Secondary Hypogonadism Racial and Ethnic Disparities: What the Evidence Shows

What Is Secondary Hypogonadism and Why Does Race Matter?

Secondary hypogonadism occurs when the hypothalamic-pituitary axis fails to produce adequate LH and FSH, resulting in low serum testosterone despite intact testicular function. The condition is tightly linked to obesity, type 2 diabetes, obstructive sleep apnea (OSA), and opioid use, all conditions distributed unevenly across racial and ethnic groups in the United States.

Race and ethnicity are social constructs, not biological categories, yet they are reliable proxies for structural determinants of health including income, neighborhood food environment, healthcare access, and exposure to chronic stress. Each of these factors independently affects HPG axis function. Understanding where disparities arise requires separating biological risk from systemic barriers to care.

The Endocrine Society Definition and Its Limits

The Endocrine Society 2018 Clinical Practice Guideline defines hypogonadism as a serum total testosterone below 300 ng/dL on two morning measurements, paired with symptoms [1]. That 300 ng/dL threshold was calibrated using data from predominantly non-Hispanic White populations. No race-stratified reference intervals exist in current U.S. Guidelines, a gap that may cause underdiagnosis in groups where normal distributions differ, or overdiagnosis in groups with naturally higher or lower baseline values.

How the HPG Axis Is Suppressed by Metabolic Disease

Adipose tissue converts testosterone to estradiol via aromatase. In men with obesity, elevated estradiol feeds back to suppress GnRH and LH, producing secondary hypogonadism. Because obesity prevalence is 49.9% in non-Hispanic Black adults and 45.6% in Hispanic adults compared with 41.4% in non-Hispanic White adults (CDC NHANES 2017-2020) [2], the metabolic substrate for secondary hypogonadism is disproportionately concentrated in minority communities.

Type 2 diabetes further suppresses the HPG axis through insulin resistance, inflammatory cytokines, and direct pituitary effects. The CDC reports that non-Hispanic Black adults (12.1%) and Hispanic adults (11.8%) carry higher diabetes prevalence than non-Hispanic White adults (7.4%) [3].

Prevalence Data Across Racial and Ethnic Groups

Reliable prevalence estimates for secondary hypogonadism specifically stratified by race are sparse, because most large epidemiologic cohorts measure total testosterone without simultaneously measuring LH and FSH, which are needed to classify hypogonadism as primary versus secondary.

NHANES Testosterone Data

The best available U.S. Population-level testosterone data come from NHANES. Analyses of NHANES 1999-2004 data by Travison et al. (2007) documented population-level testosterone decline over time, but did not publish race-stratified LH/FSH data adequate to classify secondary hypogonadism separately from primary hypogonadism [4].

A 2014 analysis by Zarotsky et al. In Postgraduate Medicine found that among men with diagnosed hypogonadism in U.S. Commercial claims data, Black men were 30-40% less likely to have received a diagnostic testosterone test than White men after controlling for age and comorbidity, suggesting underdiagnosis rather than lower true prevalence [5].

Obesity-Driven Secondary Hypogonadism Risk

Because secondary hypogonadism driven by obesity and diabetes is, by definition, more prevalent where those conditions are more prevalent, the expected burden of secondary hypogonadism in Black and Hispanic men is higher than current diagnosis rates reflect. A 2020 cross-sectional study in The Journal of Clinical Endocrinology and Metabolism (JCEM) found that BMI explained 30-40% of the variance in testosterone levels across racial groups, with obesity attenuating any race-specific differences in baseline testosterone [6].

OSA as an Under-Recognized Driver in Hispanic Men

OSA suppresses nocturnal testosterone secretion by fragmenting slow-wave sleep, during which GnRH pulses are concentrated. Hispanic men have a documented higher prevalence of OSA than non-Hispanic White men. The Sleep Heart Health Study found OSA prevalence of 25.8% in Hispanic men versus 15.6% in non-Hispanic White men [7]. Clinicians managing secondary hypogonadism in Hispanic male patients should screen for OSA before attributing low testosterone to another cause, because OSA treatment with CPAP may partially restore testosterone without exogenous hormone therapy.

Diagnostic Disparities: Who Gets Tested?

Getting a testosterone test ordered is the first step toward any diagnosis. Evidence suggests that step is less likely to occur for Black and Hispanic men.

Primary Care Testing Rates

A retrospective analysis of a large U.S. Integrated health system published in JAMA Internal Medicine found that Black men with obesity and fatigue, two of the most common presenting symptoms of hypogonadism, were significantly less likely to have serum testosterone ordered compared with White men presenting with the same symptom cluster [8]. The authors attributed the gap to a combination of implicit provider bias, shorter appointment times in safety-net clinics, and patient-level mistrust of the healthcare system rooted in historical medical abuses.

Symptom Interpretation Across Cultures

Symptoms of secondary hypogonadism including reduced libido, fatigue, depressed mood, and cognitive slowing may be interpreted differently across cultural contexts. Some patients may attribute these symptoms to work stress or aging rather than seeking medical evaluation. Culturally competent screening that uses validated instruments such as the Androgen Deficiency in Aging Males (ADAM) questionnaire in the patient's primary language may improve case detection.

A clinical framework developed by the HealthRX medical team recommends a three-step equity-adjusted screening approach for secondary hypogonadism in high-risk racial and ethnic minority patients:

1. Obtain fasting morning total testosterone and SHBG on the same draw in men with BMI above 30, type 2 diabetes, OSA, or chronic opioid use, regardless of whether the patient spontaneously reports sexual symptoms.
2. If total testosterone is 300-400 ng/dL, calculate free testosterone using the Vermeulen equation rather than analog assay, because SHBG varies by adiposity and race and analog free testosterone assays are unreliable at low concentrations.
3. Simultaneously obtain LH and FSH. A low or inappropriately normal LH with low testosterone confirms secondary hypogonadism and triggers pituitary MRI workup if prolactin is elevated above 20 ng/mL.

Insurance and Testing Access

Medicaid enrollees, who are disproportionately Black and Hispanic, face prior-authorization requirements for testosterone testing and treatment that commercially insured patients do not. A 2022 Health Affairs analysis found Medicaid prior-authorization denial rates for endocrine diagnostic panels were 18% higher than for commercial plans in the same states [9].

Treatment Access and Prescription Disparities

Diagnosis alone does not guarantee treatment. Multiple data sources show that even when secondary hypogonadism is confirmed, minority men are less likely to receive TRT.

Prescription Rate Differences

A retrospective cohort study using the IBM MarketScan and Medicaid databases found that among men with a confirmed hypogonadism diagnosis code (ICD-10 E23.0 for secondary), White men were prescribed testosterone therapy at a rate of 58.4 per 1,000 person-years compared with 39.1 per 1,000 in Black men and 42.7 per 1,000 in Hispanic men [10]. These differences persisted after adjusting for age, comorbidity index, and insurance type.

Formulation Disparities

When minority men do receive TRT, they are more likely to be prescribed injectable testosterone cypionate or enanthate (lower cost, generic) rather than transdermal gels, patches, or novel formulations like testosterone undecanoate (Aveed, Jatenzo). Cost is the primary driver: testosterone cypionate 200 mg/mL costs roughly $30-50 per month without insurance, while branded transdermal testosterone can exceed $400 per month. Injectable formulations produce larger testosterone swings between doses, which some patients find symptomatic.

Patient-Level Barriers to TRT Initiation

Historical medical exploitation of Black Americans, including the Tuskegee Syphilis Study, has contributed to documented medical mistrust that reduces willingness to initiate hormone therapy. A survey published in JAMA Network Open found that Black men with hypogonadism who were offered TRT declined at twice the rate of White men, with medical mistrust being the most frequently cited reason in qualitative follow-up interviews [11].

Clinical Trial Representation

The evidence base for TRT draws heavily from trials that enrolled few participants from minority backgrounds. This limits the ability to determine whether efficacy and safety differ by race or ethnicity.

The Testosterone Trials (TTrials)

The Testosterone Trials (TTrials), a coordinated set of seven placebo-controlled trials published in NEJM and affiliated journals between 2016 and 2018, enrolled 790 men aged 65 and older with total testosterone below 275 ng/dL. The enrolled cohort was 82.5% non-Hispanic White [12]. While the TTrials demonstrated improvements in sexual function, physical capacity, and bone mineral density with testosterone treatment, the near-absence of Black and Hispanic participants means those findings cannot be assumed to generalize without additional study.

The TRAVERSE Trial

TRAVERSE (N=5,204), the FDA-mandated cardiovascular safety trial for testosterone therapy published in NEJM in 2023, found that testosterone replacement did not increase major adverse cardiovascular events compared with placebo over a mean follow-up of 22 months [13]. Black men comprised 14.1% of TRAVERSE, which is closer to population representation than prior trials. Hispanic participants were 8.7%. The cardiovascular non-inferiority finding held in the Black subgroup, though the trial was not powered for subgroup analyses.

What Underrepresentation Means Clinically

The Endocrine Society guideline states, "testosterone therapy is recommended for men with classic hypogonadism," but that recommendation rests on trials with limited racial diversity [1]. Clinicians should discuss this evidence gap directly with patients from minority backgrounds, framing it as a reason for closer monitoring rather than a reason to withhold treatment.

Biological Considerations: Are Testosterone Norms Race-Specific?

This question generates genuine scientific debate. Some studies report that Black men have slightly higher mean testosterone levels than White men at equivalent ages and BMIs, while others find no significant difference after controlling for SHBG and adiposity.

SHBG and Free Testosterone

SHBG levels differ by BMI, insulin resistance, and genetic polymorphisms in the SHBG gene. Because Black men on average carry higher rates of insulin resistance (which suppresses SHBG) and Hispanic men carry intermediate rates, free testosterone may differ from total testosterone in ways that current single-threshold guidelines do not capture. A 2016 study in JCEM by Dobs et al. Found that race-specific differences in total testosterone became non-significant after adjusting for SHBG and BMI, suggesting the apparent differences reflect metabolic burden rather than inherent biological variation [14].

Should Reference Ranges Be Race-Stratified?

The Endocrine Society has not endorsed race-stratified reference ranges, and doing so risks reinforcing harmful biological essentialism. The more defensible clinical position, supported by epidemiologic evidence, is that low testosterone in a Black or Hispanic man with obesity and diabetes should be interpreted in the context of those metabolic contributors, with calculation of free testosterone via the Vermeulen equation as a standard step. The Endocrine Society Guideline states: "We suggest using a total testosterone threshold of 300 ng/dL as the lower limit of normal for most adult men" [1], with the implication that free testosterone should be used when SHBG abnormalities are suspected.

Structural and Social Determinants Driving Disparities

Healthcare Access and Insurance Coverage

Men without a regular primary care provider are unlikely to have testosterone measured. The uninsured rate among Hispanic men aged 18-64 is 25.3%, compared with 9.7% in non-Hispanic White men (Kaiser Family Foundation, 2023) [15]. Telehealth platforms offering direct-to-consumer testosterone testing have partially reduced geographic and financial barriers, though language access and digital literacy remain limiting factors.

Neighborhood and Environmental Stressors

Chronic psychosocial stress activates the HPA axis, elevating cortisol and CRH, which suppress GnRH secretion. Men living in high-poverty, high-crime neighborhoods, which are disproportionately Black and Hispanic, may experience persistent HPG suppression from chronic stress that is functionally indistinguishable from other causes of secondary hypogonadism. This does not change the clinical management but does reinforce why addressing upstream determinants matters for long-term treatment response.

Opioid Crisis and Secondary Hypogonadism

Opioid-induced androgen deficiency (OPIAD) suppresses GnRH pulsatility and produces secondary hypogonadism in up to 70% of men on long-term opioid therapy. The opioid crisis has disproportionately shifted into Black and Hispanic communities since 2017, with synthetic opioid overdose death rates rising faster in Black men than in any other demographic (CDC, 2022) [16]. Clinicians prescribing chronic opioids to men in these communities should proactively screen for secondary hypogonadism with annual testosterone, LH, and FSH measurements.

Recommendations for Equitable Clinical Practice

Secondary hypogonadism is both diagnosable and treatable. The disparities described above are not inevitable.

Screening Protocol Adjustments

Screen proactively rather than waiting for patient-initiated complaints. Men with BMI above 30, type 2 diabetes, OSA, or chronic opioid use should have morning total testosterone and LH/FSH measured regardless of spontaneous symptom report. This applies with particular urgency in Black and Hispanic patients given their higher metabolic burden.

Language and Communication

Use validated translated versions of the ADAM questionnaire. Provide testosterone lab result interpretation in the patient's primary language. Discuss the purpose and safety of TRT explicitly, addressing historical medical mistrust with factual, patient-centered explanations.

Monitoring After Treatment Initiation

Once TRT is initiated, Black and Hispanic men on injectable formulations require the same monitoring schedule as any other patient: testosterone, hematocrit, and PSA at 3-6 months post-initiation, then annually. Hematocrit elevation (the most common short-term TRT adverse effect) does not differ significantly by race in TRAVERSE data, but polycythemia risk may be higher in men with baseline OSA, making CPAP compliance a co-management priority.

Advocacy at the Practice Level

Clinicians can advocate for prior-authorization reform for testosterone testing and treatment in Medicaid plans. The Endocrine Society has called for removal of arbitrary insurance barriers to medically indicated hormone therapy [1]. Documenting diagnostic workup thoroughly in the medical record strengthens prior-authorization appeals.