I’ve come across some more information on hormones and MS. This is the abstract (emphasis added) of an extensive (and highly scientific) review article focused primarily on estrogen. Most of this information has already been posted. What may be new is the information about fluasterone, an analogue of DHEA.
Neuroimmunoprotective effects of estrogen and derivatives in experimental autoimmune encephalomyelitis: Therapeutic implications for multiple sclerosis.
J Neurosci Res. 2004-Oct 28 PMID 15515048
Department of Neurology, Oregon Health and Science University, and Neuroimmunology Research, Veterans Affairs Medical Center, Portland, Oregon.
The extensive literature and the work from our laboratory illustrate the large number of complex processes affected by estrogen that might contribute to the striking ability of 17beta-estradiol (E2) and its derivatives to inhibit clinical and histological signs of experimental autoimmune encephalomyelitis (EAE) in mice. These effects require sustained exposure to relatively low doses of exogenous hormone and offer better protection when initiated prior to induction of EAE. However, oral ethinyl estradiol (EE) and fluasterone, which lacks estrogenic side effects, could partially reverse clinical EAE when given after the onset of disease. The three main areas discussed in this review include E2-mediated inhibition of encephalitogenic T cells, inhibition of cell migration into central nervous system tissue, and neuroprotective effects that promote axon and myelin survival. E2 effects on EAE were mediated through Esr1 (alpha receptor for E2) but not Esr2 (beta receptor for E2), as were its antiinflammatory and neuroprotective effects. A novel finding is that E2 up-regulated the expression of Foxp3 and CTLA-4 that contribute to the activity of CD4(+)CD25(+) Treg cells. The protective effects of E2 in EAE suggest its use as therapy for MS, although the risk of cardiovascular disease may complicate treatment in postmenopausal women. This risk could be minimized by using subpregnancy levels of exogenous E2 that produced synergistic effects when used in combination another immunoregulatory therapy. Alternatively, one might envision using EE or fluasterone metabolites alone or in combination therapies in both male and female MS patients.
For women concerned about the risks of oral contraceptives (EE, ethinyl estradiol, is the basis of many birth control pills) and cardiovascular disease, there’s some good news. An article on the topic, from Medscape, entitled New WHI Analysis: Oral Contraceptives May Reduce CVD Risk
, can be accessed at http://www.medscape.com/viewarticle/491753
. I think you have to register, but it’s free.
Now, even though I don’t have a scientific background, the extensive review article by Offner also contains some really interesting tidbits:
Because of the increased susceptibility of females to autoimmune diseases, some have assumed that female sex hormones, including estrogen, actively facilitate the disease process. In contrast to this view, our studies clearly demonstrate an important regulatory role of estrogen in EAE. Both estrogen and testosterone had inhibitory effects on immunity, and it may be that the enhanced susceptibility to autoimmune disease in females vs. males is due simply to less potent natural inhibition by estrogen than by testosterone.
Also, the abstract referenced fluasterone (a synthetic analogue) of DHEA, yet another hormone. Here’s what the article says in part about that:
DHEA is one of the three principal adrenal steroids, a precurosor of both androgens and estrogens, including 17b-estradiol, which is the focus of this review. Along with its active metabolites, DHEA has been described as a natural “antiglucocorticoid”, “immune stimulatory”, and “anti-inflammatory agent, attenuating many of the undesirable effects of glucocorticoid (GC) hormones…….
DHEA and its synthetic analogue fluasterone are steroidal compounds that attenuate disease in several mouse models of EAE with an efficiency similar to that reported for IFN-b. However, benefit in the rodent is observed only at high doses of fluasterone, which may not be readily achievable in man. Other metabolites might be more potent in limiting EAE than the parent compound and would therefore require lower doses to provide therapeutic benefit, a distinct advantage for possible MS trials. This would drive the development of more practical therapeutic strategies, (i.e., tansmucosal (buccal), transdermal, or s.c. administration ) to ameliorate MS in man. Because the steroid-like compounds are nontoxic, are inexpensive to produce, and are as good as or better than IFN-b in limiting EAE, similar or greater efficacy in man, at more readily achievable doses, would provide real clinical as well as economic benefit to patients with MS.
Researchers at Vanderbilt University (including Sriram) found that DHEA suppressed EAE in mice. http://www.mult-sclerosis.org/news/Jan2 ... lOfMS.html
a very small “non-traditional” study of DHEA found low levels in people with MS. http://www.itmonline.org/arts/dhea.htm
And, remember, even though DHEA is available over the counter in the US, just like any hormone, it should only be taken under the supervision of a physician.
Lastly guys, I haven’t forgotten about you. I’m hoping to post more about testosterone soon.
Here’s to healthy and balanced hormone levels for everyone.