Endocrine Support

The stress axis (HPA) and the sex hormone axis (HPG) share a common control center in the hypothalamus. They compete for resources.

When cortisol is chronically elevated, it:

• Suppresses GnRH at the hypothalamus
• Reduces pituitary LH sensitivity to GnRH
• Inhibits testicular Leydig cells from making testosterone

Result: chronic HPA activation — from any cause — produces HPG suppression and falling testosterone.

This matters clinically. A man with low testosterone may have:

• Primary hypogonadism — testicular failure
• Secondary hypogonadism — pituitary failure
• Functional hypogonadism — HPA-driven suppression from stress, sleep loss, or overtraining

These need different treatments. Starting TRT without addressing a functional HPA cause misses the root mechanism.

This is why we run a 4-point diurnal cortisol as part of the evaluation for unexplained low testosterone.

T4 (inactive) becomes T3 (active) through enzymes called deiodinases. These enzymes are blocked by glucocorticoids.

When cortisol is high:

• Less T4 becomes active T3
• More T4 becomes inactive reverse T3
• The result: normal TSH, normal T4, but low Free T3

This is tissue-level hypothyroidism despite a "normal" TSH. The patient feels cold, tired, and slow — with lab results that look fine on a standard panel.

Our approach:

• Address the causes of impaired conversion — cortisol management, selenium adequacy, inflammation reduction
• If on levothyroxine, target TSH in the lower-normal range (0.5–2.0 mIU/L) instead of just anywhere in range
• In appropriate patients with documented low Free T3 despite adequate T4, consider combination T4/T3 therapy per American Thyroid Association framework

"Adrenal fatigue" is not a recognized medical diagnosis. It groups several different patterns under one unsupported label.

The clinically meaningful patterns we look for:

• Morning cortisol insufficiency — blunted cortisol awakening response
• Elevated evening cortisol — disrupts sleep and testosterone
• Elevated total daily cortisol output — chronic HPA activation
• Low DHEA-S with high cortisol — adrenal "pregnenolone steal" where the adrenal prioritizes cortisol over DHEA

Each pattern has a different presentation and different management. Generic "adrenal support" is the wrong answer.

DHEA-S supplementation is appropriate when labs confirm deficiency. The Endocrine Society recommends it for adrenal insufficiency. Grade B evidence supports DHEA in women with low DHEA-S for well-being, sexual function, and bone density.

For cortisol pattern abnormalities, the first-line intervention is root-cause correction: sleep optimization, stress management, exercise periodization — not supplements.