DHEA

DHEA Hormone Basics
The DHEA hormone remains at low levels throughout a child’s life until age 7 at which time the DHEA level will start climbing. The hormone will peak at its maximum by the time a human being is between 20 and 30 years old for an adult male and it peaks at about age 32 for an adult female. From those ages on, the hormone will consistently go down until the time a person is 60 to 70 years old. There will be approximately 5-10% of the total amount of hormone available as compared to the individual when they were at their prime at age 30.

This hormone serves as the pro hormone to the ovaries. Without it, the ovaries cannot make any estrogen or methyltestosterone and without it, the testicles cannot make very much testosterone. DHEA also goes to the liver and there is converted into estrogen. The DHEA hormone, as far as we know, is controlled by another hormone produced at the liver site by the name of somatomedin-C, also known currently in the medical literature as insulin-like growth factor- I. It is suspected that there is a hormone from the hypothalamus also controlling it. However, this hormone has never been found to our know ledge. ACTH controls cortisone production from the adrenal and dopamine controls aldosterone production out of the adrenal, but smatomedin-C from the liver is what controls DHEA.

From a physiologic standpoint, DHEA during pregnancy is the hormone that stimulates collagenase stimulation at the cervical site and is responsible for cervical ripening at the time a woman goes into labor. It is felt by the GYN endocrinologists that this is why the cervix will not dilate at the time of labor when the hormone is low or deficient.

In looking at a review of systems, what we would find for the skin is that DHEA, thyroid, and vitamin A control oil production on the human skin and that DHEA in the female body is the only hormone that controls hair production from the neck down to the toes. Hence, we have had some episodes at FFP of women who have come in telling us that they are losing their pubic hair when they are age 27 (premature loss of pubic hair) or women who have told us that they were no longer shaving their legs or underarms suggesting that there was a DHEA deficiency as the major cause.

It does seem like DHEA controls probably about l/3 of the hair on the top of the head which may explain some of the problems with balding that we see in women as they age. From a metabolic standpoint, DHEA is used by the body to stimulate the production of NADH, an energy substance inside the cytoplasm of the cells to stimulate DNA production inside the mitochondria and hence all the enzymes that are necessary for proper functioning of the Krebs cycle. The DHEA works in conjunction with thyroid free T3 at the mitochondrial level to help control mitochondrial function and is responsible for many of the actions that occur inside the mitochondria.

DHEA as a hormone also helps to control the utilization of lipids (fats) as a major fuel through the mitochondria. Both glucose (sugar) and lipids all end up as citrate to be burned for fuel. The body uses DHEA as the determining factor to decide whether to burn citrate from lipids vs. citrate from carbohydrates as the main source of fuel for the Krebs cycle. DHEA is the hormone that helps to control this. This helps us to understand the concept of patients who will walk in and tell us that they have problems with obesity. They restrict their total calorie intake and a week later come back in and tell us that they have lost no weight. Frequently what we find is that they don’t have enough DHEA or thyroid T3 to burn their lipids, especially through the Krebs cycle. Also in lipid metabolism, we have noted that DHEA lowers the LDL cholesterol and helps to explain why there is virtually very little atherosclerosis in the younger population and why DHEA deficiency is vary much associated with atherosclerosis as one gets older.

DHEA is also responsible for maintaining bone growth and development. Without DHEA, the bones develop problems such as osteoporosis. This has been very well classified in the past medical literature showing that the 17 ketosteroids, of which DHEA is the major player, are responsible for maintaining bone integrity. We have seen in some patients that when given DHEA, the patients’ magnesium levels climb. The opposite is that many patients lose magnesium as their DHEA level drops.

From the medical literature, there has been evidence to show that when an animal is deprived of calcium in their diet, that the animal goes on to develop osteopenia (reduced bone mass), but when an animal is deprived of magnesium in their diet the animal goes on to develop osteoporosis (porous bones – weak/brittle). This may explain why we are having much difficulty with using calcium replacement therapy for treatment of osteoporosis when we should be treating with the use of magnesium and DHEA.

In immunology, we have seen that in an acute infection, DHEA will go down and cortisone production will go up. This occurs as a result of what is called adrenal adaptation syndrome where the adrenals will adapt to the infection by decreasing DHEA production. In the presence of a chronic infection, this process of adrenal adaptation becomes pathological since DHEA is a very crucial hormone for many normal functions of the body. In addition, we find that in the presence of chronic infection or even chronic stress that this adaptation syndrome becomes pathological.

DHEA as a hormone has been documented to stop the herpes viruses from reactivating and is responsible for herpes virus immune suppression via the immune system.

Also, in the AIDS literature, there has been evidence to suggest that patients who have high levels of DHEA can survive with their AIDS for a long time without very many of the complicating problems that are normally seen in AIDS, but the lower levels of DHEA that these AIDS patients have, the higher the death rate. DHEA as a hormone also controls cytokine expression on the T cells and as a result can help T cells to determine whether they should behave as a T helper cell vs. a T suppressor cell. Once more, Dr. Raymond Daynes is most responsible for this research.

In diseases where there is autoimmune expression of diseases such as seen in lupus or diabetes, especially in animal models, DHEA has been very successful at stopping the expression of these genetic traits. In animal studies it has been shown that if you take an animal who has already expressed lupus and give them DHEA, the disease has been reversed.

From a cancer standpoint, there have been studies showing that in populations where there are very low levels of DHEA, there is very high incidence of breast cancer in the population. Not only breast cancer, but also tumors in colon cancer, prostate cancers, etc. It is felt that this anti-cancer activity is mediated through the glucose 6-P04 dehydrogenase system which plays a major role in DNA synthesis, cell proliferation and cell carcinogen activation. DHEA is a potent inhibitor of mammalian glucose 6 phosphate dehydrogenase which is the rate controlling enzyme in time pentose pathway shunt and a major source of extra mitochondrial NADPH. I would refer you to Dr. Regelson`s paper from the Annals of the New York Academy of Science, published in 1988 on Hormonal Intervention of Buffer Hormones or State Dependency of DHEA, thyroid Hormone, Estrogen, and Hypophysectomy in Aging.

From a neurological standpoint, we have seen that DHEA as a hormone is 6 times greater in concentration of brain tissue than any other tissue in the body except for the adrenals. With a lack of DHEA, the cognitive function of the brain goes down, and hence we see losses of short term memory, increased mental agitation, etc. It has been shown that DHEA does enhance the memory of humans and animals and reduces neuronal death in animal models. It has been also seen that 48% of all patients with Alzheimer’s disease are DHEA deficient.

From a sex drive standpoint, DHEA is the major hormone that controls the human sex drive. Without it, we have noticed that men have problems with impotency and women have problems with being able to get turned on.

From a GI standpoint, we have noticed in this office that a lack of this hormone has been causing patients to have problems with loose bowel movements. We haven’ t seen many patients who have had problems with constipation. We have noted that the problems with diarrhea do disappear as soon as the DHEA hormone is given.

From my standpoint, the work up for patients with potential DHEA deficiency would go as follows: I will measure the somatomedin-C blood level, DHEA blood level, and DHEA-sulfate blood level. If there are problems with recurrent vaginal yeast infections, I will measure the IgM to IgG ratio of antibodies produced against Candida albicans to check the integrity of the immune system. I find that if the IgM level is much higher than the IgG in the presence of a long term chronic infection such as Candida, that one would expect a DHEA deficiency to be present. We have been doing work here at our office which has shown that there is a reversal of the IgM to IgG ratio with treatment of DHEA.

If a patient shows normal DHEA and DHEA-sulfate blood levels yet the somatomedin-C blood level is low, then these levels of DHEA may not be the “normal” level for this particular patient since somatomedin-C is the major stimulating hormone for DHEA production. Therefore, higher levels of DHEA may be necessary for “normal” function for this patient. It is my contention that the people who have no evidence for atherosclerosis, cancer, hyperlipidemia, etc. (the population in their 30’s) should be the population that we should model as far as normal blood values for DHEA. There is sufficient evidence from the literature at this point to suggest that we do not have to allow our aging population to suffer the consequences of cancer and heart disease and a lot of other illnesses of aging which are DHEA related.

There are two excellent medical books by Dr. Lawrence Parker (1) and Dr. William Regelson (2) on DHEA. These medical text books provide a greater understanding as to how this hormone works.

1. Dr. L. Parker is a GYN endocrinologist. His book title is Adrenal Androgens in Clinical Medicine, published by Academic Press in 1989.

2. Dr. Regelson’ s book is the Biological Role of Dehyroepiandrosterone. This is published by a Walter de Gruyter Publishing Co. in New York , 1990.

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