Low testosterone: real causes and how to reverse them

Most men who receive a low testosterone diagnosis do not have a problem with their testes. In the majority of cases, they have excess visceral fat, poor sleep quality, or are training too hard on too little fuel. Dr. Jordan Feigenbaum and Dr. Austin Baraki of the Barbell Medicine podcast break down the real mechanisms behind declining testosterone and the modifiable levers to bring it back, in episode 3 of their series on their book Signal.

Body composition: the single biggest driver

A man with obesity is roughly nine times more likely to be testosterone deficient than a man at a healthy weight. The data are clear:

• An overweight man (BMI 25 to 30) has on average 66 ng/dL less testosterone.
• A man with obesity (BMI over 30) has on average 147 ng/dL less.
• A 10% reduction in body weight produces an average testosterone increase of 84 ng/dL.
• Metabolic bariatric surgery, with weight loss of 20 to 30%, produces average increases on the order of 250 ng/dL.

This is not a story about aging or generational decline. It is a direct consequence of body composition.

The aromatase-leptin loop: the invisible trap

Excess visceral fat suppresses the hypothalamic-pituitary-gonadal (HPG) axis through two simultaneous pathways:

Peripheral pathway (aromatase): Visceral fat is rich in the enzyme aromatase, which converts testosterone into estradiol before it can do its job. More visceral fat means more aromatase and more conversion. The resulting estradiol then inhibits the HPG axis more potently than testosterone itself does. The outcome is a self-reinforcing cycle: more fat drives more aromatase, which lowers testosterone, which in turn promotes more visceral fat storage.

Central pathway (leptin): Fat tissue also produces leptin. Chronically elevated leptin levels down-regulate kisspeptin neurons in the hypothalamus, reducing GnRH production and, in cascade, LH, FSH, and ultimately testosterone. This is not leptin resistance in the appetite sense. The hypothalamus detects elevated leptin correctly, but its response is hormonal suppression, not reduced hunger.

Sleep: the second major driver that almost nobody asks about

Testosterone production depends on sleep. It is tied to REM cycles. The evidence is clear:

• One week of sleep restricted to five hours in healthy young men reduced testosterone by 15% on average.
• In military recruits with similar sleep restriction, the drop reached 50%.
• Morning testosterone levels in older men are independently predicted by measured sleep duration, even after controlling for age and body composition.

The key to drawing blood at the right point in the circadian cycle is not simply drawing it in the morning, but within the first one to two hours after waking, regardless of what time that is. This is especially relevant for night shift workers, whose testosterone peak may occur in the afternoon.

Obstructive sleep apnea: the most underdiagnosed contributor

Obstructive sleep apnea is extremely common in middle-aged men, particularly those with obesity, and it is massively underdiagnosed. A man can sleep eight hours and wake up exhausted because his brain pulls him toward consciousness 30 to 100 times per hour to reopen his airway.

Treating apnea with CPAP or autoPAP improves daytime sleepiness and sexual function but does not reliably move the testosterone number on its own, because most of the effect on testosterone comes from the excess visceral fat that drives both conditions. Even so, prescribing TRT to a man with untreated sleep apnea is contraindicated, as exogenous testosterone can relax the soft tissue of the airway and worsen apnea.

The opposite extreme: low energy availability and the overtrained athlete

Not only excess fat suppresses testosterone. The opposite extreme produces the same result through the opposite mechanism. When energy availability drops below roughly 30 calories per kilogram of lean body mass per day, the hypothalamus reads scarcity and shuts down non-essential systems, including reproduction.

This affects:

• Natural bodybuilders in extreme competition prep.
• Endurance athletes with high training volumes and insufficient caloric intake.
• Men who train hard, sleep poorly, and eat just enough to maintain weight.

In these cases, a low-normal testosterone level is an adaptation, not a deficiency. The fix is more food and/or adjusting training load, not exogenous testosterone. Prescribing TRT in this scenario may function more like a performance-enhancing drug riding on top of an artificially suppressed baseline.

GLP-1s and testosterone: what changes as weight drops

GLP-1 receptor agonists such as semaglutide and tirzepatide raise testosterone by roughly 20 to 30% in men with obesity, proportional to weight loss. For a man already on TRT who starts a GLP-1, the prescribing physician should monitor hormone levels: as visceral fat decreases, aromatase activity drops and SHBG tends to rise, meaning the effective dose of prescribed testosterone may need to be adjusted downward.

A clinical trial with over 1,000 men (the T4DM trial) demonstrated that adding testosterone on top of an effective lifestyle program produces no meaningful additional improvement in quality of life. The benefits track with weight loss, not hormone levels.

Conclusion

Low testosterone is not a sentence, nor an inevitable sign of aging. In most adult men, low levels are a direct downstream consequence of modifiable factors: body composition, sleep quality, and energy availability. Understanding these mechanisms before seeking a TRT prescription can be the difference between treating the cause and simply masking the symptom.