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Arthritis - Rheumatoid

Hormones and Rheumatoid Arthritis

The role of steroid hormones in autoimmunity is evidenced by differences between men and women in both immune function and incidence of autoimmune disease. For example, estrogen actions tend to be pro-inflammatory, while progesterone, androgens, and glucocorticoids are anti-inflammatory (Cutolo 2004). Studies have documented low progesterone levels in women with autoimmune diseases, suggesting that a relative imbalance in favor of estrogen may contribute to immune reactivity in some female patients (Shabanova 2008). In RA and other autoimmune diseases, estrogen levels appear to be driven too high by actions of inflammatory mediators like TNF-α and IL-6 (Cutolo 2006). In some studies, lower levels of testosterone have been observed in male patients with RA than in controls (Masi, 2006). Testosterone and progesterone functions to promote immune tolerance in males and females, respectively (Cutolo 2006). Therefore, ensuring adequate levels of progesterone to balance excess estrogen in women and sufficient levels of testosterone in men may modulate some underlying immunologic features of RA (Karlson 2009; Cutolo 2009). Medications used to treat RA symptoms have been shown to suppress sex hormone production as well, potentially compounding an existing hormone insufficiency or imbalance (Weitoft 2008).

While large-scale clinical trials have yet to evaluate the efficacy of bioidentical hormone replacement therapy in RA patients, Life Extension suggests that the potential for considerable benefit outweighs the minimal risk. Taking measures to achieve and maintain optimal levels of sex hormones may soon emerge as an effective strategy for the symptomatic management of RA. Those interested in reading more about natural bioidentical hormone replacement therapy should review the Male or Female Hormone Restoration protocols.

The role and therapeutic potential of the hormone dehydroepiandrosterone (DHEA) in male and female RA patients is supported by a broad base of evidence. Between ages 25 and 75, levels of the multifunctional hormone DHEA decrease by approximately 80% (Weiss 2011). Moreover, glucocorticoid therapy often employed in RA suppresses DHEA levels significantly (Yukioka 2006). The implications of low levels of DHEA may be considerable in RA, especially since DHEA counteracts the inflammatory cytokines TNF-α and IL-6 in the synovium. Conversely, local TNF-α suppresses DHEA levels in the synovium; thus, the relationship between the anti-inflammatory effects of DHEA and the pro-inflammatory effects of TNF-α are reciprocal in nature. In a one year, double-blinded, placebo controlled trial, 125 men and women aged 65 – 75 received 50 mg of DHEA daily. Treatment resulted in improved insulin sensitivity and lower levels of TNF-α and IL-6 in blood samples (Weiss 2011). These results were maintained during an additional year of open-label continuation.