The Wisdom of Menopause

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The Wisdom of Menopause Page 56

by Christiane Northrup


  Bones Constantly Remodel Themselves to Adapt to

  Physical Stress and Strain

  Among the amazing properties of the basic bone cell, the osteocyte, is its ability to act like a strain sensor, evaluating the amount of stress placed on a bone. Though the exact mechanism by which this happens isn’t entirely understood, stress on a bone sets up a tiny electrical current that attracts calcium and other minerals to the site. This is known as a piezoelectric effect and is similar to the mechanism by which quartz crystals operate in electronics and clocks.

  What is fascinating about this process is that it takes into account precisely where bone is needed and where it needs to be reduced. The old song about how “the hip bone’s connected to the thigh bone” is about more than mere anatomical proximity. All our bones, like every other cell in our bodies, are functionally connected to one another. A strain on a bone in our leg not only helps build that bone, but also helps determine the bone density in our spine and shoulders.5 Regular stress on bones is absolutely essential to maintain strong bone. It’s a case of use it or lose it. It’s well documented, for example, that the weightlessness experienced by astronauts results in significant bone loss, as does prolonged bed rest.

  One more piece of the puzzle falls into place when you know that osteoblasts and osteoclasts, the builders and the destroyers, communicate via proteins known as osteoprotegerin (OPG) and OPGligand. As one researcher explains it, “OPG-ligand is like the accelerator of your car. If you step on OPG-ligand, you lose bone. OPG is the brake of the system. If you step on OPG, then you have more bone. The balance between the two determines how much bone we have.”6 Scientists are now finding that almost all the substances that stimulate bone loss do so by slashing production of OPG, boosting creation of OPG-ligand, or both. For example, the drug prednisone can set off quick and dramatic bone loss. In the lab, treating osteoblasts (bone builders) with prednisone inhibits their ability to make OPG but heightens their OPG-ligand production. In contrast, estrogen stimulates osteoblasts to produce OPG.

  Immune status and bone health are also closely connected—which is not surprising, given that both are under the influence of the first chakra. Osteoclasts (the bone destroyers) are derived from the same bone marrow cells that make white blood cells. This helps explain why individuals with such seemingly unrelated diseases as rheumatoid arthritis, lupus, diabetes, multiple sclerosis, hepatitis, depression, and lymphoma often have osteoporosis in addition to their other symptoms. Scientists have found that anything that stirs quiescent T cells, a ubiquitous part of our immune system, into action—such as chronic infections and autoimmune disorders—also triggers them to make OPG-ligand, which results in bone loss.

  The function of both osteoclasts and osteoblasts is influenced by many other factors as well, including levels of estrogen, testosterone, thyroid hormone, and insulin; nutritional status; and hormones (such as norepinephrine and cortisol) produced by emotional stress.7 There is also some evidence to suggest that OPG-ligand may stimulate osteoclasts or other substances, such as cytokines (one of the inflammatory chemicals), to degrade cartilage. This translates over time into joint destruction and arthritis. Clinical trials are now under way using a type of synthetic long-acting OPG to turn off osteoclasts and thus halt bone loss.

  FIGURE 17: BONE REMODELING

  The Ups and Downs of Bone over the Life Cycle

  We begin developing our skeleton in utero, and it rapidly increases in size throughout childhood, adolescence, and young adulthood. It reaches its maximum size and density (known as peak bone mass) somewhere between the ages of twenty-five and thirty. Over her lifetime a woman may lose 38 percent of her peak bone mass, while a man may lose only 23 percent of his.8 But some individuals are resistant to bone loss.9 One study, for example, showed that 38 percent of men and 2 percent of women age fifty-five to sixty-four lost almost no bone over a period of eleven years.10 Nevertheless, many women begin to lose bone in their late thirties, long before estrogen levels begin to fall. This loss tends to accelerate perimenopausally. The average Caucasian woman loses 2–4 percent of her bone mass per year in the first five years after menopause. After that, loss slows down markedly or disappears.11 In men, accelerated bone loss is more apt to begin in the late sixties.

  It’s important to remember that healthy women can lose some bone during menopause and not be at risk for fracture. Thousands of people walk around daily with very low bone density—yet only a small percentage of them experience fractures. It has been shown, for example, that in Japan hip bone density is markedly lower than it is in the United States, but the incidence of hip fractures is two and a half times less than it is here. And the Japanese consume less calcium than we do.12

  What is the difference between bones that fracture and those that don’t? The difference concerns two factors: basic bone architecture and the repair capability of bone. It appears that even those with osteoporosis still have enough bone mass to withstand the stresses and strains of daily life. Research has shown, for example, that a vertebra that has lost 50 percent of its bone mass is still strong enough to withstand five times the strain load that it would normally be subjected to. If the bone were otherwise normal, in other words, it shouldn’t fracture. This means that many women who are diagnosed with low bone density will never go on to get fractures.

  Still, we all know that bone fractures do occur in women with osteoporosis, even at very low strain levels—in fact, it has been documented that some women spontaneously fracture their hips and then fall as a result, not the other way around. So osteoporotic fractures must involve more than decreased bone mineral density. There must be something else wrong with the quality of the bone and its self-repair process.13 Poor bone quality results from factors such as nutritional deficiencies, lack of exercise, too little vitamin D, and too much insulin.14

  The Anatomy of Bone

  Bone comes in two types: trabecular and cortical bone. Cortical bone is the tough, protective outer layer of bone. It is more calcified than inner trabecular bone, which is spongy and includes the marrow, where blood cells are made. About 80 percent of all bone in our bodies is cortical and 20 percent is trabecular. The arms and legs are mostly cortical bone; hips are a half and half mixture; the spine, ribs, jaw, and lower two-thirds of the wrist are mainly trabecular bone. Because trabecular bone is more loosely packed and porous and has more surface area than cortical bone, it is more susceptible to bone loss, which is one reason why fractures from osteoporosis tend to occur earlier in the spine and wrist, while hip fractures occur later.

  Bones have to be strong enough to withstand hundreds of pounds of pressure, but flexible enough to withstand twisting and turning without breaking. This flexibility is provided by the living protein collagen, which makes up about 23 percent of all bone. (This is the same substance that gives skin its elasticity and thickness. Thin skin is also associated with thin bones.) The minerals attached to the collagen matrix are arranged in a crystalline structure that gives bone its rigidity and strength.

  We were designed to maintain strong, heavy bones throughout our lives, as do all animals. If we have reached peak bone mass in our twenties, then we can stand a certain amount of bone loss as we age without being at risk for fractures. But because of the vagaries of our modern lifestyle, including lack of exercise or overexercise, smoking, poor diet, lack of vitamin D, or anorexia and bulimia, many women never reach their peak bone mass by age thirty. And it appears that the matrix of the bone that is present may not be normal. So many women begin perimenopause with a deficit in their bone banks.

  Medical anthropologist Susan Brown, Ph.D., director of the Osteoporosis Education Project and author of the groundbreaking book Better Bones, Better Body: Beyond Estrogen and Calcium (Keats Publishing, 2000), points out that the bones of people who are living in Westernized countries are growing ever weaker, and that we now face a virtual epidemic of poor bone health.15 Research shows that women living several centuries ago had stronger bones than
modern women and that Near Eastern populations of some 12,000 years ago had a bone mass that was nearly 20 percent higher than it is today.16 (And they didn’t consume lots of cow’s milk!)

  Strength isn’t the whole story with bone health—body alignment and flexibility play an important role, too. Every time we walk or move, we place what are called “vertical vectors of force” on our bones. As discussed earlier, these forces create a mini-electrical current throughout our bones, but this piezoelectric effect also involves the fascia, connective tissue that encases all your muscles, nerves, and organs—almost as if they were wearing a tight sweater. The tiniest movement in one area of the body is both mechanically and electrically transmitted throughout the entire body instantaneously. If our bones, ligaments, tendons, fascia, and muscles are all properly aligned, then our movement is graceful and pain free and our bones and supporting structures remain healthy.

  However, if our posture is poor (for example, if we’re hunched over and never fully expand our rib cage), then our shoulders become tight, and we are more at risk for shoulder, neck, and back problems. The same is true for our hips. In fact, the shoulder girdle and hip girdle mirror each other—tight hips, tight shoulders. I am convinced that if women focused on moving with proper alignment, there would be far fewer hip replacements after the age of sixty! For more information about posture and alignment, I recommend The New Rules of Posture: How to Sit, Stand, and Move in the Modern World (Healing Arts Press, 2007) by Mary Bond as well as Ageless Spine, Lasting Health (Synergy Books, 2006) by Kathleen Porter. (I also recommend visiting Kathleen’s website at www.naturalposturesolutions.com.)

  I know that I personally would have a chronic right hip problem—and probably an eventual hip replacement—if it hadn’t been for Pilates. I started doing Pilates more than ten years ago because I wanted an exercise program I could do on the road and in a hotel room. Back then I didn’t realize how transformational this practice is. Now, not only am I taller than I was back then, I am also far more flexible. Most important, my posture and alignment have improved immensely.

  ARE YOU AT RISK FOR OSTEOPOROSIS?

  To determine your personal risk for thinning, poor-quality bones, review the following list. If none of the risk factors applies to you, chances are good that your bones are just fine. You can simply continue the healthy lifestyle you are following. If, on the other hand, you can identify with several of them, you need to take steps right now to ensure that you’ll be able to literally take steps in the future! Note that some of the risk factors for osteoporosis overlap those for heart disease.17 As you get a handle on your bone health, you’ll also be helping your heart.

  ~ Your mother has been diagnosed with osteoporosis or has had a hip or other osteoporotic fracture. Osteoporosis tends to run in families, but there’s still a lot you can do to prevent it.

  ~ You are fair-skinned and blue-eyed. Because of genetic factors, blue-eyed blondes and those with red hair have less collagen in both their bones and skin than do those with brown, black, or yellow skin tones. This gives them less bony matrix on which to lay down minerals. Black women have the least risk for osteoporosis because they tend to have thicker bones and more robust collagen stores than Caucasian women.

  ~ You are quite thin or tall, or have a slight build and/or less than 18 percent body fat. Tall women, especially those with small bones, may be at risk for purely mathematical reasons: they enter menopause with less bone to lose. In addition, body fat is where much of a woman’s natural estrogen during and after perimenopause is manufactured. The less fat she has, the less estrogen her body will produce to support her bones.

  ~ You smoke. Chemicals in cigarette smoke poison the ovaries and decrease your hormone levels prematurely. Estrogen, testosterone, and progesterone all have bone-protective effects.

  ~ You spend most of your time indoors. Women who are exposed to very little natural sunlight may be deficient in the natural vitamin D normally produced in sun-drenched skin. Vitamin D is necessary for healthy bone mineralization. Increasingly, we’re finding that women who get osteoporotic fractures are the ones with serum vitamin D levels of 20 or lower. The sunlight–bone health link is so important that I’ve devoted an entire section to it later in this chapter.

  ~ You are sedentary and spend fewer than four hours per day on your feet. Bones stay healthy only when they have vertical vectors of force placed on them regularly. A sedentary lifestyle provides insufficient weight-bearing exercise to stimulate bone growth. Many studies have shown that bed rest is associated with osteoporosis. In contrast, weight training has been shown to build bone density even in postmenopausal women who aren’t on estrogen.

  ~ You are (or were) a “fitness fanatic,” that is, you become irritable and unreasonable if you are unable to get in your daily run or other exercise. The lifestyle of the fitness fanatic includes dieting for weight loss and/or engaging regularly in strenuous exercise such as marathon training. Dietary restrictions and the chronic stress of overtraining can impair mineral intake and absorption. It also messes up what is known as the hypothalamic-pituitary-ovarian-adrenal axis—the exquisite feedback loop between the brain, the body, and our hormone levels. Chronic overexercise without adequate caloric or mineral intake results in stress fractures in ballet dancers, gymnasts, soccer players, and competitive runners, among others. Such fractures are currently on the rise in young athletes and can set the stage for later osteoporosis.

  ~ You have a history of amenorrhea (no periods) associated with excessive exercise and/or anorexia nervosa.18 Amenorrhea results in a derangement of the hypothalamic-pituitary-ovarian-adrenal axis similar to that seen in depression. The end result is lower estrogen, androgen, and progesterone, and an eicosanoid profile that favors osteoporosis and other diseases.19

  ~ You drink more than 25 g of alcohol per day. (The following servings each contain about 10 g of alcohol: 12 oz of beer, 4 oz of wine, and 1.5 oz of 80-proof beverage.)20 Alcohol interferes with the function of both osteoblasts and osteoclasts, thus inhibiting your body’s ability to lay down new bone and to remodel old bone.21

  ~ Your liver is overstressed. The liver’s ability to produce and metabolize estrogen is essential for the growth and maintenance of strong bones at any age. Drinking more than two alcoholic drinks per day, taking medication known to be hard on the liver (such as certain cholesterol-lowering drugs), and infection with viral hepatitis are among the significant liver stressors that can harm bone health.

  ~ You drink more than two units of caffeine per day (8 oz of coffee = 1 unit; 12 oz of cola = 0.4 units). Caffeine results in increased urinary excretion of calcium; the more you consume, the more calcium you lose. If your calcium intake is relatively low to begin with, regular caffeine consumption could result in significant loss of bone over time. If, on the other hand, your calcium and mineral intake is high, a couple of cups of coffee a day probably won’t matter much. Note: Even though tea contains caffeine, both green and black tea have been shown to build bone mass—probably because of their phytoestrogen content.

  ~ You are or have been clinically depressed for a significant period of time. Numerous studies have shown that depression is an independent risk factor for osteoporosis. Depressed people have high levels of the immune system chemical known as IL-6, which overstimulates the osteoclasts (cells responsible for breaking down bone). Depression is also associated with abnormalities in the hypothalamic-pituitary-ovarian-adrenal axis and with elevated cortisol secretion, which predispose one to bone loss.22

  ~ Your diet is poor—little fresh food, few leafy green vegetables, and lots of junk food. Such a diet doesn’t provide minerals and other nutrients necessary to support the growth and maintenance of a solid bone foundation.23

  ~ You went through premature menopause (before age forty), have had your ovaries removed surgically, went through menopause as a result of radiation or chemotherapy, and/or have prematurely gray hair. A woman who enters menopause prematurely for any reason is at increased risk for
osteoporosis unless she gets adequate hormone therapy during the years when her body would normally have been producing higher levels of hormones. Nonsurgical premature menopause, and the premature graying of the hair that often accompanies it, are the result of an autoimmune reaction affecting the ovaries and hair follicles. The cause of these reactions isn’t clear.

  ~ You take steroid drugs regularly for conditions such as asthma or lupus. Steroid drugs result in accelerated breakdown of tissue in the body—including the collagen matrix for both skin and bone.24 Steroids also diminish the sensitivity of the bowel to vitamin D, which in turn reduces calcium absorption.25 Prolonged steroid use may also significantly decrease estrogen and androgen levels.26

  ~ You’ve taken high doses or been on a long-term regimen of any of the prescription or over-the-counter drugs known as proton pump inhibitors (PPIs), including esomeprazole (Nexium), omeprazole (Prilosec, Zegerid), lansoprazole (Prevacid), rabeprazole (Aciphex), dexlansoprazole (Dexilant, Kapidex), or pantoprazole (Protonix). These popular drugs, which block the production of stomach acid, are commonly used to treat gastroesophageal reflux disease (GERD), stomach and small intestine ulcers, and inflammation of the esophagus. Recent evidence shows that they may increase risk for hip, wrist, and spine fractures. This makes sense because having some acid in the stomach is absolutely crucial for absorbing bone-building nutrients such as calcium. So when you block the acid with drugs, digestion is also impaired.

 

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