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  1. <html>
  2. <head><title>Bone Density: First Do No Harm</title></head>
  3. <body>
  4. <h1>
  5. Bone Density: First Do No Harm
  6. </h1>
  7. <article class="posted">
  8. <p>
  9. No topic can be understood in isolation. People frequently ask me what they should do about their
  10. diagnosed osteoporosis/osteopenia, and when they mention “computer controlled” and “dual photon x-ray”
  11. bone density tests, my attention tends to jump past their bones, their diet, and their hormones, to the
  12. way they must perceive themselves and their place in the world. Are they aware that this is an x-ray
  13. that’s powerful enough to differentiate very opaque bones from less opaque bones? The soft tissues
  14. aren’t being studied, so they are allowed to be “overexposed” until they appear black on the film. If a
  15. thick area like the thigh or hip is to be measured, are they aware that the x-ray dose received at the
  16. surface where the radiation enters might be 20 times more intense than the radiation that reaches the
  17. film, and that the 90 or 95% of the missing energy has been absorbed by the person’s cells? If I limited
  18. my response to answering the question they thought they had asked me, I would feel that I had joined a
  19. conspiracy against them. My answer has to assume that they are really asking about their health, rather
  20. than about a particular medical diagnosis.
  21. </p>
  22. <p>
  23. Neurologists are famous for making exquisitely erudite diagnoses of problems that they can’t do anything
  24. to remedy. The owners of expensive dual photon x-ray absorptiometer diagnostic machines are in a very
  25. different position. The remedies for osteoporosis are things that everyone should be doing, anyway, so
  26. diagnosis makes no difference in what the physician should recommend to the patient.
  27. </p>
  28. <p>
  29. Most often, estrogen is prescribed for osteoporosis, and if the doctors didn’t have their bone density
  30. tests, they would probably prescribe estrogen anyway, “to protect the heart,” or “to prevent Alzheimer’s
  31. disease.” Since I have already written about estrogen and those problems, there’s no need to say more
  32. about it here, except that estrogen is the cause of a variety of tissue atrophies, including the
  33. suppression of bone formation.[1]
  34. </p>
  35. <p>
  36. General Electric, a major advocate of x-ray screening for osteoporosis and breast cancer, has advertised
  37. that 91% of breast cancers could be cured if everyone used their technology. Breast cancer has not
  38. decreased despite the massive application of the technology, though the US government and others (using
  39. crudely deceptive statistis) claim that the War on Cancer is being won. Similarly, during the last
  40. decades when the “high technology” x-ray machines have been more widely used, the age-specific incidence
  41. of osteoporosis has increased tremendously. This apparently includes a higher rate of shortening of
  42. stature with aging than in earlier generations.[2]
  43. </p>
  44. <p>
  45. I think there are several reasons for avoiding x-ray tests of bone density, besides the simple one that
  46. everyone should eat a bone-protective diet, regardless of the present density of their bones.
  47. </p>
  48. <p>
  49. Even seemingly identical x-ray machines, or the same machine at a different time, can give very
  50. different estimates of bone density.[3-10] Radiologists evaluating the same images often reach very
  51. different conclusions.[11] Changes in the tissue water and fat content can make large differences in
  52. apparent bone density,[12] and estrogen, which affects those, could appear to cause improved bone
  53. density, when it is merely causing a generalized inflammatory condition, with edema. A machine that is
  54. accurate when measuring an aluminum model, won’t necessarily give meaningful results when the
  55. composition of the tissue, including the bone marrow, has changed. Calcification of soft tissues can
  56. create the impression of increased bone density.[13] Studies of large groups of people show such small
  57. annual losses of bone density (around 1%), especially in the neck of the femur (which is important in
  58. hip fractures) that the common technical errors of measurement in an individual seem very large.
  59. </p>
  60. <p>
  61. Ultrasound devices can do an extremely good job of evaluating both bone density and strength [14-16],
  62. rather than just density.
  63. </p>
  64. <p>Ultrasound stimulates bone repair.</p>
  65. <p>X-rays accelerate the rate of bone loss.</p>
  66. <p>X-rays do their harm at any dose; there is no threshold at which the harm begins.</p>
  67. <p>
  68. X-ray damage is not limited to the area being investigated. Deflected x-rays affect adjacent areas, and
  69. toxins produced by irradiated cells travel in the bloodstream, causing systemic effects. Dental x-rays
  70. cause thyroid cancer and eye cancer. Recent experiments have shown that low doses of radiation cause
  71. delayed death of brain cells. The action of x-rays produces tissue inflammation, and diseases as
  72. different as Alzheimer’s disease and heart disease result from prolonged inflammatory processes.
  73. </p>
  74. <p>
  75. I have never known a physician who knew, or cared, what dose of radiation his patients were receiving. I
  76. have never known a patient who could get that information from their doctors.
  77. </p>
  78. <p>
  79. The radiation exposure used to measure bone density may be higher (especially when the thigh and hip are
  80. x-rayed) than the exposure in dental x-rays, but dental x-rays are known to increase the incidence of
  81. cancer. Often, dentists have their receptionists do the x-rays, which probably doesn’t matter, since the
  82. dentist is usually no more concerned than the receptionist about understanding, and minimizing, the
  83. dose. Even radiological specialists seldom are interested in the doses they use diagnostically.
  84. </p>
  85. <p>
  86. It was only after a multitude of dentists had a finger amputated that it became standard practice to ask
  87. the patient to hold the film, while the dentist stood safely back away from the rays.
  88. </p>
  89. <p>
  90. Just after the beginning of the century, Thomas Edison was helping to popularize x-rays, but the
  91. horrible death of his chief technician turned Edison into an enemy of the technology. By the 1940s, the
  92. dangers of radiation were coming to be understood by the general public, and it was only the
  93. intervention of the US government, to popularize atomic bombs and nuclear power, that was able to
  94. reverse the trend.
  95. </p>
  96. <p>
  97. In 1956 and 1957, Linus Pauling was the only well known scientist who opposed the government’s policies.
  98. The government took away his passport, and his opportunities to write and speak were limited by a
  99. boycott imposed by a variety of institutions, but instigated by the nuclear industry and its agent, the
  100. Atomic Energy Commission. The government which considered Pauling a threat to national security, had
  101. placed thousands of German and Hungarian “ex”-Nazis in high positions in industry and government
  102. agencies, after protecting them from prosecution as war criminals. The official government policy,
  103. directed by the financier Admiral Strauss who controlled the Atomic Energy Commision, was to tell the
  104. public that radiation was good. Their extreme secrecy regarding their radiation experiments on
  105. Americans, however, indicated that they were aware of the malignant nature of their activities<strong
  106. >;</strong> many of the records were simply destroyed, so that no one could ever know what had been
  107. done. Scientists who worked for the government, Willard Libby, John Goffman, and many others, were
  108. working to convince the public that they shouldn’t worry. Of the multitude of scientists who served the
  109. government during that time, only a few ever came to oppose those policies, and those who did were
  110. unable to keep their jobs or research grants. Gofman has become the leader in the movement to protect
  111. the public against radiation, especially, since 1971, through the Committee for Nuclear Responsibility,
  112. PO Box 421993, San Francisco, CA 94132..
  113. </p>
  114. <p>
  115. Gofman has said<strong>: "I was stupid in those days. In 1955, '56, people like Linus Pauling were
  116. saying that the bomb fallout would cause all this trouble. I thought, 'We're not sure. If you're not
  117. sure, don't stand in the way of progress.' I could not have thought anything more stupid in my life.
  118. </strong>
  119. </p>
  120. <p>
  121. <strong>
  122. "The big moment in my life happened while I was giving a health lecture to nuclear engineers. In the
  123. middle of my talk it hit me! What the hell am I saying? If you don't know whether low doses are safe
  124. or not, going ahead is exactly wrong. At that moment, I changed my position entirely."[17]
  125. </strong>
  126. </p>
  127. <p>
  128. <strong>
  129. In 1979, Gofman said: "There is no way I can justify my failure to help sound an alarm over these
  130. activities many years sooner than I did. I feel that at least several hundred scientists trained in
  131. the biomedical aspect of atomic energy - myself definitely included - are candidates for
  132. Nuremburg-type trials for crimes against humanity for our gross negligence and irresponsibility. Now
  133. that we know the hazard of low-dose radiation, the crime is not experimentation - it's murder." [18]
  134. </strong>
  135. </p>
  136. <p>
  137. Many ordinary people were making exactly that argument in the 1950s, but government censorship kept the
  138. most incriminating evidence from the public. The climate of intimidation spread throughout the culture,
  139. so that teachers who spoke about the dangers of radiation were called disloyal, and were fired. Now,
  140. people who don’t want x-rays are treated as crackpots. Probably because of this cultural situation,
  141. Gofman’s recommendations are very mild--simply for doctors to use good technology and to know what they
  142. are doing, which could lead to ten-fold or even hundred-fold dose reduction. Even with such mild
  143. restraint in the use of diagnostic x-rays, Gofman’s well founded estimate is that 250,000 deaths caused
  144. by radiation could be prevented annually. I believe many more deaths would be prevented if ultrasound
  145. and MRI were used consistently instead of x-rays. Using Gofman’s estimate, I think we can blame at least
  146. ten million deaths on just the medical x-rays that have been used inappropriately because of the
  147. policies of the U.S. government in the last half century. That wouldn’t include the deaths caused by
  148. radioactive fallout from bomb tests and leaks from nuclear power plants, or the vast numbers of people
  149. mentally impaired by all sorts of toxic radiation.<strong></strong>
  150. </p>
  151. <p>
  152. <strong>Although nearly all the people who committed the radiation crimes of the 1950s and 1960s have
  153. died or retired, the culture they created remains in the mass media and scientific journals, and in
  154. the medical and academic professions.
  155. </strong>
  156. </p>
  157. <p>
  158. Medical journals describe ways to minimize diagnostic x-ray exposure, and they advocate many seemingly
  159. effective treatments for osteoporosis, giving an impression that progress is being made in “managing”
  160. osteoporosis, but the real situation is very different. Fractures resulting from osteoporosis are
  161. increasing, and osteoporosis is affecting younger and younger people. I think it would be reasonable to
  162. say that a woman with osteoporosis is usually better off when it’s not diagnosed, because of the
  163. dangerous things prescribed for it. Estrogen has become the main “treatment” for osteoporosis, but many
  164. of the other ways of “managing” osteoporosis are both ineffective and unsafe.
  165. </p>
  166. <p>
  167. Many women are told to stop taking a thyroid supplement when osteoporosis is diagnosed, but
  168. hypothyroidism often leads to hyperprolactinema and hypercortisolemia, which are two of the most clearly
  169. established causes of osteoporosis. Calcitonin, vitamin D-active metabolite, and estrogen-”HRT”
  170. treaments can cause respiratory alkalosis (relative hyperventilation),[19-24] and hypothyroidism
  171. produces a predisposition to hyperventilation.[25] Hyperventilation tends to cause calcium loss. In
  172. respiratory alkalolis, CO2 (and sometimes bicarbonate) are decreased, impairing calcium retention, and
  173. in “<strong><em>metabolic</em></strong> alkalosis,” with <strong><em>increased</em></strong>
  174. bicarbonate, calcium is retained more efficiently and bone formation is stimulated, and its dissolution
  175. is suppressed.
  176. </p>
  177. <p>
  178. Other women are told to reduce their protein consumption, or to take fluoride or whatever drug has been
  179. most recently promoted. A protein deficiency is a clear cause of osteoporosis, and bone density
  180. corresponds to the amount of protein consumed. Milk protein, especially, protects against osteoporosis,
  181. independently of milk’s other important nutrients. Too much fluoride clearly increases the risk of bone
  182. fractures,[26] and the side effects of other drugs haven’t been properly studied in humans, while they
  183. often have dangerous effects in animals.
  184. </p>
  185. <p>
  186. Calcium, magnesium, vitamin A, vitamin B6- , vitamin K, and vitamin D are important for the development
  187. and maintenance of bones. For example, a vitamin A deficiency limits the synthesis of progesterone and
  188. proteins. In calcium deficiency, parathyroid hormone is increased, and tends to cause the typical
  189. changes of aging, shifting calcium from hard tissues to soft, and decreasing the ratio of extracellular
  190. to intracellular (excitatory) calcium.
  191. </p>
  192. <p>
  193. Polyunsaturated fats are converted to prostaglandins (especially under the influence of estrogen), and
  194. several prostaglandins have toxic effects on bone. Those fats also suppress the formation of thyroid
  195. hormone and progesterone. The increased use of the unsaturated oils has coincided with the increase of
  196. osteoporosis.
  197. </p>
  198. <p>
  199. The oxidation of proteins caused by free radicals is increased with aging and by the use of unsaturated
  200. fats, and it contributes to tissue atrophy, including the age-related shrinkage of the bones. In animal
  201. studies, “adequate” dietary protein, 13.8% of the diet (equivalent to about 80 grams per day for a
  202. person) is associated with more oxidative damage to tissue proteins than the very high protein diets,
  203. 25.7% or 51.3%, that would be equivalent to about 150 or 300 grams of protein daily for a person.[27]
  204. Yet, many physicians recommend a low protein diet to protect against osteoporosis.
  205. </p>
  206. <p>
  207. Avoiding fluoridated water and the polyunsaturated oils, and drinking two quarts of milk daily (which
  208. will provide only 66 grams of protein), and using some other nutrient-rich foods such as eggs and
  209. fruits, are probably the basic things to protect the bones. For vitamins, especially K, occasional liver
  210. can be helpful. Meats, fruits, leaves, and coffee are rich in magnesium.
  211. </p>
  212. <p>
  213. Some people have argued that the acidity of urine produced by eating meat causes calcium loss. However,
  214. a high protein diet also improves the absorption of calcium by the intestine. Another overlooked
  215. function of dietary protein is that it stimulates insulin secretion, and insulin is anabolic for
  216. bone.[28]
  217. </p>
  218. <p>
  219. The same diet that protects against osteoporosis, i.e., plenty of protein and calcium, etc., also
  220. protects against kidney stones and other abnormal calcificatons.
  221. </p>
  222. <p>&nbsp;</p>
  223. <p><strong><h3>REFERENCES</h3></strong></p>
  224. <p>
  225. 1. Proc Assoc Am Physicians 1996 Mar;108(2):155-64 <strong>Potential mechanism of estrogen-mediated
  226. decrease in bone formation: estrogen increases production of inhibitory insulin-like growth
  227. factor-binding protein-4.</strong> Kassem M, Okazaki R, De Leon D, Harris SA, Robinson JA, Spelsberg
  228. TC, Conover CA, Riggs BL.
  229. </p>
  230. <p>
  231. <strong> 2.</strong> Am J Phys Anthropol 1990 Dec;83(4):467-76. <strong>Stature loss among an older
  232. United States population and its relation to bone mineral status.</strong> Galloway A, Stini WA, Fox
  233. SC, Stein P. “With advancing age there is a gradual decrease in height apparently beginning in the
  234. mid-40s. Thereafter, there is a relatively rapid decrease in measured height. <strong>This contrasts to
  235. the much slower rates predicted from earlier populations (Trotter and Gleser: American Journal of
  236. Physical Anthropology 9:311-324, 1951).
  237. </strong>The rate of stature loss is associated with diminution of bone mineral density as well as with
  238. maximum height. Since there are suggestions of a secular trend toward greater reductions in bone mineral
  239. density, this study suggests there may be a secular trend toward an increase in statural loss with age.”
  240. </p>
  241. <p>
  242. <strong> 3.</strong> Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1994 Mar;160(3):260-5. <strong
  243. >[The quantitative determination of bone mineral content--a system comparison of similarly built
  244. computed tomographs].</strong> [Article in German] Andresen R, Radmer S, Banzer D, Felsenberg D,
  245. Wolf KJ Klinik fur Radiologie, Universitatsklinikum Steglitz der FU Berlin. An intercomparison of 4 CT
  246. scanners of the same manufacturer was performed. The bone mineral content of 11 lumbar vertebral columns
  247. removed directly post mortem was determined in a specially constructed lucite-water phantom. Even
  248. devices of the same construction were shown to yield a variation in the quantitative evaluation markedly
  249. exceeding the annual physiological mineral loss. As long as scanner adjustment by physical calibration
  250. phantoms has not yet been established, a course assessment and therapy control of bone mineral content
  251. should always be carried out on the same QCT scanner.
  252. </p>
  253. <p>
  254. <strong> 4.</strong> Osteoporos Int 1990 Oct;1(1):23-9. <strong>Vertebral bone mineral density measured
  255. laterally by dual-energy X-ray absorptiometry.</strong> Slosman DO, Rizzoli R, Donath A, Bonjour JP.
  256. “The bone mineral density (BMD) of lumbar vertebrae in the anteroposterior (AP) view may be
  257. overestimated in osteoarthritis or with aortic calcification, which are common in elderly.” “Then, we
  258. compared the capability of BMD LAT and BMD AP scans for monitoring bone loss related to age and for
  259. discriminating the BMD of postmenopausal women with nontraumatic vertebral fractures from that of young
  260. subjects. In vitro, when a spine phantom was placed in lateral position in the middle of 26 cm of water
  261. in order to simulate both soft-tissue thickness and X-ray source remoteness, the coefficient of
  262. variation (CV) of six repeated determinations of BMD was 1.0%. In vivo, the CV of paired BMD LAT
  263. measurements obtained in 20 healthy volunteers<strong> after repositioning was 2.8%.”</strong>
  264. </p>
  265. <p>
  266. <strong> 5.</strong> Eur J Nucl Med 1990;17(1-2):3-9.<strong>
  267. Comparative study of the performances of X-ray and gadolinium 153 bone densitometers at the level of
  268. the spine, femoral neck and femoral shaft.</strong> Slosman DO, Rizzoli R, Buchs B, Piana F, Donath
  269. A, Bonjour JP. “In vivo, at the spine level, with DPA, mean<strong>
  270. CV of BMD measured 6 times after repositioning in 6 healthy volunteers was 3.8% +/- 1.9% and 2.1%
  271. +/- 0.7% . . . .”
  272. </strong>
  273. </p>
  274. <p><strong> &nbsp;</strong></p>
  275. <p>
  276. <strong> 6. </strong> Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1995 Apr;162(4):269-73. <strong
  277. >[Experimental studies of the visualization of the vertebral body spongiosa by high-resolution computed
  278. tomography].</strong> Henschel MG, Freyschmidt J, Holland BR. “The measured lower limit of<strong>
  279. visualisation of cancellous bone structures is clearly worse than expected from the measurements of
  280. spatial resolution with standard phantoms used for HR-CT (0.6 versus 0.4 mm). True and exact imaging
  281. of normal cancellous bone cannot be achieved even by modern HR-CT. Noise creates structures
  282. mimicking cancellous bone.”
  283. </strong>
  284. </p>
  285. <p>
  286. 7. J Comput Tomogr 1984 Apr;8(2):91-7. <strong>Quantitative computed tomography assessment of spinal
  287. trabecular bone. I. Age-related regression in normal men and women.</strong> Firooznia H, Golimbu C,
  288. Rafii M, Schwartz MS, Alterman ER. “Computed tomography, <strong>utilized in conjunction with a
  289. calibrated phantom containing a set of reference densities</strong> (K2HPO4 and water), is capable
  290. of determining the mineral content of the trabecular bone of the spine with an<strong>
  291. accuracy of about 6%</strong> of the ash weight of the vertebrae scanned (specimen studies).”
  292. </p>
  293. <p>
  294. 8. Calcif Tissue Int 1991 Sep;49(3):174-8. <strong>Precision and stability of dual-energy X-ray
  295. absorptiometry measurements.</strong>
  296. <hr />
  297. <strong></strong>
  298. </p>
  299. <p>
  300. <strong> 9.</strong> J Comput Assist Tomogr 1993 Nov-Dec;17(6):945-51. <strong>Influence of temperature
  301. on QCT: implications for mineral densitometry.</strong> Whitehouse RW, Economou G, Adams JE.
  302. “Inaccuracies in quantitative CT (QCT) for vertebral bone mineral measurements may result from
  303. differences between the temperature of the vertebrae and the calibration standards.” “In the computer
  304. simulation, the<strong>
  305. fat error associated with single energy QCT for trabecular bone mineral densitometry was 20% less
  306. for specimens at room temperature than at body temperature.”</strong> “The fat error of
  307. single<strong>
  308. energy QCT for mineral densitometry may have been underestimated in previous in vitro studies using
  309. vertebral specimens scanned at room temperature.”</strong>
  310. </p>
  311. <p>
  312. <strong> 10.</strong> Phys Med Biol 1986 Jan;31(1):55-63. <strong>Quantitative CT measurements: the
  313. effect of scatter acceptance and filter characteristics on the EMI 7070.</strong> Merritt RB,
  314. Chenery SG “Non-linearities in projection values on computed tomography (CT) scanners <strong>cause
  315. corresponding errors in derived Hounsfield unit attenuation measurements. Existing commercial
  316. machines have been refined for clinical usefulness but not necessarily for quantitative
  317. accuracy.”</strong>
  318. <strong>“It is concluded that, irrespective of any quality assurance protocol, interpatient and
  319. interslice errors can be expected to range from 3 to 10% for water-equivalent materials and the
  320. intraslice positional dependence of the CT number can vary up to 5% for dense bone-like materials in
  321. a uniform phantom.”</strong>
  322. </p>
  323. <p>
  324. <strong> 11.</strong> Skeletal Radiol 1986;15(5):347-9. <strong>Observer variation in the detection of
  325. osteopenia.</strong> Epstein DM, Dalinka MK, Kaplan FS, Aronchick JM, Marinelli DL, Kundel HL. In
  326. order to determine observer variation in the detection of osteopenia, 15 pairs of lateral chest
  327. radiographs obtained within two weeks of each other were reviewed separately by two radiologists and one
  328. orthopedist on three separate occasions. Intra- and interobserver variations were calculated for each
  329. individual film and film pairs using Kappa values. <strong>The individual observers were not able to
  330. give consistent readings on the same film on different days</strong>
  331. <hr />
  332. <strong>additional factors of repeat films</strong>
  333. <hr />
  334. <strong>or separate observers</strong>
  335. <hr />
  336. <strong>agreement was even worse.</strong>
  337. <strong>The identification of osteopenia from the lateral view of the thoracic spine is highly
  338. subjective and variable from film to film and observer to observer.</strong>
  339. </p>
  340. <p>
  341. <strong> 12.</strong> P. Schneider and C. Reiners, Letter, JAMA 277(1), 23, Jan. 1, 1997. <strong>"The
  342. influence of fat distribution on bone mass measurements with DEXA can be of considerable magnitude
  343. and ranges up to 10% error per 2 cm of fat."</strong>
  344. </p>
  345. <p>
  346. <strong> 13.</strong> Calcif Tissue Int 1990 Apr;46(4):280-1. <strong>Effect of radiographic
  347. abnormalities on rate of bone loss from the spine.</strong> Dawson-Hughes B, Dallal GE. <strong
  348. >“Spurious rates of loss of spine BMD are likely to be found in subjects with calcification of the
  349. aorta, osteophytes or other abnormalities in the spine scan field. This should be kept in mind when
  350. serial spine scans are being considered in these subjects.”
  351. </strong>
  352. </p>
  353. <p>
  354. <strong> 14.</strong> Przegl Lek 2000;57(2):93-9. [No title available]. Jaworski M, Lorenc RS. <strong
  355. >“. . .</strong>Dual Energy X-ray Absorptiometry (DEXA) method is a reference method to diagnose
  356. osteoporosis. This method allows to <strong>measure bone density and bone mass, however bone quality can
  357. not be estimated. Quantitative ultrasound (QUS)</strong>
  358. <strong>method provides information about bone structure.”</strong>
  359. </p>
  360. <p>
  361. <strong> 15.</strong> Osteoporos Int 2000;11(4):354-60.<strong>
  362. Assessment of a new quantitative ultrasound calcaneus measurement: precision and discrimination of
  363. hip fractures in elderly women compared with dual X-ray absorptiometry.</strong> He YQ, Fan B, Hans
  364. D, Li J, Wu CY, Njeh CF, Zhao S, Lu Y, Tsuda-Futami E, Fuerst T, Genant HK.
  365. </p>
  366. <p>
  367. <strong> 16.</strong> Cas Lek Cesk 2000 Apr 26;139(8):231-6 <strong>[X-ray densitometry and
  368. ultrasonography of the heel bone--sensitivity and comparison with densitometry of the axial
  369. skeleton].</strong> [Article in Czech] Michalska D, Zikan V, Stepan J, Weichetova M, Kubova V,
  370. Krenkova J, Masatova A. “The DXA of the heel underestimates the prevalence of osteoporosis. The results
  371. of the heel QUS (Stiffness) appear to be better correlated to femoral BMD than heel BMD.”
  372. </p>
  373. <p>
  374. <strong>17.</strong> John Gofman, M.D. (biographical chapter. pages 401-412.) In Studs Terkel's book
  375. <strong><em>Coming of Age. The Story of our Century by Those Who Lived It.</em></strong> The New Press.
  376. NY. 1995.
  377. </p>
  378. <p>
  379. <strong>18.</strong> Gofman, J.W. <strong>An irreverent, illustrated view of nuclear power.</strong>
  380. Committee for Nuclear Responsibility. San Francisco, CA. pp. 227-228, 1979.
  381. </p>
  382. <p>
  383. <strong> 19.</strong> Kidney Int 1992 Sep;42(3):727-34. <strong>Chronic respiratory alkalosis induces
  384. renal PTH-resistance, hyperphosphatemia and hypocalcemia in humans.</strong> Krapf R, Jaeger P,
  385. Hulter HN Department of Medicine, Insel University Hospital, Berne, Switzerland. <strong>“The effects of
  386. chronic respiratory alkalosis on divalent ion homeostasis have not been reported in any
  387. species.”</strong> “Chronic respiratory alkalosis (delta PaCO2, -8.4 mm Hg, delta[H+] -3.2
  388. nmol/liter) resulted in a sustained decrement in plasma ionized calcium concentration (delta[IoCa++]p,
  389. -0.10 mmol/liter, P less than 0.05) and a sustained increment in plasma phosphate concentration
  390. (delta[PO4]p, +0.14 mmol/liter, P less than 0.005) <strong>associated with increased fractional
  391. excretion of Ca++ . . .”
  392. </strong>
  393. </p>
  394. <p>
  395. <strong> 20.</strong> J Clin Endocrinol Metab 1999 Jun;84(6):1997-2001 <strong>Hormone replacement
  396. therapy causes a respiratory alkalosis in normal postmenopausal women.</strong>
  397. <hr />
  398. <strong>partial pressure of carbon dioxide. . . .”</strong>
  399. <strong>“Accompanying changes in blood pH were apparent in the estrogen plus MPA group, where there was
  400. an upward trend at 1 week</strong>
  401. <hr />
  402. </p>
  403. <p>
  404. <strong> 21.</strong> Wien Klin Wochenschr 1979 Apr 27;91(9):304-7 <strong>[Investigations on the
  405. pathogenesis of distal renal tubular acidosis].</strong> Schabel F, Zieglauer H. <strong
  406. >“Bicarbonate loading is followed by a lowering of calcium excretion to within the normal range and a
  407. decrease in the uncharacteristic renal hyperaminoaciduria.”
  408. </strong>
  409. </p>
  410. <p>
  411. <strong> 22.</strong> Calcif Tissue Int 1984 Sep;36(5):604-7. <strong>Respiratory alkalosis and reduced
  412. plasmatic concentration of ionized calcium in rats treated with 1,25
  413. dihydroxycholecalciferol.</strong> Locatto ME, Fernandez MC, Caferra DA, Gimenez MC, Vidal MC, Puche
  414. RC. “The daily administration of supraphysiological doses of 1,25 dihydroxycholecalciferol (0.1-2.5
  415. micrograms/d/100 g body weight) to rats, produced respiratory alkalosis. With the doses of 0.1-0.2
  416. micrograms/d/100 g and feeding a diet with 0.7% of calcium, calcemias did not exceed 2.75 mM, and
  417. significantly reduced plasma ionized calcium levels were measured. The latter<strong>
  418. phenomenon was found associated with increased urinary excretion of cAMP, soft tissue calcium
  419. content,</strong> and polyuria with hypostenuria, all known effects of parathyroid hormone.”
  420. </p>
  421. <p>
  422. <strong> 23.</strong> Am J Physiol 1996 Jul;271(1 Pt 2):F216-22. <strong>Metabolic alkalosis decreases
  423. bone calcium efflux by suppressing osteoclasts and stimulating osteoblasts.</strong> Bushinsky
  424. DA.<strong>
  425. “In vivo and in vitro evidence indicates that metabolic acidosis, which may occur prior to complete
  426. excretion of end products of metabolism, increases urinary calcium excretion.</strong>
  427. <strong>The additional urinary calcium is almost certainly derived from bone mineral.”</strong> “To
  428. determine whether metabolic alkalosis alters net calcium efflux (JCa+) from bone and bone cell function,
  429. we cultured neonatal mouse calvariae for 48 h in either control medium (pH approximately equal to
  430. 7.4,<strong> [HCO3-] approximately equal to 24</strong>), medium simulating mild alkalosis (pH
  431. approximately equal to 7.5, [HCO3-] approximately equal to 31), or severe alkalosis (pH approximately
  432. equal to 7.6,<strong> [HCO3-] approximately equal to 39) </strong>and measured JCa+ and the release of
  433. osteoclastic beta-glucuronidase and osteoblastic collagen synthesis. Compared with control, metabolic
  434. alkalosis caused a <strong>progressive decrease in JCa+</strong>, which was correlated inversely with
  435. initial medium pH (pHi). Alkalosis caused <strong>a decrease in osteoclastic beta-glucuronidase
  436. release,</strong> which was correlated inversely with pHi and directly with JCa+. Alkalosis also
  437. caused an increase in osteoblastic collagen synthesis, which was correlated directly with pHi and
  438. inversely with JCa+. There was a strong inverse correlation between the effects alkalosis on
  439. osteoclastic beta-glucuronidase release and osteoblastic collagen synthesis. Thus metabolic alkalosis
  440. decreases JCa+ from bone, at least in part, by decreasing osteoclastic resorption and increasing
  441. osteoblastic formation. These results suggest that the provision of base to neutralize endogenous acid
  442. production may improve bone mineral accretion.”
  443. </p>
  444. <p>
  445. <strong> 24.</strong> Am J Physiol 1997 Nov;273(5 Pt 2):F698-705 <strong>The effects of respiratory
  446. alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo.</strong> Unwin
  447. R, Stidwell R, Taylor S, Capasso G.
  448. </p>
  449. <p>
  450. <strong>25.</strong> Can J Anaesth 1999 Feb;46(2):185-9. <strong>Acute respiratory alkalosis associated
  451. with low minute ventilation in a patient with severe hypothyroidism.</strong> Lee HT, Levine M.
  452. <strong>“His profoundly lowered basal metabolic rate and decreased CO2 production, resulting probably
  453. from severe hypothyroidism, may have resulted in development of acute respiratory alkalosis in spite
  454. of concurrently diminished minute ventilation.”</strong>
  455. </p>
  456. <p>
  457. <strong>26.</strong> Am J Epidemiol 1991 Apr 1;133(7):649-60.<strong>
  458. A prospective study of bone mineral content and fracture in communities with differential fluoride
  459. exposure.</strong> Sowers MF, Clark MK, Jannausch ML, Wallace RB. “Residence in the higher-fluoride
  460. community was associated with a <strong>significantly lower radial bone mass</strong> in premenopausal
  461. and postmenopausal women, an increased rate of radial bone mass loss in premenopausal women, and
  462. significantly more fractures among postmenopausal women. There was no difference in the 5-year relative
  463. risk of any fracture in the higher-calcium community versus the control community; however, <strong>the
  464. relative risk was 2.1 (95% confidence interval (CI) 1.0-4.4) in women in the higher-fluoride
  465. community compared with women in the control community.</strong>
  466. <strong>There was no difference in the 5-year risk of wrist, spine, or hip fracture in the
  467. higher-calcium community versus the control community; however, the 5-year relative risk for women
  468. in the higher-fluoride community, compared with women in the control community, was 2.2 (95% CI
  469. 1.1-4.7).</strong> Estimates of risk were adjusted for age and body size.”
  470. </p>
  471. <p>
  472. <strong>27.</strong> J Nutr 2000 Dec;130(12):2889-96.<strong>
  473. Long-term high protein intake does not increase oxidative stress in rats.</strong> Petzke KJ, Elsner
  474. A, Proll J, Thielecke F, Metges CC. <strong></strong>
  475. </p>
  476. <p>
  477. <strong>28.</strong> Med Hypotheses 1995 Sep;45(3):241-6.<strong>
  478. Anabolic effects of insulin on bone suggest a role for chromium picolinate in preservation of bone
  479. density.</strong> McCarty MF. “Physiological levels of insulin reduce the ability of PTH to activate
  480. protein kinase C in osteoblasts, suggesting that insulin may be a physiological antagonist of bone
  481. resorption. In addition, insulin is known to promote collagen production by osteoblasts.” <strong>[I
  482. think chromium is too toxic to use as a supplement.]</strong>
  483. </p>
  484. <p>&nbsp;</p>
  485. <p>
  486. 29: Anesthesiology 1998 Dec;89(6):1389-400. <strong>Effects of hyperventilation and
  487. hypocapnic/normocapnic hypoxemia on renal function and lithium clearance in humans.</strong>
  488. Vidiendal Olsen N, Christensen H, Klausen T, Fogh-Andersen N, Plum I, Kanstrup IL, Hansen JM Department
  489. of Neuroanaesthesia, Copenhagen University Hospital, Denmark. NVO@DADLNET.DK BACKGROUND: Using the renal
  490. clearance of lithium as an index of proximal tubular outflow, this study tested the hypothesis that
  491. acute hypocapnic hypoxemia decreases proximal tubular reabsorption to the same extent as hypocapnic
  492. normoxemia (hyperventilation) and that this response is blunted during normocapnic hypoxemia. METHODS:
  493. Eight persons were studied on five occasions: (1) during inhalation of 10% oxygen (hypocapnic
  494. hypoxemia), (2) during hyperventilation of room air leading to carbon dioxide values similar to those
  495. with hypocapnic hypoxemia, (3) during inhalation of 10% oxygen with the addition of carbon dioxide to
  496. produce normocapnia, (4) during normal breathing of room air through the same tight-fitting face mask as
  497. used on the other study days, and (5) during breathing of room air without the face mask. RESULTS:
  498. Hypocapnic and normocapnic hypoxemia and hyperventilation increased cardiac output, respiratory minute
  499. volume, and effective renal plasma flow. Glomerular filtration rate remained unchanged on all study
  500. days. Calculated proximal tubular reabsorption decreased during hypocapnic hypoxemia and
  501. hyperventilation but remained unchanged with normocapnic hypoxemia. Sodium clearance increased<strong
  502. ></strong>slightly during hypocapnic and normocapnic hypoxemia, hyperventilation, and normocapnic
  503. normoxemia with but not without the face mask. CONCLUSIONS:<strong></strong>The results indicate
  504. that<strong>
  505. (1) respiratory alkalosis with or without hypoxemia decreases proximal tubular reabsorption and that
  506. this effect, but not renal vasodilation or natriuresis, can be abolished by adding carbon dioxide to
  507. the hypoxic gas; (2) the increases in the effective renal plasma flow were caused by</strong>
  508. increased ventilation rather than by changes in arterial oxygen and carbon dioxide levels; and (3) the
  509. natriuresis may be secondary to increased renal perfusion, but application of a face mask also may
  510. increase sodium excretion.
  511. </p>
  512. <p>
  513. 31: Wien Klin Wochenschr 1979 Apr 27;91(9):304-7. <strong>[Investigations on the pathogenesis of distal
  514. renal tubular acidosis].</strong> [Article in German] Schabel F, Zieglauer H In distal (type 1) RTA,
  515. renal acid excretion is impaired by the inability to establish adequate pH gradients between plasma and
  516. distal tubular fluid at any level of acidosis. Main clinical signs in infancy are anorexia, vomiting and
  517. failure to thrive. Despite low serum bicarbonate levels the renal threshold of bicarbonate is normal,
  518. while urinary pH levels are high even with values below the threshold. <strong>Under conditions of
  519. bicarbonate-induced systemic alkalosis urinary the pCO2 exceeds blood pCO2 in normal
  520. subjects.</strong> by contrast, the urinary pCO2 tension is not significantly greater in distal RTA,
  521. indicating a failure of the cells of the distal nephron to secrete hydrogen ions even without a
  522. gradient. Red cell carbonic anhydrase is within the normal range, whilst the inhibition of carbonic
  523. anhydrase activity has no effect on distal tubular function. Until now no histological or enzymatic
  524. defect could be detected to explain the ineffective acidification. <strong>Bicarbonate loading is
  525. followed by a lowering of calcium excretion to within the normal range</strong> and a decrease in
  526. the uncharacteristic renal hyperaminoaciduria.
  527. </p>
  528. <p>&nbsp;</p>
  529. <p>&nbsp;</p>
  530. <p></p>
  531. </article>
  532. </body>
  533. </html>