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535 lines
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<html>
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<head><title>Bone Density: First Do No Harm</title></head>
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<body>
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<h1>
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Bone Density: First Do No Harm
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</h1>
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<article class="posted">
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<p>
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No topic can be understood in isolation. People frequently ask me what they should do about their
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diagnosed osteoporosis/osteopenia, and when they mention “computer controlled” and “dual photon x-ray”
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bone density tests, my attention tends to jump past their bones, their diet, and their hormones, to the
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way they must perceive themselves and their place in the world. Are they aware that this is an x-ray
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that’s powerful enough to differentiate very opaque bones from less opaque bones? The soft tissues
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aren’t being studied, so they are allowed to be “overexposed” until they appear black on the film. If a
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thick area like the thigh or hip is to be measured, are they aware that the x-ray dose received at the
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surface where the radiation enters might be 20 times more intense than the radiation that reaches the
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film, and that the 90 or 95% of the missing energy has been absorbed by the person’s cells? If I limited
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my response to answering the question they thought they had asked me, I would feel that I had joined a
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conspiracy against them. My answer has to assume that they are really asking about their health, rather
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than about a particular medical diagnosis.
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</p>
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<p>
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Neurologists are famous for making exquisitely erudite diagnoses of problems that they can’t do anything
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to remedy. The owners of expensive dual photon x-ray absorptiometer diagnostic machines are in a very
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different position. The remedies for osteoporosis are things that everyone should be doing, anyway, so
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diagnosis makes no difference in what the physician should recommend to the patient.
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</p>
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<p>
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Most often, estrogen is prescribed for osteoporosis, and if the doctors didn’t have their bone density
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tests, they would probably prescribe estrogen anyway, “to protect the heart,” or “to prevent Alzheimer’s
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disease.” Since I have already written about estrogen and those problems, there’s no need to say more
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about it here, except that estrogen is the cause of a variety of tissue atrophies, including the
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suppression of bone formation.[1]
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</p>
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<p>
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General Electric, a major advocate of x-ray screening for osteoporosis and breast cancer, has advertised
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that 91% of breast cancers could be cured if everyone used their technology. Breast cancer has not
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decreased despite the massive application of the technology, though the US government and others (using
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crudely deceptive statistis) claim that the War on Cancer is being won. Similarly, during the last
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decades when the “high technology” x-ray machines have been more widely used, the age-specific incidence
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of osteoporosis has increased tremendously. This apparently includes a higher rate of shortening of
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stature with aging than in earlier generations.[2]
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</p>
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<p>
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I think there are several reasons for avoiding x-ray tests of bone density, besides the simple one that
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everyone should eat a bone-protective diet, regardless of the present density of their bones.
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</p>
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<p>
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Even seemingly identical x-ray machines, or the same machine at a different time, can give very
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different estimates of bone density.[3-10] Radiologists evaluating the same images often reach very
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different conclusions.[11] Changes in the tissue water and fat content can make large differences in
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apparent bone density,[12] and estrogen, which affects those, could appear to cause improved bone
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density, when it is merely causing a generalized inflammatory condition, with edema. A machine that is
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accurate when measuring an aluminum model, won’t necessarily give meaningful results when the
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composition of the tissue, including the bone marrow, has changed. Calcification of soft tissues can
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create the impression of increased bone density.[13] Studies of large groups of people show such small
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annual losses of bone density (around 1%), especially in the neck of the femur (which is important in
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hip fractures) that the common technical errors of measurement in an individual seem very large.
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</p>
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<p>
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Ultrasound devices can do an extremely good job of evaluating both bone density and strength [14-16],
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rather than just density.
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</p>
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<p>Ultrasound stimulates bone repair.</p>
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<p>X-rays accelerate the rate of bone loss.</p>
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<p>X-rays do their harm at any dose; there is no threshold at which the harm begins.</p>
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<p>
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X-ray damage is not limited to the area being investigated. Deflected x-rays affect adjacent areas, and
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toxins produced by irradiated cells travel in the bloodstream, causing systemic effects. Dental x-rays
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cause thyroid cancer and eye cancer. Recent experiments have shown that low doses of radiation cause
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delayed death of brain cells. The action of x-rays produces tissue inflammation, and diseases as
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different as Alzheimer’s disease and heart disease result from prolonged inflammatory processes.
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</p>
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<p>
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I have never known a physician who knew, or cared, what dose of radiation his patients were receiving. I
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have never known a patient who could get that information from their doctors.
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</p>
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<p>
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The radiation exposure used to measure bone density may be higher (especially when the thigh and hip are
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x-rayed) than the exposure in dental x-rays, but dental x-rays are known to increase the incidence of
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cancer. Often, dentists have their receptionists do the x-rays, which probably doesn’t matter, since the
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dentist is usually no more concerned than the receptionist about understanding, and minimizing, the
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dose. Even radiological specialists seldom are interested in the doses they use diagnostically.
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</p>
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<p>
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It was only after a multitude of dentists had a finger amputated that it became standard practice to ask
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the patient to hold the film, while the dentist stood safely back away from the rays.
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</p>
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<p>
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Just after the beginning of the century, Thomas Edison was helping to popularize x-rays, but the
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horrible death of his chief technician turned Edison into an enemy of the technology. By the 1940s, the
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dangers of radiation were coming to be understood by the general public, and it was only the
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intervention of the US government, to popularize atomic bombs and nuclear power, that was able to
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reverse the trend.
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</p>
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<p>
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In 1956 and 1957, Linus Pauling was the only well known scientist who opposed the government’s policies.
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The government took away his passport, and his opportunities to write and speak were limited by a
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boycott imposed by a variety of institutions, but instigated by the nuclear industry and its agent, the
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Atomic Energy Commission. The government which considered Pauling a threat to national security, had
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placed thousands of German and Hungarian “ex”-Nazis in high positions in industry and government
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agencies, after protecting them from prosecution as war criminals. The official government policy,
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directed by the financier Admiral Strauss who controlled the Atomic Energy Commision, was to tell the
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public that radiation was good. Their extreme secrecy regarding their radiation experiments on
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Americans, however, indicated that they were aware of the malignant nature of their activities<strong
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>;</strong> many of the records were simply destroyed, so that no one could ever know what had been
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done. Scientists who worked for the government, Willard Libby, John Goffman, and many others, were
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working to convince the public that they shouldn’t worry. Of the multitude of scientists who served the
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government during that time, only a few ever came to oppose those policies, and those who did were
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unable to keep their jobs or research grants. Gofman has become the leader in the movement to protect
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the public against radiation, especially, since 1971, through the Committee for Nuclear Responsibility,
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PO Box 421993, San Francisco, CA 94132..
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</p>
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<p>
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Gofman has said<strong>: "I was stupid in those days. In 1955, '56, people like Linus Pauling were
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saying that the bomb fallout would cause all this trouble. I thought, 'We're not sure. If you're not
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sure, don't stand in the way of progress.' I could not have thought anything more stupid in my life.
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</strong>
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</p>
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<p>
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<strong>
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"The big moment in my life happened while I was giving a health lecture to nuclear engineers. In the
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middle of my talk it hit me! What the hell am I saying? If you don't know whether low doses are safe
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or not, going ahead is exactly wrong. At that moment, I changed my position entirely."[17]
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</strong>
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</p>
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<p>
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<strong>
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In 1979, Gofman said: "There is no way I can justify my failure to help sound an alarm over these
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activities many years sooner than I did. I feel that at least several hundred scientists trained in
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the biomedical aspect of atomic energy - myself definitely included - are candidates for
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Nuremburg-type trials for crimes against humanity for our gross negligence and irresponsibility. Now
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that we know the hazard of low-dose radiation, the crime is not experimentation - it's murder." [18]
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</strong>
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</p>
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<p>
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Many ordinary people were making exactly that argument in the 1950s, but government censorship kept the
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most incriminating evidence from the public. The climate of intimidation spread throughout the culture,
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so that teachers who spoke about the dangers of radiation were called disloyal, and were fired. Now,
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people who don’t want x-rays are treated as crackpots. Probably because of this cultural situation,
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Gofman’s recommendations are very mild--simply for doctors to use good technology and to know what they
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are doing, which could lead to ten-fold or even hundred-fold dose reduction. Even with such mild
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restraint in the use of diagnostic x-rays, Gofman’s well founded estimate is that 250,000 deaths caused
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by radiation could be prevented annually. I believe many more deaths would be prevented if ultrasound
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and MRI were used consistently instead of x-rays. Using Gofman’s estimate, I think we can blame at least
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ten million deaths on just the medical x-rays that have been used inappropriately because of the
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policies of the U.S. government in the last half century. That wouldn’t include the deaths caused by
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radioactive fallout from bomb tests and leaks from nuclear power plants, or the vast numbers of people
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mentally impaired by all sorts of toxic radiation.<strong></strong>
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</p>
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<p>
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<strong>Although nearly all the people who committed the radiation crimes of the 1950s and 1960s have
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died or retired, the culture they created remains in the mass media and scientific journals, and in
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the medical and academic professions.
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</strong>
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</p>
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<p>
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Medical journals describe ways to minimize diagnostic x-ray exposure, and they advocate many seemingly
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effective treatments for osteoporosis, giving an impression that progress is being made in “managing”
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osteoporosis, but the real situation is very different. Fractures resulting from osteoporosis are
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increasing, and osteoporosis is affecting younger and younger people. I think it would be reasonable to
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say that a woman with osteoporosis is usually better off when it’s not diagnosed, because of the
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dangerous things prescribed for it. Estrogen has become the main “treatment” for osteoporosis, but many
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of the other ways of “managing” osteoporosis are both ineffective and unsafe.
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</p>
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<p>
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Many women are told to stop taking a thyroid supplement when osteoporosis is diagnosed, but
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hypothyroidism often leads to hyperprolactinema and hypercortisolemia, which are two of the most clearly
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established causes of osteoporosis. Calcitonin, vitamin D-active metabolite, and estrogen-”HRT”
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treaments can cause respiratory alkalosis (relative hyperventilation),[19-24] and hypothyroidism
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produces a predisposition to hyperventilation.[25] Hyperventilation tends to cause calcium loss. In
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respiratory alkalolis, CO2 (and sometimes bicarbonate) are decreased, impairing calcium retention, and
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in “<strong><em>metabolic</em></strong> alkalosis,” with <strong><em>increased</em></strong>
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bicarbonate, calcium is retained more efficiently and bone formation is stimulated, and its dissolution
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is suppressed.
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</p>
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<p>
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Other women are told to reduce their protein consumption, or to take fluoride or whatever drug has been
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most recently promoted. A protein deficiency is a clear cause of osteoporosis, and bone density
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corresponds to the amount of protein consumed. Milk protein, especially, protects against osteoporosis,
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independently of milk’s other important nutrients. Too much fluoride clearly increases the risk of bone
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fractures,[26] and the side effects of other drugs haven’t been properly studied in humans, while they
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often have dangerous effects in animals.
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</p>
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<p>
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Calcium, magnesium, vitamin A, vitamin B6- , vitamin K, and vitamin D are important for the development
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and maintenance of bones. For example, a vitamin A deficiency limits the synthesis of progesterone and
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proteins. In calcium deficiency, parathyroid hormone is increased, and tends to cause the typical
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changes of aging, shifting calcium from hard tissues to soft, and decreasing the ratio of extracellular
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to intracellular (excitatory) calcium.
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</p>
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<p>
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Polyunsaturated fats are converted to prostaglandins (especially under the influence of estrogen), and
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several prostaglandins have toxic effects on bone. Those fats also suppress the formation of thyroid
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hormone and progesterone. The increased use of the unsaturated oils has coincided with the increase of
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osteoporosis.
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</p>
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<p>
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The oxidation of proteins caused by free radicals is increased with aging and by the use of unsaturated
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fats, and it contributes to tissue atrophy, including the age-related shrinkage of the bones. In animal
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studies, “adequate” dietary protein, 13.8% of the diet (equivalent to about 80 grams per day for a
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person) is associated with more oxidative damage to tissue proteins than the very high protein diets,
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25.7% or 51.3%, that would be equivalent to about 150 or 300 grams of protein daily for a person.[27]
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Yet, many physicians recommend a low protein diet to protect against osteoporosis.
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</p>
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<p>
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Avoiding fluoridated water and the polyunsaturated oils, and drinking two quarts of milk daily (which
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will provide only 66 grams of protein), and using some other nutrient-rich foods such as eggs and
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fruits, are probably the basic things to protect the bones. For vitamins, especially K, occasional liver
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can be helpful. Meats, fruits, leaves, and coffee are rich in magnesium.
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</p>
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<p>
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Some people have argued that the acidity of urine produced by eating meat causes calcium loss. However,
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a high protein diet also improves the absorption of calcium by the intestine. Another overlooked
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function of dietary protein is that it stimulates insulin secretion, and insulin is anabolic for
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bone.[28]
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</p>
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<p>
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The same diet that protects against osteoporosis, i.e., plenty of protein and calcium, etc., also
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protects against kidney stones and other abnormal calcificatons.
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</p>
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<p> </p>
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<p><strong><h3>REFERENCES</h3></strong></p>
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<p>
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1. Proc Assoc Am Physicians 1996 Mar;108(2):155-64 <strong>Potential mechanism of estrogen-mediated
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decrease in bone formation: estrogen increases production of inhibitory insulin-like growth
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factor-binding protein-4.</strong> Kassem M, Okazaki R, De Leon D, Harris SA, Robinson JA, Spelsberg
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TC, Conover CA, Riggs BL.
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</p>
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<p>
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<strong> 2.</strong> Am J Phys Anthropol 1990 Dec;83(4):467-76. <strong>Stature loss among an older
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United States population and its relation to bone mineral status.</strong> Galloway A, Stini WA, Fox
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SC, Stein P. “With advancing age there is a gradual decrease in height apparently beginning in the
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mid-40s. Thereafter, there is a relatively rapid decrease in measured height. <strong>This contrasts to
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the much slower rates predicted from earlier populations (Trotter and Gleser: American Journal of
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Physical Anthropology 9:311-324, 1951).
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</strong>The rate of stature loss is associated with diminution of bone mineral density as well as with
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maximum height. Since there are suggestions of a secular trend toward greater reductions in bone mineral
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density, this study suggests there may be a secular trend toward an increase in statural loss with age.”
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</p>
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<p>
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<strong> 3.</strong> Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1994 Mar;160(3):260-5. <strong
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>[The quantitative determination of bone mineral content--a system comparison of similarly built
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computed tomographs].</strong> [Article in German] Andresen R, Radmer S, Banzer D, Felsenberg D,
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Wolf KJ Klinik fur Radiologie, Universitatsklinikum Steglitz der FU Berlin. An intercomparison of 4 CT
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scanners of the same manufacturer was performed. The bone mineral content of 11 lumbar vertebral columns
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removed directly post mortem was determined in a specially constructed lucite-water phantom. Even
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devices of the same construction were shown to yield a variation in the quantitative evaluation markedly
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exceeding the annual physiological mineral loss. As long as scanner adjustment by physical calibration
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phantoms has not yet been established, a course assessment and therapy control of bone mineral content
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should always be carried out on the same QCT scanner.
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</p>
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<p>
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<strong> 4.</strong> Osteoporos Int 1990 Oct;1(1):23-9. <strong>Vertebral bone mineral density measured
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laterally by dual-energy X-ray absorptiometry.</strong> Slosman DO, Rizzoli R, Donath A, Bonjour JP.
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“The bone mineral density (BMD) of lumbar vertebrae in the anteroposterior (AP) view may be
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overestimated in osteoarthritis or with aortic calcification, which are common in elderly.” “Then, we
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compared the capability of BMD LAT and BMD AP scans for monitoring bone loss related to age and for
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discriminating the BMD of postmenopausal women with nontraumatic vertebral fractures from that of young
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subjects. In vitro, when a spine phantom was placed in lateral position in the middle of 26 cm of water
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in order to simulate both soft-tissue thickness and X-ray source remoteness, the coefficient of
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variation (CV) of six repeated determinations of BMD was 1.0%. In vivo, the CV of paired BMD LAT
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measurements obtained in 20 healthy volunteers<strong> after repositioning was 2.8%.”</strong>
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</p>
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<p>
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<strong> 5.</strong> Eur J Nucl Med 1990;17(1-2):3-9.<strong>
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Comparative study of the performances of X-ray and gadolinium 153 bone densitometers at the level of
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the spine, femoral neck and femoral shaft.</strong> Slosman DO, Rizzoli R, Buchs B, Piana F, Donath
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A, Bonjour JP. “In vivo, at the spine level, with DPA, mean<strong>
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CV of BMD measured 6 times after repositioning in 6 healthy volunteers was 3.8% +/- 1.9% and 2.1%
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+/- 0.7% . . . .”
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</strong>
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</p>
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<p><strong> </strong></p>
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<p>
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<strong> 6. </strong> Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1995 Apr;162(4):269-73. <strong
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>[Experimental studies of the visualization of the vertebral body spongiosa by high-resolution computed
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tomography].</strong> Henschel MG, Freyschmidt J, Holland BR. “The measured lower limit of<strong>
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visualisation of cancellous bone structures is clearly worse than expected from the measurements of
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spatial resolution with standard phantoms used for HR-CT (0.6 versus 0.4 mm). True and exact imaging
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of normal cancellous bone cannot be achieved even by modern HR-CT. Noise creates structures
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mimicking cancellous bone.”
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</strong>
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</p>
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<p>
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7. J Comput Tomogr 1984 Apr;8(2):91-7. <strong>Quantitative computed tomography assessment of spinal
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trabecular bone. I. Age-related regression in normal men and women.</strong> Firooznia H, Golimbu C,
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Rafii M, Schwartz MS, Alterman ER. “Computed tomography, <strong>utilized in conjunction with a
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calibrated phantom containing a set of reference densities</strong> (K2HPO4 and water), is capable
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of determining the mineral content of the trabecular bone of the spine with an<strong>
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accuracy of about 6%</strong> of the ash weight of the vertebrae scanned (specimen studies).”
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</p>
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<p>
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8. Calcif Tissue Int 1991 Sep;49(3):174-8. <strong>Precision and stability of dual-energy X-ray
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absorptiometry measurements.</strong>
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<hr />
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<strong></strong>
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</p>
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<p>
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<strong> 9.</strong> J Comput Assist Tomogr 1993 Nov-Dec;17(6):945-51. <strong>Influence of temperature
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on QCT: implications for mineral densitometry.</strong> Whitehouse RW, Economou G, Adams JE.
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“Inaccuracies in quantitative CT (QCT) for vertebral bone mineral measurements may result from
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differences between the temperature of the vertebrae and the calibration standards.” “In the computer
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simulation, the<strong>
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fat error associated with single energy QCT for trabecular bone mineral densitometry was 20% less
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for specimens at room temperature than at body temperature.”</strong> “The fat error of
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single<strong>
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energy QCT for mineral densitometry may have been underestimated in previous in vitro studies using
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vertebral specimens scanned at room temperature.”</strong>
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</p>
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<p>
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<strong> 10.</strong> Phys Med Biol 1986 Jan;31(1):55-63. <strong>Quantitative CT measurements: the
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effect of scatter acceptance and filter characteristics on the EMI 7070.</strong> Merritt RB,
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Chenery SG “Non-linearities in projection values on computed tomography (CT) scanners <strong>cause
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corresponding errors in derived Hounsfield unit attenuation measurements. Existing commercial
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machines have been refined for clinical usefulness but not necessarily for quantitative
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accuracy.”</strong>
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<strong>“It is concluded that, irrespective of any quality assurance protocol, interpatient and
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interslice errors can be expected to range from 3 to 10% for water-equivalent materials and the
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intraslice positional dependence of the CT number can vary up to 5% for dense bone-like materials in
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a uniform phantom.”</strong>
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</p>
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<p>
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<strong> 11.</strong> Skeletal Radiol 1986;15(5):347-9. <strong>Observer variation in the detection of
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osteopenia.</strong> Epstein DM, Dalinka MK, Kaplan FS, Aronchick JM, Marinelli DL, Kundel HL. In
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order to determine observer variation in the detection of osteopenia, 15 pairs of lateral chest
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radiographs obtained within two weeks of each other were reviewed separately by two radiologists and one
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orthopedist on three separate occasions. Intra- and interobserver variations were calculated for each
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individual film and film pairs using Kappa values. <strong>The individual observers were not able to
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give consistent readings on the same film on different days</strong>
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<hr />
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<strong>additional factors of repeat films</strong>
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<hr />
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<strong>or separate observers</strong>
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<hr />
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<strong>agreement was even worse.</strong>
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<strong>The identification of osteopenia from the lateral view of the thoracic spine is highly
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subjective and variable from film to film and observer to observer.</strong>
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</p>
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<p>
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<strong> 12.</strong> P. Schneider and C. Reiners, Letter, JAMA 277(1), 23, Jan. 1, 1997. <strong>"The
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influence of fat distribution on bone mass measurements with DEXA can be of considerable magnitude
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and ranges up to 10% error per 2 cm of fat."</strong>
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</p>
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<p>
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<strong> 13.</strong> Calcif Tissue Int 1990 Apr;46(4):280-1. <strong>Effect of radiographic
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abnormalities on rate of bone loss from the spine.</strong> Dawson-Hughes B, Dallal GE. <strong
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>“Spurious rates of loss of spine BMD are likely to be found in subjects with calcification of the
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aorta, osteophytes or other abnormalities in the spine scan field. This should be kept in mind when
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serial spine scans are being considered in these subjects.”
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</strong>
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</p>
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<p>
|
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<strong> 14.</strong> Przegl Lek 2000;57(2):93-9. [No title available]. Jaworski M, Lorenc RS. <strong
|
||
>“. . .</strong>Dual Energy X-ray Absorptiometry (DEXA) method is a reference method to diagnose
|
||
osteoporosis. This method allows to <strong>measure bone density and bone mass, however bone quality can
|
||
not be estimated. Quantitative ultrasound (QUS)</strong>
|
||
<strong>method provides information about bone structure.”</strong>
|
||
</p>
|
||
<p>
|
||
<strong> 15.</strong> Osteoporos Int 2000;11(4):354-60.<strong>
|
||
Assessment of a new quantitative ultrasound calcaneus measurement: precision and discrimination of
|
||
hip fractures in elderly women compared with dual X-ray absorptiometry.</strong> He YQ, Fan B, Hans
|
||
D, Li J, Wu CY, Njeh CF, Zhao S, Lu Y, Tsuda-Futami E, Fuerst T, Genant HK.
|
||
</p>
|
||
<p>
|
||
<strong> 16.</strong> Cas Lek Cesk 2000 Apr 26;139(8):231-6 <strong>[X-ray densitometry and
|
||
ultrasonography of the heel bone--sensitivity and comparison with densitometry of the axial
|
||
skeleton].</strong> [Article in Czech] Michalska D, Zikan V, Stepan J, Weichetova M, Kubova V,
|
||
Krenkova J, Masatova A. “The DXA of the heel underestimates the prevalence of osteoporosis. The results
|
||
of the heel QUS (Stiffness) appear to be better correlated to femoral BMD than heel BMD.”
|
||
</p>
|
||
<p>
|
||
<strong>17.</strong> John Gofman, M.D. (biographical chapter. pages 401-412.) In Studs Terkel's book
|
||
<strong><em>Coming of Age. The Story of our Century by Those Who Lived It.</em></strong> The New Press.
|
||
NY. 1995.
|
||
</p>
|
||
<p>
|
||
<strong>18.</strong> Gofman, J.W. <strong>An irreverent, illustrated view of nuclear power.</strong>
|
||
Committee for Nuclear Responsibility. San Francisco, CA. pp. 227-228, 1979.
|
||
</p>
|
||
<p>
|
||
<strong> 19.</strong> Kidney Int 1992 Sep;42(3):727-34. <strong>Chronic respiratory alkalosis induces
|
||
renal PTH-resistance, hyperphosphatemia and hypocalcemia in humans.</strong> Krapf R, Jaeger P,
|
||
Hulter HN Department of Medicine, Insel University Hospital, Berne, Switzerland. <strong>“The effects of
|
||
chronic respiratory alkalosis on divalent ion homeostasis have not been reported in any
|
||
species.”</strong> “Chronic respiratory alkalosis (delta PaCO2, -8.4 mm Hg, delta[H+] -3.2
|
||
nmol/liter) resulted in a sustained decrement in plasma ionized calcium concentration (delta[IoCa++]p,
|
||
-0.10 mmol/liter, P less than 0.05) and a sustained increment in plasma phosphate concentration
|
||
(delta[PO4]p, +0.14 mmol/liter, P less than 0.005) <strong>associated with increased fractional
|
||
excretion of Ca++ . . .”
|
||
</strong>
|
||
</p>
|
||
<p>
|
||
<strong> 20.</strong> J Clin Endocrinol Metab 1999 Jun;84(6):1997-2001 <strong>Hormone replacement
|
||
therapy causes a respiratory alkalosis in normal postmenopausal women.</strong>
|
||
<hr />
|
||
<strong>partial pressure of carbon dioxide. . . .”</strong>
|
||
<strong>“Accompanying changes in blood pH were apparent in the estrogen plus MPA group, where there was
|
||
an upward trend at 1 week</strong>
|
||
<hr />
|
||
</p>
|
||
<p>
|
||
<strong> 21.</strong> Wien Klin Wochenschr 1979 Apr 27;91(9):304-7 <strong>[Investigations on the
|
||
pathogenesis of distal renal tubular acidosis].</strong> Schabel F, Zieglauer H. <strong
|
||
>“Bicarbonate loading is followed by a lowering of calcium excretion to within the normal range and a
|
||
decrease in the uncharacteristic renal hyperaminoaciduria.”
|
||
</strong>
|
||
</p>
|
||
<p>
|
||
<strong> 22.</strong> Calcif Tissue Int 1984 Sep;36(5):604-7. <strong>Respiratory alkalosis and reduced
|
||
plasmatic concentration of ionized calcium in rats treated with 1,25
|
||
dihydroxycholecalciferol.</strong> Locatto ME, Fernandez MC, Caferra DA, Gimenez MC, Vidal MC, Puche
|
||
RC. “The daily administration of supraphysiological doses of 1,25 dihydroxycholecalciferol (0.1-2.5
|
||
micrograms/d/100 g body weight) to rats, produced respiratory alkalosis. With the doses of 0.1-0.2
|
||
micrograms/d/100 g and feeding a diet with 0.7% of calcium, calcemias did not exceed 2.75 mM, and
|
||
significantly reduced plasma ionized calcium levels were measured. The latter<strong>
|
||
phenomenon was found associated with increased urinary excretion of cAMP, soft tissue calcium
|
||
content,</strong> and polyuria with hypostenuria, all known effects of parathyroid hormone.”
|
||
</p>
|
||
<p>
|
||
<strong> 23.</strong> Am J Physiol 1996 Jul;271(1 Pt 2):F216-22. <strong>Metabolic alkalosis decreases
|
||
bone calcium efflux by suppressing osteoclasts and stimulating osteoblasts.</strong> Bushinsky
|
||
DA.<strong>
|
||
“In vivo and in vitro evidence indicates that metabolic acidosis, which may occur prior to complete
|
||
excretion of end products of metabolism, increases urinary calcium excretion.</strong>
|
||
<strong>The additional urinary calcium is almost certainly derived from bone mineral.”</strong> “To
|
||
determine whether metabolic alkalosis alters net calcium efflux (JCa+) from bone and bone cell function,
|
||
we cultured neonatal mouse calvariae for 48 h in either control medium (pH approximately equal to
|
||
7.4,<strong> [HCO3-] approximately equal to 24</strong>), medium simulating mild alkalosis (pH
|
||
approximately equal to 7.5, [HCO3-] approximately equal to 31), or severe alkalosis (pH approximately
|
||
equal to 7.6,<strong> [HCO3-] approximately equal to 39) </strong>and measured JCa+ and the release of
|
||
osteoclastic beta-glucuronidase and osteoblastic collagen synthesis. Compared with control, metabolic
|
||
alkalosis caused a <strong>progressive decrease in JCa+</strong>, which was correlated inversely with
|
||
initial medium pH (pHi). Alkalosis caused <strong>a decrease in osteoclastic beta-glucuronidase
|
||
release,</strong> which was correlated inversely with pHi and directly with JCa+. Alkalosis also
|
||
caused an increase in osteoblastic collagen synthesis, which was correlated directly with pHi and
|
||
inversely with JCa+. There was a strong inverse correlation between the effects alkalosis on
|
||
osteoclastic beta-glucuronidase release and osteoblastic collagen synthesis. Thus metabolic alkalosis
|
||
decreases JCa+ from bone, at least in part, by decreasing osteoclastic resorption and increasing
|
||
osteoblastic formation. These results suggest that the provision of base to neutralize endogenous acid
|
||
production may improve bone mineral accretion.”
|
||
</p>
|
||
<p>
|
||
<strong> 24.</strong> Am J Physiol 1997 Nov;273(5 Pt 2):F698-705 <strong>The effects of respiratory
|
||
alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo.</strong> Unwin
|
||
R, Stidwell R, Taylor S, Capasso G.
|
||
</p>
|
||
<p>
|
||
<strong>25.</strong> Can J Anaesth 1999 Feb;46(2):185-9. <strong>Acute respiratory alkalosis associated
|
||
with low minute ventilation in a patient with severe hypothyroidism.</strong> Lee HT, Levine M.
|
||
<strong>“His profoundly lowered basal metabolic rate and decreased CO2 production, resulting probably
|
||
from severe hypothyroidism, may have resulted in development of acute respiratory alkalosis in spite
|
||
of concurrently diminished minute ventilation.”</strong>
|
||
</p>
|
||
<p>
|
||
<strong>26.</strong> Am J Epidemiol 1991 Apr 1;133(7):649-60.<strong>
|
||
A prospective study of bone mineral content and fracture in communities with differential fluoride
|
||
exposure.</strong> Sowers MF, Clark MK, Jannausch ML, Wallace RB. “Residence in the higher-fluoride
|
||
community was associated with a <strong>significantly lower radial bone mass</strong> in premenopausal
|
||
and postmenopausal women, an increased rate of radial bone mass loss in premenopausal women, and
|
||
significantly more fractures among postmenopausal women. There was no difference in the 5-year relative
|
||
risk of any fracture in the higher-calcium community versus the control community; however, <strong>the
|
||
relative risk was 2.1 (95% confidence interval (CI) 1.0-4.4) in women in the higher-fluoride
|
||
community compared with women in the control community.</strong>
|
||
<strong>There was no difference in the 5-year risk of wrist, spine, or hip fracture in the
|
||
higher-calcium community versus the control community; however, the 5-year relative risk for women
|
||
in the higher-fluoride community, compared with women in the control community, was 2.2 (95% CI
|
||
1.1-4.7).</strong> Estimates of risk were adjusted for age and body size.”
|
||
</p>
|
||
<p>
|
||
<strong>27.</strong> J Nutr 2000 Dec;130(12):2889-96.<strong>
|
||
Long-term high protein intake does not increase oxidative stress in rats.</strong> Petzke KJ, Elsner
|
||
A, Proll J, Thielecke F, Metges CC. <strong></strong>
|
||
</p>
|
||
<p>
|
||
<strong>28.</strong> Med Hypotheses 1995 Sep;45(3):241-6.<strong>
|
||
Anabolic effects of insulin on bone suggest a role for chromium picolinate in preservation of bone
|
||
density.</strong> McCarty MF. “Physiological levels of insulin reduce the ability of PTH to activate
|
||
protein kinase C in osteoblasts, suggesting that insulin may be a physiological antagonist of bone
|
||
resorption. In addition, insulin is known to promote collagen production by osteoblasts.” <strong>[I
|
||
think chromium is too toxic to use as a supplement.]</strong>
|
||
</p>
|
||
<p> </p>
|
||
<p>
|
||
29: Anesthesiology 1998 Dec;89(6):1389-400. <strong>Effects of hyperventilation and
|
||
hypocapnic/normocapnic hypoxemia on renal function and lithium clearance in humans.</strong>
|
||
Vidiendal Olsen N, Christensen H, Klausen T, Fogh-Andersen N, Plum I, Kanstrup IL, Hansen JM Department
|
||
of Neuroanaesthesia, Copenhagen University Hospital, Denmark. NVO@DADLNET.DK BACKGROUND: Using the renal
|
||
clearance of lithium as an index of proximal tubular outflow, this study tested the hypothesis that
|
||
acute hypocapnic hypoxemia decreases proximal tubular reabsorption to the same extent as hypocapnic
|
||
normoxemia (hyperventilation) and that this response is blunted during normocapnic hypoxemia. METHODS:
|
||
Eight persons were studied on five occasions: (1) during inhalation of 10% oxygen (hypocapnic
|
||
hypoxemia), (2) during hyperventilation of room air leading to carbon dioxide values similar to those
|
||
with hypocapnic hypoxemia, (3) during inhalation of 10% oxygen with the addition of carbon dioxide to
|
||
produce normocapnia, (4) during normal breathing of room air through the same tight-fitting face mask as
|
||
used on the other study days, and (5) during breathing of room air without the face mask. RESULTS:
|
||
Hypocapnic and normocapnic hypoxemia and hyperventilation increased cardiac output, respiratory minute
|
||
volume, and effective renal plasma flow. Glomerular filtration rate remained unchanged on all study
|
||
days. Calculated proximal tubular reabsorption decreased during hypocapnic hypoxemia and
|
||
hyperventilation but remained unchanged with normocapnic hypoxemia. Sodium clearance increased<strong
|
||
></strong>slightly during hypocapnic and normocapnic hypoxemia, hyperventilation, and normocapnic
|
||
normoxemia with but not without the face mask. CONCLUSIONS:<strong></strong>The results indicate
|
||
that<strong>
|
||
(1) respiratory alkalosis with or without hypoxemia decreases proximal tubular reabsorption and that
|
||
this effect, but not renal vasodilation or natriuresis, can be abolished by adding carbon dioxide to
|
||
the hypoxic gas; (2) the increases in the effective renal plasma flow were caused by</strong>
|
||
increased ventilation rather than by changes in arterial oxygen and carbon dioxide levels; and (3) the
|
||
natriuresis may be secondary to increased renal perfusion, but application of a face mask also may
|
||
increase sodium excretion.
|
||
</p>
|
||
<p>
|
||
31: Wien Klin Wochenschr 1979 Apr 27;91(9):304-7. <strong>[Investigations on the pathogenesis of distal
|
||
renal tubular acidosis].</strong> [Article in German] Schabel F, Zieglauer H In distal (type 1) RTA,
|
||
renal acid excretion is impaired by the inability to establish adequate pH gradients between plasma and
|
||
distal tubular fluid at any level of acidosis. Main clinical signs in infancy are anorexia, vomiting and
|
||
failure to thrive. Despite low serum bicarbonate levels the renal threshold of bicarbonate is normal,
|
||
while urinary pH levels are high even with values below the threshold. <strong>Under conditions of
|
||
bicarbonate-induced systemic alkalosis urinary the pCO2 exceeds blood pCO2 in normal
|
||
subjects.</strong> by contrast, the urinary pCO2 tension is not significantly greater in distal RTA,
|
||
indicating a failure of the cells of the distal nephron to secrete hydrogen ions even without a
|
||
gradient. Red cell carbonic anhydrase is within the normal range, whilst the inhibition of carbonic
|
||
anhydrase activity has no effect on distal tubular function. Until now no histological or enzymatic
|
||
defect could be detected to explain the ineffective acidification. <strong>Bicarbonate loading is
|
||
followed by a lowering of calcium excretion to within the normal range</strong> and a decrease in
|
||
the uncharacteristic renal hyperaminoaciduria.
|
||
</p>
|
||
<p> </p>
|
||
<p> </p>
|
||
<p></p>
|
||
</article>
|
||
</body>
|
||
</html>
|