DHEA - this hormone is available as an OTC dietary supplement in the USA.┬ If you Google for DHEA and inflammation or anti-inflammatory there's quite a few interesting articles.┬ Women, in particular, should only take very small amounts unless under medical supervision. http://www.lef.org/protocols/metabolic_health/dhea_replacement_01.htm
DHEA: Fighting Inflammation
Inflammation is an insidious condition, and we are learning more every year about its association with a host of diseases. Inflammation is caused by internal chemicals called inflammatory cytokines that are released as part of the immune system response. These chemicals, including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin 1(beta) [IL-1(β)] and/or leukotriene, are present in greater concentrations as we age. Reducing the concentration of inflammatory cytokines to reduce the risk of serious disease is one goal of nutrient and hormone therapy. DHEA supplementation has been shown to improve several aspects of the immune system
―cytokine production and T-cell, B-cell, natural killer cell, and monocyte function―in postmenopausal women and elderly men (Khorram O et al 1997). DHEA appears to be especially valuable against IL-6 and TNF, both of which are elevated in patients with inflammatory arthritis (James K et al 1997; Straub RH et al 1998; Straub RH et al 2002a; Leowattana W 2001). Systemic lupus erythematosus is another chronic inflammatory condition, affecting approximately 1 in every 700 women, usually younger women (Sullivan KE 1999-2000). Treatment of this type of lupus with DHEA (50 to 200 mg daily) caused clinical improvement and decreased lupus flares by 16% (van Vollenhoven RF et al 1998; Chang DM et al 2002).
I found some possibly interesting research citations in Pubmed http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11600195&dopt=Abstract
Dehydroepiandrosterone attenuates the spontaneous elevation of serum IgE level in NC/Nga mice.
Sudo N, Yu XN, Kubo C.
Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, 812-8582, Fukuoka, Japan. firstname.lastname@example.org
Dehydroepiandrosterone (DHEA) and its sulfate derivatives are known to affect host immune function; however if such hormones influence the development of atopic dermatitis has not yet been clarified. In this study, we examined the effects of DHEA on the allergic process using NC/Nga mouse, a model animal of human atopic dermatitis. The administration of DHEA profoundly suppressed the spontaneous elevation of both serum IgE and interleukin-6 levels in NC/Nga mice during the observation period.
These results indicate that DHEA promotes a shift in Thl/Th2 balance toward Th1-dominant immunity, and thus may be one of the effective alternatives in treating atopic dermatitis.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9248620&query_hl=3&itool=pubmed_docsum
Dehydroepiandrosterone may be one of the regulators of cytokine production in atopic dermatitis.
Tabata N, Tagami H, Terui T.
Department of Dermatology, Tohoku University, School of Medicine, Sendai, Japan.
Previous studies in mice have shown that dehydroepiandrosterone (DHEA) increases the production of Th1-associated lymphokines, and of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), by lymphocytes. However, there are no reports concerning the effect of DHEA on the production of Th2-associated lymphokines, IL-4 and IL-5, by lymphocytes in humans. We examined serum DHEA levels in patients with atopic dermatitis (AD), which is thought to be associated with a higher activity of Th2 cells than of Th1 cells. We also studied the effects of DHEA on the production of IL-4 and IL-5 by human lymphocytes. Serum DHEA concentrations in 47 adult male patients with AD aged 19-30 years were significantly lower than those of 53 age-matched healthy male controls. Preincubation of peripheral blood mononuclear cells (PBMCs) with DHEA reduced the IL-4 production by concanavalin A-stimulated PBMCs. Their IL-5 production also showed a tendency to decrease. These results suggest that DHEA may be one of the regulators of IgE synthesis and eosinophil proliferation in patients with AD
and it may act by controlling IL-4, IL-5 and IL-2 production by lymphocytes.