During a visit to my physician 20 years ago, my doctor said “You don’t want to get osteoporosis – It’s a painful disease.” I did not think that would be in my future!
As a young woman, I started taking daily calcium supplements, watched my diet and exercised. I was taking care of myself.
A painful fall started to raise concern. My physician was alarmed because the x-rays taken showed a very old skeletal structure in a young woman.
As the years went by, I decided to get a bone density. The results were not good… I had osteopenia as well as osteoporosis. I started taking an osteoporosis medication to help with the bone loss…. Did it help… no!
My first fracture was in the 1980s, a fractured rib from a hug. Hmmm …. Then ten years later… another broken rib occurred while leaning over the arm of a chair, I felt my ribs “Pop”! Another rib fracture in again less than 6 months! More pain…
Fast forward to today… 15 episodes of fractured ribs…. Yes … this is a painful disease!
So how did this happen to me? Is it simply osteoporosis? It is not, I was exposed to the drug DES (Diethylstilbestrol) in utero. I believe that is why I have this painful disease.
Do you know if you are a DES Daughter or Son? If so, do you know if DES effected your skeletal structure like mine was… you need to know!
Research excerpts for the article….
Researchers from NIEHS has demonstrated that in utero DES exposure did affect the skeletal tissue…
“In research, it was shown that DES induces permanent changes in skeletal tissue in adulthood, such as shorter femurs and increase in the amount of bone in the femurs and vertebrae, suggesting that physiological exposure to estrogens in childhood might be one of the key factors in determining the final peak bone density in adulthood.
Fetal exposure to DES had significant effects on lumbar bone in terms of the percentage of bone volume, trabecular separation, trabecular number and the distance between the lumbars.
Humans were typically exposed to DES throughout gestation until birth. The brief exposure in this study was chosen at a time of organogenesis; however, the overall dose of DES in this study is much less than the comparable dose used on pregnant women. Therefore, the present results are more likely to underestimate the effects of DES because the exposure was brief and at a lower cumulative dose.”
“DES is traditionally thought of as a pure estrogen agonist, but can actually have an antagonistic effect in some circumstances. It has an agonistic effect on ERα but an antagonistic effect on ERR-γ. DES was most studied in terms of its effect on the reproductive system, and it was found to have a net agonist effect on these tissues (endometrium, breast, prostate).
How a tissue responds to DES would largely be determined by the receptor distribution in that tissue. A prevalence of ERα in articular cartilage, for example, would lead us to suspect an agonistic effect. Furthermore, it should be noted that the effects observed in this study are due to "priming" with DES at a critical stage, which differs from exposing an adult animal to DES. This priming can change the receptor distribution in a particular tissue or in the downstream pathways that a particular receptor stimulates. These exact effects are not known at present and must be further elucidated.”
“DES exposed should benefit from earlier screening for signs of osteopenia or degenerative changes of their bones”
Arthritis Research & Therapy 2012 14:R17
“It may be clinically important to further investigate the possibility that exposure of the human population to exogenous estrogens could permanently affect skeletal tissue. In particular, it will be clinically relevant to evaluate whether low or high doses of these steroids could affect the skeleton in different manner, for instance increasing peak bone density or inducing skeletal malformations at higher doses.
In conclusion, our results show for the first time that developmental exposure to estrogens during certain stages can permanently influence bone tissue in an animal model.
The observed changes appear to be due to an effect on bone cell programming since differences in bone cell number and activity are retained through adulthood.”
National Institute of Environmental Health Sciences
Authors: Silvia Migliaccio, Retha R. Newbold, John A. McLachlan, and Kenneth S. Korach