Imbalance of the DHEA hormone could be affecting how you respond to stress.

We use Labrix Clinical Services Inc. who is dedicated to providing the most accurate and physiologically relevant hormone testing available. In keeping with our dedication to accuracy we have chosen to measure DHEA rather than DHEAS in saliva. We are aware that many laboratories choose to measure DHEAS in spite of the overwhelming evidence that points to DHEA being the only form of DHEA accurately measured in saliva and additionally more clinically relevant.

DHEA exists in two forms – free DHEA (DHEA) and sulphated DHEA (DHEAS). DHEAS is the inactive stored reservoir form of DHEA. DHEAS levels do not reflect biologically active DHEA levels. It must be desulfated by the enzyme DHEA sulfotransferase (SULT2A1) in order to be active.

Since DHEA is the biologically active form of the hormone, it is the only form which can be converted into androgens and estrogen and only DHEA (not DHEAS) is protective for the brain. The active form of DHEA is produced in the adrenal glands and its free levels in the body can be measured accurately in the saliva. Measuring salivary levels of DHEA is a precise evaluation of the circadian secretions of this hormone by the adrenal cortex.

Salivary DHEA reflects the unbound, biologically active fraction of the hormone in the general circulation and shows excellent correlation with free plasma levels of DHEA. DHEA (like other steroid hormones) is a non-polar molecule. Non-polar molecules are transported very easily through the salivary gland and their concentration in saliva matches that of the free circulating levels in the body. DHEAS on the other hand is a polar molecule. Its concentration in saliva is not a reflection of its concentration in the body.

Dehydroepiandrosterone (DHEA) is the most abundant hormone in the body. It is primarily produced in the zona reticularis of the adrenal cortex and small amounts of DHEA are produced in the brain. DHEA serves as a metabolic intermediate (prohormone) in the pathway for synthesis of testosterone, androstendione, estrone, and estradiol. All the enzymes required to transform DHEA into androgens and/or estrogens are expressed in a cell-specific manner in a large series of peripheral target tissues (breast, prostate, skin, bone etc.), thus permitting all androgen-sensitive and estrogen-sensitive tissues to make sex steroids locally and control the intracellular levels according to their local needs.

DHEA also serves a very important role in the stress response (hence its formation is triggered by ACTH, the same chemical messenger that triggers cortisol formation). DHEA has been shown to elevate mood,calm emotions and increase alertness – all essential qualities for responding well to stress. Additionally, DHEA’s affect on mood helps us cope more evenly with the stress and also helps improve memory.


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DHEA and DHEAS levels do not correlate well in pathological conditions i.e. high DHEA levels do not necessarily lead to high DHEAS levels. It appears that the enzyme that converts DHEA to DHEAS (SULT2A1) is often impaired during ill health. This leads to a reduction in DHEAS levels and a marked increase in DHEA levels.

This again underscores the necessity of testing DHEA not DHEAS when evaluating patient and especially for those who are chronically ill.

Reference List

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3. No evidence for hepatic conversion of dehydroepiandrosterone sulfate fo DHEA – in vivo and in vitro studies. Hammer F, Subtil S, Lux P, et al. J Clin Endocrinol Metab 2005;Mar 8

4. Hormones in Saliva. Vining RF and McGinley RA. Critical Reviews in Clinical Laboratory Sciences. (1986)


5. Is dehydroepiandrosterone a hormone? Labrie F, Luu-The V, Belanger A, Lin SX, Simard J, Pelletier F, Labrie C. J Endocrinol. 2005 Nov;187(2):169-96.

6. Functions and mechanisms of dehydroepiandrosterone in nervous system. Xie L, Sun HY, Gao J. Liao H.. Shen Li Ke XueJin Zhan. 2006 Oct;37(4):335-8.

7. Suppression of DHEA sulfotransferase (Sult2A1) during the acute-phase response. Kim MS, Shigenaga J, Moser A, Grunfeld C, Feingold KR. Am J Physiol Endocrinol Metab. 2004 Oct:287(4):E731-8.

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The Endocrinologist. Issue 77. Autumn 2005.