Tuesday, August 08, 2006

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FOR YOUR HEALTH:Dairy products are a health hazard. They contain no fiber or complex carbohydrates and are laden with saturated fat and cholesterol. They are contaminated with cow's blood and pus and are frequently contaminated with pesticides, hormones, and antibiotics. Dairy products are linked to allergies, constipation, obesity, heart disease, cancer, and other diseases. The late Dr. Benjamin Spock, America's leading authority on child care, spoke out against feeding cow's milk to children, saying it can cause anemia, allergies, and insulin-dependent diabetes and in the long term, will set kids up for obesity and heart disease, America's number one cause of death.And dairy products may actually cause osteoporosis, not prevent it, since their high-protein content leaches calcium from the body. Population studies, backed up by a groundbreaking Harvard study of more than 75,000 nurses, suggest that drinking milk can actually cause osteoporosis. Find out more by visiting our links page....................................Milk: No Longer Recommended or Required A substantial body of scientific evidence raises concerns about health risks from cow’s milk products. These problems relate to the proteins, sugar, fat, and contaminants in dairy products, and the inadequacy of whole cow’s milk for infant nutrition.Health risks from milk consumption are greatest for infants less than one year of age, in whom whole cow’s milk can contribute to deficiencies in several nutrients, including iron, essential fatty acids, and vitamin E. The American Academy of Pediatrics1 recommends that infants under one year of age not receive whole cow’s milk.Cow’s milk products are very low in iron,2 containing only about one-tenth of a milligram (mg) per eight-ounce serving. To get the U.S. Recommended Daily Allowance of 15 mg of iron, an infant would have to drink more than 31 quarts of milk per day. Milk can also cause blood loss from the intestinal tract, which, over time, reduces the body’s iron stores. Researchers speculate that the blood loss may be a reaction to proteins present in milk.3 Pasteurization does not eliminate the problem. Researchers from the University of Iowa recently wrote in the Journal of Pediatrics that “in a large proportion of infants, the feeding of cow milk causes a substantial increase of hemoglobin loss. Some infants are exquisitely sensitive to cow milk and can lose large quantities of blood.”3 Although concerns are greatest for children in the first year of life, there are also health concerns related to milk use among older children and some problems associated with cow’s milk formulas.Milk Proteins and DiabetesSeveral reports link insulin-dependent diabetes to a specific protein in dairy products. This form of diabetes usually begins in childhood. It is a leading cause of blindness and contributes to heart disease, kidney damage, and amputations due to poor circulation.Studies of various countries show a strong correlation between the use of dairy products and the incidence of diabetes.4 A recent report in the New England Journal of Medicine5 adds substantial support to the long-standing theory that cow’s milk proteins stimulate the production of the antibodies6 which, in turn, destroy the insulin-producing pancreatic cells.7 In the new report, researchers from Canada and Finland found high levels of antibodies to a specific portion of a cow’s milk protein, called bovine serum albumin, in 100 percent of the 142 diabetic children they studied at the time the disease was diagnosed. Non-diabetic children may have such antibodies, but only at much lower levels. Evidence suggests that the combination of a genetic predisposition and cow’s milk exposure is the major cause of the childhood form of diabetes, although there is no way of determining which children are genetically predisposed. Antibodies can apparently form in response to even small quantities of milk products, including infant formulas.Pancreatic cell destruction occurs gradually, especially after infections, which cause the cellular proteins to be exposed to the damage of antibodies. Diabetes becomes evident when 80 to 90 percent of the insulin-producing beta cells are destroyed.Milk proteins are also among the most common causes of food allergies. Often, the cause of the symptoms is not recognized for substantial periods of time.Milk Sugar and Health ProblemsMany people, particularly those of Asian and African ancestry, are unable to digest the milk sugar, lactose. The result is diarrhea and gas. For those who can digest lactose, its breakdown products are two simple sugars: glucose and galactose. Galactose has been implicated in ovarian cancer8 and cataracts.9,10 Nursing children have active enzymes that break down galactose. As we age, many of us lose much of this capacity.Fat ContentWhole milk, cheese, cream, butter, ice cream, sour cream, and all other dairy products aside from skim and non-fat products contain significant amounts of saturated fat, as well as cholesterol, contributing to cardiovascular diseases and certain forms of cancer. The early changes of heart disease have been documented in American teenagers. While children do need a certain amount of fat in their diets, there is no nutritional requirement for cow’s milk fat. On the contrary, cow’s milk is high in saturated fats, but low in the essential fatty acid linoleic acid.ContaminantsMilk contains frequent contaminants, from pesticides to drugs. About one-third of milk products have been shown to be contaminated with antibiotic traces. The vitamin D content of milk has been poorly regulated. Recent testing of 42 milk samples found only 12 percent within the expected range of vitamin D content. Testing of ten samples of infant formula revealed seven with more than twice the vitamin D content reported on the label, one of which had more than four times the label amount.11 Vitamin D is toxic in overdose.12OsteoporosisDairy products offer a false sense of security to those concerned about osteoporosis. In countries where dairy products are not generally consumed, there is actually less osteoporosis than in the United States. Studies have shown little effect of dairy products on osteoporosis.13 The Harvard Nurses’ Health Study followed 78,000 women for a 12-year period and found that milk did not protect against bone fractures. Indeed, those who drank three glasses of milk per day had more fractures than those who rarely drank milk.14There are many good sources of calcium. Kale, broccoli, and other green leafy vegetables contain calcium that is readily absorbed by the body. A recent report in the American Journal of Clinical Nutrition found that calcium absorbability was actually higher for kale than for milk, and concluded that “greens such as kale can be considered to be at least as good as milk in terms of their calcium absorbability.”15 Beans are also rich in calcium. Fortified orange juice supplies large amounts of calcium in a palatable form.16Calcium is only one of many factors that affect the bone. Other factors include hormones, phosphorus, boron, exercise, smoking, alcohol, and drugs.17-20 Protein is also important in calcium balance. Diets that are rich in protein, particularly animal proteins, encourage calcium loss.21-23RecommendationsThere is no nutritional requirement for dairy products, and there are serious problems that can result from the proteins, sugar, fat, and contaminants in milk products. Therefore, the following recommendations are offered:Breast-feeding is the preferred method of infant feeding. As recommended by the American Academy of Pediatrics, whole cow’s milk should not be given to infants under one year of age. Parents should be alerted to the potential risks to their children from cow’s milk use. Cow’s milk should not be required or recommended in government guidelines. Government programs, such as school lunch programs and the WIC program, should be consistent with these recommendations. References1. American Academy of Pediatrics, Committee on Nutrition. The use of whole cow’s milk in infancy. Pediatrics 1992;89:1105-9.2. Pennington JAT, Church HN. Food values of portions commonly used. New York, Harper and Row, 1989.3. Ziegler EE, Fomon SJ, Nelson SE, et al. Cow milk feeding in infancy: further observations on blood loss from the gastrointestinal tract. J Pediatr 1990;116:11-8.4. Scott FW. Cow milk and insulin-dependent diabetes mellitus: is there a relationship? Am J CLin Nutr 1990;51:489-91.5. Karjalainen J, Martin JM, Knip M, et al. A bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. N Engl J Med 1992;327:302-7.6. Roberton DM, Paganelli R, Dinwiddie R, Levinsky RJ. Milk antigen absorption in the preterm and term neonate. Arch Dis Child 1982;57:369-72.7. Bruining GJ, Molenaar J, Tuk CW, Lindeman J, Bruining HA, Marner B. Clinical time-course and characteristics of islet cell cytoplasmatic antibodies in childhood diabetes. Diabetologia 1984;26:24-29.8. Cramer DW, Willett WC, Bell DA, et al. Galactose consumption and metabolism in relation to the risk of ovarian cancer. Lancet 1989;2:66-71. 9. Simoons FJ. A geographic approach to senile cataracts: possible links with milk consumption, lactase activity, and galactose metabolism. Digestive Diseases and Sciences 1982;27:257-64.10. Couet C, Jan P, Debry G. Lactose and cataract in humans: a review. J Am Coll Nutr 1991;10:79-86.11. Holick MF, Shao Q, Liu WW, Chen TC. The vitamin D content of fortified milk and infant formula. New Engl J Med 1992;326:1178-81.12. Jacobus CH, Holick MF, Shao Q, et al. Hypervitaminosis D associated with drinking milk. New Engl J Med 1992;326:1173-7.13. Riggs BL, Wahner HW, Melton J, Richelson LS, Judd HL, O’Fallon M. Dietary calcium intake and rates on bone loss in women. J Clin Invest 1987;80:979-82. 14. Feskanich D, Willett WC, Stampfer MJ, Colditz GA. Milk, dietary calcium, and bone fractures in women: a 12-year prospective study. Am J Publ Health 1997;87:992-7. 15. Heaney RP, Weaver CM. Calcium absorption from kale. Am J Clin Nutr 1990;51:656-7.16. Nicar MJ, Pak CYC. Calcium bioavailability from calcium carbonate and calcium citrate. J Clin Endocrinol Metab 1985;61:391-3. 17. Dawson-Hughes B. Calcium supplementation and bone loss: a review of controlled clinical trials. Am J Clin Nutr 1991;54:274S-80S.18. Mazess RB, Barden HS. Bone density in premenopausal women: effects of age, dietary intake, physical activity, smoking, and birth control pills. Am J Clin Nutr 1991;53:132-42.19. Nelson ME, Fisher EC, Dilmanian FA, Dallal GE, Evans WJ. A 1-y walking program and increased dietary calcium in postmenopausal women: efect on bone. Am J Clin Nutr 1991;53:1304-11. 20. Nielsen FH, Hunt CD, Mullen LM, Hunt JR. Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women. FASEB J 1987;1:394-7. 21. Zemel MB. Role of the sulfur-containing amino acids in protein-induced hypercalciuria in men. J Nutr 1981;111:545. 22. Hegsted M. Urinary calcium and calcium balance in young men as affected by level of protein and phosphorus intake. J Nutr 1981;111:553. 23. Marsh AG, Sanchez TV, Mickelsen O, Keiser J, Mayor G. Cortical bone density of adult lacto-ovo-vegetarian and omnivorous women. J Am Dietetic Asso 1980;76:148-51.Many Americans, including some vegetarians, still consume large amounts of dairy products. Here are eight great reasons to eliminate dairy products from your diet.1. OsteoporosisMilk is touted for preventing osteoporosis, yet clinical research shows otherwise. The Harvard Nurses’ Health Study,1 which followed more than 75,000 women for 12 years, showed no protective effect of increased milk consumption on fracture risk. In fact, increased intake of calcium from dairy products was associated with a higher fracture risk. An Australian study2 showed the same results. Additionally, other studies3,4 have also found no protective effect of dairy calcium on bone. You can decrease your risk of osteoporosis by reducing sodium and animal protein intake in the diet,5-7 increasing intake of fruits and vegetables,8 exercising,9 and ensuring adequate calcium intake from plant foods such as leafy green vegetables and beans, as well as calcium-fortified products such as breakfast cereals and juices.2. Cardiovascular DiseaseDairy products—including cheese, ice cream, milk, butter, and yogurt—contribute significant amounts of cholesterol and fat to the diet.10 Diets high in fat and saturated fat can increase the risk of several chronic diseases including cardiovascular disease. A low-fat vegetarian diet that eliminates dairy products, in combination with exercise, smoking cessation, and stress management, can not only prevent heart disease, but may also reverse it.11 Non-fat dairy products are available, however, they pose other health risks as noted below.3. CancerSeveral cancers, such as ovarian cancer, have been linked to the consumption of dairy products. The milk sugar lactose is broken down in the body into another sugar, galactose. In turn, galactose is broken down further by enzymes. According to a study by Daniel Cramer, M.D., and his colleagues at Harvard,12 when dairy product consumption exceeds the enzymes’ capacity to break down galactose, it can build up in the blood and may affect a woman’s ovaries. Some women have particularly low levels of these enzymes, and when they consume dairy products on a regular basis, their risk of ovarian cancer can be triple that of other women.Breast and prostate cancers have also been linked to consumption of dairy products, presumably related, at least in part, to increases in a compound called insulin-like growth factor (IGF-I).13-15 IGF-I is found in cow’s milk and has been shown to occur in increased levels in the blood by individuals consuming dairy products on a regular basis.16 Other nutrients that increase IGF-I are also found in cow’s milk. A recent study showed that men who had the highest levels of IGF-I had more than four times the risk of prostate cancer compared with those who had the lowest levels.144. DiabetesInsulin-dependent diabetes (Type I or childhood-onset) is linked to consumption of dairy products. Epidemiological studies of various countries show a strong correlation between the use of dairy products and the incidence of insulin-dependent diabetes.17,18 Researchers in 199218 found that a specific dairy protein sparks an auto-immune reaction, which is believed to be what destroys the insulin-producing cells of the pancreas.5. Lactose IntoleranceLactose intolerance is common among many populations, affecting approximately 95 percent of Asian Americans, 74 percent of Native Americans, 70 percent of African Americans, 53 percent of Mexican Americans, and 15 percent of Caucasians.19 Symptoms, which include gastrointestinal distress, diarrhea, and flatulence, occur because these individuals do not have the enzymes that digest the milk sugar lactose. Additionally, along with unwanted symptoms, milk-drinkers are also putting themselves at risk for development of other chronic diseases and ailments.6. Vitamin D ToxicityConsumption of milk may not provide a consistent and reliable source of vitamin D in the diet. Samplings of milk have found significant variation in vitamin D content, with some samplings having had as much as 500 times the indicated level, while others had little or none at all.20,21 Too much vitamin D can be toxic and may result in excess calcium levels in the blood and urine, increased aluminum absorption in the body, and calcium deposits in soft tissue.7. ContaminantsSynthetic hormones such as recombinant bovine growth hormone (rBGH) are commonly used in dairy cows to increase the production of milk.13 Because the cows are producing quantities of milk nature never intended, the end result is mastitis, or inflammation of the mammary glands. The treatment requires the use of antibiotics, and traces of these and hormones have been found in samples of milk and other dairy products. Pesticides and other drugs are also frequent contaminants of dairy products.8. Health Concerns of Infants and ChildrenMilk proteins, milk sugar, fat, and saturated fat in dairy products may pose health risks for children and lead to the development of chronic diseases such as obesity, diabetes, and formation of athersclerotic plaques that can lead to heart disease.The American Academy of Pediatrics recommends that infants below one year of age not be given whole cow’s milk, as iron deficiency is more likely on a dairy-rich diet. Cow’s milk products are very low in iron. If they become a major part of one’s diet, iron deficiency is more likely.10 Colic is an additional concern with milk consumption. One out of every five babies suffers from colic. Pediatricians learned long ago that cows’ milk was often the reason. We now know that breastfeeding mothers can have colicky babies if the mothers are consuming cow’s milk. The cows’ antibodies can pass through the mother’s bloodstream into her breast milk and to the baby.22 Additionally, food allergies appear to be common results of milk consumption, particularly in children. A recent study23 also linked cow’s milk consumption to chronic constipation in children. Researchers suggest that milk consumption resulted in perianal sores and severe pain on defecation, leading to constipation.Milk and dairy products are not necessary in the diet and can, in fact, be harmful to your health. Consume a healthful diet of grains, fruits, vegetables, legumes, and fortified foods including cereals and juices. These nutrient-dense foods can help you meet your calcium, potassium, riboflavin, and vitamin D requirements with ease—and without the health risks.References1. Feskanich D, Willet WC, Stampfer MJ, Colditz GA. Milk, dietary calcium, and bone fractures in women: a 12-year prospective study. Am J Public Health 1997;87:992-7.2. Cumming RG, Klineberg RJ. Case-control study of risk factors for hip fractures in the elderly. Am J Epidemiol 1994;139:493-505.3. Huang Z, Himes JH, McGovern PG. Nutrition and subsequent hip fracture risk among a national cohort of white women. Am J Epidemiol 1996;144:124-34.4. Cummings SR, Nevitt MC, Browner WS, et al. Risk factors for hip fracture in white women. N Engl J Med 1995;332:767-73.5. Finn SC. The skeleton crew: is calcium enough? J Women’s Health 1998;7(1):31-6.6. Nordin CBE. Calcium and osteoporosis. Nutrition 1997;3(7/8):664-86.7. Reid DM, New SA. Nutritional influences on bone mass. Proceed Nutr Soc 1997;56:977-87.8. Tucker KL, Hannan MR, Chen H, Cupples LA, Wilson PWF, Kiel DP. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr 1999;69:727-36.9. Prince R, Devine A, Dick I, et al. The effects of calcium supplementation (milk powder or tablets) and exercise on bone mineral density in postmenopausal women. J Bone Miner Res 1995;10:1068-75.10. Pennington JAT. Bowes and Churches Food Values of Portions Commonly Used, 17th ed. New York: Lippincott, 1998.11. Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA. Can lifestyle changes reverse coronary heart disease? Lancet 1990;336:129-33.12. Cramer DW, Harlow BL, Willet WC. Galactose consumption and metabolism in relation to the risk of ovarian cancer. Lancet 1989;2:66-71.13. Outwater JL, Nicholson A, Barnard N. Dairy products and breast cancer: the IGF-1, estrogen, and bGH hypothesis. Medical Hypothesis 1997;48:453-61.14. Chan JM, Stampfer MJ, Giovannucci E, et al. Plasma insulin-like growth factor-1 and prostate cancer risk: a prospective study. Science 1998;279:563-5.15. World Cancer Research Fund. Food, Nutrition, and the Prevention of Cancer: A Global Perspective. American Institute of Cancer Research. Washington, D.C.: 1997. 16. Cadogan J, Eastell R, Jones N, Barker ME. Milk intake and bone mineral acquisition in adolescent girls: randomised, controlled intervention trial. BMJ 1997;315:1255-69.17. Scott FW. Cow milk and insulin-dependent diabetes mellitus: is there a relationship? Am J Clin Nutr 1990;51:489-91.18. Karjalainen J, Martin JM, Knip M, et al. A bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. N Engl J Med 1992;327:302-7.19. Bertron P, Barnard ND, Mills M. Racial bias in federal nutrition policy, part I: the public health implications of variations in lactase persistence. J Natl Med Assoc 1999;91:151-7.20. Jacobus CH, Holick MF, Shao Q, et al. Hypervitaminosis D associated with drinking milk. N Engl J Med 1992;326(18):1173-7.21. Holick MF. Vitamin D and bone health. J Nutr 1996;126(4suppl):1159S-64S.22. Clyne PS, Kulczycki A. Human breast milk contains bovine IgG. Relationship to infant colic? Pediatrics 1991;87(4):439-44.23. Iacono G, Cavataio F, Montalto G, et al. Intolerance of cow’s milk and chronic constipation in children. N Engl J Med 1998;339(16):1100-4......Milk - it DOESN'T do your body goodMilk - much vaunted by nutritionists and fitness gurus as a "perfect food" may actually be the most atherosclerotic food in existence. Ah, you say - but I drink skim or low fat milk. It's the fat in the milk that clogs up the arteries. Well, yes and no. It's true that dairy fat is one of the more unhealthier fats out there, but it seems that the protein from milk is actually causing more harm. Stephen Seely, a leading researcher in the field, examined data obtained by the World Health Organization and the Organization of Economic Cooperation and Development about the correlation of coronary mortality with the consumption of various foods. Guess what topped the list? Not meat. Not eggs. Not animal fats. First on the list was milk protein, second was milk fats, and third was sugar. Milk protein consumption had an almost perfect correlation (r=0.93) to coronary mortality. I know that correlation does not necessarily mean cause and effect, but Seely actually discussed some very plausible theories by which milk protein could cause heart disease. The first theory is the estrogen theory. Milk is the leading cause of estrogens in our diet. Exogenous estrogen has been shown to be associated with a higher risk of both stroke and heart disease in men being treated with estrogens for various conditions. Furthermore, the liver usually clears away endogenous estrogens from the bloodstream pretty quickly, but exogenous estrogens can linger in the blood for a while, and can thus cause their damage. A second theory is the antibody theory. It is known that the body makes antibodies against milk proteins (especially casein), since they essentially act as antigens. Scientists in Wales observed that men who had heart attacks had higher levels of these milk antibodies than the controls. These antibodies not only activate platelets and thus act as a thrombogenic agent, but also cause inflammation of the artery walls, which initiates atherosclerosis[1]. Other researchers at the NASA Langely Research Center found that the highest correlation of any food to heart disease was non-fatmilk and milk carbohydrates depending on the age group (as an aside, for women under 64, the highest association between diet and heart disease was with sugar intake). Among their proposed mechanisms was: 1. increased homocysteine production from the milk protein, which, unlike meat has low levels of B vitamins, rendering it unable to neutralize the potential harmful effects of the homocysteine, and 2. The lactose increasing the absorption of a concentrated source of calcium promoting calcification of the arteries [2]. To be fair though, despite the high correlation between milk and heart disease, there is no one mechanism that has been proven without a doubt, and so more research needs to be done to uncover what’s going on.Milk is also a cause of malabsorption disorders[3], may be a cause of some mental illnesses[4],[5], as well as juvenile diabetes[6][7][8], and may promote prostate and testicular cancer[9].From the perspective of the TBK diet, the above information makes perfect sense. Not only are we the only species to consume another species' milk, but cow's milk is meant to foster rapid growth in calves, not to feed adult human beings.Finally, an important point to be made is that newborns and babies SHOULD be preferably breast fed or at the very least given formula. Although dairy products are not on the TBK diet, hunter-gatherer babies ARE breast fed. Mother's milk is very important nutritionally for babies, and dairy products are only harmful for children and adults. Children can get any calcium they need from other sources such as fortified orange or grapefruit juices, green leafy vegetables, or, if so inclined, sardines or canned salmon (yummy).ReferencesSeely, Stephen, et al. Diet Related Diseases - The Modern Epidemic.The AVI publishing company. Westport, Connecticut. 1985. pp. 43-70. Grant, WB. Milk and other dietary influences on coronary heart disease. Alternative Medicine Review. 3(4):281-294. Shils, Maurice E. Olson, James A. Shike, Moshe. Ross, Catherine A.(eds). Modern Nutrition in Health and Disease. Williams and Wilkins. Baltimore, Maryland. 1999. pg. 1506 Seely, Stephen, et al. Diet Related Diseases - The Modern Epidemic.The AVI publishing company. Westport, Connecticut. 1985. pp. 247-248. Autism 1999;3:67-83, 85-95. Saukkonen T. Virtanen SM. Karppinen M. Reijonen H. Ilonen J. Rasanen L. Akerblom HK. Savilahti E.Institution Children's Hospital, University of Helsinki, Finland. Significance of cow's milk protein antibodies as risk factor for childhood IDDM: interactions with dietary cow's milk intake and HLA-DQB1 genotype. Childhood Diabetes in Finland Study Group. Diabetologia. 41(1):72-8, Jan. 1998. Scott FW, Norris JM and Kolb H. Milk and Type 1 Diabetes – Examining the evidence and broadening the focus. Diabetes Care. April 1996 19(4):379-383. Gerstein, HC. Cow’s Milk Exposure and Type 1 Diabetes Mellitus – A critical overview of the clinical literature. Diabetes Care. January 1994 17(1):13-19. Davies TW et al. Adolescent milk, dairy product and fruit consumption and testicular cancer. British Journal of cancerAugust 1996 74(4):657-60. Excessive Calcium Causes OsteoporosisThe older you get, the higher your risk of osteoporosis.Obviously, osteoporosis is about aging.Osteoporosis patients originally had very strong bones, like everybody else. Osteoporosis is not about the inability to build strong bones, but about premature degeneration of the bones. What makes the bones degenerate prematurely?Somehow, osteoporotic bones have degenerated more than healthy bones of the same age. In osteoporotic patients, the bones have obviously aged faster. Osteoporosis is about prematurely aged bones. So, the key question is:What accelerates aging of the bones?All our organs age. In all our organs cells constantly replicate themselves; they wear out and are replaced by new ones. And because the number of times cells can replicate is fixed, organs eventually age. Like the skin eventually becomes wrinkled when there are less cells available to replace the dehydrated old skin-cells.We all know that if we expose our skin to the sun too much, that we will look older sooner. Excessive sun-exposure accelerates he aging of the skin. It does so because the sun burns the outer skin cells, which must be replaced by new cells sooner. And the sooner cells must be replaced, the sooner the moment will come that these cells cannot replicate anymore.Accelerated aging of cells is about a higher turnover of cells; new cells replacing old cells more frequently.What causes old bone-cells to be replaced by new ones sooner?We know that estrogen is protective. (and androgens to a lesser extent) All bone-scientists acknowledge that if the female body has sufficient estrogen at it's disposal all the time, osteoporosis risk is far lower.That is why osteoporosis risk is 3-fold higher in women: In women the estrogen level is far lower every 4th week, and the bones are less protected at that time. And in post-menopausal women, estrogen level is permanently decreased.If we knew exactly how estrogen protects against premature aging of the bones, we would also know how the opposite process enhances osteoporosis.So, how exactly is bone-metabolism influenced by estrogen? Estrogen inhibits both the uptake of calcium into the bones (1) and deportation of calcium from the bones. (See Calcium Hormones) But how exactly can processing more calcium cause osteoporosis?The absorption of calcium requires the activity of specialized cells: osteoblasts. These osteoblasts also compose pre-calcified bone-matrix, upon which the calcium can precipitate. Deportation of calcium from the bones requires the activity of osteoclasts.If more calcium is absorbed into the bones, like due to a lack of estrogen (2), the production and activity of both osteoblasts and osteoclasts is increased (3) (as in hyperparathyroidism). If much calcium is absorbed, much calcium is deported. But 50 to 70% of the composing osteoblasts die in the composition of new matrix. (4) The more their activity is stimulated, the more they die (5). And since estrogen inhibits uptake of calcium, estrogen prevents the death of osteoblasts (6). If you consume higher amounts of calcium all your life, the replacement of osteoblasts maybe increased all this time; many people succeed in increasing bone-mineral density by consuming more calcium. (7) That is why the average BMD is higher in residents of countries where much milk is consumed.Since the number of times a cell can be replaced is fixed, the replicative capacity will be exhausted sooner if much calcium is absorbed on a regular basis. And if replacement capacity is exhausted, there will be a lack of new osteoblasts. And since only these osteoblasts can compose bone-matrix, too little new bone-matrix can be composed. But without the matrix, the calcium cannot precipitate, and new bone cannot be composed, while old bone is constantly being decomposed anyway, to be replaced by new bone. Since there is a lack of pre-calcified bone matrix upon which to build, replacement cannot occur, and porous holes will begin to appear. And this is exactly what happens in osteoporosis: in osteoporotic bone the osteoblasts cannot be replaced adequately anymore, and thus less osteoblasts are available (8) and/or the activity of osteoblasts is at least impaired, (9) like ‘exaggeratedly aged’ bones. (10) In osteoporotic bones there is less matrix available that can yet be calcified than in healthy bones. (11) In osteoporosis dead cells cannot be replaced and micro-fractures cannot be repaired. (12)Does that mean that dietary calcium causes osteoporosis?Only if too much calcium is actually absorbed into the bones. As with all minerals, the body normally absorbs just as much calcium from our food as it needs. Only about 200 mg is absorbed into the blood, on the average, whether we consume 300 mg or 700 mg calcium daily, or sometimes even when we consume up to 1200 mg supplementary calcium daily. (13) In order to absorb the right amount of calcium, absorption rate decreases when we consume more calcium. But if we consume too much calcium, the absorption rate cannot be sufficiently decreased; about 5% of dietary calcium on top of 1500 mg a day is yet absorbed into the blood. For example: Consuming 5-fold more calcium than before, a group of girls did, in fact, absorb twice as much calcium (as before) into the blood. (14)But why is this extra calcium absorbed in the bones?This is to prevent blood-calcium level from rising too much. Muscles can only function if calcium from inside the muscle cells can be deported outside the cells. If blood-calcium level were too high, this wouldn't be possible; it would be lethal since breathing requires muscle-action. To save your life excessive dietary calcium is temporarily stored in the bones, prior to excretion. Normally the blood contains a total of 500 mg calcium. The difference between highest and lowest blood-calcium level is only 26%, thanks to the three different hormones that prevent our blood from containing too much (or too little) calcium. After the calcium has been absorbed into the bones two of these hormones stimulate deportation of calcium from the bones, and the third one stimulates excretion of calcium into urine. But why don’t the bones hold on to that extra calcium?According to the old doctrine, we can prevent osteoporosis by stacking more calcium in the bones. “The more calcium your bones contain, the longer it will take before they are empty.”This would be a simple solution if the bones did indeed hold on to that extra calcium, but…Our bones are built according to a plan - just like a house, and the amount of calcium in the bones has to be according to that plan. Just as piling up bricks in your living room does not make your house better or stronger, stacking extra calcium in the bones is not an improvement either. To be able to watch TV and clean your house properly, you throw the bricks out. The redundant calcium in your bones is always deported eventually. To preserve redundant calcium in your bones, you have to keep on consuming lots of calcium daily. But no matter how much milk you drink, or supplementary calcium you take (or not at all), your bones always contain less calcium at the age of 70 than at the age of 30.The problem is that all this extra calcium is processed by osteoblasts and osteoclasts. If you have been absorbing 400 mg instead of 200 mg dietary calcium into the blood daily, these cells have had to process 2.9 million mg more calcium during these 40 years. Since all this extra calcium is absorbed due to the action of osteoblasts, these osteoblasts die sooner, leaving you with too little new bone-matrix and too many porous holes once you are old. Similarly, excessive vitamin A, and also the administration of corticosteroids (15) and elevated cortisol levels can cause osteoporosis by killing osteoblasts; all prematurely exhaust the capacity to produce new osteoblasts. If less calcium is consumed, the bone-cells age slower, and a low calcium intake throughout adolescence has been shown to both retard and prolong longitudinal bone growth in rats. (16)So, yes, you can increase your bone mineral density (BMD) by consuming much calcium, but that will exhaust your bones sooner. Yes, a high BMD means (temporarily) stronger bones, but not healthier bones. Just as bodybuilders have stronger muscles, but not healthier muscles. Actually, as they grow older, they experience more muscle problems.The same is true for the bones; the more their aging is accelerated, the sooner their bone modeling capacity will be exhaustedThat is why in those countries where the average BMD is highest, the hip fracture incidence is highest too.Does this mean that a low BMD is preventive?If BMD is low because you consume little calcium all your life; yes. If calcium intake is very low, there will still not be a lack of calcium for the calcification of bone-matrix. (17) The only difference will be that the bones will not age prematurely, and that they will not contain redundant calcium.But if the BMD is low as the result of exhausted osteoblasts; no. BMD is decreased in osteoporosis due to the lack of new bone-matrix. Holes do not contain calcium.So BMD can be low in very strong bones and in weakened bones, which is what makes it so confusing for so many scientists.ProofSupplementary calcium / milk has short term ‘beneficial’ effects on bone-mineral density (BMD) and adverse long-term (lifetime-) effects.One can increase BMD by a high-calcium intake (7) or not. (18) The average short term effect of extra calcium is the increase in bone-mineral density, and thus strength. That is why average BMD is highest in those countries where much milk is consumed.If you investigate this correlation, extra calcium will have ‘beneficial’ effects on bone-strength (19) or not. (20)But this does not say anything about the lifetime effects; it just confirms what initially happens if you consume much calcium; this is just the first effects, not the eventual result. But is there no other way to find proof?Yes there is. Compared to other foods, only dairy products (or supplements of course) can be consumed in such large quantities on a daily basis that their consumption strongly increases calcium intake, which is proven by the fact that average BMD is highest in those countries where the most milk is consumed. There is, in fact, a tradition of consuming high amounts of milk in these countries..And there also many scientific studies about hip-fracture incidence per country.If extra calcium eventually has adverse effects, osteoporosis / hip-fracture incidence should be clearly higher in those countries where the most milk is consumed…StatisticsAnd yes….For example:In Greece the average milk consumption doubled from 1961 to 1977 (21) (and was even higher in 1985), and during the period 1977 - 1985 the age adjusted osteoporosis incidence almost doubled too. (22) In Hong Kong in 1989 twice as much dairy products were consumed as in 1966 (21) and osteoporosis incidence tripled in the same period. (23) Now their milk consumption level is almost “European”, and so is osteoporosis incidence. (24)It is very simple: where the most milk is consumed, the osteoporosis incidence is highest. Compared to other countries, the most milk is consumed in Sweden, Finland, Switzerland and The Netherlands (300 to 400 kg / cap / year), and osteoporosis incidence in these countries has sky rocketed. (25)Like Australians and New Zealanders, (26) Americans consume three fold more milk than the Japanese, and hip-fracture incidence in Americans is therefore 2½ fold higher. (27) Among those within America that consume less milk, such as the Mexican-Americans and Black Americans, osteoporosis incidence is two-fold lower than in white Americans, (28) which is not due to genetic differences. (29)In Venezuela and Chile much less milk is consumed than in the US, Finland, Sweden and Switzerland, while the hip fracture incidence in Venezuela and Chile is over 3 fold lower. (61)Chinese consume very little milk (8 kg / year), and hip-fracture incidence, therefore, is among the lowest in the world; hip-fracture incidence in Chinese women is 6 fold lower than in the US. (30) (The average American consumes 254 kg milk / year)The less milk consumed, the lower is the osteoporosis rate. (31)In other countries where very little milk is consumed, on the average, as in Congo (32), Guinea (33) and Togo (34) (6 kg / year) osteoporosis is extremely rare too. In the Dem. Rep. Congo, Liberia, Ghana, Laos and Cambodia even less milk is consumed (average person: 1 to 3 kg a year !!), and they've never even heard of age-related hip fracture. See:milk consumption per country in 1998 Of course, 'they' will say : "that's because blacks and Asians are genetically different from whites", but that is rubbish ; Osteoporosis incidence in female Asians is much lower than in Asian females living in the USA (35) just like osteoporosis incidence (and calcium consumption) in African Bantu women (36) is much lower than in Bantu women living in the USA. (37) And both calcium intake and hip-fracture rate is far lower in South African Blacks than in African Americans. (38)Response on these findings Alternative hypotheses about osteoporosis incidence;The excessive-phosphorus hypothesis Water fluoridation and fracture incidence Osteoporosis and protein- and soy consumption Some think it is because of low milk-calcium bio-availabilityThe magnesium-calcium ratio hypothesis Osteoporosis and a high-fat diet Smarter Than Nature''Nature has made a mistake but fortunately we are smarter than nature, and know how to correct this; Mother's milk, by mistake, contains far too little calcium, which has to be corrected through giving to humans cow's milk which contains 4 times as much calcium.''Of course this is nonsense.If calcium requirements really were four fold higher, pre-historic infants would never have been able to grow up, and ultimately, to have children. If we really need cows' milk, man could never have existed.Why ? Because we have already been on this planet for millions of years. And we have only consumed milk for a maximum of 0.01 million years. This means that we did not drink a single drop of milk from other animals in more than 99% of human existence; in our entire development from ape to modern human being, we never drank, nor needed animals' milk.1.6 million years ago there were already humans well over 6 feet tall (39), with apparently strong bones.Some argue that our prehistoric diet contained more calcium, but that is not trueBabies' FoodOf all humans, babies need the most calcium because their bones are still weak and need to be calcified much more. And mothers' milk does, of course, contain all the calcium (and other nutrients) babies need in their first two years. Babies fed on mother’s milk are perfectly able to increase bone-mineral density (BMD).So, exactly how much calcium does mothers' milk contain ? Not much:Calcium in mg / 100 g226 Hazelnuts140 Egg yolk132 Brazil nuts96 Olives, green87 Walnuts54 Figs44 Black berries42 Orange40 Raspberries38 Kiwi33 Mandarin32 Human milk 20 Coconut 18 Grapes16 Apricot16 Pineapple14 Plum13 Salmon12 Mackerel12 Mango11 Watermelon10 Avocado9 Banana6 MuskmelonWhat does this mean?Adults and infants always need less calcium than babies (per kg bodyweight). Food for adults therefore does not need to contain as much calcium (in %) as mother’s milk.And because our natural foods, on the average, contain about as much calcium as mother's milk, it is absolutely impossible that these natural foods contain too little calcium. If they did, mother’s milk would contain too little calcium too, and babies would not be able to increase BMD on mother’s milk.And because many foods contain more calcium than mother’s milk, the average calcium absorption rate is low, to prevent the uptake of excessive calcium. Vitamin DThe body needs broad daylight to transform cholesterol into vitamin D. The hormone that increases dietary calcium absorption (calcitriol), is composed of vitamin D.Some say osteoporosis incidence is, therefore, higher in countries with little sunlight.However, if you consume some fish and / or egg yolk once in a while, you'll absorb all the vitamin D you need - even living in Greenland, Canada or Northern Europe.Is osteoporosis incidence really lower in countries with more sunlight?

Not necessarily. Though Italy is much sunnier than Poland, hip-fracture incidence in Italy is much higher (40) than in Poland (and Spain) (41), simply because in Italy 25% more dairy products are consumed. (21) Kuwait is extremely sunny, but, nevertheless, osteoporosis incidence in Kuwait is about as high as in Great Britain and France (35), because in Kuwait, also, lots of milk is consumed. (21)Furthermore, the effects of this vitamin D-hormone can be very different.This hormone increases calcium absorption from food and absorption of calcium into the bones, (42) and therefore induces death of osteoblasts (43). Calcitriol also stimulates deportation of calcium from the bones into the blood. (See The Calcium-hormones") On the other hand, this hormone also inhibits secretion of PTH (excessive PTH strongly accelerates ageing of the bones). (See hyperparathyroidism) Thus, indirectly, this hormone can be protective, per saldo decreasing both uptake of calcium into the bones and deportation of calcium from the bones. (44) (See "The Calcium-hormones")However, since supplementary vitamin D / calcitriol increases the blood-calcium level (45), this extra calcium can precipitate in arteries and on the outside of the bones, causing arteriosclerosis and bone-deformities (46). It can also settle in joints and ligaments, and can cause muscle-cramps because the blood-calcium level needs to be low enough to deport calcium from muscle cells. It can even kill muscles cells (if the calcium cannot be deported), eventually causing fibromyalgia.Osteoporosis is often accompanied with a very low vitamin D level. (47) This can have multiple causes: Osteoporosis is caused by consuming too much calcium year after year. The body tries to counteract this by taking up as little calcium as possible. Vitamin D increases the calcium-absorption rate. So to prevent the uptake of excessive calcium, the body composes as little vitamin D as possible. · Hyperparathyroidism strongly increases both uptake of calcium into the bones and deportation from the bones, eventually causing osteoporosis. If too little calcitriol is available, the secretion of PTH is not sufficiently inhibited.· If always very, very little calcium is consumed (less than 300 mg / day which is a very hard thing to achieve), a lack of vitamin D / calcitriol can cause osteoporosis by making it impossible to increase calcium absorption.In general, it is not a problem at all to have little vitamin D / calcitriol at our disposal. This even protects us against absorbing too much calcium. In 52% of examined Saudi Arabian females for example, vitamin D level was extremely low (because of clothes that block almost all sunlight), but their bones were not affected. (48)In alcoholics the levels of the vitamin D-hormones were decreased by3 to 48%, but BMD was not affected. (49)In general, we do not need much vitamin D to either inhibit PTH secretion or to increase calcium absorption.In fact, in countries where the people consume high amounts of fish and eggs (which are the only vitamin D containing foods), the hip fracture rates are high too; because when both the intake of calcium (due to consuming dairy products) and vitamin D is high, the vitamin D causes a high uptake ratio of the calcium (accelerating the aging of osteoblasts.ExerciseIf osteoporosis was about a lack of exercise, all healthy but physical inactive people would have osteoporosis, which is not the case. That is why bone-loss with age cannot be explained by declining physical activity levels. (50)Loading determines the maintenance of bone-strength. If the bones are not loaded at all (like in space), they rapidly lose calcium. If we are normally active, our bones contain sufficient calcium to cope with incidental falls. Furthermore, a lack of exercise does not accelerate the aging of osteoblasts, so it cannot possibly be the cause osteoporosis. If one lacks exercise, one can easily increase BMD through exercise. In osteoporosis the lack of osteoblast activity is irreversible.

Exercise causes microfractures which stimulates the osteoblasts to increase their activity. Logically, then exercise also increases the death rate of osteoblasts. (51) (excessive exercise is detrimental (52))But exercise can increase bone-strength in elderly, can’t it?Yes, but only as long as osteoblast reproductivity is not almost totally exhausted. Exercise increases activity and reproduction of the remaining osteoblasts, temporarily increasing bone-strength (exercise does not guarantee future bone-strength (53)), but also accelerating aging of the bones.If osteoblast reproductivity is almost totally exhausted, one cannot increase BMD through exercise (or extra calcium) anymore, which is often the case in osteoporotic patients. (54) That is why the possible exercise-induced bone mass gain is far less than the disuse-induced bone loss. (55) This is why in osteoporosis exercise only partially (20 – 40%) decreases hip-fracture risk - even in the short term. (56) The later in life, the smaller the effects of exercise will be. (57)Normal activities are all the exercise you need to maintain bone health. Increased physical activity accelerates aging of the bones. On the other hand, exercising specific muscles can be effective since strong muscles can absorb the shock when falling. (58).





Athletes & Stress-fracturesOverweight & OsteoporosisThat menopause favors osteoporosis and obesity inhibits it, are well-known clinical observations.In menopause the estrogen level is lower, and adequate natural estrogen levels areprotective because estrogeninhibits uptake of calcium in the bones and bone-formation by osteoblasts. (1)In obesity the leptin level is elevated (59) and leptin also inhibits bone-formation by the osteoblasts. (60) Some think that obesity is protective because there is more loading on the bones, increasing their strength, but if that would be the case, osteoporosis could easily be stopped and even reversed by increasing physical activity / loading of the bones. Osteoporosis however is irreversible. Osteoporosis is not caused by a decreased bone mass, but is due to the exhaustion of osteoblasts, which is irreversible since it is about aging. The low bone mass is the result of the lack of new matrix, not the cause.For related topics, see index © 2000 Copyright Artists Cooperative Groove Union U.A.SourcesAbstracts of most sources can be found at the National Library of Medicine ; (1) Bryant HU, et al, An estrogen receptor basis for raloxifene action in bone. J Steroid Biochem Mol Biol 1999 / 69 (1-6) / 37-44. , Jilka RL, et al, Loss of estrogen upregulates osteoblastogenesis in the murine bone marrow. Evidence for autonomy from factors released during bone resorption. J. Clin. Invest. 1998 / 101 (9) / 1942-1950. , Sims NA, et al, Estradiol treatment transiently increases trabecular bone volume in ovariectomized rats. Bone1996 / 19 (5) / 455-461. , Westerlind KC, et al, Estrogen does not increase bone formation in growing rats. Endocrinology1993 / 133 (6) / 2924-2934. , Smith, G.R. et al, Inhibitory action of oestrogen on calcium-induced mitosis in rat bone marrow and thymus. J. Endocrinol. 1975 / 65 (1) / 45-53.(2)Erben RG, et al, Androgen deficiency induces high turnover osteopenia in aged male rats: a sequential histomorphometric study. J. Bone Miner. Res. 2000 / 15 (6) / 1085-1098. , Yeh JK, et al, Ovariectomy-induced high turnover in cortical bone is dependent on pituitary hormone in rats. Bone1996 / 18 (5) / 443-540. , Garnero P, et al, Increased bone turnover in late postmenopausal women is a major determinant of osteoporosis. J. Bone Miner. Res.1996 / 11 (3) / 337-349.(3) Taguchi Y, et al, Interleukin-6-type cytokines stimulate mesenchymal progenitor differentiation toward the osteoblastic lineage. Proc. Assoc. Am. Physicians 1998 / 110 (6) / 559-574. , Jilka RL, et al, Loss of estrogen upregulates osteoblastogenesis in the murine bone marrow. Evidence for autonomy from factors released during bone resorption. J. Clin. Invest. 1998 / 101 (9) / 1942-1950. , Tau KR, et al, Estrogen regulation of a transforming growth factor-beta inducible early gene that inhibits deoxyribonucleic acid synthesis in human osteoblasts. Endocrinology1998 / 139 (3) / 1346-1353. , Hietala EL, The effect of ovariectomy on periosteal bone formation and bone resorption in adult rats. Bone Miner. 1993 / 20 (1) / 57-65. , Egrise D, et al, Bone blood flow and in vitro proliferation of bone marrow and trabecular bone osteoblast-like cells in ovariectomized rats. Calcif. Tissue Int. 1992 / 50 (4) / 336-341.(4) Jilka RL, et al, Osteoblast programmed cell death (apoptosis): modulation by growth factors and cytokines. J. Bone Miner. Res. 1998 / 13 (5) / 793-802.(5) Mogi M, et al, Involvement of nitric oxide and biopterin in proinflammatory cytokine-induced apoptotic cell death in mouse osteoblastic cell line MC3T3-E1. Biochem. Pharmacol. 1999 / 58 (4) / 649-654. , Kobayashi ET, et al, Force-induced rapid changes in cell fate at midpalatal suture cartilage of growing rats. J. Dent. Res.1999 / 78 (9) / 1495-1504.(6) Vegeto E, et al, Estrogen and progesterone induction of survival of monoblastoid cells undergoing TNF-alpha-induced apoptosis. FASEB J.1999 / 13 (8) / 793-803. , Tomkinson A, et al, The role of estrogen in the control of rat osteocyte apoptosis. J. Bone Miner. Res. 1998 / 13 (8) / 1243-1250.(7) Davis JW, et al, Ethnic, anthropometric, and lifestyle associations with regional variations in peak bone mass. Calcif Tissue Int 1999 Aug;65(2):100-5. , Ulrich CM, et al, Lifetime physical activity is associated with bone mineral density in premenopausal women. J Womens Health 1999 Apr;8(3):365-75. , Boot AM, et al, Bone mineral density in children and adolescents: relation to puberty, calcium intake, and physical activity. J Clin Endocrinol Metab 1997 Jan;82(1):57-62. , Hu JF, et al, Dietary calcium and bone density among middle-aged and elderly women in China. Am J Clin Nutr 1993 Aug;58(2):219-27.(8) Weinstein RS, et al, Apoptosis and osteoporosis.Am. J. Med. 2000 / 108 (2) / 153-164. , Manolagas SC, Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. Endocr. Rev. 2000 / 21 (2) / 115-137. , Rodriguez JP, Abnormal osteogenesis in osteoporotic patients is reflected by altered mesenchymal stem cells dynamics. J. Cell. Biochem. 1999 / 75 (3) / 414-423. , Gazit D, et al, Bone loss (osteopenia) in old male mice results from diminished activity and availability of TGF-beta. J. Cell. Biochem. 1998 / 70 (4) / 478-488. , Ikeda T, et al, Age-related reduction in bone matrix protein mRNA expression in rat bone tissues: application of histomorphometry to in situ hybridization. Bone1995 / 16 (1) / 17-23. , Parfitt AM, et al, Relations between histologic indices of bone formation: implications for the pathogenesis of spinal osteoporosis. J. .Bone Miner. Res.1995 / 10 (3) / 466-473. , Neidlinger-Wilke C, et al, Human osteoblasts from younger normal and osteoporotic donors show differences in proliferation and TGF beta-release in response to cyclic strain. J. Biomech. 1995 / 28 (12) / 1411-1418. , Marie PJ, Decreased DNA synthesis by cultured osteoblastic cells in eugonadal osteoporotic men with defective bone formation. J Clin Invest 1991 Oct;88(4):1167-1172.(9) Byers RJ, et al, Differential patterns of osteoblast dysfunction in trabecular bone in patients with established osteoporosis. J. Clin. Pathol. 1997 / 50 (9) / 760-764. , Mullender MG, et al, Osteocyte density changes in aging and osteoporosis. Bone1996 / 18 (2) / 109-113. , Ikeda T, et al, Age-related reduction in bone matrix protein mRNA expression in rat bone tissues: application of histomorphometry to in situ hybridization. Bone1995 / 16 (1) / 17-23. , Hills E, et al, Bone histology in young adult osteoporosis. J. Clin. Pathol. 1989 / 42 (4) / 391-397. (10) Kassem M, et al, Demonstration of cellular aging and senescence in serially passaged long-term cultures of human trabecular osteoblasts. Osteoporos. Int. 1997 / 7 (6) / 514-524. , de Vernejoul MC, Bone remodelling in osteoporosis. Clin. Rheumatol.1989 / 8 Suppl. 2 / 13-15.(11) Delany AM, et al, Osteopenia and decreased bone formation in osteonectin-deficient mice. J. Clin. Invest. 2000 / 105 (7) / 915-923. , Gazit D, et al, Bone loss (osteopenia) in old male mice results from diminished activity and availability of TGF-beta. J. Cell. Biochem. 1998 / 70 (4) / 478-488. , Arlot M, et al, Impaired osteoblast function in osteoporosis: comparison between calcium balance and dynamic histomorphometry. Br. Med. J. (Clin. Res. Ed.) 1984 / 289(6444) / 517-520.(12) Namkung-Matthai H, et al, Osteoporosis influences the early period of fracture healing in a rat osteoporotic model. Bone2001 / 28 (1) / 80-86. , Dunstan CR, et al, Bone death in hip fracture in the elderly. Calcif. Tissue Int. 1990 / 47 (5) / 270-275. (13) Kung AW, Age-related osteoporosis in Chinese: an evaluation of the response of intestinal calcium absorption and calcitropic hormones to dietary calcium deprivation. Am. J. Clin. Nutr. 1998 / 68 (6) / 1291-1297. , Wang MC, et al, Associations of vitamin C, calcium and protein with bone mass in postmenopausal Mexican American women. Osteoporos Int 1997 / 7(6) / 533-8.(14) O'Brien, K.O. et al, Increased efficiency of calcium absorption from the rectum and distal colon of humans. American Journal of Clinical Nutrition 1996 / 63 (4) / 579-583.(15) Weinstein, RS, et al, Apoptosis of osteocytes in glucocorticoid-induced osteonecrosis of the hip. J. Clin. Endocrinol. Metab. 2000 / 85 (8) / 2907-2912. , Silvestrini, G, et al, Evaluation of apoptosis and the glucocorticoid receptor in the cartilage growth plate and metaphyseal bone cells of rats after high-dose treatment with corticosterone. Bone2000 / 26 (1) / 33-42. , Gohel A, et al, Estrogen prevents glucocorticoid-induced apoptosis in osteoblasts in vivo and in vitro. Endocrinology1999 / 140 (11) / 5339-5347.(16) Peterson CA, et al, Alterations in calcium intake on peak bone mass in the female rat. J. Bone Miner. Res. 1995 / 10 (1) / 81-95.(17) Pazzaglia UE, Experimental osteoporosis in the rat induced by a hypocalcic diet. Ital. J. Orthop. Traumatol.1990 / 16 (2) / 257-265.(18) Bonofiglio D, et al, Critical years and stages of puberty for radial bone mass apposition during adolescence. Horm Metab Res 1999 Aug ;31 (8) : 478-82. , Maggiolini M, et al, The effect of dietary calcium intake on bone mineral density in healthy adolescent girls and young women in southern Italy. Int J Epidemiol 1999 Jun;28 (3): 479-84. , van Mechelen W, et al, Longitudinal relationships between lifestyle and cardiovascular and bone health status indicators in males and females between 13 and 27 years of age; a review of findings from the Amsterdam Growth and Health Longitudinal Study. Public Health Nutr 1999 Sep;2 (3A) :419-27. , Kardinaal AF, et al, Dietary calcium and bone density in adolescent girls and young women in Europe. J Bone Miner Res 1999 Apr ;14(4) :583-92. , Cheng JC, et al, Determinants of axial and peripheral bone mass in Chinese adolescents. Arch Dis Child 1998 Jun;78 (6) :524-30. , Shaw CK, An epidemiologic study of osteoporosis in Taiwan. Ann Epidemiol 1993 May ;3 (3) :264-71. , Kroger H, et al, Development of bone mass and bone density of the spine and femoral neck--a prospective study of 65 children and adolescents. Bone Miner 1993 Dec;23 (3) :171-82.(19) Holbrook TL, et al, Dietary calcium and risk of hip fracture: 14-year prospective population study. Lancet 1988 / 2 (8619) / 1046-1049. , Lau EM, et al, Epidemiology and prevention of osteoporosis in urbanized Asian populations. Osteoporos Int 1993 / 3 (Suppl 1) / 23-26. , Ribot C, et al, Risk factors for hip fracture. MEDOS study: results of the Toulouse Centre. Bone 1993 / 14 (Suppl 1) / S77-80. , Perez Cano R, et al, Risk factors for hip fracture in Spanish and Turkish women. Bone 1993 / 14 (Suppl 1) / S69-72. , Kreiger N, et al, Dietary factors and fracture in postmenopausal women: a case-control study. Int J Epidemiol 1992 / 21 (5) / 953-958.(20) Turner, L.W. et al, Dairy-product intake and hip fracture among older women : issues for health behaviour. Psychol. Rep. 1999 / 85 (2) / 423-430. , Mussolino ME, et al, Risk factors for hip fracture in white men: the NHANES I Epidemiologic Follow-up Study. J Bone Miner Res 1998 / 13 (6) / 918-924. , Turner LW, et al, Osteoporotic fracture among older U.S. women: risk factors quantified. J Aging Health 1998 / 10 (3) / 372-391. , Owusu W, et al, Calcium intake and the incidence of forearm and hip fractures among men. J Nutr 1997 / 127 (9) / 1782-1787. , Feskanich, D. et al, Milk ,dietary calcium ,and bonefractures in women, a 12 year prospective study. Am. J. Public Health 1997 / 87 (6) / 992-997. , Meyer HE, et al, Dietary factors and the incidence of hip fracture in middle-aged Norwegians. A prospective study. Am J Epidemiol 1997 / 145 (2) / 117-123. , Tavani A, et al, Calcium, dairy products, and the risk of hip fracture in women in northern Italy. Epidemiology 1995 / 6 (5) / 554-557. , Meyer HE, Risk factors for hip fracture in a high incidence area: a case-control study from Oslo, Norway. Osteoporos Int 1995 / 5 (4) / 239-246. , Michaelsson K, et al, Diet and hip fracture risk: a case-control study. Study Group of the Multiple Risk Survey on Swedish Women for Eating Assessment. Int J Epidemiol 1995 / 24 (4) / 771-782. , Cumming RG, et al, Case-control study of risk factors for hip fractures in the elderly. Am J Epidemiol 1994 / 139 (5) / 493-503. , Nieves JW, et al, A case-control study of hip fracture: evaluation of selected dietary variables and teenage physical activity. Osteoporos Int 1992 / 2 (3) / 122-127. , Wickham CA, et al, Dietary calcium, physical activity, and risk of hip fracture: a prospective study. BMJ 1989 / 299 (6704) / 889-92. , Cooper C, et al, Physical activity, muscle strength, and calcium intake in fracture of the proximal femur in Britain. BMJ 1988 / 297 (6661) / 1443-1446. (21) FAO database on the internet ; www.fao.org/ Statistical Database / Food Balance Sheet Reports. Hong Kong has been removed from the database since the unification with China.(22) Paspati, I. et al, Hip fracture epidemiology in Greece during 1977-1992. Calcif. Tissue Int. 1998 / 62 (6) / 542-547. (23) Lau, E.M. & C. Cooper, Epidemiology and prevention of osteoporosis in urbanized Asian populations. Osteoporosis 1993 / 3 / suppl. 1 : 23-26.(24) Ho SC, et al, The prevalence of osteoporosis in the Hong Kong Chinese female population. Maturitas 1999 Aug 16;32(3):171-8.(25) Versluis, R.G. et al, Prevalence of osteoporosis in post-menopausal women in family practise (in Dutch). Ned. Tijdschr. Geneesk. 1999 / 143 (1) / 20-24. , Oden, A. et al, Lifetime risk of hip fractures is underestimated. Osteoporosis Int. 1998 / 8 (6) / 599-603. , Smeets-Goevaars, C.G. et al, The prevalence of low bone-meineral density in dutch perimenopausal women : the Eindhoven perimenopausal osteoporosis study. Osteoporosis Int. 1998 / 8 (5) / 404-409. , Lippuner, K.o et al, Incidence and direct medical costs of hospitilizations due to osteoporotic fractures in Switzerland. Osteoporosis Int. 1997 / 7 (5) / 414-425. , Lips, P. ,Epidemiology and predictors of fractures associated with osteoporosis. Am. J. Med. 1997 / 103 (2A) / 3S-8S / discussion 8S-11S. , Parkkari, J. et al, Secular trends in osteoporotic pelvic fractures in Finland : number and incidence of fractures in 1970-1991 and prediction for the future. Calcif. Tissue Int. 1996 / 59 (2) / 79-83. , Nydegger, V. et al, Epidemiology of fractures of the proximal femur in Geneva ; incidence, clinical and social aspects. Osteoporosis Int. 1991 / 2 (1) / 42-47. , Van Hemert, A.M. et al, Prediction of osteoporotic fractures in the general population by a fracture risk score. A 9-year follow up among middle aged women. Am.J.Epidemiol. 1990 / 132 (1) / 123-135.)(26) Lau, E.M. et al, Admission rates for hip fracture in Australia in the last decade. The New South Wales scene in a world perspective. Med.J.Aust. 1993 / 158 (9) / 604-606.(27) Fujita, T. and M. Fukase, Comparison of osteoporosis and calcium intake between Japan and the United States. Proc.Soc.Exp.Biol.Med. 1992 / 200 (2) / 149-152.(28) Bauer RL, Ethnic differences in hip fracture: a reduced incidence in Mexican Americans. Am J Epidemiol 1988 Jan;127(1):145-9.(29) Kessenich CR, Osteoporosis and african-american women. Womens Health Issues 2000 / 10 (6) / 300-304.(30) Xu. L. et al, Very low rates of hip fracture in Beijing, People's Republic of China ; The Beijing Osteoprosis Project. Am.J.Epedemiol. 1996 / 144 (9) / 901-907.(31) Schwartz, A.V. et al, International variation in the incidence of hip fractures : cross-national project on osteoporosis for the World Health Organization Program for Research on Ageing. Osteoporosis Int. 1999 / 9 (3) / 242-253.Rowe, S.M. et al, An epidemiological study of hip fracture in Honan, Korea. Int. Orthop. 1993 / 17 (3) / 139-143.(32) Bwanahali, K. et al, Etiological aspects of low back pain in rheumatic patients in Kinshasa (Zaire). Apropos of 169 cases. (in French) Rev. Rhum. Mal. Osteoartic. 1992 / 59 (4) / 253-257.(33) Barss, P., Fractured hips in rural Melanesians : a nonepidemic. Trop. Geogr. 1985 / 37 (2) / 156-159.(34) Mijiyawa, M.A. et al, Rheumatic diseases in hospital outpatients in Lome. Rev. Rhum. Mal. Osteoartic. 1991 / 58 (5) / 349-354.(35) Memon, A. et al, Incidence of hip fracture in Kuwait. Int.J.Epidemiol.1998 / 5 / 860-865.(36) Walker, A., Osteoporosis and Calcium Deficiency, Am. J. Clin. Nutr. 1965 / 16 / 327. (37) Smith, R., Epidemiologic Studies of Osteoporosis in Women of Puerto Rico and South-eastern Michigan ... Clin. Ortho. 1966 / 45 /32.(38) Abelow BJ, et al, Cross-cultural association between dietary animal protein and hip fracture: a hypothesis. Calcif. Tissue Int.1992 / 50 (1) / 14-18.(39) Holly Smith in : Leakey, R. & Lewin, R., Origins Reconsidered : In Search of what Makes Us Human, London 1992 / 144-145. , Mc Henry, H.M. ,Femoral lengths and stature in Plio-Pleistocene hominids. Am. J. Phys. Anthropol. 1991 / 85 (2) / 149-158. , Brown, F. et al, Early Homo erectus skeleton from west Lake-Turkana, Kenya. Nature 1985 / 316 (6031) / 788-792.(40) Mazzuoli, G.F. et al, Hip fracture in Italy : Epidemiology and preventive effeicacy of bone active drugs. Bone 1993 / 14 / suppl. /581-584.(41) Lips, P., Epidemiology and predictors of fractures associated with osteoporosis. Am. J. Med. 1997 / 103 (2A) / 3S-8S / discussion 8S-11S.(42) Erben RG, et al, Therapeutic efficacy of 1alpha,25-dihydroxyvitamin D3 and calcium in osteopenic ovariectomized rats: evidence for a direct anabolic effect of 1alpha,25-dihydroxyvitamin D3 on bone. Endocrinology1998 / 139 (10) / 4319-4328.(43) Pascher E, et al, Effect of 1alpha,25(OH)2-vitamin D3 on TNF alpha-mediated apoptosis of human primary osteoblast-like cells in vitro. Horm. Metab. Res.1999 / 31 (12) / 653-656.(44) Sairanen S, et al, Bone mass and markers of bone and calcium metabolism in postmenopausal women treated with 1,25-dihydroxyvitamin D (Calcitriol) for four years. Calcif. Tissue Int. 2000 / 67 (2) / 122-127.(45) Sairanen S, et al, Bone mass and markers of bone and calcium metabolism in postmenopausal women treated with 1,25-dihydroxyvitamin D (Calcitriol) for four years. Calcif. Tissue Int. 2000 / 67 (2) / 122-127. , Gurlek A, et al, Comparison of calcitriol treatment with etidronate-calcitriol and calcitonin-calcitriol combinations in Turkish women with postmenopausal osteoporosis: a prospective study. Calcif. Tissue Int. 1997 / 61 (1) / 39-43.(46) Giunta, D.L. ,Dental changes in hypervitaminosis D. Oral. Surg. Pathol. Oral. Radiol. Endod. 1998 / 85 (4) / 410-413. , Uehlinger, P. et al, Differential diagnosis of hypercalcemia - a retrospective study of 46 dogs. (duitst.) Schweiz. Arch. Tierheilkd. 1998 / 140 (5) / 188-197. , Qin, X. et al, Altered phosphorylation of a 91-kDa protein in particulate fractions of rat kidney after protracted 1,25-dihydroxyvitamin D3 or estrogen treatment. Arch. Biochem. Biophys. 1997 / 348 (2) / 239-246. , Niederhoffer, N. et al, Calcification of medical elastic fibers and aortic elasticity. Hypertension 1997 / 29 (4) / 999-1006. , Selby, P.L. et al, Vitamin D intoxication causes hypercalcemia by increased bone resorption with responds to pamidronate. Clin. Endocrinol. (Oxf.) 1995 / 43 (5) / 531-536. , Ito, M. et al, Dietary magnesium effect on swine coronary atherosclerosis induced by hypervitaminosis D. Acta Pathol. Jpn. 1987 / 37 (6) / 955-964.(47) Le Boff, M.S., Occult vitamin D deficiency in postmenopausal US women with acute hip fracture. J. Am. Med. Assoc. 1999 / 281 (16) / 1505-1511. , Scharla SH, et al, Prevalence of low bone mass and endocrine disorders in hip fracture patients in Southern Germany. Exp. Clin. Endocrinol. Diabetes 1999 / 107 (8) / 547-554.(48) Ghannam NN, et al, Bone mineral density of the spine and femur in healthy Saudi females: relation to vitamin D status, pregnancy, and lactation. Calcif Tissue Int 1999 Jul;65(1):23-8(49) Laitinen K, et al, Deranged vitamin D metabolism but normal bone mineral density in Finnish noncirrhotic male alcoholics. Alcohol Clin Exp Res 1990 Aug;14(4):551-6.(50) Rutherford OM, et al, The relationship of muscle and bone loss and activity levels with age in women. Age Ageing 1992 / 21 (4) / 286-293.(51) Meyer T, et al, Identification of apoptotic cell death in distraction osteogenesis. Cell. Biol. Int.1999 / 23 (6) / 439-446. , Landry P, et al, Apoptosis is coordinately regulated with osteoblast formation during bone healing. Tissue Cell 1997 / 29 (4) / 413-419.(52) Cromer B, et al, Adolescents: at increased risk for osteoporosis? Clin. Pediatr. (Phila) 2000 / 39 (10) / 565-574. , Judex S, et al, Does the mechanical milieu associated with high-speed running lead to adaptive changes in diaphyseal growing bone? Bone 2000 Feb;26(2):153-9.(53) Rutherford OM. , Is there a role for exercise in the prevention of osteoporotic fractures? Br J Sports Med 1999 / 33 (6) / 378-386.(54) Kerschan-Shindl K, et al, Long-term home exercise program: effect in women at high risk of fracture. Arch. Phys. Med. Rehabil. 2000 / 81 (3) / 319-323. , Greendale GA, et al, Lifetime leisure exercise and osteoporosis. The Rancho Bernardo study. Am. J. Epidemiol. 1995 / 141 (10) / 951-959. , Jaglal SB, et al, Past and recent physical activity and risk of hip fracture. Am. J. Epidemiol. 1993 / 138 (2) / 107-118.(55) Chesnut CH, Bone mass and exercise. Am. J. Med. 1993 / 95 (5A) / 34S-36S.(56) Gregg EW, et al, Physical activity, falls, and fractures among older adults: a review of the epidemiologic evidence. J. Am. Geriatr. Soc. 2000 / 48 (8):883-93. , Layne JE, et al, The effects of progressive resistance training on bone density: a review. Med. Sci. Sports Exerc. 1999 / 31 (1) / 25-30. , Preisinger E, et al, Therapeutic exercise in the prevention of bone loss. A controlled trial with women after menopause. Am. J. Phys. Med. Rehabil. 1995 / 74 (2) / 120-123. , Lau EM, et al, The effects of calcium supplementation and exercise on bone density in elderly Chinese women. Osteoporos. Int.1992 / 2 (4) / 168-173.(57) Rutherford OM, Is there a role for exercise in the prevention of osteoporotic fractures? Br. J. Sports Med. 1999 / 33 (6) / 378-386. , Commandre F, et al, [Physical activities and bone mass in women]. [Article in French] Bull. Acad. Natl. Med. 1995 / 179 (7) / 1483-1491; discussion 1491-1492.(58) Kaastad TS, et al, Training increases the in vivo fracture strength in osteoporotic bone. Protection by muscle contraction examined in rat tibiae. Acta Orthop. Scand. 1996 / 67 (4) / 371-376.(59) Chu NF, et al, Plasma leptin concentrations and four-year weight gain among US men. Int. J. Obes. Relat. Metab. Disord. 2001 / 25 (3) / 346-353. , Szymczak E, et al, The role of leptin in human obesity. Med. Wieku. Rozwoj. 2001 / 5 (1) / 17-26. , Hu FB, et al, Leptin concentrations in relation to overall adiposity, fat distribution, and blood pressure in a rural Chinese population. Int. J. Obes. Relat. Metab. Disord. 2001 / 25 (1) / 121-125. , Bahceci M, et al, The effect of high-fat diet on the development of obesity and serum leptin level in rats. Eat. Weight. Disord. 1999 / 4 (3) / 128-132. , Milewicz A, et al, Plasma insulin, cholecystokinin, galanin, neuropeptide Y andleptin levels in obese women with and without type 2 diabetes mellitus. Int. J. Obes. Relat. Metab. Disord. 2000 / 24 / Suppl 2 / S152-3. , Nakamura M, et al, Association between basal serum and leptin levels and changes in abdominal fat distribution during weight loss. J. Atheroscler. Thromb. 2000 / 6 (1) / 28-32. , Bunger L, et al, Leptin levels in lines of mice developed by long-term divergent selection on fat content. Genet`. Res. 1999 / 73 (1) / 37-44.(60) Takeda S, et al, Leptin regulates bone formation via the sympathetic nervous system. Cell 2002 Nov 1;111(3):305-17. , Burguera B. et al, Leptin reduces ovariectomy-induced bone loss in rats. Endocrinology 2001 / 142 (8) / 3546-3553. , Takeda S, et al, Central control of bone formation. J. Bone Miner. Metab. 2001 / 19 (3) / 195-198. , Anselme K, et al, Comparative study of the in vitro characteristics of osteoblasts from paralytic and non-paralytic children. Spinal Cord 2000 / 38 (10) / 622-629. , Ducy P, et al, Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass. Cell 2000 / 100 (2) / 197-207.(61) Bacon WE, et al, International comparison of hip fracture rates in 1988-89. Osteoporos Int. 199 / 6 (1) / 69-75.
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