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Doug Maready, MD
Treatments

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Obesity & Hormones

Male Obesity-Associated Hypogonadism

Distinguishing true hypogonadism from low testosterone in men with obesity — and what to actually do about it.

AR
Adapted from Aman Rajpal, MD, DABOM
Obesity Medicine 2026 · The Heart of Obesity Care
By the numbers
2.4×
Higher odds of hypogonadism in men with obesity vs. normal weight peers.
Bhasin et al., J Clin Endocrinol Metab, 2018
Core Concepts

Six ideas that change how you treat low T in obesity.

Click any card for a quick reference summary with key pearls and references.

01

The MOSH Cycle

How obesity and low testosterone reinforce each other through aromatase, leptin, and GnRH suppression.

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02

Symptoms & Signs

Specific vs. suggestive vs. nonspecific. Knowing the difference changes who you treat.

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03

Why SHBG Matters

Obesity lowers SHBG, which lowers total T without true deficiency. Free T tells the truth.

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04

TRAVERSE & CV Safety

The 5,246-man RCT that settled the cardiovascular safety question for testosterone replacement.

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05

Monitoring on TRT

Endocrine Society guidance on hematocrit, PSA, and hitting the target T range.

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06

Fertility Considerations

Why GLP-1s may replace TRT for MOSH patients who want children.

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Clinical Algorithms

Procedural workflows that deserve a full screen.

These open dedicated walkthroughs with step-by-step reasoning.

Diagnostic Workup

Step-by-step decision tree from symptoms through labs to diagnosis. Click each step to expand the rationale.

Open walkthrough

TRT Formulations Compared

Visual comparison across injectable, transdermal, and oral options with practical pros and cons.

Open walkthrough
Hypogonadism / Diagnostic Workup
Clinical Algorithm

Diagnostic Workup of Suspected Hypogonadism

Click each step to expand the rationale and key decision points. The workup follows Endocrine Society guidance, adapted by Dr. Rajpal for the MOSH patient.

01History & Physical — Symptoms and Signs

+

Establish whether the patient has clinical features of hypogonadism. Specific signs (small testes, eunuchoid features) carry the most weight. Suggestive signs (low libido, ED) are common but nonspecific. Nonspecific symptoms alone are insufficient.

Pitfall: labs without symptoms = not hypogonadism, regardless of the number.

02Morning Total T (8 AM, fasting)

+

Diurnal variation is real. Test in the patient's morning — for night shift workers, that means after their shift, not 8 AM clock time.

Lab normal range: 250-1100 ng/dL.

Normal total T? Hypogonadism essentially ruled out (unless high SHBG suspected — see step 3).

03Suspect altered SHBG? Check Free T

+

Obesity is the most common cause of low SHBG, which lowers total T artifactually.

Always check free T when: obesity is present, total T is borderline (250-300 ng/dL), or any SHBG-altering condition is suspected.

Bioavailable T (free + albumin-bound) is the most accurate functional measure.

04Repeat Low T + Add LH and FSH

+

Endocrine Society requires "unequivocally and consistently low" — a single low value is not enough. Always repeat to confirm.

LH and FSH localize the problem:

• Low/normal LH+FSH → secondary (hypothalamic/pituitary) — includes MOSH

• High LH+FSH → primary (testicular) — Klinefelter, post-orchitis, testicular insult

05Classify and Investigate Cause

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Secondary causes: obesity/T2DM/MetS (functional), pituitary/hypothalamic disease (organic), opioids, glucocorticoids, marijuana, severe acute illness.

Primary causes: Klinefelter (karyotype), prior chemo/radiation, orchitis, trauma, advanced age.

MRI in selected cases: severe hypogonadism (T < 150 ng/dL), visual symptoms, hyperprolactinemia, low cortisol/free T4.

06Semen Analysis if Fertility Concern

+

Critical step before any TRT. TRT suppresses spermatogenesis — once started in a fertility-seeking patient, you've narrowed his options.

Document baseline volume, count, motility, morphology.

Final synthesis
MOSH = obesity + clinical features + low total T (or low free T if low SHBG) confirmed twice + low/normal LH/FSH + other causes systematically excluded.
Hypogonadism / TRT Formulations
Pharmacology

Testosterone Replacement Therapy: Formulations Compared

Six routes, very different patient experiences. Match formulation to patient lifestyle, fertility goals, and tolerance for self-administration.

Parenteral / Implants

Testosterone Cypionate

100-200 mg/mL · q1-2 weeks · IM/SC
+ Most common; cost-effective
– Peaks and troughs in mood/energy

Testosterone Enanthate

50-200 mg in sesame oil · weekly · SC/IM
+ Flexible dosing schedule
– Level fluctuations

Testosterone Undecanoate

750 mg / 3 mL castor oil · q10 weeks · IM
+ Infrequent dosing
– Injection site reactions; in-office

Implant Pellets

75 mg/pellet · 3-6 months
+ Long-acting; set and forget
– Procedure required for insertion

Topical / Transdermal

Testosterone Patch

2 or 4 mg · daily · back/abdomen/arms
+ Easy use; steady levels
– Skin irritation common

Testosterone Gel

1% / 1.62% / 2% lotion · daily · shoulders/arms
+ Convenient; flexible dosing
– Transfer risk to children/partners

Buccal / Nasal / Oral

Buccal Tablets

30 mg BID · gum
+ Discrete
– Gum irritation

Nasal Gel

11 mg gel · 2-3× daily · intranasal
+ Rapid absorption
– Frequent dosing required

Oral Testosterone Undecanoate Capsules

40 mg capsules 2-3× daily, OR 158-396 mg BID · with food
+ No injection, no skin transfer
– Food-dependent absorption; pill burden
Practical pearl
Match the route to the man. Cypionate q2 weeks works for most. Gels for needle-averse. Pellets for the "set and forget" patient. Avoid TRT entirely if fertility is on the table.
References

Shenoy MT et al. World J Exp Med. 2024;14(2):93689.

Bhasin S et al. J Clin Endocrinol Metab. 2018;103(5):1715-1744.