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Raloxifene, DHEA, and Osteoporosis

James Howard jmhoward at sprynet.com
Fri Sep 12 11:26:46 EST 1997


Raloxifene, DHEA, and Osteoporosis
James Howard

Associated Press, Sept 12: "A new drug could give aging women all the 
benefits of estrogen replacement, such as stronger bones, but have fewer 
side  effects, according to a study released Thursday.    The study 
suggests the drug, an "anti-estrogen" called raloxifene, helps  increase 
bone mass and reduce blood cholesterol levels like estrogen, said  Dr. 
Edward Lufkin, the study's lead author."

I suggest all raloxifene may be doing is increasing production of the 
natural, adrenal hormone, DHEA, a commonly available, cheap hormone.  
This is easily demonstrated.

A single injection of raloxifene significantly increases the production 
of the pituitary hormone, prolactin (Prostate 1993;23(3):245-262).  
Prolactin is not only specific for stimulating DHEA (Endocrinology 1985; 
117: 1968), but prolactin stimulates DHEA more than the usual hormone, 
ACTH, thought to stimulate the adrenal glands (American Journal of 
Obstetrics and Gynecology 1987; 156: 1275).

Osteoporosis is the loss of bone mineral (BMD) density in aging.  
"Estrogen" is usually given credit for helping with BMD in aging women. 
 However, "estrogen" is a combination of compounds that includes 
estradiol (E2) and estrone (E1).  It has been proven that "chronic 
administration of estrone significantly enhanced the bone mineral 
density of femur in aged animals" (In Vivo 1996 Jul;10(4):455-457).  The 
connection of estrone with DHEA is that "DHEA, is converted to E1 in 
osteoblasts [[the primary bone-forming cells] 
and important to maintain 
BMD in the 6 to 7th decade, after menopause." (J Steroid Biochem Mol 
Biol 1995 Jun;53(1-6):165-174).  

DHEA begins to naturally decline around age twenty and reaches very low 
levels in old age, when osteoporosis occurs.  I suggest that raloxifene 
is stimulating production of DHEA, which is converted into estrone, by 
bone-forming cells.  This estrone causes the osteoblasts to increase the 
bone mineral density that was lost in old age, because of the loss of 
DHEA.  Raloxifene also reduces cholesterol levels.  Again, this is 
another of the effects of DHEA.  When given to 60- to 70-year-old women, 
DHEA causes a decrease in total cholesterol (J Endocrinol 1996 Sep;150 
Suppl:S43-S50). 

It may well be that all raloxifene is doing is increasing DHEA in women, 
whose DHEA has declined to very low levels.  Another study found that: 
"DHEA in appropriate replacement doses appears to have remedial effects 
with respect to its ability to induce an anabolic growth factor, 
increase muscle strength and lean body mass, activate immune function, 
and enhance quality of life in aging men and women, with no significant 
adverse effects." (Annals of the New York Academy of Science 1995; 774: 
128).  Perhaps before physicians start prescribing raloxifene, they 
should consider DHEA.




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