BONE DENSITY AND OSTEOPOROSIS ISSUES

Dr,….But what about bone density??

This is a question I am confronted with daily, when we discuss women’s health.

After 40yrs in medical practice as a general practitioner, and diagnostic radiologist, doing BMD testing on many patients since 1996, it is reasonable to expect that I am able to have certain strong opinions about this issue:

When we started to do BMD testing on women, the availability of BMD machines were few and far apart. Initially we did BMD testing on older women who had fractures after injury. They were mostly post menopausal women in their seventies and aighties. We found many to be osteoporotic. We thus assumed that it is a disease caused by “estrogen deficiency” as a detriment of the menopause.

As BMD machines became more available and more utilized, a different picture emerged: It was found that low bone density is also seen in younger women before the menopause and also in men. New thoughts about the causes of low bone density were formulated, and some of there are discussed below:

    • It as a disease of changing lifestyle.

When one exercise a muscle to be stronger, it enlarges (hypertrophy) if the muscle is not used, it atrophies and becomes smaller. The same happens to bone. If you do not use it and do not put weight and stress on it, why then the need to be strong. We now live sedentary lives of sitting and inactivity. We do not carry heavy weights any more and machines or computers are doing the job. Why need our bones to be heavy and strong?

  • Our children are much less active during their bone building years up to 25 than before. Kids in the 1920-1980ties had to do many tasks and activities that bear weight and build their bone mass. Without these activities, the peek bone mass is lower than 50 yrs ago. They start off with a bone mass deficit, and will reach osteoporosis levels at an earlier age than before.
  • Exposure to sun (Vit. D) is much less, being indoor kids.
  • Our diet today lacks the essential raw and green vegetables so essential for good bone nutrition.
  • Our affluent society consumes too much animal proteins that suppress Calcium uptake in bone.
  • Our society is exposed to many drugs and chemicals that are detrimental to bone growth. Steroids are often used indiscriminately, and these drugs weaken our bones. Diuretics cause us to lose calcium. Overuse of antibiotics kills our intestinal flora responsible for Vit. K production. Many other drugs are detrimental for our bone health, and toxic, like chemotherapeutics.
  • Toxic agents like alcohol, smoking, break down our bones and are socially acceptable today.

Taking there facts into consideration, one could clearly understand the following:

  1. Overweight women carry an extra burden, and are less likely to develop osteoporosis.
  2. Alcohol abuse and smoking cause low BMD.
  3. Anorexics develop osteoporosis.
  4. Chinese and Japanese women, although of small built, are less likely to develop osteoporosis. They eat more vegetarian and are more active into age.
  5. African women in rural communities are seldom affected by low BMD. They also go through menopause and hardly ever use HRT.

HORMONES AND THE BONE

Let us consider the graph below, depicting our bone density over a lifespan:

Life time bone density

  1. Men reach a higher peek bone mass at age 25 than women(perhaps more active and less likely to have dietary preferences)
  2. Women start to lose bone younger (35), long before the menopausal estrogen decline. She still has her full ovarian function at this age. Surely nothing to do with estrogen “deficiency”
  3. She loses bone faster than men in the menopausal years, but look at what happens after 60 when her estrogen levels are even lower: She stop the fast decline and now loses bone at the same tempo than men. This is strange and do not fit in with the “estrogen deficiency” hypothesis.
  4. Having a lower peek bone mass than males, she is more likely to reach the osteoporosis levels, when she loses bone in the later years(like men)

BONE STRENGTH DYNAMICA

Bone strength is a function of breakdown and new bone formation. The osteoclasts break down old bone and the osteoblasts fill the gap with new healthy bone. There are no estrogen receptors on the osteoblasts and thus no stimulation of new bone formation. At the most, estrogen inhibit breakdown of old bone by the osteoclasts. Bone density is thus seemingly preserved or decline slowed, but new bone is prevented from being formed.

Let us hear what is Prof.W.J. Serfontein (M.Sc. PhD) view on this:

Among the other arguments in favor of HRT as it is currently used is the assumed reduced risk of osteoporosis and heart attack. The former assumption is only partly true and the latter is not true. Bone density is determined by the balanced activity of two types of bone cells: osteoclasts that constantly break down bone, and osteoblasts that remodel new bone. Estrogens suppress osteoclastic activity, thus suppressing the rate at which bone is broken down, but they have no effect on osteoblastic activity. There are no estrogen receptors on osteoblasts. For this reason, estrogen therapy is initially beneficial for a period of 7 – 10 years. The protective effect wanes and women who had been on HRT were found to lose bone faster when HRT was stopped than those who had not been on HRT.6 Since HRT has to be stopped at some stage because of increased cancer risk, it has been shown that whether a woman had been on HRT during her menopausal years makes no difference to her bone density in later life when the danger of osteoporosis is greatest.7 HRT therefore has only temporary advantages at best.8
The fact that estrogen is not a major role player in osteoporosis is further supported by the well-known fact that osteoporosis starts at age 30 at a stage when estrogen

Levels are still high.

What were the conclusion of the WHI study regarding osteoporosis prevention and hormone replacement?

Medscape: at this point, what are the primary indications for estrogen-alone therapy?

Dr. Rossouw: According to the FDA, the indications for estrogens-only therapy are the treatment of moderate to severe hot flashes and night sweats, the treatment of vulvovaginal atrophy (but topical estrogen is preferred), and the prevention of osteoporosis. For osteoporosis prevention [with] estrogen and estrogen plus progestin, the FDA advises that the need for treatment must be clearly established, and that other treatments must first be carefully considered. In other words, hormones are no longer a first-line treatment for the prevention of osteoporosis

BOTTOM-LINE CONCLUSIONS REGARDING OSTEOPOROSIS

    • Too much emphasis is placed on HRT for the prevention and treatment of osteoporosis.
    • Many factors play a role in prevention, and more emphasis should be placed on lifestyle changes, diet and exercise.
    • There are good bone support drug available for treatment and prevention other than HRT which have many undesirable side effect.
    • Bone density measurement should be started well before the menopause to identify those women at risk and to start specific measures to prevent their declining into the fracture risk category.

EMERGING TRENDS IN THE DIAGNOSIS AND TREATMENT OF OSTEOPOROSIS

MEDICOGRAPHIA,  VOL. 28, No. 1, 2006 23

The need for long-term treatments in order to achieve clinically meaningful benefits 2 decades later, when the risk of fracture becomes high, contrasts with two recent observations. The duration of hormone therapy in clinical practice is much shorter: It has been estimated that only about 10% of American women continue treatment for more than 1 year.’ In addition, the results of the Women’s Health Initiative (WHI) study’ indicate a benefit- side effect ratio that is particularly negative the longer the duration and the older the age of the patients! As a consequence of these obvious contra­dictions, the European Agency for the Evaluation of Medicinal Products (EMEA) decided to modify the label of hormone replacement therapy, deleting the indication of prevention and treatment of osteoporosis. These various considerations have suggested that interventions might be more optimally targeted in later life, perhaps with the use of non- hormonal treatment modalities.” The risk of osteoporosis might still be considered when deciding on the appropriateness of initiating hormonal therapy at the menopause, but only as an additional reason to the main aim of relieving menopausal symptoms. Gynaecologists should become aware of this new philosophy and redesign their approach to osteoporosis prevention. Who will manage the diagnosis and treatment of osteoporosis?—Adami