use: Tribulus terrestris has been used in Ayurvedic medicine under the name gokshura as a rejuvenating tonic and aphrodisiac, and in traditional Chinese medicine for conditions related to kidney and liver "deficiency." It was also used in traditional Bulgarian folk medicine. Aerial parts and fruits were used in preparations.

Scientific Evidence: Despite widespread commercial use, the evidence for a testosterone-raising effect in humans is largely negative. A systematic review examining all Tribulus studies found that the evidence indicated it is ineffective at increasing testosterone concentrations in humans. The use of tribulus was not scientifically supported to improve serum testosterone levels in men based on available controlled trial evidence.

Some evidence suggests it may have effects on sexual function independent of testosterone. A prospective, randomized, double-blind, placebo-controlled clinical trial published in Journal of Urology enrolled 172 patients and found improvements in IIEF (erectile function) scores compared to placebo.

Evidence strength: Weak to negative for testosterone-raising effects in humans. Some preliminary evidence exists for effects on subjective sexual function outcomes, but this does not appear to be hormonally mediated. The body of evidence does not support Tribulus as an androgen-modulating agent in men.

Mucuna pruriens (Velvet Bean)

Traditional Use: Mucuna pruriens, known in Ayurveda as Kapikachhu, has been used for centuries as a rejuvenating aphrodisiac and to support male fertility and nervous system function. Seeds are the primary part used, traditionally processed to reduce irritant compounds.

Scientific Evidence: Moderate evidence supports the use of mucuna (Mucuna pruriens) to increase total testosterone levels in men. The primary proposed mechanism involves the seed's high content of L-DOPA (levodopa), a dopamine precursor. Dopamine stimulates GnRH and LH secretion, thereby supporting testosterone production. Additionally, mucuna has been shown to reduce prolactin levels, which — when elevated — suppresses testosterone production. Small RCTs in infertile and subfertile men have shown improvements in testosterone levels and sperm parameters, though evidence in the specific population of aging men with LOH is limited.

Evidence strength: Moderate but limited to specific populations (infertile men). Data on aging men with LOH specifically is sparse. Larger, well-designed trials are needed.

Panax Ginseng

Traditional Use: Panax ginseng (Korean or Asian ginseng) has been used in traditional Chinese and Korean medicine for over 2,000 years as a tonic for energy, vitality, and male sexual function. The root is the part used, prepared as decoctions, tinctures, or standardized extracts (typically standardized to ginsenoside content).

Scientific Evidence: Panax ginseng has been reported to enhance libido and sperm quality through hormonal and antioxidant mechanisms. Clinical trials have focused more on erectile function outcomes than on testosterone levels per se. The ginsenosides are thought to influence nitric oxide synthesis in erectile tissue and modulate HPA axis activity. Evidence for direct testosterone elevation in aging men is limited; effects on sexual function symptoms are more consistent in the literature.

Evidence strength: Moderate for erectile function outcomes; weak for direct androgenic effects on testosterone levels in aging men.

Dietary Factors Discussed in the Literature

Mediterranean Dietary Pattern

Mediterranean dietary patterns emphasizing whole foods, healthy fats, and antioxidant-rich plants support endogenous testosterone production while reducing systemic inflammation. The anti-inflammatory properties of Mediterranean dietary patterns may contribute to their beneficial effects on testosterone levels by reducing systemic inflammation that can interfere with steroidogenesis. Additionally, the high antioxidant content of these dietary patterns helps combat oxidative stress, which represents a significant contributor to age-related testosterone decline and testicular dysfunction.

These findings support the implementation of Mediterranean-style dietary approaches as components of comprehensive natural interventions for age-related testosterone decline.

Dietary Fat and Cholesterol

Testosterone is a steroid hormone synthesized from cholesterol. Extremely low-fat diets may therefore limit the substrate availability for steroidogenesis. Dietary fat quality — particularly the intake of monounsaturated fatty acids (MUFAs) from sources such as olive oil and avocados, and omega-3 polyunsaturated fatty acids from fatty fish — is considered more relevant than total fat intake. Only a select few nutritional agents have had promising results for supporting testosterone production, including zinc, vitamin D (in cases of hypovitaminosis D), l-arginine, mucuna, and ashwagandha, based on well-controlled randomized clinical trials. Except for l-arginine, these natural agents, as well as tribulus and omega-3 fatty acids, can improve some degree of sperm parameters in infertile men.

Protein Intake

While traditional Mediterranean patterns provide adequate protein for general health, optimization for aging men may require targeting higher protein intakes of 1.2–1.6 g/kg/day distributed across meals to overcome age-related anabolic resistance.

Ultra-Processed and Western Dietary Patterns

Dietary compounds have demonstrated the ability to modulate testosterone levels in the body, and clinical studies have identified variations in testosterone levels among individuals with distinct dietary patterns. Western dietary patterns, characterized by high consumption of ultra-processed foods, refined carbohydrates, and trans-fatty acids, are associated with obesity, insulin resistance, and systemic inflammation — all of which are independently associated with suppressed testosterone in aging men.

Lifestyle Factors Discussed in Authoritative Sources

Physical Activity and Exercise

Serum testosterone levels in obese males were lower than those in age-matched non-obese males. Lifestyle modification-induced weight reduction, through a combination of aerobic exercise training and dietary modification, increases serum testosterone levels in overweight and obese men.

Significant correlations between testosterone and frailty in men have been confirmed by numerous cross-sectional studies. Many randomized controlled studies have also supported the beneficial effect of testosterone replacement therapy on muscle volume and strength among men with low to normal testosterone levels. In the world's aging society, maintaining testosterone levels can be a tool for preventing the onset of sarcopenia in older adult men.

The effect of exercise type on testosterone is nuanced. Resistance training in particular has been associated with acute testosterone elevations, and regular aerobic exercise supports weight maintenance and metabolic health, which indirectly supports the HPG axis. There is conflicting evidence on the effect of physical activity on hormone levels, depending on the kind and duration of activity, and there is no clear consensus evidence of a sustained testosterone-raising effect.

Weight Management

Obesity-driven aromatization is one of the most potent modifiable drivers of testosterone deficiency in aging men. Excess adipose tissue increases local aromatase activity, converting testosterone to estradiol and reducing circulating androgens. Adequate sleep, exercise, and weight loss in patients with obesity are imperative before implementing nutraceutical agents for hormonal support.

Sleep Quality

Testosterone secretion is strongly tied to sleep architecture, with the largest pulsatile releases occurring during slow-wave (deep) sleep and during REM periods. Sleep deprivation and/or reduced sleep quality result in a modest but functionally important activation of the HPA axis. HPA hyperactivity is clearly associated with metabolic, cognitive, and psychiatric disorders and could be involved in well-documented associations between sleep disturbances and the risk of obesity, diabetes, and cognitive dysfunction. Research published in JAMA (Leproult et al., 2011) demonstrated that even one week of sleep restriction significantly reduced testosterone levels in young healthy men.

Stress Management

The inverse relationship between cortisol and testosterone is well established. Chronic stress sustains cortisol elevation, which suppresses GnRH pulsatility and reduces Leydig cell responsiveness to LH stimulation. Tongkat ali supplementation trials suggest that it may be an effective approach to moderating the detrimental effects of chronic stress from daily stressors, dieting for weight loss, sleep deprivation, and intense exercise training on the cortisol/testosterone ratio.

Alcohol and Substance Use

Chronic heavy alcohol consumption is associated with direct Leydig cell toxicity, elevated aromatase activity in the liver, and suppression of LH secretion — all of which can exacerbate age-related testosterone decline. The effects of non-pharmacologic interventions on testosterone levels are modest and hence do not directly translate into clinical benefits in isolation; comprehensive lifestyle modification addressing multiple factors simultaneously is consistently recommended in the research literature.

Evidence Summary

• Well-established physiology: The HPG axis disruption, Leydig cell decline, rising SHBG, and associations with obesity, metabolic syndrome, and sleep disruption are firmly supported in peer-reviewed literature.
• Nutrients with conditional evidence: Zinc (in deficiency states) and vitamin D (in frank deficiency) show conditional evidence for supporting testosterone; neither is supported for supplementation in replete individuals.
• Herbs with moderate evidence: Ashwagandha, Eurycoma longifolia, fenugreek, and mucuna pruriens have the highest quality evidence base among botanicals, with multiple RCTs showing positive — but modest and heterogeneous — effects, primarily in men with suboptimal testosterone or fertility issues. Studies are often small, short-term, and use proprietary extracts.
• Herbs with weak or negative evidence: Tribulus terrestris has consistently failed to demonstrate testosterone-raising effects in controlled human trials despite widespread traditional and commercial use.
• Lifestyle factors: Weight loss, resistance and aerobic exercise, improved sleep hygiene, and stress reduction are supported by convergent lines of evidence as the most potent modifiable influences on testosterone in aging men.

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