RE: Adrenal and gonadal steroid hormone deficiency in the etiopathogenesis of rheumatoid arthritis

[Guest guest]

<<In summary, a

growing body of data indicate that RA develops as a consequence of a

deficiency in both adrenal and gonadal steroid hormone production. This

hypothesis clearly has potential clinical implications.>>

Yikes! And then we're given prednisone which suppresses our adrenal gland

more? It certainly is a vicious cycle.

Since my hysterectomy at 30, I've become pretty experienced in hormone

replacement. We've tried various combinations of estrogen, progesterone and

testosterone. I've read other places that testosterone should help RA, at

least in theory, and it certainly makes sense. But I've used small (small

even for a female) amounts of testosterone, and couldn't tolerate it for any

length of time. It made me feel aggressive, and didn't really help my RA.

I have noticed that natural progesterone (not progestins) does help my

symptoms somewhat, but only if it is balanced with a little estrogen. I

find with RA and hormones, less is more. The dosages most women take cause

me to flare (even worse), so my compounded dosage is about half the

strength.

As far as DHEA, I've tried the supplement in the health food store years

ago, and felt terrible. I know my compounding pharmacist does DHEA, but I

would never try it without having the cortisol/DHEA testing done first.

Right now, I'm sticking with what I'm on. But it is an interesting area to

watch.

Love and hugs,

Carol

[Carol]

[ ] Adrenal and gonadal steroid hormone deficiency in

the etiopathogenesis of rheumatoid arthritis

Adrenal and gonadal steroid hormone deficiency in the etiopathogenesis of

rheumatoid arthritis

Journal of Rheumatology (Canada), 1996, 23/SUPPL. 44 (10-12

Rheumatoid arthritis (RA) is a multifactonal disease in which both

environmental and genetic factors play a role. Data also suggest that

neuroendocrine factors are involved. I briefly summarize observations that

support this hypothesis. RA is characterized by striking age-sex

disparities. The incidence of disease in women increases steadily from the

age of menarche to its maximal incidence around menopause. The disease is

uncommon in men under age 45, but its incidence increases rapidly in older

men and approaches the incidence in women. These observations strongly

suggest that androgens play a major suppressive role, and, in fact,

testosterone levels are depressed in most men with RA. Mechanistically,

many

data indicate that testosterone suppresses both cellular and humoral

immune

responses. Dehydroepiandrosterone (DHEA), an adrenal product, is the major

androgen in women. Its production is strikingly dependent upon age. Peak

production is in the 2nd and 3rd decades, but levels decline precipitously

thereafter. DHEA levels are low in both men and women with RA, and recent

data show that levels of this hormone may be depressed before the onset of

disease. The role of DHEA in immune diseases, however, is controversial.

The

menopausal peak of RA onset suggests estrogen and/or progesterone

deficiency

play-a role in the disease, and many data Indicate that estrogens suppress

cellular immunity but stimulate humoral immunity, i.e., deficiency

promotes

cellular (Th1-type) immunity. Recent data also indicate that progesterone

stimulates a switch for Th1 to Th2-type immune responses, RA often

develops

or flares in the postpartum period, particularly if the mother

breastfeeds.

This is again consistent with gonadal steroid deficiency playing a role in

the onset of disease. Breastfeeding Is associated with blunted

hypothalamic-pitu itary-adrenal function and elevated prolactin synthesis.

Gonadal and adrenal steroid hormone deficiency, plus elevated prolactin,

probably greatly facilitates the expression of Th1-type immunity, which is

widely believed to be critical in the pathogenesis of RA. By contrast, RA

typically remits during pregnancy, in parallel with the increasing levels

of

corticosteroids, estrogens, and progesterone. Pregnancy is characterized

by

a shift in immune function from Th1-type to Th2-type. Oral contraceptives,

which generate a condition of pseudopregnancy, also decrease the risk of

RA.

These data argue that adrenal and gonadal steroid hormones suppress the

development. of RA. Several studies indicate that corticosteroid

production

is inappropriately low in patients with RA, and are reminiscent of

observations in rat models of chronic erosive arthritis. In summary,

a

growing body of data indicate that RA develops as a consequence of a

deficiency in both adrenal and gonadal steroid hormone production. This

hypothesis clearly has potential clinical implications.