A study of 659 young men linked testosterone and SHBG with metabolic risk markers. Learn the findings, limits and implications for interpreting results.
On 2026-10-16, Medscape reported on a study published online in the Journal of Endocrinological Investigation that linked testosterone-related biomarkers with metabolic risk measures in young men. The research was led by Davide Menafra of the University of Naples Federico II.
This article is for informational purposes only and is not medical advice. Personal testing and treatment decisions belong with a qualified clinician.
According to Medscape, the analysis included 659 men aged 18 to 35 who were recruited through an awareness campaign in Italy from 2013 to 2018. Their mean age was 22.7. The researchers assessed total testosterone, SHBG and calculated free testosterone alongside metabolic and cardiovascular risk markers.
The study was a retrospective observational cohort analysis with a cross-sectional design. It compared hormone measurements with body size, blood pressure and blood lipids within the participating group. The researchers also examined patterns across total-testosterone and SHBG tertiles, grouping participants according to their hormone measurements.
The central question was broader than whether a testosterone result fell below a particular threshold. It concerned how an androgenic profile appeared alongside other measurements relevant to metabolic health. That distinction is important when reading the specific findings below.
Medscape reported that higher total testosterone tracked with lower weight, BMI and waist circumference across tertiles. Higher levels also tracked with lower diastolic blood pressure and triglycerides. HDL cholesterol showed the opposite pattern, with higher total testosterone accompanying higher HDL cholesterol.
The pattern therefore involved several measurements rather than body weight alone. Differences appeared across body size and blood lipids as well as one blood-pressure measure. This is why the study is best understood as an examination of a broader biomarker profile.
Higher SHBG tracked with lower weight, BMI and waist circumference. It also tracked with lower triglycerides and lower systolic and diastolic blood pressure. As with total testosterone, higher SHBG accompanied higher HDL cholesterol.
The reported blood-pressure patterns were not identical for the two hormone markers. The total-testosterone tertile findings included diastolic pressure, while the SHBG findings included both systolic and diastolic pressure. Keeping those results separate avoids reducing the study to a single claim about testosterone.
In the adjusted analyses described by Medscape, total testosterone and SHBG were each associated with HDL cholesterol. SHBG was also associated with systolic and diastolic blood pressure.
These findings give SHBG a distinct place in the reported metabolic pattern. Total testosterone was not the only measurement associated with the risk markers under study. For interpretation, the useful detail is which marker was associated with which outcome rather than whether the overall hormone profile looked more or less favorable.
The researchers also compared participants using a total-testosterone threshold. Medscape reported that 111 men had total testosterone ≤12 nmol/L, while 548 were above that threshold.
The reported obesity prevalence differed between those groups:
A separate comparison examined mean total testosterone by weight category. Men with overweight or obesity had a mean total testosterone of 16.5 nmol/L. Men of normal weight had a mean of 18.3 nmol/L.
These comparisons describe the findings from different directions. One groups participants by testosterone and compares obesity prevalence. The other groups participants by weight category and compares average testosterone. Preserving that distinction helps readers avoid mixing a group average with a prevalence figure.
The young-men study fits within a wider clinical discussion about testosterone results and body weight. In its statement dated 2026-09-24, the Endocrine Society separately noted that men with obesity are more likely to have low total testosterone on blood tests.
That observation provides context for the study's emphasis on metabolic profiling. The findings belong within a discussion of overlapping hormonal and health concerns, rather than an interpretation of testosterone in isolation.
The useful connection is not simply that body size and hormone measurements appeared together. It is that the study examined blood pressure and blood lipids alongside them. Those measurements help define the broader clinical picture the authors considered relevant.
The cross-sectional design cannot establish whether the hormone pattern preceded or followed the metabolic differences. It also cannot prove that lower testosterone or SHBG caused obesity or less favorable blood-pressure and lipid measurements.
This boundary applies to the whole set of associations. A statistical relationship between measurements does not establish which one drove the other. The practical interpretation is to consider the findings together without assigning a causal direction.
Low testosterone in this study was based on a single morning measurement. There was no follow-up confirmation or thorough symptom evaluation. According to Medscape, the authors emphasized that sexual symptoms remain essential to diagnosing clinical hypogonadism.
The study's ≤12 nmol/L grouping should therefore remain a research comparison rather than a personal diagnostic rule. Neither a single result nor a change in weight or waist circumference establishes hypogonadism. Keeping symptoms separate from risk factors helps preserve the distinction between a laboratory finding and a clinical diagnosis.
The participants came from a community-based awareness campaign. According to the study report, they may not represent young men more broadly. The age range also limits how directly the findings can be applied to men outside that group.
The sample was too young to assess major adverse cardiovascular events. The findings concern risk markers rather than demonstrated differences in those events. That matters because a study of body measurements and blood tests answers a different question from a study tracking clinical cardiovascular outcomes.
This was not a trial of testosterone replacement therapy. It does not establish that TRT improves the metabolic pattern or prevents cardiovascular problems. Calculated free testosterone was assessed, but the total-testosterone and SHBG findings described here should not be treated as interchangeable with a separate cFT result.
Personal decisions about further assessment or treatment therefore belong with a qualified clinician reviewing the full clinical picture. The study supplies context for that review rather than a treatment pathway.
This study does not warrant an immediate change in medical practice. Its contribution is to support a contextual reading of testosterone-related biomarkers alongside metabolic measurements. It does not introduce a new diagnostic rule or treatment recommendation.
For a clinical conversation about a low testosterone result, the useful questions concern how the pieces fit together:
These are questions for interpretation rather than instructions to pursue a particular test or treatment. They keep attention on the problem the study actually examined: the relationship between a hormone profile and several other health measurements.
The authors' emphasis on metabolic profiling is clinically relevant because it resists treating testosterone as a standalone measure of health. At the same time, their emphasis on sexual symptoms preserves the distinction between a biomarker pattern and clinical hypogonadism.
The bottom line is a more complete reading of the evidence, not an immediate change in care. A clinician can place the hormone results within the person's symptoms and broader assessment. The study adds support for that contextual approach.
A population-level association leaves an individual hormone result needing clinical context. Testostra explains total testosterone, free testosterone and SHBG through evidence-led education that addresses confusion about related biomarkers and helps readers prepare clearer questions for a qualified clinician, without assigning a diagnosis or directing personal treatment.
Testostra follows testosterone research, clinical guidance and emerging evidence without turning general information into personal treatment advice.
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