Why DHEA and T3/rT3 Testing Matters, & why everyone should be aware of DHEA deficiency and Intracellular Hypothyroidism

Free post, for everyone: background information, for “Aging, Due to DHEA Deficiency”

A: In a current, standard family practice

An otherwise healthy patient presents with nonspecific symptoms (fatigue, anxiety, poor sleep): → Standard lab tests return within normal limits → No intervention
→ DHEA & T3/R T3 are not tested → Deficiency is missed → Symptoms persist

B: in a family practice aware of DHEA and thyroid 3 insufficiency syndromes

An otherwise healthy patient presents with nonspecific symptoms (fatigue, anxiety, poor sleep) → Standard lab tests, plus DHEA & T3/rT3 are tested and Age group is noted → Deficiency of DHEA and/or T3 confirmed → Therapy trial is initiated, beginning with DHEA supplementation.
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Symptom profile, serum DHEA and the serum FT3 are reassessed after 2 weeks (DHEA will have improved)
T3 may have improved: if T3 >4.0 pmol/litre, continue on DHEA only: If T3 = <4.0 pmol/L, start therapy trial with SRT3
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After one month on SRT3, the patient’s symptoms, serum FT3 and serum DHEA are reassessed .

C: Caveat
(1) T3 insufficiency (the Low T3 Syndrome, “LT3S”) may have resulted from DHEA insufficiency: if so, it may resolve when DHEA rises to, or exceeds, normal limits for a 25-year-old. Therefore if serum T3 rises to >4.0 with DHEA supplementation, LT3S has cleared and DHEA monotherapy can be continued, pending reassessment after 3 months
(2) If serum FT3 = <4.0 pmol/L in spite of DHEAsupplementation, T3/rT3 should be reassessed and SRT3 supplementation should be started. Please see “undiagnosed hypothyroidism”, for a full explanation of the LT3S and the protocol for its therapy.

D: Comment

(1) DHEA and intracellular T3 deficiency contribute to the aging process itself—not merely as markers, but as drivers!
DHEA and T3/rT3 ratio testing economically differentiates easily-treatable hormone deficiency from more virulent causes of nonspecific symptoms, such as Lyme disease, heavy-metal overload, AIDS, etc., which are more expensive to investigate.

(2) Early testing avoids mislabeling the symptoms as psychological or untreatable.

(3) Beginning At age 25 – 26, undisturbed humans reduce DHEA production by one percent per annum and begin to show evidence of insufficiency by age 30 – 40; but individuals who have been subjected to childhood stress or trauma may enter adulthood already deficient in DHEA and already “lumbered” by the Low T3 Syndrome: those unfortunates develop symptoms earlier (sometimes, in the teens).

(4) Improvement in the symptoms of DHEA deficiency is usually seen within a few days of starting supplementation, but improvement in LT3S symptoms may be delayed for several weeks.

(5) Intracellular T3 deficiency (IH), a failure of intracellular T3 production due to stress-related hypercortisolism, with blockade of deiodinase 1 and enhancement of deiodinase 3, causing impaired cellular metabolism, causes LT3S symptoms (fatigue, constipation, low motivation, hair loss, brittle fingernails, brain fog and anxiety). It is a vastly under-recognized metabolic condition: standard blood tests, TSH and T4, are normal, because the pituitary gland is exempt from the effects of cortisol and it keeps TSH and T4 levels normal, masking the deficiency in the peripheral tissues.

(6) IH can only be diagnosed with the T3/rT3 ratio, which isn’t flagged in standard thyroid panels. So most family doctors miss the diagnosis.

E: Nota Bene

In 585 patients whom I tested for DHEA deficiency, between 2006 and 2014, I observed that the presenting symptoms tended to vary according to the patient’s age, so (for purposes of descriptive stratification) I utilized a system of age grouping, as follows:
🔹 Group A (<15 years of age) DHEA is normally low: stress may cause low T3.
🔹 Group B (15–20 years) DHEA, testosterone, estrogen, progesterone etc. normally rise, but severe stress in childhood (? PTSD) may hold neurosteroids and T3 down.
🔹 Group C (21–25 years) DHEA still sits near peak levels, but is on the cusp of decline.
🔸 Group D (26–40 years) the 26th year marks the beginning of noticeable symptoms, particularly hair loss, greying, weak fingernails, constipation etc. For many, fatigue, cognitive dulling and mood shifts signal stress-related overproduction of cortisol and IH.
🔸 Group E (41–60 years) often sees cumulative effects of ongoing DHEA deficiency: sleep disturbances, weight gain, anxiety, IH-linked issues and the onset of more aggressive autoimmune diseases and cancer.
🔹 Group F (61-70 years) experience severe DHEA depletion, where age-related diseases ramp up dramatically.
🔹 Group G (70+years)

Thus, routine DHEA and thyroid profile testing becomes more important to patient assessment, as the individual ages: I do not suggest that everyone needs supplementation, but symptoms without biochemical confirmation lead to misdiagnosis and missed opportunities. An adequate investigation protocol, begun at the patient’s first presentation to the doctor’s office, saves time, results in earlier diagnosis and in summary, is less costly to our publicly-administered healthcare system, in the long run.

F: Summary Chart: DHEA-Related Symptoms by Age Group

This is a rough guide: there is considerable overlap, in all parameters

G: A personal note

I started taking DHEA at age 67: brain fog and anxiety disappeared within two days, and over the following two weeks, recent-onset cardiac arrhythmia stopped. Over a month or so, the graying of my hair slowed to a minimum, previous symptoms of fibromyalgia settled down. Tendon and joint deteriorations (flexor tendon nodules in the hands, Heberden’s nodes and multiple exostoses due to DISH) improved slowly over the following 15 years. in addition, my skin has not thinned and stretched as it usually does with aging: now aged 86, I have no wrinkles.