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骨密度:第一步-停止伤害

Bone Density: First Do No Harm

骨密度:第一步-停止伤害

by Raymond Peat

No topic can be understood in isolation. People frequently ask me what they should do about their diagnosed osteoporosis/osteopenia, and when they mention “computer controlled” and “dual photon x-ray” bone density tests, my attention tends to jump past their bones, their diet, and their hormones, to the way they must perceive themselves and their place in the world. Are they aware that this is an x-ray that’s powerful enough to differentiate very opaque bones from less opaque bones? The soft tissues aren’t being studied, so they are allowed to be “overexposed” until they appear black on the film. If a thick area like the thigh or hip is to be measured, are they aware that the x-ray dose received at the surface where the radiation enters might be 20 times more intense than the radiation that reaches the film, and that the 90 or 95% of the missing energy has been absorbed by the person’s cells? If I limited my response to answering the question they thought they had asked me, I would feel that I had joined a conspiracy against them. My answer has to assume that they are really asking about their health, rather than about a particular medical diagnosis.

任何事物都不能被单角度解读。人们经常问我他们应该做什么来应对他们的骨质疏松症/骨量减少。但当他们提到“计算机控制”和“双光子射线”骨密度测试时，我的注意力往往会越过他们的骨问题，饮食和他们的荷尔蒙。他们必须先理解自己和自己在世界上的地位。他们是否意识到这是一种足够强大的x光片可以区分不透明的骨骼和不透明的骨骼?软组织没有被研究，所以允许“过度曝光”，直到它们在胶片上呈现黑色。如果厚区域喜欢大腿或臀部来衡量，他们是否意识到在地表接收到的x射线剂量辐射进入可能是20倍比辐射到电影更强烈，而90或95%的失踪能源已经被人的细胞吸收? 如果我只回答他们自以为问过我的问题，我就会觉得自己加入了一个反对他们的阴谋。我的回答必须假设他们真的是在问自己的健康问题，而不是某个特定的医学诊断。

Neurologists are famous for making exquisitely erudite diagnoses of problems that they can’t do anything to remedy. The owners of expensive dual photon x-ray absorptiometer diagnostic machines are in a very different position. The remedies for osteoporosis are things that everyone should be doing, anyway, so diagnosis makes no difference in what the physician should recommend to the patient.

神经学家以对他们无能为力的问题做出细致而博学的诊断而闻名。昂贵的双光子x射线吸收仪诊断机器的所有者处于一个非常不同的位置。无论如何，治疗骨质疏松症的方法是每个人都应该做的，所以诊断对医生给病人的建议没有什么区别。

Most often, estrogen is prescribed for osteoporosis, and if the doctors didn’t have their bone density tests, they would probably prescribe estrogen anyway, “to protect the heart,” or “to prevent Alzheimer’s disease.” Since I have already written about estrogen and those problems, there’s no need to say more about it here, except that estrogen is the cause of a variety of tissue atrophies, including the suppression of bone formation.[1]

通常情况下，医生开雌激素是为了治疗骨质疏松症，如果医生没有进行骨密度测试，他们可能还是会开雌激素处方，“保护心脏”或“预防阿尔茨海默病”。因为我已经写了关于雌激素和这些问题的文章，这里就不需要再多说了，除了雌激素是各种组织萎缩的原因，包括抑制骨形成。[1]

General Electric, a major advocate of x-ray screening for osteoporosis and breast cancer, has advertised that 91% of breast cancers could be cured if everyone used their technology. Breast cancer has not decreased despite the massive application of the technology, though the US government and others (using crudely deceptive statistis) claim that the War on Cancer is being won. Similarly, during the last decades when the “high technology” x-ray machines have been more widely used, the age-specific incidence of osteoporosis has increased tremendously. This apparently includes a higher rate of shortening of stature with aging than in earlier generations.[2]

作为骨质疏松症和乳腺癌x射线筛查的主要倡导者，通用电气(General Electric)曾宣称，如果每个人都使用他们的技术，91%的乳腺癌可以治愈。尽管这项技术的大规模应用，尽管美国政府和其他国家(使用粗略的欺骗性统计数据)声称对癌症的战争正在取得胜利，但乳腺癌并没有减少。同样，在过去的几十年里，当“高科技”x光机得到更广泛的应用时，特定年龄的骨质疏松症发病率也大幅增加。这显然包括随着年龄增长身材缩短的比率比前几代人高。

I think there are several reasons for avoiding x-ray tests of bone density, besides the simple one that everyone should eat a bone-protective diet, regardless of the present density of their bones.

我认为有几个原因可以避免对骨密度进行x光检查，除了一个简单的原因，那就是每个人都应该吃保护骨骼的饮食，不管他们目前的骨密度如何。

Even seemingly identical x-ray machines, or the same machine at a different time, can give very different estimates of bone density.[3-10] Radiologists evaluating the same images often reach very different conclusions.[11] Changes in the tissue water and fat content can make large differences in apparent bone density,[12] and estrogen, which affects those, could appear to cause improved bone density, when it is merely causing a generalized inflammatory condition, with edema. A machine that is accurate when measuring an aluminum model, won’t necessarily give meaningful results when the composition of the tissue, including the bone marrow, has changed.

Calcification of soft tissues can create the impression of increased bone density.[13] Studies of large groups of people show such small annual losses of bone density (around 1%), especially in the neck of the femur (which is important in hip fractures) that the common technical errors of measurement in an individual seem very large.

即使是看起来一模一样的x光机，或同一台机器在不同的时间，也能给出非常不同的骨密度估计。[3-10]放射科医生在评估相同的图像时往往会得出截然不同的结论组织中水和脂肪含量的变化可以在表观骨密度、[12]和雌激素方面产生很大的差异，而影响这些的雌激素可能会导致骨密度的改善，当它仅仅引起广泛性炎症和水肿时。当包括骨髓在内的组织成分发生变化时，一台测量铝模型的仪器就不一定能给出有意义的结果。软组织钙化可造成骨密度增加的印象对大量人群的研究表明，每年的骨密度损失很小(约1%)，尤其是在股骨颈(这在髋部骨折中很重要)，以至于测量个人的常见技术错误似乎非常大。

Ultrasound devices can do an extremely good job of evaluating both bone density and strength [14-16], rather than just density.

Ultrasound stimulates bone repair.

X-rays accelerate the rate of bone loss.

超声设备可以很好地评估骨密度和强度[14-16]，而不仅仅是骨密度。

超声波刺激骨修复。

x射线会加速骨质流失。

X-rays do their harm at any dose; there is no threshold at which the harm begins.

x射线无论剂量多大都会造成伤害;伤害没有开始的门槛。

X-ray damage is not limited to the area being investigated. Deflected x-rays affect adjacent areas, and toxins produced by irradiated cells travel in the bloodstream, causing systemic effects. Dental x-rays cause thyroid cancer and eye cancer. Recent experiments have shown that low doses of radiation cause delayed death of brain cells. The action of x-rays produces tissue inflammation, and diseases as different as Alzheimer’s disease and heart disease result from prolonged inflammatory processes.

x射线损伤并不局限于正在调查的区域。偏转的x射线会影响邻近区域，受辐射细胞产生的毒素会在血液中流动，造成全身效应。牙科x光会导致甲状腺癌和眼癌。最近的实验表明，低剂量的辐射会导致脑细胞的延迟死亡。x光的作用会引起组织炎症，而像阿尔茨海默病和心脏病这样不同的疾病都是由长期的炎症过程引起的。

I have never known a physician who knew, or cared, what dose of radiation his patients were receiving. I have never known a patient who could get that information from their doctors.

我从未见过一位医生知道或关心他的病人接受了多大剂量的辐射。我从来没见过哪个病人能从医生那里得到这些信息。

The radiation exposure used to measure bone density may be higher (especially when the thigh and hip are x-rayed) than the exposure in dental x-rays, but dental x-rays are known to increase the incidence of cancer. Often, dentists have their receptionists do the x-rays, which probably doesn’t matter, since the dentist is usually no more concerned than the receptionist about understanding, and minimizing, the dose. Even radiological specialists seldom are interested in the doses they use diagnostically.

用于测量骨密度的辐射照射可能比牙科x光照射要高(特别是当对大腿和臀部进行x光照射时)，但牙科x光照射众所周知会增加癌症的发病率。通常情况下，牙医会让他们的接待员做x光检查，这可能并不重要，因为牙医通常比接待员更关心理解和减少剂量。即使是放射专家也很少对他们在诊断中使用的剂量感兴趣。

It was only after a multitude of dentists had a finger amputated that it became standard practice to ask the patient to hold the film, while the dentist stood safely back away from the rays.

直到许多牙医的一根手指被截肢后，要求病人拿着胶片，而牙医则安全地站在远离射线的地方，这才成为标准做法。

Just after the beginning of the century, Thomas Edison was helping to popularize x-rays, but the horrible death of his chief technician turned Edison into an enemy of the technology. By the 1940s, the dangers of radiation were coming to be understood by the general public, and it was only the intervention of the US government, to popularize atomic bombs and nuclear power, that was able to reverse the trend.

就在本世纪初，托马斯·爱迪生(Thomas Edison)还在帮助普及x射线，但他的首席技术人员的惨死却让他成了这项技术的敌人。到了20世纪40年代，核辐射的危害逐渐被公众所认识，只有美国政府的干预，普及了原子弹和核能，才扭转了这一趋势。

In 1956 and 1957, Linus Pauling was the only well known scientist who opposed the government’s policies. The government took away his passport, and his opportunities to write and speak were limited by a boycott imposed by a variety of institutions, but instigated by the nuclear industry and its agent, the Atomic Energy Commission. The government which considered Pauling a threat to national security, had placed thousands of German and Hungarian “ex”-Nazis in high positions in industry and government agencies, after protecting them from prosecution as war criminals. The official government policy, directed by the financier Admiral Strauss who controlled the Atomic Energy Commision, was to tell the public that radiation was good. Their extreme secrecy regarding their radiation experiments on Americans, however, indicated that they were aware of the malignant nature of their activities; many of the records were simply destroyed, so that no one could ever know what had been done. Scientists who worked for the government, Willard Libby, John Goffman, and many others, were working to convince the public that they shouldn’t worry. Of the multitude of scientists who served the government during that time, only a few ever came to oppose those policies, and those who did were unable to keep their jobs or research grants. Gofman has become the leader in the movement to protect the public against radiation, especially, since 1971, through the Committee for Nuclear Responsibility, PO Box 421993, San Francisco, CA 94132..

在1956年和1957年，莱纳斯鲍林是唯一一个反对政府政策的著名科学家。政府没收了他的护照，他写作和演讲的机会受到了各种机构的抵制，但这是由核工业及其代理机构原子能委员会煽动的。政府认为鲍林对国家安全构成威胁，在保护他们免受战争罪犯起诉后，将数千名德国和匈牙利“前”纳粹分子安置在工业和政府机构的高位。由掌管原子能委员会的金融家、海军上将施特劳斯指导的政府官方政策是告诉公众辐射是有益的。然而，他们对对美国人进行的辐射实验极度保密，这表明他们知道其活动的恶性性质;许多记录都被销毁了，所以没人知道发生了什么事。为政府工作的科学家威拉德·利比(Willard Libby)、约翰·戈夫曼(John Goffman)和其他许多人正在努力说服公众，他们不应该担心。在当时为政府服务的众多科学家中，只有少数人反对这些政策，而那些反对的人都无法保住工作或研究经费。戈夫曼已成为保护公众免受辐射运动的领袖，特别是自1971年以来，通过核责任委员会，邮政信箱421993，旧金山，CA 94132..

Gofman has said: “I was stupid in those days. In 1955, '56, people like Linus Pauling were saying that the bomb fallout would cause all this trouble. I thought, 'We're not sure. If you're not sure, don't stand in the way of progress.' I could not have thought anything more stupid in my life.

戈夫曼曾说过:“那些日子我很愚蠢。在1955年和1956年，像莱纳斯·鲍林这样的人说原子弹的余波会引起所有这些麻烦。我想，‘我们不确定。如果你不确定，就不要阻碍进步。”我这辈子想不出比这更蠢的事了。

“The big moment in my life happened while I was giving a health lecture to nuclear engineers. In the middle of my talk it hit me! What the hell am I saying? If you don't know whether low doses are safe or not, going ahead is exactly wrong. At that moment, I changed my position entirely.”[17]

“我生命中的重要时刻发生在我给核工程师做健康讲座的时候。我说到一半突然想到!我到底在说什么?如果你不知道低剂量是否安全，那就大错特错了。在那一刻，我完全改变了立场。“[17]

In 1979, Gofman said: “There is no way I can justify my failure to help sound an alarm over these activities many years sooner than I did. I feel that at least several hundred scientists trained in the biomedical aspect of atomic energy - myself definitely included - are candidates for Nuremburg-type trials for crimes against humanity for our gross negligence and irresponsibility. Now that we know the hazard of low-dose radiation, the crime is not experimentation - it's murder.” [18]

1979年，戈夫曼说:“我没有办法为自己的失败辩护，没有提前多年就这些活动发出警告。我认为，至少有几百名在原子能生物医学方面受过训练的科学家- -当然包括我本人- -是因我们的严重疏忽和不负责任而对危害人类罪进行纽伦堡式审判的候选国。既然我们知道了低剂量辐射的危害，犯罪就不是实验，而是谋杀。”［18］

Many ordinary people were making exactly that argument in the 1950s, but government censorship kept the most incriminating evidence from the public. The climate of intimidation spread throughout the culture, so that teachers who spoke about the dangers of radiation were called disloyal, and were fired. Now, people who don’t want x-rays are treated as crackpots. Probably because of this cultural situation, Gofman’s recommendations are very mild–simply for doctors to use good technology and to know what they are doing, which could lead to ten-fold or even hundred-fold dose reduction. Even with such mild restraint in the use of diagnostic x-rays, Gofman’s well founded estimate is that 250,000 deaths caused by radiation could be prevented annually. I believe many more deaths would be prevented if ultrasound and MRI were used consistently instead of x-rays. Using Gofman’s estimate, I think we can blame at least ten million deaths on just the medical x-rays that have been used inappropriately because of the policies of the U.S. government in the last half century. That wouldn’t include the deaths caused by radioactive fallout from bomb tests and leaks from nuclear power plants, or the vast numbers of people mentally impaired by all sorts of toxic radiation.

在20世纪50年代，许多普通人都在提出同样的观点，但政府审查制度将最具罪证的证据隐瞒了出来。恐吓的气氛蔓延到整个文化中，因此，教师谁谈论辐射的危险被称为不忠，并被解雇。现在，不想要x光的人会被视为疯子。可能因为这种文化环境，Gofman的建议非常温和——只是让医生使用好的技术，并知道他们在做什么，这可能导致10倍甚至100倍的剂量减少。即使对诊断x射线的使用有如此温和的限制，Gofman有充分根据的估计是，每年可以避免25万人因辐射而死亡。我相信，如果始终如一地使用超声波和核磁共振，而不是x光，就可以避免更多的死亡。根据Gofman的估计，我认为我们可以将至少1000万人的死亡归咎于医疗x光片，这些x光片由于美国政府在过去半个世纪的政策而被不当使用。这还不包括核弹试验的放射性沉降物和核电站泄漏造成的死亡，以及大量因各种有毒辐射而精神受损的人。

Although nearly all the people who committed the radiation crimes of the 1950s and 1960s have died or retired, the culture they created remains in the mass media and scientific journals, and in the medical and academic professions.

尽管几乎所有在20世纪50年代和60年代犯下辐射罪行的人都已经去世或退休，但他们创造的文化仍然存在于大众媒体和科学期刊，以及医学和学术领域。

Medical journals describe ways to minimize diagnostic x-ray exposure, and they advocate many seemingly effective treatments for osteoporosis, giving an impression that progress is being made in “managing” osteoporosis, but the real situation is very different. Fractures resulting from osteoporosis are increasing, and osteoporosis is affecting younger and younger people. I think it would be reasonable to say that a woman with osteoporosis is usually better off when it’s not diagnosed, because of the dangerous things prescribed for it. Estrogen has become the main “treatment” for osteoporosis, but many of the other ways of “managing” osteoporosis are both ineffective and unsafe.

医学杂志描述了减少诊断x射线照射的方法，他们提倡许多表面上有效的骨质疏松症治疗方法，给人一种“管理”骨质疏松症正在取得进展的印象，但实际情况是非常不同的。骨质疏松引起的骨折正在增加，骨质疏松症正在影响越来越年轻的人。我认为，有骨质疏松症的女性在没有被诊断出来的情况下通常会更好，这是合理的，因为医生会给她开一些危险的药。雌激素已成为骨质疏松症的主要“治疗”手段，但许多其他“管理”骨质疏松症的方法既无效又不安全。

Many women are told to stop taking a thyroid supplement when osteoporosis is diagnosed, but hypothyroidism often leads to hyperprolactinema and hypercortisolemia, which are two of the most clearly established causes of osteoporosis. Calcitonin, vitamin D-active metabolite, and estrogen-”HRT” treaments can cause respiratory alkalosis (relative hyperventilation),[19-24] and hypothyroidism produces a predisposition to hyperventilation.[25] Hyperventilation tends to cause calcium loss. In respiratory alkalolis, CO2 (and sometimes bicarbonate) are decreased, impairing calcium retention, and in “metabolicalkalosis,” with increased bicarbonate, calcium is retained more efficiently and bone formation is stimulated, and its dissolution is suppressed.

许多女性在确诊骨质疏松时被告知停止服用甲状腺补充剂，但甲状腺功能减退通常会导致泌乳素和高皮质醇血症，这两种疾病是骨质疏松最明显的原因。降钙素、维生素d活性代谢物和雌激素- HRT治疗可导致呼吸性碱中毒(相对过度通气)[19-24]，甲状腺功能减退可导致过度通气的易感性过度通气往往会导致钙流失。在呼吸性碱中毒中，CO2(有时是碳酸氢盐)减少，损害钙潴留，而在“代谢性碱中毒”中，碳酸氢盐增加，钙潴留更有效，刺激骨形成，抑制其溶解。

Other women are told to reduce their protein consumption, or to take fluoride or whatever drug has been most recently promoted. A protein deficiency is a clear cause of osteoporosis, and bone density corresponds to the amount of protein consumed. Milk protein, especially, protects against osteoporosis, independently of milk’s other important nutrients. Too much fluoride clearly increases the risk of bone fractures,[26] and the side effects of other drugs haven’t been properly studied in humans, while they often have dangerous effects in animals.

其他女性则被告知要减少蛋白质摄入，或者服用氟化物或任何最近被推广的药物。缺乏蛋白质是骨质疏松症的一个明显原因，而骨密度与摄入的蛋白质量相对应。牛奶中的蛋白质，尤其能预防骨质疏松症，与牛奶中的其他重要营养成分无关。过多的氟化物显然会增加骨折的风险，[26]和其他药物的副作用还没有在人类身上进行适当的研究，而它们在动物身上通常会有危险的影响。

Calcium, magnesium, vitamin A, vitamin B6- , vitamin K, and vitamin D are important for the development and maintenance of bones. For example, a vitamin A deficiency limits the synthesis of progesterone and proteins. In calcium deficiency, parathyroid hormone is increased, and tends to cause the typical changes of aging, shifting calcium from hard tissues to soft, and decreasing the ratio of extracellular to intracellular (excitatory) calcium.

钙、镁、维生素A、维生素B6-、维生素K和维生素D对骨骼的发育和维护都很重要。例如，缺乏维生素a会限制孕酮和蛋白质的合成。钙缺乏时，甲状旁腺激素增加，往往引起典型的衰老变化，钙从硬组织转移到软组织，细胞外钙与细胞内(兴奋性)钙的比例降低。

Polyunsaturated fats are converted to prostaglandins (especially under the influence of estrogen), and several prostaglandins have toxic effects on bone. Those fats also suppress the formation of thyroid hormone and progesterone. The increased use of the unsaturated oils has coincided with the increase of osteoporosis.

多不饱和脂肪转化为前列腺素(尤其是在雌激素的影响下)，几种前列腺素对骨骼有毒性作用。这些脂肪还会抑制甲状腺激素和黄体酮的形成。不饱和油脂的增加与骨质疏松症的增加相一致。

The oxidation of proteins caused by free radicals is increased with aging and by the use of unsaturated fats, and it contributes to tissue atrophy, including the age-related shrinkage of the bones. In animal studies, “adequate” dietary protein, 13.8% of the diet (equivalent to about 80 grams per day for a person) is associated with more oxidative damage to tissue proteins than the very high protein diets, 25.7% or 51.3%, that would be equivalent to about 150 or 300 grams of protein daily for a person.[27] Yet, many physicians recommend a low protein diet to protect against osteoporosis.

自由基引起的蛋白质氧化会随着年龄增长和使用不饱和脂肪而增加，它会导致组织萎缩，包括与年龄有关的骨骼萎缩。在动物实验中,“足够”膳食蛋白质,13.8%的饮食(相当于每天约80克一个人)与氧化损伤组织蛋白质比高蛋白质饮食,25.7%或51.3%,相当于每天约150或300克蛋白质。[27]然而，许多医生推荐低蛋白饮食来预防骨质疏松症。

Avoiding fluoridated water and the polyunsaturated oils, and drinking two quarts of milk daily (which will provide only 66 grams of protein), and using some other nutrient-rich foods such as eggs and fruits, are probably the basic things to protect the bones. For vitamins, especially K, occasional liver can be helpful. Meats, fruits, leaves, and coffee are rich in magnesium.

避免含氟水和多不饱和油，每天喝两夸脱牛奶(这只能提供66克蛋白质)，吃一些其他营养丰富的食物，如鸡蛋和水果，这些可能是保护骨骼的基本方法。对于维生素，尤其是K，偶尔的肝脏是有帮助的。肉类、水果、树叶（绿叶菜）和咖啡都富含镁。

Some people have argued that the acidity of urine produced by eating meat causes calcium loss. However, a high protein diet also improves the absorption of calcium by the intestine. Another overlooked function of dietary protein is that it stimulates insulin secretion, and insulin is anabolic for bone.[28]

有些人认为，吃肉产生的酸性尿液会导致钙流失。然而，高蛋白饮食也能提高肠道对钙的吸收。膳食蛋白质的另一个被忽视的功能是刺激胰岛素分泌，而胰岛素是骨骼的合成代谢产物

The same diet that protects against osteoporosis, i.e., plenty of protein and calcium, etc., also protects against kidney stones and other abnormal calcificatons.

预防骨质疏松症的饮食，即大量的蛋白质和钙等，也可以预防肾结石和其他异常钙化。

REFERENCES引用

  1. Proc Assoc Am Physicians 1996 Mar;108(2):155-64 Potential mechanism of estrogen-mediated decrease in bone formation: estrogen increases production of inhibitory insulin-like growth factor-binding protein-4. Kassem M, Okazaki R, De Leon D, Harris SA, Robinson JA, Spelsberg TC, Conover CA, Riggs BL.
  2. Am J Phys Anthropol 1990 Dec;83(4):467-76. Stature loss among an older United States population and its relation to bone mineral status. Galloway A, Stini WA, Fox SC, Stein P. “With advancing age there is a gradual decrease in height apparently beginning in the mid-40s. Thereafter, there is a relatively rapid decrease in measured height. This contrasts to the much slower rates predicted from earlier populations (Trotter and Gleser: American Journal of Physical Anthropology 9:311-324, 1951). The rate of stature loss is associated with diminution of bone mineral density as well as with maximum height. Since there are suggestions of a secular trend toward greater reductions in bone mineral density, this study suggests there may be a secular trend toward an increase in statural loss with age.”
  3. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1994 Mar;160(3):260-5. [The quantitative determination of bone mineral content–a system comparison of similarly built computed tomographs]. [Article in German] Andresen R, Radmer S, Banzer D, Felsenberg D, Wolf KJ Klinik fur Radiologie, Universitatsklinikum Steglitz der FU Berlin. An intercomparison of 4 CT scanners of the same manufacturer was performed. The bone mineral content of 11 lumbar vertebral columns removed directly post mortem was determined in a specially constructed lucite-water phantom. Even devices of the same construction were shown to yield a variation in the quantitative evaluation markedly exceeding the annual physiological mineral loss. As long as scanner adjustment by physical calibration phantoms has not yet been established, a course assessment and therapy control of bone mineral content should always be carried out on the same QCT scanner.
  4. Osteoporos Int 1990 Oct;1(1):23-9. Vertebral bone mineral density measured laterally by dual-energy X-ray absorptiometry. Slosman DO, Rizzoli R, Donath A, Bonjour JP. “The bone mineral density (BMD) of lumbar vertebrae in the anteroposterior (AP) view may be overestimated in osteoarthritis or with aortic calcification, which are common in elderly.”“Then, we compared the capability of BMD LAT and BMD AP scans for monitoring bone loss related to age and for discriminating the BMD of postmenopausal women with nontraumatic vertebral fractures from that of young subjects. In vitro, when a spine phantom was placed in lateral position in the middle of 26 cm of water in order to simulate both soft-tissue thickness and X-ray source remoteness, the coefficient of variation (CV) of six repeated determinations of BMD was 1.0%. In vivo, the CV of paired BMD LAT measurements obtained in 20 healthy volunteers after repositioning was 2.8%.”
  5. Eur J Nucl Med 1990;17(1-2):3-9. Comparative study of the performances of X-ray and gadolinium 153 bone densitometers at the level of the spine, femoral neck and femoral shaft. Slosman DO, Rizzoli R, Buchs B, Piana F, Donath A, Bonjour JP. “In vivo, at the spine level, with DPA, mean CV of BMD measured 6 times after repositioning in 6 healthy volunteers was 3.8% +/- 1.9% and 2.1% +/- 0.7% . . . .”
  6. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1995 Apr;162(4):269-73. [Experimental studies of the visualization of the vertebral body spongiosa by high-resolution computed tomography]. Henschel MG, Freyschmidt J, Holland BR. “The measured lower limit of visualisation of cancellous bone structures is clearly worse than expected from the measurements of spatial resolution with standard phantoms used for HR-CT (0.6 versus 0.4 mm). True and exact imaging of normal cancellous bone cannot be achieved even by modern HR-CT. Noise creates structures mimicking cancellous bone.”
  7. J Comput Tomogr 1984 Apr;8(2):91-7. Quantitative computed tomography assessment of spinal trabecular bone. I. Age-related regression in normal men and women.Firooznia H, Golimbu C, Rafii M, Schwartz MS, Alterman ER. “Computed tomography, utilized in conjunction with a calibrated phantom containing a set of reference densities(K2HPO4 and water), is capable of determining the mineral content of the trabecular bone of the spine with an accuracy of about 6% of the ash weight of the vertebrae scanned (specimen studies).”
  8. Calcif Tissue Int 1991 Sep;49(3):174-8. Precision and stability of dual-energy X-ray absorptiometry measurements. Johnson J, Dawson-Hughes B. “The phantom was scanned repeatedly in 15.2, 20.3, and 27.9 cm of water over a 9 month period. In 15.2 and 20.3 cm of water, phantom BMD did not vary significantly whereas in 27.9 cm of water (equivalent to a human over 30 cm thick), phantom BMD increased 2.3% (P = 0.01) over the 9 months.”
  9. J Comput Assist Tomogr 1993 Nov-Dec;17(6):945-51. Influence of temperature on QCT: implications for mineral densitometry. Whitehouse RW, Economou G, Adams JE. “Inaccuracies in quantitative CT (QCT) for vertebral bone mineral measurements may result from differences between the temperature of the vertebrae and the calibration standards.” “In the computer simulation, the fat error associated with single energy QCT for trabecular bone mineral densitometry was 20% less for specimens at room temperature than at body temperature.” “The fat error of single energy QCT for mineral densitometry may have been underestimated in previous in vitro studies using vertebral specimens scanned at room temperature.”
  10. Phys Med Biol 1986 Jan;31(1):55-63. Quantitative CT measurements: the effect of scatter acceptance and filter characteristics on the EMI 7070. Merritt RB, Chenery SG “Non-linearities in projection values on computed tomography (CT) scanners cause corresponding errors in derived Hounsfield unit attenuation measurements. Existing commercial machines have been refined for clinical usefulness but not necessarily for quantitative accuracy.”“It is concluded that, irrespective of any quality assurance protocol, interpatient and interslice errors can be expected to range from 3 to 10% for water-equivalent materials and the intraslice positional dependence of the CT number can vary up to 5% for dense bone-like materials in a uniform phantom.”
  11. Skeletal Radiol 1986;15(5):347-9. Observer variation in the detection of osteopenia.Epstein DM, Dalinka MK, Kaplan FS, Aronchick JM, Marinelli DL, Kundel HL. In order to determine observer variation in the detection of osteopenia, 15 pairs of lateral chest radiographs obtained within two weeks of each other were reviewed separately by two radiologists and one orthopedist on three separate occasions. Intra- and interobserver variations were calculated for each individual film and film pairs using Kappa values. The individual observers were not able to give consistent readings on the same film on different days (average Kappa = 0.54). When the additional factors of repeat films(average kappa = 0.47), or separate observers (average Kappa = 0.38) were analyzed, agreement was even worse.The identification of osteopenia from the lateral view of the thoracic spine is highly subjective and variable from film to film and observer to observer.
  12. P. Schneider and C. Reiners, Letter, JAMA 277(1), 23, Jan. 1, 1997. “The influence of fat distribution on bone mass measurements with DEXA can be of considerable magnitude and ranges up to 10% error per 2 cm of fat.”
  13. Calcif Tissue Int 1990 Apr;46(4):280-1. Effect of radiographic abnormalities on rate of bone loss from the spine. Dawson-Hughes B, Dallal GE. “Spurious rates of loss of spine BMD are likely to be found in subjects with calcification of the aorta, osteophytes or other abnormalities in the spine scan field. This should be kept in mind when serial spine scans are being considered in these subjects.”
  14. Przegl Lek 2000;57(2):93-9. [No title available]. Jaworski M, Lorenc RS. “. . .Dual Energy X-ray Absorptiometry (DEXA) method is a reference method to diagnose osteoporosis. This method allows to measure bone density and bone mass, however bone quality can not be estimated. Quantitative ultrasound (QUS)method provides information about bone structure.”
  15. Osteoporos Int 2000;11(4):354-60. Assessment of a new quantitative ultrasound calcaneus measurement: precision and discrimination of hip fractures in elderly women compared with dual X-ray absorptiometry. He YQ, Fan B, Hans D, Li J, Wu CY, Njeh CF, Zhao S, Lu Y, Tsuda-Futami E, Fuerst T, Genant HK.
  16. Cas Lek Cesk 2000 Apr 26;139(8):231-6 [X-ray densitometry and ultrasonography of the heel bone–sensitivity and comparison with densitometry of the axial skeleton].[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.”
  17. John Gofman, M.D. (biographical chapter. pages 401-412.) In Studs Terkel's book Coming of Age. The Story of our Century by Those Who Lived It. The New Press. NY. 1995.
  18. Gofman, J.W. An irreverent, illustrated view of nuclear power. Committee for Nuclear Responsibility. San Francisco, CA. pp. 227-228, 1979.
  19. Kidney Int 1992 Sep;42(3):727-34. Chronic respiratory alkalosis induces renal PTH-resistance, hyperphosphatemia and hypocalcemia in humans. Krapf R, Jaeger P, Hulter HN Department of Medicine, Insel University Hospital, Berne, Switzerland. “The effects of chronic respiratory alkalosis on divalent ion homeostasis have not been reported in any species.” “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) associated with increased fractional excretion of Ca++ . . .”
  20. J Clin Endocrinol Metab 1999 Jun;84(6):1997-2001 Hormone replacement therapy causes a respiratory alkalosis in normal postmenopausal women. Orr-Walker BJ, Horne AM, Evans MC, Grey AB, Murray MA, McNeil AR, Reid IR. “Serum bicarbonate concentrations decreased significantly in the groups receiving either MPA or estrogen plus MPA (P = 0.008). This trend was apparent as early as 2 days and reached 2.7 and 2.3 mmol/L in the respective groups by 3 months. Similar changes were seen with partial pressure of carbon dioxide. . . .”“Accompanying changes in blood pH were apparent in the estrogen plus MPA group, where there was an upward trend at 1 week (P = 0.056) and a significant change from baseline (+0.013) at 3 months (P = 0.03).”
  21. Wien Klin Wochenschr 1979 Apr 27;91(9):304-7 [Investigations on the pathogenesis of distal renal tubular acidosis]. Schabel F, Zieglauer H. “Bicarbonate loading is followed by a lowering of calcium excretion to within the normal range and a decrease in the uncharacteristic renal hyperaminoaciduria.”
  22. Calcif Tissue Int 1984 Sep;36(5):604-7. Respiratory alkalosis and reduced plasmatic concentration of ionized calcium in rats treated with 1,25 dihydroxycholecalciferol.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 phenomenon was found associated with increased urinary excretion of cAMP, soft tissue calcium content, and polyuria with hypostenuria, all known effects of parathyroid hormone.”
  23. Am J Physiol 1996 Jul;271(1 Pt 2):F216-22. Metabolic alkalosis decreases bone calcium efflux by suppressing osteoclasts and stimulating osteoblasts. Bushinsky DA.“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.The additional urinary calcium is almost certainly derived from bone mineral.” “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, [HCO3-] approximately equal to 24), medium simulating mild alkalosis (pH approximately equal to 7.5, [HCO3-] approximately equal to 31), or severe alkalosis (pH approximately equal to 7.6, [HCO3-] approximately equal to 39) and measured JCa+ and the release of osteoclastic beta-glucuronidase and osteoblastic collagen synthesis. Compared with control, metabolic alkalosis caused a progressive decrease in JCa+, which was correlated inversely with initial medium pH (pHi). Alkalosis caused a decrease in osteoclastic beta-glucuronidase release, 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.”
  24. Am J Physiol 1997 Nov;273(5 Pt 2):F698-705 The effects of respiratory alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo. Unwin R, Stidwell R, Taylor S, Capasso G.
  25. Can J Anaesth 1999 Feb;46(2):185-9. Acute respiratory alkalosis associated with low minute ventilation in a patient with severe hypothyroidism. Lee HT, Levine M. “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.”
  26. Am J Epidemiol 1991 Apr 1;133(7):649-60. A prospective study of bone mineral content and fracture in communities with differential fluoride exposure. Sowers MF, Clark MK, Jannausch ML, Wallace RB. “Residence in the higher-fluoride community was associated with a significantly lower radial bone mass 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, 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.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). Estimates of risk were adjusted for age and body size.”
  27. J Nutr 2000 Dec;130(12):2889-96. Long-term high protein intake does not increase oxidative stress in rats. Petzke KJ, Elsner A, Proll J, Thielecke F, Metges CC.
  28. Med Hypotheses 1995 Sep;45(3):241-6. Anabolic effects of insulin on bone suggest a role for chromium picolinate in preservation of bone density. 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.” [I think chromium is too toxic to use as a supplement.]

29: Anesthesiology 1998 Dec;89(6):1389-400. Effects of hyperventilation and hypocapnic/normocapnic hypoxemia on renal function and lithium clearance in humans. Vidiendal Olsen N, Christensen H, Klausen T, Fogh-Andersen N, Plum I, Kanstrup IL, Hansen JM Department of Neuroanaesthesia, Copenhagen University Hospital, Denmark. [email protected] 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 increasedslightly during hypocapnic and normocapnic hypoxemia, hyperventilation, and normocapnic normoxemia with but not without the face mask. CONCLUSIONS:The results indicate that (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 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.

31: Wien Klin Wochenschr 1979 Apr 27;91(9):304-7. [Investigations on the pathogenesis of distal renal tubular acidosis]. [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. Under conditions of bicarbonate-induced systemic alkalosis urinary the pCO2 exceeds blood pCO2 in normal subjects. 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. Bicarbonate loading is followed by a lowering of calcium excretion to within the normal range and a decrease in the uncharacteristic renal hyperaminoaciduria.

http://raypeat.com/articles/aging/bonedensity.shtml

骨密度：首先不要伤害

没有一个主题可以孤立地理解。人们经常问我，他们应该如何处理诊断出的骨质疏松症/骨质减少症，当他们提到“计算机控制”和“双光子 X 射线”骨密度测试时，我的注意力往往会跳过他们的骨骼、饮食和激素，以他们必须感知自己和他们在世界上的位置的方式。他们是否知道这是一种强大到足以区分非常不透明的骨头和不太透明的骨头的 X 射线？软组织没有被研究，所以它们被允许“过度曝光”，直到它们在胶片上显示为黑色。如果要测量大腿或臀部等较厚的区域，他们是否意识到在辐射进入的表面处接收到的 X 射线剂量可能是到达胶片的辐射强度的 20 倍？90% 或 95% 的缺失能量是否已被人体细胞吸收？如果我只回答他们认为他们问我的问题，我会觉得我加入了一个反对他们的阴谋。我的回答必须假设他们真的在询问他们的健康状况，而不是特定的医疗诊断。

神经学家以对他们无能为力的问题做出精巧博学的诊断而闻名。昂贵的双光子 X 射线吸收仪诊断机的拥有者处于非常不同的位置。无论如何，骨质疏松症的补救措施是每个人都应该做的事情，因此诊断与医生应该向患者推荐的内容没有区别。

大多数情况下，雌激素是针对骨质疏松症开的，如果医生没有进行骨密度测试，他们可能会开雌激素，“保护心脏”或“预防阿尔茨海默病”。由于我已经写过关于雌激素和那些问题的文章，这里没有必要多说，除了雌激素是各种组织萎缩的原因，包括抑制骨形成。 [1]

通用电气公司是骨质疏松症和乳腺癌 X 射线筛查的主要倡导者，它宣称如果每个人都使用他们的技术，91% 的乳腺癌可以治愈。尽管该技术得到了广泛应用，但乳腺癌并没有减少，尽管美国政府和其他人（使用粗略的欺骗性统计数据）声称抗癌战争正在取得胜利。同样，在“高科技” X 光机得到更广泛使用的过去几十年中，骨质疏松症的年龄别发病率也大大增加。与前几代相比，这显然包括随着年龄增长而导致身材缩短的比例更高。 [2]

我认为避免对骨密度进行 X 射线检查的原因有几个，除了一个简单的原因，即每个人都应该吃骨保护饮食，不管他们目前的骨密度如何。

即使看似相同的 X 光机，或不同时间的同一台机器，也可以给出非常不同的骨密度估计值。[3-10] 评估相同图像的放射科医生通常会得出非常不同的结论。[11] 组织水和脂肪含量的变化会导致表观骨密度的巨大差异，[12] 影响这些的雌激素似乎会导致骨密度提高，但它只是引起全身性炎症，伴有水肿。在测量铝模型时准确的机器，当包括骨髓在内的组织成分发生变化时，不一定会给出有意义的结果。软组织钙化会造成骨密度增加的印象。 [13] 对大量人群的研究表明，每年骨密度的损失很小（约 1%），

超声设备可以很好地评估骨密度和强度 [14-16]，而不仅仅是密度。

超声波刺激骨骼修复。

X 射线会加速骨质流失的速度。

X 射线在任何剂量下都会造成伤害；伤害开始时没有阈值。

X 射线损伤不仅限于被调查的区域。偏转的 X 射线会影响邻近区域，受辐射细胞产生的毒素会在血液中传播，从而导致全身效应。牙科 X 射线会导致甲状腺癌和眼癌。最近的实验表明，低剂量的辐射会导致脑细胞延迟死亡。X 射线的作用会产生组织炎症，而与阿尔茨海默病和心脏病等不同的疾病是由长时间的炎症过程引起的。

我从来没有认识一位医生知道或关心他的病人接受的辐射剂量。我从来不知道有哪个病人可以从他们的医生那里得到这些信息。

用于测量骨密度的辐射暴露（尤其是大腿和臀部进行 X 光检查时）可能高于牙科 X 射线的辐射，但众所周知，牙科 X 光会增加癌症的发病率。通常，牙医会让他们的接待员做 X 光检查，这可能无关紧要，因为牙医通常并不比接待员更关心了解和减少剂量。即使是放射科专家也很少对他们用于诊断的剂量感兴趣。

直到许多牙医截掉手指后，才成为标准做法，要求患者拿着胶卷，而牙医则安全地站在远离射线的地方。

就在本世纪初，托马斯·爱迪生正在帮助普及 X 射线，但他的首席技术员的可怕死亡使爱迪生成为该技术的敌人。到了1940年代，辐射的危害逐渐被大众所了解，只有美国政府介入，普及原子弹和核能，才有可能扭转这种趋势。

在 1956 年和 1957 年，莱纳斯·鲍林是唯一一位反对政府政策的知名科学家。政府拿走了他的护照，他的写作和演讲机会受到各种机构的抵制，但受到核工业及其代理人原子能委员会的煽动。政府认为鲍林对国家安全构成威胁，在保护他们免遭作为战犯起诉后，将数千名德国和匈牙利“前”纳粹分子置于工业和政府机构的高级职位。由控制原子能委员会的金融家施特劳斯上将指挥的官方政府政策是告诉公众辐射是好的。然而，他们对美国人的辐射实验极为保密，; 许多记录被简单地销毁，因此没有人知道发生了什么。为政府工作的科学家威拉德·利比、约翰·戈夫曼和其他许多人正在努力说服公众不要担心。在那段时间为政府服务的众多科学家中，只有少数人反对这些政策，而那些反对的人也无法保住工作或研究经费。戈夫曼已成为保护公众免受辐射运动的领导者，特别是自 1971 年以来，通过核责任委员会，邮政信箱 421993，旧金山，加利福尼亚州 94132。

戈夫曼曾说过：“那些日子我很愚蠢。在 1955 年，56 年，像莱纳斯·鲍林这样的人说炸弹落下会造成所有这些麻烦。我想，‘我们不确定。如果你不确定，不要阻碍进步。在我的生活中，我想不出比这更愚蠢的事情了。

“我生命中的重要时刻发生在我给核工程师做健康讲座时。在我的演讲中，它击中了我！我到底在说什么？如果你不知道低剂量是否安全，前进是完全错误的。那一刻，我完全改变了我的立场。”[17]

1979 年，戈夫曼说：“我无法证明我未能比我早很多年就这些活动发出警报。我觉得至少有数百名接受过原子能生物医学方面培训的科学家——当然是我自己包括 - 因我们的重大过失和不负责任而对反人类罪进行纽伦堡式审判的候选人。现在我们知道低剂量辐射的危害，犯罪不是实验 - 这是谋杀。[18]

许多普通人在 1950 年代就提出了这样的论点，但政府审查制度保留了公众最有罪的证据。恐吓气氛在整个文化中蔓延，以至于谈论辐射危险的老师被称为不忠诚，并被解雇。现在，不想要 X 射线的人被视为疯子。可能是因为这种文化状况，戈夫曼的建议非常温和——只是让医生使用好的技术，知道他们在做什么，这可能导致剂量减少十倍甚至一百倍。即使在使用诊断 X 射线方面有如此温和的限制，戈夫曼有充分根据的估计是，每年可以防止 250,000 人死于辐射。我相信，如果始终使用超声波和 MRI 代替 X 射线，可以避免更多的死亡。使用戈夫曼的估计，我认为我们可以将至少一千万人的死亡归咎于由于美国政府在过去半个世纪的政策而被不当使用的医用 X 射线。这不包括炸弹试验和核电站泄漏造成的放射性沉降物造成的死亡，或者大量因各种有毒辐射而精神受损的人。

尽管几乎所有在 1950 年代和 1960 年代犯下辐射罪的人都已经死亡或退休，但他们创造的文化仍然存在于大众媒体和科学期刊以及医学和学术专业中。

医学期刊描述了最大限度减少诊断 X 射线照射的方法，并提倡许多看似有效的骨质疏松症治疗方法，给人的印象是“管理”骨质疏松症正在取得进展，但实际情况却大不相同。骨质疏松症导致的骨折正在增加，骨质疏松症正在影响越来越年轻的人。我认为可以合理地说，患有骨质疏松症的女性通常在没有被诊断出来的情况下会更好，因为给它开的处方很危险。雌激素已成为骨质疏松症的主要“治疗方法”，但许多其他“管理”骨质疏松症的方法既无效又不安全。

许多女性被告知在诊断出骨质疏松症时停止服用甲状腺补充剂，但甲状腺功能减退症通常会导致高催乳素血症和高皮质醇血症，这是骨质疏松症最明确的两个原因。降钙素、维生素 D 活性代谢物和雌激素-“HRT”治疗可引起呼吸性碱中毒（相对过度通气），[19-24] 甲状腺功能减退会导致过度通气。 [25] 过度换气往往会导致钙流失。在呼吸性碱中，CO2（有时是碳酸氢盐）减少，从而损害钙的潴留，而在“代谢性碱中毒”中，随着碳酸氢盐的增加，钙的保留效率更高，骨形成受到刺激，其溶解受到抑制。

其他女性被告知减少蛋白质消耗，或服用氟化物或最近推广的任何药物。蛋白质缺乏是骨质疏松症的一个明显原因，骨密度对应于蛋白质的消耗量。尤其是牛奶蛋白可以预防骨质疏松症，与牛奶的其他重要营养素无关。过多的氟化物显然会增加骨折的风险，[26] 并且其他药物的副作用尚未在人类身上得到适当的研究，而它们通常对动物有危险的影响。

钙、镁、维生素 A、维生素 B6-、维生素 K 和维生素 D 对骨骼的发育和维持很重要。例如，维生素 A 缺乏会限制黄体酮和蛋白质的合成。缺钙时，甲状旁腺激素升高，容易引起典型的衰老变化，钙从硬组织向软组织转移，细胞外钙与细胞内（兴奋性）钙的比例降低。

多不饱和脂肪会转化为前列腺素（特别是在雌激素的影响下），并且几种前列腺素对骨骼有毒性作用。这些脂肪还抑制甲状腺激素和黄体酮的形成。不饱和油的使用增加与骨质疏松症的增加相吻合。

自由基引起的蛋白质氧化会随着年龄的增长和不饱和脂肪的使用而增加，它会导致组织萎缩，包括与年龄相关的骨骼收缩。在动物研究中，“充足”的膳食蛋白质，即 13.8% 的膳食（相当于一个人每天约 80 克）与高蛋白膳食（25.7% 或 51.3%）相比对组织蛋白造成更多的氧化损伤，即相当于一个人每天大约 150 或 300 克蛋白质。 [27] 然而，许多医生推荐低蛋白饮食来预防骨质疏松症。

避免含氟水和多不饱和油，每天喝两夸脱牛奶（只能提供 66 克蛋白质），并使用其他一些营养丰富的食物，如鸡蛋和水果，可能是保护骨骼的基本方法。对于维生素，尤其是 K，偶尔使用肝脏可能会有所帮助。肉类、水果、树叶和咖啡富含镁。

有些人认为，吃肉产生的尿液酸度会导致钙流失。然而，高蛋白饮食也能提高肠道对钙的吸收。膳食蛋白质的另一个被忽视的功能是它刺激胰岛素分泌，而胰岛素是骨骼的合成代谢。 [28]

预防骨质疏松症的相同饮食，即大量蛋白质和钙等，也可以预防肾结石和其他异常钙化。

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