Every year more than half a million American women develop osteoporosis (brittle bones), a very serious and often debilitating disease. Of these women, 200,000 over the age of forty-five will fracture one or more bones. Forty thousand will die of complications following their injuries. Thousands of others will be disabled for the rest of their lives. With its complications, it is the twelfth most common cause of death in the United States. For women, it must be considered a major killer. Yet, with all these impressive statistics, osteoporosis seems to be neglected. An incident such as a woman over sixty-five fracturing a hip is easily dismissed as one of the inevitable consequences of getting older? Possible reasons for this are: one, that brittle bones are a natural result of the aging process; or, two, we have not been much concerned about the health of our older citizens.
Although osteoporosis is, in a sense, an exaggeration of the normal bone loss that accompanies aging in women, we can dispel any notions that it is inevitable.
Osteoporosis is simply a loss of bone. Therefore, to understand how it occurs, it is important to know the processes within our bodies that affect bone growth and bone destruction. Bone is the strongest tissue in our structures; but it is not a solid mass. Bones are tubular shaped with a central canal (marrow cavity) surrounded by a complex lattice-work of protein (collagen) and crystals made of calcium and phosphorus (hydroxyapatite). The marrow cavity contains blood-forming cells, which, though housed by bone, constitute a separate organ, the bone marrow. Most of our blood cells are produced there. These cells pass through the bone tissue into the bloodstream by traversing millions of small blood vessels. Bone tissue is not solid. It has passages for numerous blood vessels and nerve fibers.
The blood vessels are not closed conduits passing from the circulation to the marrow. They nourish the bone tissue itself. Bone tissue is in constant contact with the bloodstream. Through this contact, the blood delivers substances to the bone and the bone releases substances into the blood. The intimate relationship between blood and bone is essential. Bone is a living tissue. Its protein matrix is constantly breaking down and rebuilding. As with all body proteins, bone collagen is always in a state of flux, moving new amino acids (building blocks for proteins) from the blood into its structure and releasing used amino acids into the blood.
Within the protein matrix, bone consists of a hard substance made mostly from calcium and phosphorus. This substance, called hydroxyapatite, is constantly remodeling. Like the amino acids, calcium and phosphorus move freely from the blood into the bone and from the bone into the blood. When new bone is constructed, more calcium and phosphorus pass into the structure. When bone tissue is destroyed, more of these minerals move out of the bone. If a similar amount is moving in and out of the bone tissue, there is no net change in bone mass.
Calcium is the key element in maintaining the structural integrity of bone; but that is only one of the important functions of this mineral. Calcium is essential for every cell in the body. Without it, nerve cells cannot conduct impulses and muscle cells cannot contract. Calcium is essential for the brain to generate nerve impulses and for the heart to beat. We cannot live unless this essential mineral is available to all the tissues of the body. Ninety-nine percent of it occurs in bone; and only one percent circulates in our blood and other tissues. Yet, this one percent is so critical that the body has evolved a complex machinery to keep the tissues supplied with the precise amount of calcium. This machinery is responsible for regulating calcium within the bloodstream, ensuring that the tissues get an adequate supply. Concurrently, it protects them from receiving too much. Excess calcium within the tissues can have serious consequences. Bone plays a crucial role in this regulatory process.
The calcium in our bones is also a vast reservoir in which excess calcium can be safely stored. If calcium is not available for our tissues, it will slowly be withdrawn from our bones. The more of the mineral withdrawn the thinner our bones become. Eventually they become so thin that the everyday stresses of life are too much. Fractures may occur. When this happens, we are suffering from the effects of osteoporosis.
From the moment a calcium molecule enters our body, the regulatory machinery controls it. First, the amount absorbed is regulated by a hormone (dihydroxy-vitamin D) made in the kidney from vitamin D. This nutrient is obtained from our diet or from a precursor (pro vitamin D) which is activated by ultraviolet light in our skin. The hormone is necessary for calcium to be absorbed by the intestinal cells and passed into the bloodstream. Once in the bloodstream, the calcium molecule becomes part of a pool. If its level should fall below a critical point, the parathyroid glands (four tiny structures at the base of the thyroid gland) secrete parathyroid hormone, which increases the level of calcium in our blood by signaling the kidney to convert vitamin D to its active form. This product increases calcium absorption. It can also stimulate the breakdown of bone to release calcium into the bloodstream.
The body uses another hormone (calcitonin), produced in the thyroid gland, to protect against withdrawal of too much calcium from our bones. We do not understand how this hormone works. Somehow, it inhibits the action of cells within the bone tissues that break down the bone (osteoclasts). These three factors (parathyroid hormone, dihydroxy-vitamin D, and calcitonin) are the principal means for regulating calcium metabolism. They are sensitive to the amount of calcium in the blood, and they interact with each other. Blood-calcium levels rarely get too high or too low.
Other hormones within our bodies help in determining whether bone loss will occur.
Unlike the three hormones mentioned above, these do not regulate blood calcium directly. They are secreted for a variety of reasons, but not in response to the level of blood calcium. The most important is the female sex hormone estrogen. Estrogen is a bone-protecting hormone. Yet, it does not have any activity on bone itself. It works indirectly by blocking the action of parathyroid hormone. Thus, when estrogen is present, greater amounts of parathyroid hormone are necessary to cause bone resorption. If estrogen is absent, the brake releases, and even small amounts of parathyroid hormone will release large quantities of bone calcium. When the fine-tuning of the calcium-regulating mechanism is disrupted, more calcium gets into the blood than required. The excess is excreted in the urine and, thereby, lost to the body. Also, estrogen stimulates secretion of calcitonin (the primary bone-protecting hormone). So, when estrogen levels are low, calcitonin levels tend to be low and bone resorption increases. Finally, there is evidence that high levels of estrogen (such as those occurring during pregnancy) stimulate the kidney to convert vitamin D to its active form, thereby increasing the amounts of calcium absorbed. The absence of estrogen will produce an imbalance between the bone-resorbing hormone (parathyroid hormone) and the bone-protecting hormone (calcitonin), in favor of the former. Calcium will be lost from the bones and excreted in the urine. In addition, the one hormone that might reverse this loss, dihydroxy-vitamin D, may not be made as efficiently without estrogen. Therefore, it is not surprising that menopause, when estrogen falls to very low levels, is the key event in the development of osteoporosis in women.
The adrenocortical steroids are another group of hormones affecting bone metabolism. These hormones work directly on bone tissue, causing resorption. Both estrogen and another female sex hormone, progesterone, prevent the action of adrenal hormones on bone tissue. Thus, during menopause, when both of these sex hormones decline, the adrenal hormones are given greater license to cause breakdown of bone. Finally, two other hormones affect bone. Growth hormone from the pituitary gland promotes growth of all tissues, including bone, while thyroid hormone promotes bone resorption.
Therefore, bone tissue is under a variety of hormonal influences. Table 26 shows those hormones that promote bone growth and those which promote bone loss. When all of these regulators are in balance, bone growth and loss stabilize so that bone mass does not change. But, if the hormones that regulates bone growth predominate (as during early life), bone mass will increase. If the hormones involved in bone loss predominate (as after menopause), bone mass will decrease. Anything that promotes the action or maximizes the effect of the bone-growth hormones will lower our risk for osteoporosis. Anything that promotes the activity or maximizes the effect of the bone-loss hormones will raise our risk for osteoporosis.
Table 26. Factors Affecting Bone Growth or Loss
Bone Growth Bone Loss
Calcitonin Parathyroid hormone
Dihydroxy vitamin D
Estrogen Adrenocortical hormones
Growth hormone Thyroid hormone
Let us trace the history of a typical bone as a woman goes through her normal life cycle. During infancy and early childhood, the bone-growth hormones predominate, and calcium is deposited into the growing bones. At puberty, estrogen and progesterone levels increase sharply, further promoting bone growth. During pregnancy, levels of estrogen and progesterone again rise, promoting bone growth in the mother and fetus. In addition, the placenta makes dihydroxy-vitamin D during pregnancy, further promoting bone growth. If the mother nurses her infant, the levels of estrogen remain high and bone growth remains good.
A few years before menopause, progesterone levels begin to fall. The balance tips in favor of the bone-loss hormones. At menopause, estrogen levels fall dramatically and the bone-loss hormones become increasingly dominant. The result: bone is rapidly resorbed. At about age sixty-five, adrenal cortical activity lessens and levels of adrenal steroids drop. This tends to correct the imbalance; and bone loss slows down.
Who is at risk, and how may that risk be minimized? Osteoporosis relates to several risk factors. Some of these risks are under our control and can be modified by proper diet and certain kinds of exercise. In this sense, this disease is no different from atherosclerosis, hypertension, obesity, diabetes, and some types of cancer. Like them, certain people are more prone to get it than others.
To minimize our risk for osteoporosis, we must take advantage of the times when our hormonal balance favors bone growth. Unfortunately, most women do not become concerned until they are near menopause or later. Then, the balance of hormones is not in their favor. Under these circumstances, osteoporosis often occurs in spite of the preventive measures. Thus, women should do whatever possible to promote maximum bone growth during childhood and the childbearing years.
Certain external forces influence bone growth and resorption. Diet and exercise, particularly weight-bearing exercise, are primary. If we do not get enough calcium in our diet, no matter how efficiently our body deposits it, we will not get enough into our bones. A diet deficient in calcium will promote bone loss. The proportion of calcium in our diet that can be absorbed from the gastrointestinal tract is also important. Certain dietary elements promote calcium absorption and indirectly promote bone growth. Other elements of the diet inhibit calcium absorption and indirectly promote bone loss. We will examine these interactions when we discuss eating practices to lower our risk for osteoporosis.
Bones are made to bear weight, and weight bearing increases bone mass. When bones are not supporting weight, they lose mass. Thus, long periods of immobilization or bed rest will result in loss of bone. The importance of weight bearing has become dramatically apparent through studies of astronauts. Even a short period (two weeks) of weightlessness results in measurable amounts of bone loss. This is the most significant medical problem facing our space program. (We still do not fully understand why the state of weightlessness induces such profound changes.)
The first and most important risk factor for the disease is our gender. Women are ten times as likely to suffer from severe osteoporosis as men, largely because of testosterone, the main male sex hormone. Like estrogen, it is a bone-protecting hormone. Whether it works the same way as estrogen is not known. Since men do not undergo menopause, the balance between hormones that promote bone growth and those that promote bone loss is better maintained after men reach middle age. Another reason the ultimate toll of this disease is higher in women than in men is that women live about eight years longer than men. The older we are, the greater our risk. For that reason alone, we can expect more women than men to become osteoporotic. Beyond the sex-hormone differences, males start life with a larger bone mass and lose bone more slowly with age. Their increased weight and muscle mass place more stress on their bones. They also have higher levels of calcitonin.
However, men are not immune to the disease. As male life expectancy increases, more cases of osteoporosis will appear in men. Several of the risks for osteoporosis will pertain only to women. Others will pertain to both genders. If you are male and have enough of these risks, it would be prudent to take preventive measures. The scoring system for osteoporosis, detailed in the next section, places a woman at greater risk than a man. However, some men will reach at least the lower levels of an at-risk category. These men should modify their diets in the same manner as for women who show high risks.
The earlier women undergo menopause, the greater their risk for osteoporosis. Most women experience natural menopause between the ages of forty-five and fifty-one. Of these, about 25 percent will exhibit osteoporosis. If menopause begins before age fifty, the rate is slightly higher; and it is lower if the changes begin after age fifty. Women who have their ovaries removed before natural menopause exhibit a 50 percent risk of developing osteoporosis. Again, the earlier the ovaries are removed, the greater the risk. Estrogen therapy may reduce the risk; but any woman who undergoes surgical removal of her ovaries before undergoing natural menopause must be considered at high risk.
While the actual mechanisms by which our genes affect our bones are unknown, there is no doubt that a strong family history is an important factor. Try to fill in as many branches of your family health tree as possible. Osteoporosis may not be the listed cause of death, so it is not enough to ask what disease a relative died from. We must delve much deeper. Were there any fractures at older ages, particularly fractures of the hip or vertebrae? Did your grandmother limp? If so, at what age did she start? Was there a noticeable shortening of stature in any of your female relatives as they got older? If these symptoms appeared early, your risk for osteoporosis becomes greater. Taking a thorough family history is important for men and women. The genetic effect asserts itself in both genders.
Osteoporosis is less common among African-American women than among white women. African-American women have larger bones at skeletal maturity. They also tend to have larger muscle masses that exert more stress on their bones. African-American women also tend to lose bone at a slower rate than white women, and some studies have shown that they also have higher blood levels of calcitonin. Thus, if you are an African-American woman, you will be doubly protected. You start life with bigger bones and therefore can withstand more bone loss. You lose bone more slowly, and, hence, will sustain less loss. Interestingly, there is no such protection for African-American men.
There is less information about other ethnic groups. Women whose ancestors came from the British Isles, Northern Europe, China, or Japan are more likely to develop osteoporosis than those of African, Hispanic, or Mediterranean ancestry. The risks for Jewish women seem to fall somewhere between that of low-risk African-Americans and high-risk whites. Generally, there appears to be an association between skin pigmentation and the degree of risk. The whiter our skin, the higher our risk.
The thinner we are, the higher our risk for osteoporosis. Obese women rarely get the disease. During a woman’s reproductive life, the ovaries produce large quantities of estrogen and progesterone plus small amounts of the male sex hormones, androgens. The adrenal glands also make androgens. After menopause, the ovarian output of estrogen and progesterone drops to very low levels. However, the ovaries and adrenal glands still produce the same quantity of androgens. Fat tissue is able to convert these androgens to estrogens. The fatter a woman’s body, the more estrogen she will be able to produce before and after menopause. Fat, therefore, reduces her risk for osteoporosis.
If you are small in stature and narrow in build, your risk for osteoporosis increases. You have less bone. Given the same rate of loss, you will reach the osteoporotic, fracture-prone state sooner than your more sturdily built counterpart. This is also true for men. Another reason very thin women (and men) have an increased risk for osteoporosis is that the amount of stress exerted on their bones is less than for heavier people. This results in increased bone loss.
Oral contraceptives contain estrogen and progesterone, which stimulate bone growth. Women who take oral contraceptives, particularly if for a long time, seem to have greater bone mass when they enter menopause. Therefore, their risk may be somewhat less than that of women who have not used this form of contraception.
A woman who has never been pregnant has an increased risk for osteoporosis. During pregnancy, levels of estrogen and progesterone are very high and will promote bone growth (if calcium intake is adequate). Since higher estrogen levels increase the production of active vitamin D hormone, and because the placenta makes this hormone, calcium absorption is more efficient during pregnancy. With a diet adequate in calcium, pregnancy can be a time to acquire stronger bones. If her calcium intake is low, the increased demand for calcium during pregnancy will be supplied by the mother’s bones, leading to a reduction of bone mass. This happens in developing countries where women whose diets have been inadequate for most of their lives have repeated pregnancies. There is an old adage, “a tooth for every pregnancy.” The teeth are not considered to be part of our calcium reservoir, but this extreme can happen.
Although a woman who breast-feeds loses a large amount of calcium each day, there is no evidence that breast-feeding increases her risk for osteoporosis. The reverse may be true. Her hormonal milieu during lactation should promote bone growth. We need more knowledge on the relationship between lactation and osteoporosis, but the fear of osteoporosis is not a valid reason for avoiding breast-feeding. Breast milk will supply an infant the most highly absorbable form of calcium and give the newly forming bones a head start.
If you are confined to bed for a long period, or have to spend much time in a wheelchair, you will be at increased risk for osteoporosis. If you lead a sedentary life, your risk is higher than that of a person who is more active. Weight-bearing exercise is important for several reasons. First, such exercise places physical stress on our bones. Our bones respond by becoming larger and stronger. Second, exercise increases the flow of blood to our bones, thereby increasing the availability of bone-building nutrients. Third, exercise generates mini electrical currents that stimulate bone growth. Fourth, exercise alters our hormonal balance, favoring those hormones that protect the bones. One study showed that middle-aged women had increased estrogen levels after six-weeks of moderate exercise. Another study found that middle-aged men who rode exercise bicycles had lower levels of the bone-resorbing adrenal hormones after they exercised.
Measurements of bone density changes resulting from exercise showed—to no one’s surprise—that a number of world-class athletes had denser bones than sedentary people. Still unknown, however, is how much exercise is necessary to gain this increase in bone mass. Some studies suggest that regular exercise by middle-aged people over a sustained period of time (one year or more) will prevent the bone loss that would normally occur at this stage of life.
In summary, leading a very sedentary existence will increase our risk for osteoporosis. Regular exercise may increase our bone mass and thereby reduce our risk, or at least delay onset. It is important to note that the type of exercise that gives these results, such as walking, jogging, cycling, basketball, tennis, etc., tends to place a stress on our bones. Swimming, though excellent for cardiac fitness, does not lower our risk for osteoporosis. The buoyancy of the water takes the stress off our bones.
Smoking places you at increased risk for osteoporosis. Women who smoke generally reach menopause about five years earlier than nonsmokers, and early menopause increases their risk for osteoporosis. Smoking affects the potential of the liver for making the vitamin D hormone that increases calcium absorption. Smokers tend to be leaner than nonsmokers, and lean women are more at risk for osteoporosis. However, it is still not clear whether smoking is an independent risk for osteoporosis. We don’t know exactly how smoking increases our risk; but there are enough other reasons to stop smoking.
Heavy consumption of alcohol can result in osteoporosis in both men and women. Alcohol has a profound effect on liver function, including reduced production of the vitamin D hormone; and it can directly impair the absorption of calcium through the gastrointestinal tract. Men with alcoholism can have severe osteoporosis in their twenties, probably because of liver damage, poor diets, and low exercise levels. We are not sure whether moderate consumption of alcohol over long periods of time will increase our risk for osteoporosis. However, if we are already at high risk, this may further stack the cards against us.
Asthma, rheumatoid arthritis, and ulcerative colitis are among several chronic diseases treated over long periods of time with cortisone or derivatives of cortisone (hydrocortisone, prednisone, dexamethasone, etc.). These drugs can promote profound bone loss and result in severe osteoporosis in both genders at early ages. Cortisone and its derivatives appear to act in two ways. They increase calcium excretion and decrease calcium absorption, thus producing a net calcium loss. They also block the formation of new bone. While the osteoporosis induced by these drugs is similar to the form occurring in postmenopausal women, the drug-induced disease is often severe enough to affect bones such as the ribs, which are spared in postmenopausal osteoporosis. The two types of the disease are additive; thus, anyone treated with these drugs for a long time is at increased risk for osteoporosis.
Certain drugs such as phenytoin, phenobarbital, primidone, and phensuximide stimulate the production of enzymes that break down the vitamin D hormone produced by the liver. A relative vitamin D deficiency ensues, and calcium absorption is impaired. The result is bone loss. Anyone taking these drugs is therefore at increased risk for osteoporosis.
Millions of Americans regularly use antacids to alleviate the symptoms of everything from “acid indigestion” to peptic ulcer. Many antacids contain aluminum, which can cause an increase in the rate of calcium excretion. Sometimes antacids, together with corticosteroids, are used to prevent the gastric upset that these drugs often cause. If you often use antacids, particularly in the combinations outlined above, your risk for developing osteoporosis increases.
Any illness that keeps us in bed for a long time will increase our risk for osteoporosis, and certain specific illnesses will increase that risk over and above the effects produced by lack of weight bearing. Endocrine diseases such as hyperparathyroidism, hyperthyroidism, and overactive adrenals (Cushing’s syndrome), will increase bone loss. Chronic diseases such as diabetes, rheumatoid arthritis, and some forms of kidney disease, may also increase our risk for osteoporosis. Certain gastrointestinal problems, such as sprue or celiac disease, will result in poor calcium absorption from food and, hence, increase bone loss. If you have any of these diseases, your risk for osteoporosis increases.
In some people, periodontal disease may resemble osteoporosis. Bone resorption takes place within the jawbones. Thus, periodontal disease may be a forewarning of osteoporosis.
Of dietary factors that may contribute to the development of osteoporosis, first and most important, is calcium deficiency. No matter how favorable our hormonal balance, if our diet is too low in calcium, our bone mass will decrease. Calcium deficiency is more threatening during certain periods of life, particularly the infant year, than at other times. Bone is being produced at a rapid rate, and hormonal balance is favoring bone growth. The reserves are made ready for later life. If the diet is deficient in calcium, or if calcium cannot be adequately absorbed, the impaired bone growth can never be replaced. Breast milk is the best food for an infant. The calcium it contains is better absorbed than calcium from cow’s milk. For mothers who do not breast-feed, an infant formula that simulates breast milk, as closely as possible, is recommended for the first year of life.
Adolescence is another time when inadequate calcium intake can be very risky. It can lead to osteoporosis later in life. An adolescent undergoes the most rapid rate of bone growth that will occur during any period of his or her life. Unfortunately, the eating habits of many adolescents promote calcium deficiency. Some eat only foods that are low in calcium or high in phosphorus (which interferes with calcium absorption). Others diet so rigorously that they do not take in enough food to supply their calcium needs.
Pregnancy is another period when insufficient calcium intake can lead to a reduction of bone mass. The fetal skeleton is rapidly consuming calcium. The mother’s body is in a hormonal state that favors bone growth; but, unless adequate calcium is available from her diet, the maternal bones will be the main source of this mineral. Fetal bone growth will take place at the expense of maternal bone mass. A diet adequate in calcium will supply enough for her fetus and concurrently allow the mother’s own bones to increase in mass.
If a woman nurses her infant, her milk will have to supply large amounts of calcium. If dietary calcium is inadequate during this period, her bones must supply the calcium. Lactation is a critical time when a lack of dietary calcium can erode bones. Hormones favor bone growth during lactation. If enough calcium is available to satisfy the needs of both her infant and her bones, a woman can finish nursing with an increase in bone mass.
We have seen that the body regulates the amount of dietary calcium absorbed from the intestines into the blood and the amount excreted by the kidneys into the urine. This balance between absorption and excretion determines whether sufficient calcium is available for bone growth or if calcium must come from our bones to supply our tissues.
Several other constituents of our diet will affect our calcium balance. The first is vitamin D. It is so important that our bodies maintain two methods for supplying it. Our skin contains a substance which, when exposed to the ultraviolet rays of the sun, is converted to vitamin D. In addition, our food supply contains vitamin D, naturally (in fish oils, for example) and through fortification (as in dairy products). However, vitamin D, whether consumed in the diet or converted from the skin, has very little activity within our bodies. To become active, it must undergo two chemical modifications. The first takes place in the liver, which manufactures an intermediate form of vitamin D. This intermediate form is somewhat more active than regular vitamin D, but it is nowhere near as active as the final form made in the kidney. That form, sometimes called vitamin D hormone, is essential for calcium absorption. We have already seen how liver disease or kidney disease, by interfering with the manufacture of vitamin D hormone, can increase our risk for osteoporosis .
However, if insufficient vitamin D is available for conversion to the active hormone, even when our liver and kidneys are working perfectly, less hormone will be made. The results are poor calcium absorption, retarded bone growth, increased bone loss, and greater risk for osteoporosis. It is important, therefore, to get enough vitamin D. Too much, however, is of no advantage. The body converts only as much as it needs. An excess of vitamin D can be quite harmful. It can result in the abnormal deposition of calcium in soft tissues such as the kidney (kidney stones).
The amount of phosphorus in our diet will also affect our calcium balance. Like calcium, phosphorus is essential for life. Also like calcium, the greatest amount of phosphorus is present in bone. Unlike calcium, however, phosphorus is so abundant in our food that primary phosphorus deficiency almost never occurs. In most American diets, there is such an excess of phosphorus that it can promote negative calcium balance. This happens because calcium and phosphorus are transported from the intestines into the blood by the same system. These minerals do not diffuse passively through the intestinal wall. They are borne by protein molecules specially adapted for this work. These “carrier” molecules have a specific and limited number of sites to which a calcium or phosphorus molecule can attach itself. Phosphorus competes with calcium for transport sites into the body; the more phosphorus we take in (particularly at the same meal in which calcium is consumed), the less calcium we absorb. (The phosphorus in soft drinks cannot be ignored.) The less calcium we absorb, the more negative calcium balance, the slower bone growth, the faster our bone loss, and the greater our risk for osteoporosis.
The high-protein content of most American diets will also induce negative calcium balance. Exactly how this happens is not entirely clear, but studies have shown that subjects fed a very high-protein diet will excrete more calcium in their urine than subjects fed a lower-protein diet. The most concentrated form of protein and phosphorus in our diet is meat. Thus, heavy meat eaters will be at increased risk for osteoporosis. Several studies have shown that vegetarians, particularly ovo-lactovegetarians, have more dense bones than meat eaters. In one study, bone density was greater in vegetarian women at age seventy than in fifty-year-old women who had consumed meat for most of their lives.
Finally, the large amount of salt ingested by most Americans has a negative effect on calcium balance. The excess sodium must be excreted by the kidneys. In this process, extra calcium is excreted. Though the mechanism is indirect, the more sodium we consume the more calcium we will lose and the higher our risk for osteoporosis.
To start scoring your risks:
If you are a woman you are automatically at higher risk than if you are a man. All women therefore begin with a score of 5; all men with a score of 0.
Racial tendencies toward osteoporosis pertain only to women, not to men. If you are a man, score 0 no matter what your race or ethnic background. If you are an African-American woman, score 0. If you are of Hispanic, Mediterranean, Eastern European, or Oriental background, score 1. If you are a woman of northern European origin, or of very fair complexion, score 2.
If your mother or sister or several very close relatives have or have had osteoporosis, score 3. If a few aunts or cousins have or have had osteoporosis, score 2; if a scattering of distant relatives, 1; and if nobody in your family was affected, score 0.
If you are a woman who had surgically induced menopause before natural menopause, score 5. If natural menopause occurred before age forty-five, score 3; if between age forty-five and fifty-five, score 0. Thus, if you underwent surgical menopause before reaching the age of natural menopause, you are automatically at high risk for osteoporosis. Even if you are treated with estrogen, you should still start a program of diet and exercise designed to prevent the disease.
- If you have a large frame and broad bones, score 0; an average frame, 1; and if you are petite and slight of build, score 2.
- Anyone of either gender who is 20 percent or more below ideal weight increases his or her chances of developing osteoporosis. If you fall into this category, score 2; between 10 and 20 percent, score 1. If your body weight is above this figure (even if you are obese), score 0.
- If you have been taking oral contraceptives for a long time, it has given you some protection against osteoporosis. How much protection is unclear. If you are such an individual, subtract one point from your final score. However, if this one point is the deciding factor between whether or not to introduce preventive measures, it would still be prudent to undertake those measures.
- If you are a woman who has never been pregnant, score 3; if you have had one pregnancy, score 1; more than one, score 0. While breast-feeding one or more infants probably offers some protection, we do not know enough about it to assign a risk number. However, if your calcium intake was adequate, you can expect an added bonus in lowering your score.
- If you have been bedridden or confined to a wheelchair for a long time (months or years), score 5; this is a very significant risk factor. Lesser periods of non-weight-bearing time should be scored proportionally. If you live a sedentary existence, score 2; take moderate but occasional exercise, score 1; engage in regular exercise, score 0.
- If you are a heavy cigarette smoker, score 1.
- If you are a practicing alcoholic, you need help for many reasons, only one of which a higher risk for osteoporosis. Whether a man or a woman, if you fall into this category, score 5. If you are a woman, this score will automatically place you in the high-risk category. Heavy drinkers, even if they are not alcoholics, should score 3.
- If you have taken cortisone-like drugs for a long time, score 5, This is a very significant risk factor. It applies to both men and women. For shorter periods on these drugs, adjust your score appropriately, but those short periods can add up.
- Anticonvulsant drugs will increase our risk, but not as much as cortisone and its derivatives. Score 3 if you have been taking anticonvulsants for a long time.
- Antacids also increase our risk. If you regularly use types that contain aluminum, score 2.
- Whether a man or a woman, if you suffer from hyperparathyroidism, hyperthyroidism, or overactive adrenals (Cushing’s syndrome), score 3. If you have diabetes, rheumatoid arthritis, or certain forms of kidney disease (ask your doctor which kinds), score 2.
- If you are a vegetarian, particularly an ovo-lactovegetarian, score 0. If you eat the “typical” American diet, score 2. Heavy meat eaters should score 3. If you cannot consume foods high in calcium (that is, if you have a lactose intolerance), score 3. If you are a constant dieter, taking in 1,200 calories or less, for long periods in your life, score 2.
You are now ready to calculate your risk score for osteoporosis. If the total adds up to 10 or more, you are at enough risk to institute preventive measures. You will see that if you are a woman, your chances for reaching a high-risk score of 10 or more are much greater than if you are a man. This is not surprising. Osteoporosis is much more common in women than in men. For a woman, either surgical menopause or severe alcoholism or chronic ingestion of cortisone like drugs, alone, is enough to place her in the high-risk category. However, men can also be at high risk. For example, the heavy-drinking, very thin, slightly built man who smokes has a score of 10 or higher. Similarly, a man with a strong family history of the disease, whose diet is poor, and who takes certain medications can also be at high risk.
A score of 10 or above places either a woman or a man at high enough risk to alter his or her diet and exercise level. Since it is much easier for a woman to reach this score, many more women will find themselves at this risk level than men. However, for those men who score 10 or above, the dietary advice is as important as for women.
We cannot estimate risk precisely. The scores allotted to the various categories have been assigned to err on the side of overstatement of risk. Since preventive measures outlined in the next section are without danger and have positive health benefits other than merely lowering our risk for osteoporosis, it would be prudent to institute them more often than not.
If your score is 10 or above, your risk for osteoporosis is great enough to instigate whatever preventive measures you can. Concurrently, you may wish to undergo tests to determine actual bone density. These tests are available in many hospitals and involve newer forms of tissue-imaging that subject you to little or no radiation. They are helpful in determining if you have already undergone significant bone loss. They are also useful for measuring the degree of probable success of any preventive measures you institute. They are not designed to influence your decision to begin preventive measures. Even though the tests may reveal normal bone mass, if your score is 10 or above, you should begin a preventive program before significant bone loss has occurred. Later tests will tell you if your program is succeeding.
Thoroughly examine your score. Some of the risk factors are under your control and can be eliminated. Once these risk factors have been eliminated, to reduce your risk further, pay special attention to your diet and to the type and amount of physical activity you engage in.
The principles of a diet designed to lower our risk for osteoporosis include: Adequate calories to attain and/or maintain ideal weight; a calcium intake of 1 gram (1,000 milligrams, or mg) per day or 1,500 mg during periods of high calcium need—such as adolescence, pregnancy, and lactation; a moderately low phosphorus intake; a moderately low protein intake; avoidance of excess dietary sodium; and adequate, but not excessive, amounts of vitamin D.
Calories are important for two reasons. If we are too thin, our risk is increased. Additionally, we are unlikely to fulfill our calcium requirement when we are consuming too few calories.
Women who, for cosmetic reasons, are constantly consuming less than 1,500 calories per day, to maintain a weight that is 10 or 20 percent below their ideal weight, are endangering their bones. We often assume that the thinner we are the better. If we are at high risk for osteoporosis, this is not true. Being too thin may be as much of a health risk as being too fat.
If you are truly obese, and also are at increased risk for osteoporosis, you will need to follow the regimen outlined in Chapter 4. Avoid crash dieting or the use of fad diets. They are often very low in calcium. Emphasize foods of high nutrient density with specific attention to calcium. Choose foods of low-calorie and high-calcium content. For example, skim milk is much better than whole milk; low-fat yogurt is better than sour cream on your baked potato; cottage cheese is preferable to cream cheese. Finally, set realistic goals that you can reach and maintain without constantly restricting calories to unrealistically low levels. If you are overweight but out of the danger zone, you will reap at least one benefit of being slightly overweight. Your risk for developing osteoporosis will be lessened.
The recommended dietary intake for calcium (set by the Food and Nutrition Board of the National Academy of Sciences) for an adult woman is 800 mg per day (1,200 mg per day during periods of increased calcium demand). We recommend that the amounts be slightly higher (see the principles outlined above) because women who are at risk for osteoporosis often begin with a deficit. The levels we set are attainable by eating a proper diet. Calcium supplements are necessary only if you cannot consume adequate amounts of high-calcium foods. Table 27 lists portions that will contribute approximately 300 mg of calcium content per serving.
Table 27. Calcium Content of Foods
(Each portion provides approximately 300 mg of calcium. )
Almonds 1 cup Ice cream (reg)12/3 cup
Amaranth 4 oz. Kelp 1½ oz.
Broccoli 2¼ cups Milk:
Cheese: whole, low fat, or
cottage 12 oz buttermilk 8 oz.
sandwich style 1½ to 2 oz. Tofu 8 oz.
Custard 1 cup Tortillas (6 in.) 5
Fish (canned):* Yeast (brewer) 14 tbs.
mackerel 3½ oz.
salmon 5½ oz.
sardines 3½ oz.
*This calcium level includes the softened bones. If the bones are discarded, the calcium content is greatly reduced.
Most of the high-calcium foods fall into the category of dairy products (Americans normally get about 80 percent of their calcium from dairy products). However, by making careful food choices we can get the required amount of calcium with a much lower percentage coming from milk and milk products. For example, any daily menu that includes single portions of any two of the following will supply more than half your calcium requirement: almonds, broccoli, canned fish (with bones), kelp, tofu, tortillas, kale, turnip or collard greens, macaroni and cheese, pizza, beef tacos, or cheese or meat enchiladas.
Although the rest of your diet will supply some calcium, you will generally need some dairy foods to reach your requirement. If you cannot eat any dairy products, you should take a calcium supplement. A more complete discussion of calcium supplements will follow.
A diet high in phosphorus will inhibit calcium absorption and thereby reduce the amount of calcium getting into our bodies. For optimal calcium absorption we should strive for a dietary pattern that gives us twice as much calcium as phosphorus. The average American consumes more phosphorus than calcium. The major dietary sources of phosphorus are meat, particularly red meat, and carbonated soft drinks. These foods contain very little calcium. Thus, the calcium-phosphorus ratio is very low. It should be 2:1. Foods such as beef liver, bologna, fried chicken, corn on the cob, frankfurters, ground beef, ham, lamb chops, and pork chops have a calcium-phosphorus ratio from 1:15 to 1:45. Most phosphorylated soft drinks contain no calcium. By contrast, many green leafy vegetables, such as spinach and lettuce, have more calcium than phosphorus and hence have a favorable calcium-phosphorus ratio. Dairy products contain significant amounts of phosphorus, and their calcium-phosphorus ratio, although favorable, is not as good as that of some of the plant foods. A diet to lower our risk for osteoporosis should not only be high in calcium but also be relatively low in phosphorus.
Table 28 is a list of high-phosphorus foods and the average phosphorus content per serving.
Table 28. Phosphorus Content of Selected Foods
Food Weight Mg P
Beef liver 3 oz. 405 Milk, skim 8 oz. 233
Calf’s liver 3 oz. 456 Cottage cheese,
Lean beef 3 oz. 207 creamed 1 cup 319
Chicken, light 3 ½ oz.280 Cheddar cheese 1 oz. 136
Chicken, dark 3 oz. 188 Bread, wheat 1 slice 71
Pork, lean 3 oz. 185 Bread, white 1 slice 28
Egg, large 1 (57g)103 Peanuts 1 oz. 114
Milk, whole 8 oz 227 Kidney beans 1 cup 259
Milk, 2% fat 8 oz. 276 Almonds 1oz. 143
Besides the amount in our diet, the time we eat these two nutrients in relation to each other is important. Because calcium and phosphorus compete for the binding sites on the transport protein (“seats on the train”), the more we separate the intake of these two minerals, the better. The calcium from the sour cream in our baked-potato-and-steak meal is not absorbed as well as the calcium from our late evening ice-cream snack. The meals that emphasize calcium-rich foods are better absorbed if phosphorus-rich foods are not eaten with them. It would be good to emphasize calcium-rich snack foods, which are often eaten separate from our regular meals. An ice cream float is not a good combination!
The very high-protein diets consumed by most Americans will cause more calcium excretion in their urine than occurs in people who consume less protein. Like phosphorus, the main source of dietary protein is meat. The more meat we eat, the more calcium we lose, and the greater our risk for osteoporosis. This does not mean that we have to eliminate meat. It does mean, however, that we should use moderation. Every meal does not have to contain meat. Try to limit your meat intake to one meal a day, and cut down on the size of your portions. Emphasize calcium at other meals and during snacks. If you are consuming dairy products to supply calcium, you will automatically be getting significant amounts of protein and don’t need to worry about protein deficiency.
Vegetarians, particularly ovo-lactovegetarians, have a lower incidence of osteoporosis than meat eaters. This is probably because of the lower protein and phosphorus content of their diets. A well-balanced vegetarian diet that allows milk and milk products is probably the best plan for preventing osteoporosis. The closer you approximate such a diet, the better. However, a pure vegetarian, or vegan, diet (no meat, milk products, or eggs) can be a problem unless nondairy sources of calcium are provided. A vegetarian diet promotes good calcium absorption and low calcium excretion. Therefore, the calcium requirement is probably less than on the typical American diet.
However, even with these factors in your favor, if your risk for osteoporosis is high, you must pay special attention to your calcium intake. Diets which claim to be variations of vegetarianism but are much more restrictive—for example, macrobiotic diets—will increase our risk for osteoporosis. They will be too low in calcium to supply your body’s needs. Such diets should be discouraged for several reasons, not the least of which is their tendency to increase our risk for osteoporosis.
A very high-salt intake will force our kidneys to excrete more sodium. In the process, calcium will be excreted. You do not have to go on a low-sodium diet to protect your bones from osteoporosis, but if you are a saltaholic, you should cut back. The mild sodium restriction described in Chapter 3 is not very limiting and will not place an excessive load on your kidneys. (An occasional transgression can be tolerated without endangering your bones.) Remember the non-dietary sources of sodium, such as over-the-counter medications, and avoid them when possible.
Most American diets, particularly those adequate in calcium, will be adequate in vitamin D. Thus, a diet for preventing osteoporosis almost always supplies enough of this important vitamin. However, most of our dietary vitamin D comes from dairy products made from milk that has been fortified. If you cannot take more than small amount of these foods, you may need a supplement. Remember that vitamin D in excess amounts can be very dangerous, and since it is stored in the body, its effects can be cumulative. If you must take a supplement, take no more than the RDI (400 IU).
There are two advantages to calcium supplements for people who are at risk for osteoporosis:
1.We can guarantee an adequate amount of calcium for our body’s needs.
2.We can consume the calcium in a form and at a time that will promote maximum absorption.
Since there is no known toxicity for moderate doses of calcium, even when they are taken for a long time, we have no objection to using a supplement as an added protection for anyone at risk for osteoporosis. If your diet makes it difficult for you to get enough calcium, if you are an avid meat eater, or if you cannot do without phosphorylated soft drinks, then you need a calcium supplement. If your risk score is 15 or above, we also recommend a calcium supplement. If you cannot give up heavy drinking, you should take a calcium supplement; and if you are constantly cutting calories, a supplement will ensure that you get enough. One gram per day, in addition to that in our food, is more than adequate for our needs.
As you can see, we are advocating that most people at risk for osteoporosis take a daily calcium supplement. If your score is between 10 and 15 and you are able to eat foods that are high in calcium and moderately low in phosphorus and protein, a calcium supplement is optional. If your score is 15 or above, or if you are a heavy user of alcohol, then a calcium supplement should be taken. To minimize the dietary factors that interfere with calcium absorption, the best time to take this supplement is between meals. The use of a calcium supplement is to ensure that you get enough total calcium; it should not be used as a replacement for a high calcium diet. We believe that a diet high in calcium and low in phosphorus and protein offers considerable protection from osteoporosis. There is no evidence that supplements can replace such a diet. Dietary patterns become habitual. If you can establish a pattern that emphasizes high calcium, low protein, and low phosphorus you can stay on such a diet for the rest of your life.
Any of the available calcium supplements, with the exception of calcium phosphate, are acceptable. Calcium carbonate is usually the cheapest and contains the most calcium per tablet (Several antacid tablets are made of calcium carbonate). Calcium lactate should be avoided by people who are lactose intolerant. Calcium gluconate contains only small amounts of calcium per tablet and, hence, must be taken several times during the day. Calcium chloride irritates the stomach in some people. Bone meal and dolomite are high in calcium but these products may be contaminated by toxic substances, and they contain significant amounts of phosphorus. Whichever supplement you choose, establish a routine and take it at the same time every day.
Exercise is important for maintaining healthy bones, especially for anyone at high risk for osteoporosis. The best exercises will combine movement and stress on the long bones. Walking, bicycling, hiking, jogging, rowing, and gymnastics are excellent. But maintaining an active lifestyle is even more important than undertaking a specific exercise program. Walk when you can. Climb that flight of stairs. Stand rather than sit. Let your bones bear the weight of your body. That will lower your risk for osteoporosis.
Excessive exercise, particularly for young women, may increase the risk for osteoporosis. Although the number of women athletes studied is still small, results of tests suggest that exercising to the point where menstruation ceases may increase the risk of bone loss.
It is difficult to say how much exercise is enough. However, a regime such as those advocated for promoting cardiovascular fitness is adequate. You may derive a double benefit from such a regime.
Anyone who is at risk for osteoporosis should have bone mass assessments at regular intervals. For most, the program outlined above will show tangible results. Bone mass will stay the same or regress very slowly. The tests will reinforce your incentive to stay with your diet and exercise program. For some, however, bone loss will progress. At this point, you have to make a difficult decision, in consultation with your physician, whether to start estrogen therapy.
Estrogen therapy can help prevent the bone loss that accompanies natural menopause or removal of the ovaries. It is one of the most effective treatment available, and it can be undertaken when diet and exercise are not adequate in slowing the rate of bone loss. To be effective, estrogen therapy must continue for a long time (ten to fifteen years).
Since this treatment will increase a woman’s risk for cancer of the uterus, and perhaps of the breast, it is not a decision to be taken lightly. However, progressive osteoporosis is a very serious problem, which can lead to death and disabilities. Thus, you must balance the risk of using estrogen against the risk of not using it. A word of caution: There is an indication that women who are already at high risk for heart disease due to plaque buildup on the arteries may be put at even higher risk for heart attacks by use of HRT (hormone replacement therapy).
The incidence of cancer of the uterus among the general population is about one per thousand. The use of estrogen after menopause increases that risk four to eight times. Therefore, at most, if you undertake estrogen treatment, your risk for developing cancer of the uterus is eight per thousand. Of 1,000 women taking estrogen, 992 will not get uterine cancer. The evidence for breast cancer is not conclusive. Some studies suggest a slight increase with estrogen treatment; some suggest no change in incidence; and some suggest a decrease in incidence. Present evidence suggests that women with a family history of breast cancer, or with other known risk factors for the disease (see Chapter 6), will increase their risk with long-term estrogen treatment. It appears that if only women who show no known risk factors for either breast or uterine cancer use estrogen therapy, their risk for uterine cancer will increase from one per thousand to, at most, eight per thousand. Their risk of breast cancer will not increase significantly.
Balance these numbers against the risk of developing severe osteoporosis and its potentially debilitating fractures. Sometimes the decision is easy. Almost all physicians will treat surgically induced pre-menopausal removal of the ovaries with estrogen. Rapid bone loss in the face of dietary treatment is also an indication for treatment. But how rapid is rapid? In the last analysis, you will have to rely on your physician’s judgment. You now know what questions to ask. You can be assured that if you do start estrogen therapy, your increased risk for cancer is very small. In addition, your physician may elect to use progesterone together with estrogen, which may reduce that risk.
In summary, if your risk score is below 10, stay alert; but you do not need to take specific measures. If your score is 10 or above, take the following steps:
Eliminate those factors under your control (alcohol, smoking, and certain drugs).
Have your bone mass measured periodically.
Consume a diet with adequate calories to reach or maintain ideal weight; one that is high in calcium, low in phosphorus and protein, and not excessive in salt.
Maintain regular activities and an exercise program that will place modest stress on your bones.
Take a calcium supplement (optional for scores 10 to 15; mandatory for scores of 15 and above).
Discuss with your physician the pros and cons of estrogen treatment or more recently developed medications and decide whether such treatment would be best for you.