After menopause without the use of estrogen, a woman can lose up to 20% of her bone mass. This increases her risk for osteoporosis leading to loss of height, hip fractures, chronic pain, and disability. Of women who suffer hip fractures, 24 percent die of complications within a year of the injury. Osteoporosis of the spine leads to the familiar “dowager’s hump.” A dowager’s hump is a prominence on the back resulting from collapse of the spine from spontaneous vertebral fractures. When it’s severe, the woman is totally bent over and cannot stand up straight. It is tragic to see a woman suffering from something that could have been prevented.
A recent British study estimated the lifetime risk for any fracture to be 53.2% at age 50 among women not taking estrogen. In comparison, the estimated lifetime risk for endometrial carcinoma for a 50-year-old woman is 2.6%, for breast cancer 10%, for coronary artery disease 46%, and for stroke 20%.
Prevention of osteoporosis was the first FDA-approved indication for estrogen therapy. In the Million Women Study, a prospective, cohort study of over one million women, all taking different formulations of estrogen, including oral and transdermal, were associated with a lower risk of hip and vertebral fractures. While not FDA-approved for this indication, estrogen is also effective for treatment of osteoporosis. In a study of 75 women treated with either topical estradiol or placebo for one year, the estrogen group had an increased bone density in hip and spine and 50% fewer fractures.
Estrogen is even effective at protecting bones when started after age 75. One study in 67 elderly women over 75 years old treated with estrogen for nine months showed improvement in bone density in the hip and spine compared to placebo. Improvements in bone density are seen even with ultra low doses of estrogen, like 0.25 mg of oral estradiol or a 0.014 mg estradiol patch. At such low doses there appears to be no stimulation to the uterine lining.
How does estrogen work to prevent osteoporosis? When people think of bones, they may have a visual image of the skeleton that you studied in biology class. They see the skeleton as inanimate, solid scaffolding that simply holds up the rest of the body. Nothing could be further from the truth. Bones are active living tissues maintained by a continuous balance between two types of bone cells, osteoclasts and osteoblasts that work upon an internal collagen framework. Osteoclasts break down bone (resorption) while osteoblasts build bone onto the collagen framework. When bones are injured, osteoclasts rush in to remove the damaged bone and osteoblasts deposit new bone to repair it.
Most women are very familiar with collagen because it is an important support structure which plumps up the skin preventing wrinkles. However, few are aware that collagen is also present in fingernails, hair, tendons and importantly, in bone. Since collagen normally declines with aging, reduction in the collagen framework can further weaken the bone leading to “brittle bones” commonly seen in elderly individuals. In animal studies, loss of estrogen increases immune cells that produce a protein called tumor necrosis factor (TNF) that increases the formation of osteoclasts. With an increase in osteoclasts over osteoblasts, the net result is bone resorption or bone loss leading to osteoporosis. Estrogen decreases this accelerated bone resorption and also plays a role in improving calcium absorption in the intestine.
Lifestyle measures which will further increase bone density include weight-bearing exercise, taking in adequate dietary calcium, taking adequate vitamin D, and treating inflammatory conditions that cause increased bone loss.
Excerpt from “Outliving Your Ovaries” © 2012 by Marina Johnson MD. Dr. Johnson has no financial conflicts of interest or ties to any pharmaceutical company. Her only objective is determining the most effective, safest therapy for patients.