A reported fall in average testosterone is not a diagnosis. Understand symptoms, repeat testing, treatment evidence and the fertility implications of TRT.
On November 1, 2026, EL PAÍS reported that a study presented at a European Society of Human Reproduction and Embryology meeting found a 54% decline in average testosterone between 1972 and 2019.
This article is for informational purposes only and is not medical advice. Individual testing and treatment decisions require assessment by a qualified clinician.
According to EL PAÍS, the study included about 118,000 men of reproductive age across five countries. The sample covered the United States, Brazil and Israel alongside Finland and Denmark.
The finding concerns average testosterone in the populations studied. Clinical assessment asks a different question: does a particular man have symptoms together with confirmed evidence of testosterone deficiency? Those questions require different kinds of evidence.
The European Association of Urology, or EAU, defines male hypogonadism as a clinical syndrome involving symptoms alongside biochemical evidence of testosterone deficiency. Physical signs may also be present. A change in a population average is therefore not the clinical definition of hypogonadism.
This distinction matters because a headline and a laboratory report serve different purposes. A headline may describe a broad pattern. A clinician must interpret an individual's symptoms and measurements within that person's health context.
The EAU also describes a separate pattern involving age. It cites the European Male Ageing Study's estimates of average annual decreases of 0.4% in total testosterone and 1.3% in free testosterone. The guideline characterizes the decline in healthy aging men as small and gradual.
These findings make separating broad hormone trends from a clinical diagnosis a useful starting point. The clinical task is not to decide whether someone fits a cultural story about testosterone. It is to determine whether there is a hormone deficiency that explains relevant clinical findings.
The EAU identifies sexual symptoms as the most specific symptoms associated with late-onset hypogonadism. These include reduced libido and erectile dysfunction. Fewer spontaneous or morning erections are also among the more specific features.
The guideline also lists fatigue, low mood and concentration difficulties. Their presence belongs in a clinical assessment, but they do not carry the same diagnostic weight as the more specific sexual symptoms. A symptom list is a starting point for discussion rather than a way to establish the cause.
EL PAÍS describes several possible consequences of progressing hypogonadism. These include infertility and erectile dysfunction. The article also identifies loss of body hair, decreased muscle mass, breast-tissue growth and bone loss.
Those effects explain why genuine deficiency deserves attention. Testosterone is not relevant only to sexual interest or appearance. The Association of American Medical Colleges, or AAMC, describes roles in reproduction and sexual function as well as muscle and bone maintenance.
The useful distinction is between taking symptoms seriously and assigning them a cause. The EAU's approach connects the symptom history with biochemical evidence rather than treating either as sufficient by itself.
The EAU recommends measuring testosterone with a reliable assay in the fasting morning. Its usual testing window is between 7 a.m. and 10 a.m. A low morning result should be confirmed on at least two occasions as part of the diagnostic assessment.
The guideline identifies 12 nmol/L (3.5 ng/mL) as a reliable threshold for assessing late-onset hypogonadism in the context of symptoms. That context is part of the recommendation. The threshold is not a stand-alone instruction to begin treatment.
This is where putting an isolated result in context becomes important. A flagged value provides information for assessment. It does not replace the symptom history or the confirmation required by the guideline.
The EAU also recommends checking for diseases, medicines and substances that could affect testosterone production or action. That expands the question beyond whether a laboratory number is below a threshold. It asks what may be contributing to the result and how it relates to the patient's health.
For someone preparing for a clinical conversation, the relevant information includes when the sample was taken and whether it was fasting. It also includes whether a low result has been repeated. Understanding why clinicians confirm low measurements helps distinguish a screening result from a completed assessment.
These are features of clinical evaluation rather than a home diagnostic protocol. Personal interpretation remains the clinician's responsibility.
Establishing a diagnosis and deciding on treatment are related but separate tasks. The EAU discusses potential treatment benefits in symptomatic men with low testosterone. It reports that the greatest benefits in the evidence it reviews were seen in men with more severe deficiency.
The AAMC's summary of the Testosterone Trials shows why treatment outcomes need to be considered individually. Among men aged 65 and older with hypogonadism, the trials found improvements in sexual function and bone density. Hemoglobin also improved.
However, the same summary reports little or no improvement in energy or cognitive function. That is a more specific picture than the idea that testosterone treatment improves every symptom associated with low testosterone. The outcome being discussed matters as much as the hormone measurement.
Fertility adds another important consideration. The EAU says testosterone therapy suppresses gonadotropins and sperm production. It considers the therapy contraindicated for men who desire fertility.
That warning is especially relevant when infertility appears in a list of possible consequences of hypogonadism. Testosterone's role in reproduction does not mean that testosterone therapy preserves sperm production. Fertility goals therefore belong in the clinical discussion before treatment decisions are made.
The decision is not simply whether to raise a number. It requires weighing the diagnosis and the intended benefits alongside the patient's circumstances and reproductive goals.
The population estimate has methodological limits. EL PAÍS notes that some analysts have questioned the methods behind striking estimates of testosterone decline. The reported percentage should therefore remain attributed to that account rather than presented as a settled worldwide measurement.
The sample also concerns men of reproductive age in the countries studied. It does not establish that every man experienced the same change. A group average cannot assign an individual's hormone level or clinical status.
The age-related findings cited by the EAU answer a different question from the historical population estimate. An average annual change associated with age is not interchangeable with a change reported across calendar years. Neither supplies a personal forecast of future testosterone levels.
The treatment evidence has a separate boundary. The AAMC's Testosterone Trials summary concerns men aged 65 and older with hypogonadism. Its findings should not be automatically transferred to younger men or to men without confirmed deficiency.
Testing guidance also has a scheduling qualification. The EAU notes that a 10 a.m. cutoff may not fit night-shift workers because sleep patterns influence the daily rhythm. That is a reason for clinicians to account for sleep schedules when interpreting test timing.
Finally, the population report does not establish what caused the trend or support conclusions about social behavior. EL PAÍS explicitly rejects the leap from lower averages to claims that men are becoming feminized. Cultural labels do not resolve questions about hormone deficiency.
The reported population decline does not justify an immediate change in medical practice. The appropriate clinical framework remains the EAU's assessment of compatible symptoms alongside reliable and repeated testosterone measurements. Treatment decisions follow that assessment rather than a population headline.
For men concerned about symptoms or a laboratory result, a qualified clinician is the appropriate person to connect those pieces. Useful questions for that discussion include:
These questions focus attention on the evidence needed for an individual decision. They also leave room to investigate symptoms without assuming that testosterone is their explanation.
The bottom line is neither to dismiss genuine deficiency nor to turn a broad trend into a personal diagnosis. The report adds a population-level question. It does not replace the clinical standards used to decide whether an individual has hypogonadism or would benefit from treatment.
A falling population average is not a personal laboratory assessment, a distinction reflected in Testostra's separation of research education from medical advice. Its coverage of total testosterone, free testosterone and SHBG gives men clearer language for discussing related biomarkers with a qualified clinician rather than interpreting a headline as a diagnosis.
Testostra follows testosterone research, clinical guidance and emerging evidence without turning general information into personal treatment advice.
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