Does DHEA work for bodybuilding purposes

DHEA: Notes from Laboratory Medicine
by Priv.-Doz. Dr. med. habil. W. P. Bieger, Munich


DHEA is largely sulfated to DHEAS (DHEA sulfate) already in the adrenal cavity and secreted into the plasma as a prohormone, which, unlike DHEA, has no androgenic activity of its own. Only the non-sulfated, free DHEA has biological activity.
Since the plasma half-life of DHEAS clearly exceeds that of DHEA, the serum concentration of DHEAS is many times that of DHEA: approx. 500 times,
i.e. 0.2% of the total DHEA / S is present as bioactive DHEA.


The plasma relation of DHEA and DHEAS remains constant throughout life. However, new findings show that the situation in the CNS is different (Guazzo et al., 1996). Here, the proportion of DHEA compared to DHEAS is significantly higher. In the CSF (cerebrospinal fluid), DHEA reaches approx. 5.4% of the serum concentration, DHEAS only 0.15%. The CNS thus contains five to six times more DHEA than any other organ.

In contrast to the periphery, DHEAS itself appears to be biologically active in the CNS, possibly more effective than DHEA. From Baulieu, the 'discoverer' of DHEA, DHEAS is therefore called a neurosteroid. DHEAS is also synthesized locally in the CNS and in local peripheral nerves, the rate of synthesis can reach the level of the adrenal gland.


The DHEAS serum levels vary greatly from person to person, with genetic disposition, race, weight and stress factors being decisive. The serum concentration of DHEAS in men is about 4 times higher than in women. It falls continuously in both sexes from the age of 30. The so-called 'adrenopause' with approx. 10% residual production is reached between the ages of 70 and 80:

DHEAS is free or bound in the serum (albumin SHBG), DHEA predominantly bound. The concentration of DHEA in saliva correlates highly significantly with the total amount of hormone (free + bound) in the serum, and even more closely with the free DHEA in the serum. The saliva concentration is independent of local factors such as the amount of saliva, flow rate, pH or protein content. Since only the biologically active, free steroid hormones (DHEA) are present in saliva, saliva measurement is increasingly being used in diagnostics.

DHEAS functions as a peripheral prohormone pool of male and female sex hormones, as androstenedione, testosterone and dihydrotestosterone or estradiol and estrone can be formed from DHEAS after desulfation.

DHEA = "Mother of All Hormones"
The DHEAS sulfatase, which is responsible for the desulfation of DHEAS, occurs in numerous tissues with different levels of activity. The age-related decrease in the peripheral DHEA / S concentration is obviously largely due to the decrease in the key enzyme in DHEA synthesis, 17,20-desmolase (Longcope, 1995). Adrenal DHEAS production is primarily regulated by corticotropin / ACTH.

However, the serum concentrations of DHEAS and cortisol show significant differences. DHEAS is not subject to any daily rhythm. The age-dependent decline in DHEA / DHEAS production finds no parallel in glucocorticoid production. Treatment with glucocorticoids suppresses DHEAS.

A stress-related increase in ACTH and cortisol is accompanied by a decrease in the DHEAS concentration. The two steroid hormones thus identify themselves as functional antagonists. In fact, when plasma cortisol is high, low DHEA / S levels are regularly found. The quotient of cortisol and DHEA + DHEAS, determined in serum or saliva, is therefore often used as a stress indicator. The determination of the cortisol in saliva also allows a daily profile to be determined in a simple manner, which optimizes the informative value of the quotient.

immune system
Steroids, especially glucocorticoids (GK), are potent modulators of the cellular immune system. The anti-inflammatory effect of the GK's is mainly due to the modulation of the cytokine production of T-lymphocytes. Both CD4 helper cells and CD8 suppressor cells switch to type 2 cytokines (interleukin 4, interleukin 10) with simultaneous suppression of the type 1 cytokines interleukin 2 and g-interferon under the influence of GK. In particular, the suppression of the pro-inflammatory g-IFN is characteristic of cortisol, which also inhibits the activity of inflammatory cells such as granulocytes and macrophages. DHEA has an antagonistic effect on cortisol and increases the activity of the cellular immune defense by inducing type 1 cells (IL 2, IL 12, g-IFN).

Metabolic effect
In parallel with the age-related decrease in DHEA / S, the fasting levels of insulin in the plasma increase. Insulin slows down the production of DHEA, probably by inhibiting the
17,20 lyase and additional increase in the activity of DHEA-degrading enzymes.
DHEA, for its part, has no direct influence on the production and effects of insulin. Substances that are able to improve age-related insulin resistance can also improve the availability of DHEA. For Benfluorex it has been shown that the DHEA levels of 30 to 50 year olds can be reached in 60 to 80 year olds under treatment (Nestler, 1996).

DHEA also promotes fat burning. With substitution (> 40 y.), The muscle mass increases, the body fat percentage decreases - but obviously only in men. In women, the androgenic component of DHEA predominates during menopause (lack of estrogen):
  • increased truncal fat accumulation
  • Hyperinsulinemia
  • Drop in SHBG concentration
  • Increase in free testosterone
  • Fat accumulation.
Such a cycle is suggested by new results on the relationship of androgenic / estrogenic hormone effects, fat mass / insulin sensitivity and hyperinsulinemia / SHGB / testosterone (Ebeling and Koivisto, 1994).

DHEA increases the effectiveness of growth hormones. After the administration of DHEA, the age-related decline in IGF-1 is inhibited. In addition to the direct or indirect (testosterone) androgenic effect of DHEA, this effect also contributes to building muscles and increasing physical fitness.

Anti-atherosclerotic effect
The DHEAS concentration in the blood is significantly correlated with the incidence of atherosclerosis. The antiatherogenic effect of DHEA in men is mediated at least in part by influencing the lipid metabolism. DHEA lowers cholesterol, increases HDL and suppresses LDL cholesterol. The opposite can be observed in women.

Anti-aging effect / life extension
So far it has only been possible to show in animal models that the administration of DHEA increases survival time. There are no conclusive data on humans. DHEA substitution in older women and men significantly increased the growth hormone effector IGF-1, while HGH itself and IGFBP-3 remained unchanged.

During the administration of DHEA (50 mg / orally), the plasma DHEA and DHEAS concentrations stabilized within 14 days at values ​​of young adults. The androgen concentration in women increased two-fold (androstenedione, testosterone, dihydrotestosterone), in men only androstenedione increased slightly, the estrogen concentrations (estrone, estradiol) and SHBG remained unchanged in both sexes (Morales et al., 1994).

substitution
The most important recommendations for substitution therapy:

  1. If substitution therapy is planned, DHEAS and cortisol in the serum or - better - DHEA and cortisol in saliva should be determined beforehand on an empty stomach. As a rule, DHEA is saturated to the lower concentration values ​​of young adults within 2-4 weeks. The typical DHEAS serum concentration in 20-year-olds is 3000-5000 ng / ml.

  2. Lately, the sublingual application has increasingly been suggested, since almost the entire amount of hormones is absorbed. With conventional oral intake, up to 90% of the absorbed DHEA can be metabolized in the liver before the target cells are reached. DHEA creams that are absorbed transdermally also serve the same purpose. Absorbed DHEA is converted into DHEAS within 30 minutes, the plasma half-life of DHEAS is given as 12 hours. The individual maintenance dose is determined by checking the serum or saliva concentrations until the steady state is reached, initially every 2 to 4 weeks, later every 3 to 6 months. To this day it is absolutely unclear whether it makes sense to saturate up to the maximum adolescent values ​​in old age. Some experienced authors therefore recommend significantly lower doses of 5-15 mg / for women and 10-25 mg / for men, each for 5 days, in order to maintain the natural DHEA production. In the sick, the dosage may be increased up to the clinical maintenance dose.

  3. In addition, antioxidants are recommended, among other things to neutralize the potentially toxic effects of high DHEA doses, because DHEA is classified as a prooxidant (in order of suitability): Vitamin E> Ubiquinone / Coenzyme Q10> Green tea extract> Vitamin C (fat-soluble ascorbic acid palmitate) .

  4. Other supplements discussed: Melatonin - because of its protective effect against mammary and ovarian CA in estrogen substitution during menopause. Menopausal women should also take estrogens to counteract the more androgenic effect of DHEA on women. The current alternative to DHEA is pregnenolone, recently sometimes referred to as the 'grandmother of all hormones'.
Criticism:
All the effects of DHEA / S postulated to date come from animal experiments or studies on small numbers of cases. Most of the studies were carried out on rats, which in turn are unable to synthesize DHEA in the adrenal gland and which are therefore likely to be particularly sensitive to DHEA supplementation. Long-term results are not available to date. Possible positive effects contrast with possible negative risks such as increased breast and prostate CA risk.

Diagnosis:
Saliva: DHEA and possibly cortisol in 2 ml saliva each.
Material collection in special salivettes (to be requested from the laboratory!) - approx. 8 a.m.
Before collecting saliva, rinse your mouth twice with water, empty it and then take the filter cylinder from the Salivette into your mouth and chew gently for about 5 minutes! Put the filter back in the tube and close it. For the ASI / adrenal stress index, 4 saliva samples are required: 8 a.m. - 12 p.m. - 4 p.m. - 8 p.m. for the morning DHEA determination and the daily cortisol profile.

Other steroid hormones (free hormones!) Can also be determined from saliva:
Testosterone, progesterone, estradiol

Serum: 0.5 ml each of serum for steroid hormone determinations and, if necessary, HGH / growth hormone. Frozen serum / plasma is required for IGF-1.

Recommended intake:
5 - 50 mg DHEA for women and 25 - 100 mg for men, each orally in the morning.
However, various recommendations point to taking half the dose twice a day - early in the morning and late in the evening. DHEA capsules are available from 5 - 50 mg as imported medicinal products.

PreventNetwork Notice:
If you want to obtain case-related information from one of our hotline partners, be sure to state your age and gender as well as any hormone substitutions.

Notes on importing: international medicinal products subject to prescription, which the pharmacy can obtain by individual import: e.g. from Centropa Pharma, Tel. (+49) (0) 1805 33 11 60; Fax (+49) (0) 1805 33 11 69; e-mail: [email protected]

For:
anyone who is low in DHEA from age 35 and up;
Patients with malignant tumors (except for tumors that are themselves under hormonal influence: mammary, ovarian, uterine CA in women, prostate CA in men);
Crohn's disease
Allergies, asthma etc .;
CMS / Chronic Fatigue Syndrome, Multiple Sclerosis, Lupus Erythematosus, RA / Rheumatoid Arthritis; AIDS, primary / secondary immunodeficiency.

literature
  1. Barrett-Connor E, Khaw KT, Yen SSC: A prospective study of dehydroepiandrosterone sulfate, mortality and cardiovascular disease. New Engl J Med 1986; 315: 1519-1524.
  2. Ebeling P, Koivisto VA: Physiological importance of dehydroepiandrosterone. Lancet 1994; 343: 1479-1481.
  3. Guazzo EP, Kirkpatrick PJ, Goodyer IM, Shiers HM, Herbert J: Cortisol, Dehydroepiandrosterone (DHEA) and DHEA sulfate in the cerebrospinal fluid of man: relation to blood levels and the effect of age. J Clin Endocrinol Metab 1996; 81: 3951-3960.
  4. Lamberts SWJ, van den Beld AW, van der Lely AJ: The endocrinology of aging. Science 1997; 419-424.
  5. Longcope C: The metabolism of dehydroepiandrosterone sulfate. Sem Reprod Medicine 1995; 13: 270-275.
  6. Van Vollenhoven RF, Engleman EG, McGuire JL: An open study of dehydroepiandrosterone in systemic lupus erythematosus. Arthritis Rheum 1994; 37: 1305-1310.
  7. Morales AJ, Nolan JJ, Nelson JC, Yen SS: Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age. J Clin Endocrinol Metab 1994; 78: 1360-1367.