Understand primary, secondary and functional low testosterone, how LH and SHBG inform evaluation, and why the cause matters for treatment and fertility.
On September 24, 2026, the Endocrine Society published a statement addressing the Defense Health Agency’s guideline on testosterone deficiency. The statement described a recommendation to offer testosterone therapy alongside weight-management care for men with obesity and low testosterone.
This article is for informational purposes only and is not medical advice. Individual decisions about hormone testing and treatment belong with a qualified clinician.
The European Association of Urology (EAU) places cause-finding within its guidance on male hypogonadism. Its distinctions between primary and secondary hypogonadism describe where the hormone system is affected. The term functional addresses a different question: whether testosterone suppression occurs without a recognised structural or organic abnormality and alongside a contributing condition.
These terms are therefore not simply three competing labels for the same blood result. A useful way to read them is to separate the location of the problem from its underlying explanation. That distinction helps explain why similar testosterone results can lead to different investigations and treatment discussions.
The EAU defines primary hypogonadism as impaired testicular function. Low testosterone together with high luteinizing hormone, or LH, supports this pattern. The testosterone result and the signalling hormone are interpreted together rather than as isolated findings.
The guideline lists testicular injury and some congenital conditions among possible causes. Other examples include orchitis, torsion and chemotherapy. These examples show why a medical history matters alongside bloodwork; Testostra’s explanation of conditions affecting the testes provides related educational context.
Secondary hypogonadism involves inadequate stimulation of the testes by the hypothalamus-pituitary system. According to the EAU, low testosterone with low or inappropriately normal LH supports a secondary pattern. A laboratory result within the LH reference range therefore needs to be read alongside testosterone.
The EAU lists pituitary or hypothalamic disorders and hyperprolactinaemia among secondary causes. It also includes opioids and other medicines. Systemic disease and acute or critical illness can contribute as well. This category directs attention beyond the testes to the systems and circumstances affecting their stimulation.
The EAU describes functional hypogonadism as testosterone suppression without recognised organic alterations in the hormone axis. Obesity and coexisting medical conditions are leading suggested contributors. The guideline also lists chronic illness, some medicines and eating disorders. Endurance exercise and acute illness appear among the other possible contributors.
In the EAU’s approach, functional hypogonadism is considered after organic causes have been ruled out. The label does not mean symptoms are imaginary or that a low result is irrelevant. It identifies a different explanation to investigate and a potentially different management discussion.
The EAU’s diagnostic approach combines compatible symptoms with consistently low testosterone. For late-onset hypogonadism, it recommends morning measurements taken while fasting on at least two occasions using a reliable assay. The aim is to establish a clinical pattern rather than attach a diagnosis to an isolated number.
Cause-finding then involves additional information. The guideline recommends LH and follicle-stimulating hormone, or FSH, to help distinguish hypogonadism types. It also recommends measuring LH and prolactin when pathological total testosterone is detected. These markers contribute different pieces to the assessment.
The distinction matters because confirming low testosterone and explaining it are separate tasks. Repeat testosterone testing addresses whether the finding is consistent. LH and FSH help frame the primary-versus-secondary question. Prolactin can help identify whether further investigation of a central cause is indicated.
SHBG adds another layer. The EAU notes that obesity can lower sex hormone-binding globulin, which can complicate total testosterone interpretation. Measuring SHBG and calculating free testosterone may therefore be relevant when SHBG is altered.
A discussion about a low total result may consequently include questions about binding proteins as well as hormone production. Understanding the relationship between total and free testosterone can make that discussion easier to follow. These measurements belong within the broader clinical assessment rather than competing for the title of the single decisive test.
A secondary pattern can lead to investigation of the pituitary. The EAU recommends pituitary MRI when secondary hypogonadism accompanies high prolactin or symptoms suggesting a pituitary mass. Other anterior pituitary hormone deficiencies are another indication. The guideline gives a weaker recommendation for MRI in severe secondary hypogonadism.
The management discussion also depends on the explanation. The EAU advises treating indicated organic causes and addressing coexisting conditions. It recommends lifestyle changes and weight reduction where appropriate. For overweight or obese men with hypogonadism, it places weight loss and lifestyle changes first.
Medicines and recent illness also belong in the review. The EAU advises avoiding testosterone measurement during acute illness because illness can be associated with functional suppression. It also recommends withdrawing potentially contributing medicines when possible before starting testosterone therapy. Any medication change requires clinician oversight rather than stopping a prescription independently.
This is why identifying a potentially changeable contributor is useful: it gives the clinician something specific to assess and address. Testostra’s discussion of clinical context and potentially reversible contributors explains this distinction between recognising a possible contributor and deciding on treatment.
The cause of low testosterone is especially relevant when fertility matters. The EAU states that exogenous testosterone suppresses gonadotropins and sperm production. It advises against testosterone therapy in men seeking fertility.
For men with secondary hypogonadism who desire paternity, the EAU identifies gonadotropin therapy as the standard treatment. This is a guideline distinction between treatment pathways, not a recommendation for an individual to select a medicine or construct a hormone regimen.
Near-term and longer-term plans for children therefore belong in the treatment conversation from the beginning. The relevant discussion is broader than whether testosterone rises on treatment. It also includes how the proposed approach relates to sperm production and the man’s underlying diagnosis.
The September 2026 Endocrine Society statement highlights a difference in management recommendations. In the Society’s account, the Defense Health Agency guideline calls for men with obesity and low testosterone to be offered testosterone therapy alongside weight-management care. That differs from the EAU’s first approach of weight loss and lifestyle changes for overweight or obese men with hypogonadism.
The Society also raises a specific objection to the Defense Health Agency guideline’s fertility-related hCG approach. Its statement says hCG suppresses FSH, which is needed for normal sperm production. It argues that this could reduce sperm production in men with obesity-induced hypogonadism who typically have normal FSH.
This disagreement concerns the treatment proposed as well as the population receiving it. It makes the cause of testosterone suppression and fertility priorities important parts of the discussion. Both positions should be understood through their respective sources rather than combined into one treatment rule.
These sources provide clinical guidance and a professional society’s statement, not a new trial comparing every cause or treatment pathway. The Endocrine Society statement reports and challenges aspects of another guideline. It should not be read as evidence that all clinicians agree on obesity-related low testosterone management.
The EAU uses a total testosterone threshold of 12 nmol/L as a diagnostic criterion for late-onset hypogonadism when symptoms are present. It recommends repeat testing below that level before treatment. This threshold belongs to that diagnostic framework, including its symptom assessment and testing requirements. It is not a universal cutoff detached from clinical context.
The categories themselves also have limits. The EAU notes that chronic disease and some other conditions can affect the hormone axis at more than one level. Obesity does not establish that low testosterone is functional, and a potentially changeable contributor does not establish that every case will resolve. The practical implication is to complete the clinical evaluation rather than self-assign a category.
The bottom line is that this information should not trigger an automatic change in treatment. It supports a cause-focused assessment before deciding what treatment and follow-up should involve. The September statement adds a specific management disagreement to that conversation rather than replacing the need to understand the hormone pattern.
Useful questions for a clinical discussion include:
The practical value of the categories is not the label itself. It is the next clinical question the label helps identify. For one man that may involve investigating a central disorder; for another it may involve addressing a contributing condition. Personal treatment decisions require that fuller assessment rather than a low testosterone number alone.
Sorting a testicular cause from functional suppression requires clinical assessment; Testostra takes up the separate task of explaining the evidence. For men unsure how SHBG relates to total and free testosterone, its educational coverage makes the biomarker discussion easier to follow without offering personal diagnosis or treatment.
Testostra follows testosterone research, clinical guidance and emerging evidence without turning general information into personal treatment advice.
Send us a question, research idea or topic suggestion. Reader questions help shape future Testostra content.
Contact Testostra