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Controversies

Why Experts Don't Always Agree

Patients are usually given one answer. In reality the major professional societies disagree with each other on several of the most consequential questions in this field, and those disagreements change who gets treated.

This page is not a soft "reasonable people differ." It names who disagrees with whom, and why it matters to you.

1. What counts as low

There is no agreed threshold. The spread is wide enough that the same man is deficient in one country and normal in another.

SourceThreshold for total testosterone
VA/DoD (January 2026)264 ng/dL (9.2 nmol/L)
Endocrine Society (July 2026 statement)"near 300 ng/dL" (10.4 nmol/L)
AUA300 ng/dL (10.4 nmol/L)
EAUBelow 12 nmol/L (346 ng/dL) likely hypogonadal; below 8 nmol/L (231 ng/dL) confirmed; 8–12 a gray zone

A 2025 cross-society analysis documented thresholds spanning roughly231 to 346 ng/dL. A man at 320 ng/dL is normal under the AUA and the Endocrine Society, and potentially hypogonadal under the EAU. He has not changed. The threshold has.

This is not a failure of measurement. Testosterone is a continuous distribution with no natural break between "deficient" and "sufficient," so any threshold is a decision about how to trade off treating men who don't need it against missing men who do. Different societies weighed that differently, with different populations in mind.

More on testing and thresholds →

2. Does "functional hypogonadism" exist?

This is the sharpest disagreement in the field right now, and almost no patient is told it exists.

The Endocrine Society's July 2026 statement rejects the term outright: terms like "age-related," "late-onset" and "functional" hypogonadism "are hard to define operationally and blur the line between treatable disease and normal aging." Where obesity with a BMI above 27 is the only identified cause, its position is that weight loss is typically first-line therapy.

The European Academy of Andrology built a guideline around functional hypogonadism as a distinct, treatable entity.

The stakes are not semantic. If obesity-associated low testosterone is a disease, it warrants treatment. If it is a physiological consequence of obesity, it warrants treating the obesity. Millions of men sit in that category.

More on causes →

3. When free testosterone matters

Six positions, roughly:

  • AUA — does not routinely recommend it for initial diagnosis.
  • Endocrine Society — uses it for borderline total testosterone.
  • EAU and the British Society for Sexual Medicine — measure it routinely in the 8–12 nmol/L gray zone, especially when SHBG is abnormal.
  • Italian endocrine and andrology societies — formalize it within the diagnostic algorithm.
  • UK Society for Endocrinology — sceptical of the assays.
  • VA/DoD — recommends it when SHBG-altering conditions are present, and is explicit that direct immunoassay free testosterone has poor accuracy.

There is far more agreement about how to measure it than about when. On method the guidelines are unanimous: equilibrium dialysis or a calculated value, never a direct analog immunoassay.

4. Older men

The Endocrine Society insists the diagnostic criteria are the same at every age and pushes back on age-framed labels. VA/DoD frames the decline as largely physiologic, noting that around 63% of men over 70 remain within the reference interval, and relaxes PSA screening requirements for the oldest patients rather than changing the threshold.

Different rhetoric, similar practice — but it determines whether a 72-year-old is told he has a disease or that he is 72.

5. Estradiol monitoring and aromatase inhibitors

Routine aromatase inhibition alongside testosterone is common clinic practice. It has no guideline support and a real downside: estradiol is the dominant regulator of bone resorption in men, and aromatase inhibitor trials show adverse bone-turnover signals.

This is less a disagreement between societies than a gap between what guidelines say and what a substantial part of the market does.

6. hCG alongside testosterone

Widely used to preserve fertility, mechanistically well-founded — hCG maintains intratesticular testosterone when the pituitary is suppressed — and supported by small retrospective series rather than randomized trials. The most-cited study included 26 men. No RCT exists.

Reasonable practice on thin evidence is not the same as established practice, and the distinction should be made to patients rather than glossed.

More on fertility →

What to do with this

Two practical consequences.

A threshold is a prompt to think, not a trigger to prescribe. If your result sits near a cutoff, which cutoff your clinician uses is partly a matter of where they trained.

Confident answers should make you more suspicious, not less. Anyone who tells you the field has settled these questions is either not following it or is selling something.