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Osteoporosis information
Introduction
There are many conditions in Western industrialised societies today that were unheard of, or at least very rare, just a century ago. The same conditions are still unheard of in primitive peoples who do not have the 'benefits' of our knowledge. There is a very good reason for this: They eat what Nature intended; we don't. The diseases caused by our incorrect and unnatural diets are those featured on these pages.
Dietary causes of osteoporosis:
Bran; cereal fibre; soya; vegetarian diet; low intake of meat; fizzy drinks (sodas)Osteoporosis
By the end of the 1980s, post-menopausal women in Britain stood a one in two chance of suffering from osteoporosis (brittle bone disease) and one in five of them died as a direct result.[i] That was twice as many fractures as there were in the 1950s.[ii] And the numbers aren't going down. Yet there are many cultures in the world where postmenopausal women are fit, active and healthy right up the end of their lives. It is also noticeable that the women in these cultures do not suffer from osteoporosis.
Central American Indian women, for example, live for an average of thirty years after the menopause but they don't get osteoporosis, they don't lose height, they don't develop a dowager's hump and they don't get fractures. A research team analysed their hormone levels and bone density and found that their oestrogen levels were no higher than those of white American women — in some cases they were even lower. Bone density tests by a research team showed that bone loss occurred in these women at the same rate as their US counterparts.[iii] So why didn't they suffer fractures?
To understand this, it is important to understand the nature of bones. Bone might appear to be static, but it is a living tissue which undergoes constant renewal and replacement. At any given time, in every one of us, there are up to ten million sites where small segments of old bone are being dissolved and new bone is being laid down to replace it.[iv]
Bone-forming cells are of two different kinds: osteoclasts and osteoblasts. The job of osteoclasts is to find old bone that is in need of renewal: they dissolve bone and leave behind tiny unfilled spaces. Osteoblast cells then move into these spaces in order to build new bone. In this way, bone heals and renews itself in a process called remodelling. It is imbalances in this remodelling process that contribute to osteoporosis: when more old bone is eaten up than new bone is laid down, bone loss occurs.
The process of remodelling continues throughout our lives. But after the age of about fifty, although the rate increases, the bone-building osteoblasts become less and less capable of completely refilling the spaces made by the osteoclasts.[v]
The correct term for low bone density is osteopenia. And density is only one factor in osteoporosis and the fractures that result from it. Another factor which tends to be forgotten is the micro-architecture of the bone. As osteoclasts absorb more bone than is rebuilt, the micro-architecture becomes fragile. As it weakens, the wrist and hip become more vulnerable to fracture. Vertebrae don't really fracture or crack, they collapse, causing loss of height, and if enough vertebrae collapse, a 'dowager's' hump is created.
The medical definition of osteoporosis used to be 'fractures caused by thin bones'. In 1991, it was redefined to 'a disease characterised by low bone mass and micro-architectural deterioration of bone tissue which lead to increased bone fragility and a consequent increase in fracture risk'.[vi] However, there is a problem with defining osteoporosis as a disease rather than a fracture because low bone mass is only a 'risk-factor' for osteoporosis, not osteoporosis itself. It's like defining heart disease as having high cholesterol rather than having a heart attack. Needless to say, this new definition has increased the number of women and men who 'have osteoporosis'.
Osteoporosis really has two components: bone density and micro-architecture. But all we hear about is bone density; micro-architecture is virtually ignored. This is probably because only bone density can be measured. But just measuring bone density can be misleading, for not everyone with low bone density will get fractures. Asian women, for example, tend to have low bone density yet have very few bone fractures; and if you have had a high intake of fluoride, your bone density will be higher — but so will your fracture risk because fluoride is more brittle!
The general assumption has been that once bone reaches a certain level of thinness, it becomes subject to fractures more easily. Now that more is known about bone physiology, it is clear that this is not the full story. Bone does not fracture due to thinness alone. Leading bone expert, Dr Susan E. Brown, states: 'Osteoporosis by itself does not cause bone fractures. This is documented simply by the fact that half of the population with thin osteoporotic bones in fact never fracture.'[vii]
And Lawrence Melton of the Mayo Clinic noted as early as 1988: 'Osteoporosis alone may not be sufficient to produce such osteoporotic fracture, since many individuals remain fracture-free even within the sub-groups of lowest bone density. Most women aged 65 and over and men 75 and over have lost enough bone to place them at significant risk of osteoporosis, yet many never fracture any bones at all. By age 80, virtually all women in the United States are osteoporotic with regard to their hip bone density, yet only a small percentage of them suffer hip fractures each year.'[viii]
So why does there seem to be many more women now with osteoporosis than in the past? Part of it may be nothing more than the change in definition. However, that doesn't alter the fact that the numbers of bone fractures in both women and men have increased since 'healthy eating' was introduced. And that is the clue.
How can one avoid osteoporosis?
The recommended way to prevent osteoporosis is to supplement with calcium, usually with low-fat, calcium fortified milk. But a lack of calcium causes osteomalacia (see below), not osteoporosis. This is a common misconception. And it may actually be counterproductive as many studies have shown that calcium supplementation may actually make the condition worse. As osteoporosis is caused by a weakening of the protein matrix of the bones, the best preventative measure is not calcium supplementation but a high-protein diet.
So it should not be a surprise that the overwhelming majority of epidemiological studies show low bone density to be more closely associated with low protein intakes, and high bone density with high protein intakes.[ix]
Bone density varies widely in different individuals. It is determined by the peak amount of bone you started with and the rate of this loss. That is why it is important to eat plenty of bone-forming foods and do weight-bearing exercise to build up bone density when young. It is too late to do either of those things when symptoms appear in your 70s.
In England alone, a fifth of all orthopaedic beds were already occupied by patients with broken hips and the direct hospital costs alone amounted to more than £160 million a year nearly two decades ago.[x] And that figure did not include other breakages, personal costs and, of course, the pain and hardship brought on by the disease. Is it coincidence that the incidence of osteoporosis has increased by about 10% a year for the past two decades as we have been told to reduce our intakes of meat, and to replace this with fibre-rich cereals?
Protein and bone health
In certain sections of the nutritional world, there seems to be a belief that if we eat animal protein this will cause our bones to lose calcium. This question is of particular interest in light of Palaeolithic diet research for two reasons: The first is because estimates of the levels of animal protein in the hominid diet during at least the last 1.7 million years of human evolution (from the time of Homo erectus) are much higher than considered prudent in some sectors of the nutritional research community today; the second is because the fossil evidence shows that Palaeolithic humans had a higher bone mass that would have been more robust and fracture-resistant than modern Western humans' bones.
Studies published in the 1980s of people eating a high-protein diet have also detected no calcium loss even over a long period of time, provided that meat is eaten with its fat.[xi] And subsequent studies confirmed that:
- meat eating does not adversely affect calcium balance,[xii] [xiii]
- protein actually promotes stronger bones.[xiv]
- men and women who eat the most animal protein have better bone mass than those who avoid it.[xv] [xvi]
Increasing protein intake also helped elderly patients who were taking vitamin D and calcium supplements. Drs B. Dawson-Hughes and S. S. Harris of the Calcium and Bone Metabolism Laboratory, Tufts University, Boston, Massachusetts, tested associations between protein intake and change in bone mass density in 342 healthy men and women aged 65 or over who had completed a 3-year, randomised, placebo-controlled trial of calcium and vitamin D supplementation.[xvii] They found that higher protein intake was significantly associated with a favourable 3-year change in total-body bone mass density in the supplemented group but not in the placebo group.
Protein powders are the culprit proteins
What is significant in the various studies of protein intake and bone density is that the studies which purported to show protein intake caused calcium loss were not conducted with real foods but with isolated amino acids and fractionated protein powders of the sort used by low-carb dieters and athletes. The reason why these amino acids and fat-free protein powders caused calcium loss while the fat meat diet did not is because protein, calcium, and minerals require the fat-soluble vitamins A and D for their assimilation and utilisation by the body. When protein is consumed without these factors it upsets the normal biochemistry of the body and mineral loss results.[xviii] True vitamin A and full-complex vitamin D are only found in animal fats. Furthermore, saturated fats that are present with meat are essential for proper calcium deposition in the bones.[xix] It should be no surprise, therefore that vegan diets have been shown to place women at the greatest risk for osteoporosis.[xx] [xxi]
References
[i]. Fractured neck of femur: prevention and management. A report of the Royal College of Physicians, London. 1989.
[ii]. Bengner U. Changes in the incidence of fracture of the upper humerus during a 30-year period: A study of 2125 fractures. Clin Orthop 1988; 231: 179-82.
[iii]. Love S. Dr Susan Love's Hormone Book. Random House, New York, 1997, p. 85.
[iv]. Frost H. The pathomechanics of osteoporosis. Clin Orthop 1985; 200: 198-225.
[v]. Love S. op. cit., p 77.
[vi]. Consensus Development Conference. Prophylaxis and treatment of osteoporosis. Conference Report. Am J Med 1991: 107-110.
[vii]. Brown S. Better Bones, Better Body. Keats Publishing, Connecticut, USA, 1996, p.38.
[viii]. Ibid.
[ix]. Kerstetter, et al. Low protein intake: The impact on calcium and bone homeostasis in humans. J Nutr 2003; 133: 855S-861S.
[x]. Fehily A M. Dietary determinants of bone mass and fracture risk: a review. J Hum Nutr and Diet 1989; 2: 299.
[xi]. Spencer H, Kramer L. Factors contributing to osteoporosis. J Nutr 1986; 116:316-319.; Further studies of the effect of a high protein diet as meat on calcium metabolism. Amer J Clin Nutr 1983; 37:6: 924-9.
[xii]. Hunt J, et al. High- versus low-meat diets: Effects on zinc absorption, iron status, and calcium, copper, iron, magnesium, manganese, nitrogen, phosphorus, and zinc balance in postmenopausal women. Am J Clin Nutr 1995; 62: 621-32.
[xiii]. Spencer H, et al. Do protein and phosphorus cause calcium loss? J Nutr 1988;118:657-60.
[xiv]. Cooper C, et al. Dietary protein and bone mass in women. Calcif Tiss Int 1996; 58:320-5.
[xv]. Munger RG, et al. Prospective study of dietary protein intake and risk of hip fracture in postmenopausal women. Am J Clin Nutr 1999; 69: 147-52.
[xvi]. Hannan MT, et al. Effect of dietary protein on bone loss in elderly men and women: The Framingham Osteoporosis Study. J Bone & Min Res 2000; 15: 2504-2512.
[xvii]. Dawson-Hughes B, Harris SS. Calcium intake influences the association of protein intake with rates of bone loss in elderly men and women. Am J Clin Nutr 2002; 75: 773-9
[xviii]. Fallon S, Enig M. Dem bones — do high protein diets cause osteoporosis? Wise Traditions 2000; 1: 4: 38-41. Also posted at http://www.westonaprice.org
[xix]. Watkins BA, et al. Importance of vitamin E in bone formation and in chondrocyte function. American Oil Chemists Society Proceedings 1996, at Purdue University.; Food Lipids and Bone Health in McDonald and Min, Eds Food Lipids and Health. Marcel Dekker Co. NY, 1996.
[xx]. Chiu JF, et al. Long-term vegetarian diet and bone mineral density in postmenopausal Taiwanese women. Calcif Tissue Int 1997; 60: 245-9.
[xxi]. Lau EM, et al. Bone mineral density in Chinese elderly female vegetarians, vegans, lacto-vegetarians and omnivores. Eur J Clin Nutr 1998; 52: 60-4.
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