Your Hypogonadism is Most Likely a New Development
Your sudden onset of symptoms 6 months ago, combined with your elevated SHBG (90 nmol/L) and normal-to-elevated LH/FSH levels, strongly suggests this is acquired secondary hypogonadism rather than a longstanding condition. Your previous year of normal sexual function provides clear evidence that this represents a recent change in your hormonal status.
Understanding Your Laboratory Results
Your hormone pattern reveals secondary (hypogonadotropic) hypogonadism, which occurs when the hypothalamic-pituitary-gonadal axis is impaired, resulting in low testosterone with normal or low LH/FSH levels 1. In your case:
- Total testosterone of 40 nmol/L (~1154 ng/dL) appears to be a transcription error - this would be supraphysiologic and inconsistent with your symptoms. If you meant 4.0 nmol/L (~115 ng/dL), this confirms severe hypogonadism 1.
- LH 7.7 and FSH 10 are inappropriately normal for someone with symptomatic testosterone deficiency, confirming secondary rather than primary hypogonadism 1, 2.
- SHBG of 90 nmol/L is significantly elevated, which further reduces your bioavailable testosterone 3.
Why This Developed Recently
Your elevated SHBG is the critical clue. Hypothyroidism causes elevated SHBG levels 3, and even "well-controlled" hypothyroidism on thyroid hormone replacement can paradoxically increase SHBG 3. This creates a vicious cycle where:
- High SHBG binds more testosterone, reducing free/bioavailable testosterone
- Despite adequate total testosterone production, insufficient free testosterone reaches tissues
- The pituitary doesn't respond appropriately because total testosterone may appear adequate
- Your symptoms emerge despite seemingly "normal" LH/FSH levels 1
Diabetes, even when well-controlled, is another major contributor - it causes secondary hypogonadism through increased aromatization of testosterone to estradiol in adipose tissue, with subsequent estradiol-mediated negative feedback suppressing pituitary LH secretion 1.
Evidence This is New-Onset
Your clinical history of normal function one year ago is the strongest evidence this is acquired hypogonadism 4. Acquired hypogonadotropic hypogonadism is characterized by postnatal onset of disorders that alter GnRH neuron or pituitary gonadotroph function 4. The sudden 6-month onset pattern is classic for acquired rather than congenital disease 4, 5.
Men with long-standing hypogonadism develop physical signs like diminished facial/body hair, reduced muscle mass, fine facial wrinkles, and hypotrophic testes 4. If you lack these physical findings, this further confirms recent onset 4.
Critical Next Steps
Confirm your actual total testosterone level with repeat morning measurements (8-10 AM) on at least two separate occasions 1. Given your elevated SHBG, you absolutely need free testosterone measured by equilibrium dialysis 1. Your calculated free testosterone is likely severely low despite whatever your total testosterone actually is.
Review your thyroid medication dosing and timing - overreplacement with thyroid hormone increases SHBG 3. Work with your endocrinologist to optimize thyroid replacement, as this may lower SHBG and improve bioavailable testosterone.
Evaluate for other acquired causes of secondary hypogonadism: medications (opiates, glucocorticoids), obesity/metabolic syndrome, sleep apnea, pituitary lesions, or recent head trauma 1, 2, 4.
Treatment Considerations
If you desire fertility now or in the future, you are an absolute contraindication to testosterone therapy 3, 1. Exogenous testosterone suppresses spermatogenesis and can cause oligospermia or azoospermia 3.
For men with secondary hypogonadism seeking fertility, gonadotropin therapy with hCG (500-2500 IU, 2-3 times weekly) is first-line treatment, followed by FSH if needed after testosterone normalizes on hCG 3, 1. This approach can restore both testosterone levels and fertility 1.
If fertility is not a concern, testosterone replacement therapy combined with lifestyle modifications (weight loss, exercise, optimizing diabetes control) can reverse symptoms 1, 2. However, address the SHBG issue first, as high SHBG may blunt your response to treatment.
Common Pitfall to Avoid
Do not accept "well-controlled" diabetes and hypothyroidism as the end of the story - these conditions are likely driving your secondary hypogonadism through elevated SHBG and metabolic dysfunction 3, 1. The interplay between thyroid replacement, SHBG, and bioavailable testosterone requires careful optimization, not just TSH normalization.