When doctors won't tell . . . Of all the online nutritional information, nutritional facts, medical and dietary sites there are to choose from, in an article entitled "How to ease the pain" The Sunday Times magazine, Culture, published a list of just five websites it considered reliable and informative.
This site was one of that five.
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Barry Groves, PhD
Exposing dietary misinformation
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TITLE
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Perhaps one reason for the wide acceptance of the suggestion
that fibre is an important, if not essential, dietary component is
that it had the enthusiastic support of commercial interests.
PROFESSOR JOHN YUDKIN
Introduction
On this site and in my books, I have talked about a radical change from the 'healthy' diet that is currently recommended. By cutting out carbohydrate-rich foods like bread, pasta, breakfast cereals and rice and reducing our intake of other plant foods, does the food that is left constitute a balanced diet? Or could we be at risk of deficiency diseases?
Current recommendations suggest that we should increase our intake of 'whole grains'; soya is promoted as a useful source of protein, a healthy replacement for the meat we are told to eat less of. But soya, cereals and to a lesser extent other foods of vegetable origin all contain anti-nutrients built into the plants by Nature to protect them from predators. As a consequence, many are toxic if not adequately fermented or cooked.
These anti-nutrients have adverse effects on us not just as poisons but also by inhibiting the absorption of many minerals and other nutrients.
Fibre and mineral absorption
The fibre hypothesis was based on the fact that an increase in dietary fibre moved food through the gut faster. However, all the nutrients in food are absorbed through the gut wall and this takes time. If the food travels through faster, there is less time for its absorption and consequently less is absorbed. Because of this all fibre, whether it is from fruit, vegetables or cereals, inhibits the absorption of such nutrients as zinc,[1] iron, calcium, phosphorus, magnesium, energy, proteins, fats and vitamins A, D, E and K.[2] Now this doesn't matter too much if you eat a good nutrient-dense diet which contains plenty of these nutrients. But there is another problem with cereal fibre (bran): phytate.
Phytate
The American Journal of Clinical Nutrition is arguably the most important journal of nutrition. In 1992 Professor Harold H. Sandsted, its Editor-in-Chief, noted that:
'the evidence seems overwhelming that high intakes of fiber sources that are also rich in phytate can have adverse effects on mineral nutrition of humans. . . In view of the data, it appears that some health promoters who suggest that [we] should consume 30-35 g dietary fiber daily either have not done their homework or have simply ignored carefully done research on this topic'.[3]
What he was talking about was the phytic acid that cereals, soya and other seeds have in their husks. Phytic acid is a chemical that forms strong bonds with several minerals to form compounds called phytates.[4] These phytates are insoluble salts which are not absorbed from the gut. It is well known that by this mechanism wholegrain cereals decrease the absorption of these minerals and that this leads to a variety of deficiency diseases in both the developed and the undeveloped countries. Phytic acid is also an important cause of mineral deficiencies in vegetarians.[5] It seems that our bodies do not adapt to continual high intakes of phytic acid.[6]
This is because we have no evolutionary history of eating such foods. As Dr E J Moynahan pointed out in 1977:
'Man's ancestors forsook the fringe of the rain forest, where his nearest primate relatives still dwell, for the open savannah to join the large carnivorous predators (lions, leopards and cheetahs) preying on the deer and other herbivores of the savannah and other grasslands. Conservation of water and salt is essential for survival in this habitat and his colon adapted for this purpose. It is not designed to scavenge calcium, trace metals, or any other micronutrient that may be bound to the undigested cellulose.'[7]
The minerals mostly affected by phytic acid are calcium, iron,[8] and zinc.[9] For example, subjects absorbed more iron from white bread than from wholemeal bread even though their intakes of iron were fifty percent higher with the wholemeal bread.[10] And while white bread must have added calcium, the law does not require it of wholemeal bread.
Bran fibre has also been shown to cause faecal losses,[11] and what the medical profession calls 'negative balances' of calcium,[12] iron, zinc, phosphorus,[13] nitrogen, fats, fatty acids and sterols. A negative balance is where more is lost from the body than is absorbed. What this means is that by eating bran is depleting you lose minerals from your body.[14]
As a consequence, since the advent of 'healthy eating' we have seen the re-emergence of previously rare deficiency diseases such as rickets, caused by calcium deficiency, iron-deficiency anaemia, and low birth-weight babies. Low birth-weight is particularly serious as it leads to serious ill health in later life.
Osteoporosis
Post-menopausal women in Britain today stand a one in two chance of suffering from osteoporosis (brittle bone disease) and one in five of them will die as a direct result.[15] That is twice as many fractures as there were in the 1950s.[16] And yet there are many cultures in the world where postmenopausal women are fit, active and healthy until the end of their lives. It is also noticeable that the women in these cultures do not suffer from osteoporosis.
Mayan 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.[17] 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.[18]
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.[19]
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. Your vertebrae don't really fracture or crack, they collapse, causing loss of height, and if enough vertebrae collapse, a dowager 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'.[20] 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 — and so will your fracture risk!
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.'[21]
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.'[22]
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 has increased since 'healthy eating' was introduced. And that is the clue.
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 seventies.
How can one avoid osteoporosis?
Osteoporosis is caused by a number of things, but one aspect is calcium deficiency when bones are forming. Very few surveys have concentrated on intake of any nutrient other than calcium and more research is needed on this subject. However, as the eating of bran both inhibits the absorption of calcium from food and depletes the body of the calcium it has, is it coincidence that the incidence of osteoporosis has increased by about ten percent a year for the past two decades? 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 over a decade ago.[23] And that figure did not include other breakages, personal costs and, of course, the pain and hardship brought on by the disease.
Thus avoiding bran intake should help avoid the risk.
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.
When studies were done with people eating meat with its fat, no calcium loss was detected, even over a long period of time.[24] Other studies confirmed that meat eating did not adversely affect calcium balance,[25] and that protein actually promotes stronger bones.[26] 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 sixty-five or over who had completed a three-year, randomised, placebo-controlled trial of calcium and vitamin D supplementation.[27] They found that higher protein intake was significantly associated with a favourable three-year change in total-body bone mass density in the supplemented group but not in the placebo group.
Studies that purported to show protein intake caused calcium loss were not conducted with real foods but with isolated amino acids and fractionated protein powders. The reason why the 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.[28] 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.[29] Recent evidence shows that men and women who eat the most animal protein have better bone mass compared to those who avoid it.[30] The evidence also shows that vegan diets place women at a greater risk for osteoporosis.[31]
Soft drinks also hurt bones
Girls who drink colas and other fizzy drinks have a heightened risk of fracture, according to a report by Dr. Grace Wyshak. Her study tracked 460 ninth- and tenth-grade American schoolgirls. The girls completed questionnaires detailing physical activity, behavioural habits, fizzy drink consumption and history of bone fracture. Findings revealed that girls who drank colas and other fizzy drinks had more than three times the risk of fracture, compared with their peers who did not drink these. The results were especially pronounced among physically active girls who drank cola. Specifically, drinking cola boosted the risk of fracture by nearly five-fold in active girls. Experts speculate that the abundance of phosphorus in cola inhibits calcium metabolism, in turn weakening bones and making them more likely to break.[32] There is probably no better example of what's wrong with today's materialistic attitudes than school boards' acceptance of cash for vending machines, which amounts to a sellout of the birthright of thousands of growing children.
Arthritis
There can be few if any who have not suffered from pain in their lower backs at some time in their lives. Back troubles are some of the most common complaints seen in a doctor's office. In each year, about two percent of any general practitioner's patients consult him with backache.
Beverly had suffered intermittent mild to severe lower back pain for over ten years. She told me that within a week of starting eating the way I recommend, she found that her pain cleared up completely. She said 'It only comes back when I have slipped off the wagon. I put it down to wheat, as my odd foray into chocolate land doesn't seem to bring it on.'
This case illustrates a simple case of cause and effect as, apart from studies of ancient peoples, clinical trials have also shown that carbohydrates, particularly cereals, in the diet cause arthritis.[33] They may also be responsible for other conditions.
Arthritis, a common plague of modern society, exists in two major forms:
· osteoarthritis which is caused by wear and tear and, consequently, is generally present only in the middle-aged or elderly, and
· rheumatoid arthritis which may be present at all ages.
Osteoarthritis has been found in the most ancient skeletal remains of man and animals. But evidence of rheumatoid arthritis did not appear until about 2750 bc, a time when consumption of cereal grains had become widespread.
Osteoarthritis
Osteoarthritis tends to accompany osteoporosis. Researchers at Wayne State University School of Medicine tested the hypothesis that women with arthritis had a lower bone density.[34] They found a significant decrease in bone density in the legs of female patients with relatively mild osteoarthritis of the knee whether or not they had osteoporosis based on a spine bone density measurement. Osteoarthritis is known to be more prevalent in those who are obese.[35] It's not surprising that joints protest at having to support a heavier body.
Rheumatoid arthritis
Rheumatoid arthritis is never found in animal remains. Neither has it ever been found in skeletal remains of corn-eating peoples, such as Central American Indians. But it has been found to be present equally in all races and cultures eating wheat, rye and oats. This finding suggests that rheumatoid arthritis is a gluten-induced condition similar to coeliac disease.[36]
Today, arthritis and other rheumatic conditions are among the most prevalent diseases and the most frequent cause of disability.[37] An American mortality and morbidity report published in 2001 estimated that some 43 million persons had arthritis in 1997. This was up from 35 million in 1985 — an increase of nearly a quarter. All age groups were affected, including the working-age population, and rates increased with age. Females had higher arthritis rates than males overall and for each age group. There is no reason to suppose that the situation is not similar in Britain.
In a survey of North American Indians in 1932, Dr Weston Price, looked specifically for the presence of arthritis in the more isolated groups. He found not one case, neither did he hear of a case, however, he says 'at the point of contact with the foods of modern civilization many cases were found including ten bed-ridden cripples in a series of about twenty Indian homes.'[38]
One five-year-old boy had been in bed in hospitals with rheumatic fever, arthritis and an acute heart involvement for the past two and a half years. His mother had been told that her boy would not recover, so severe were the complications. She asked Dr Price's assistance in planning a nutritional program for her boy. He writes:
'The important change that I made in this boy's dietary program was the removal of the white flour products and in their stead the use of freshly cracked or ground wheat and oats used with whole milk to which was added a small amount of specially high vitamin butter produced by cows pasturing on green wheat. Small doses of a high-vitamin, natural cod liver oil were also added. At this time the boy was so badly crippled with arthritis, in his swollen knees, wrists, and rigid spine, that he was bedfast and cried by the hour. With the improvement in his nutrition which was the only change made in his care, his acute pain rapidly subsided, his appetite greatly improved, he slept soundly and gained rapidly in weight.'[39]
Rheumatoid arthritis is a complex autoimmune disease involving numerous environmental and genetic components, and similar to a number of other autoimmune diseases is found more often in coeliac patients.[40] Many studies of arthritic patients have demonstrated elevated antibody levels for gliadin (a protein found in gluten).[41] While no large clinical trials have been undertaken specifically to examine the effectiveness of gluten-free diets in the treatment of arthritis, there are numerous case studies reporting alleviation of arthritis symptoms with grain-free diets.[42] In view of this, I suspect that the valuable part of Dr Price's nutritional changes in the case outlined above were the addition of butter and cod liver oil.
Vilhjalmur Stefansson's experience
The anthropologist, Vilhjalmur Stefansson, didn't always take his own advice. As an explorer, he had lived for many years in the early twentieth century with the Inuit in northern Canada and Alaska, eating their no-carb diet. He, like they, was supremely healthy on it and actively promoted such a diet. However, from about 1927 to 1955 he tended to eat a conventional western diet as it was more socially convenient. Over time he put weight — it rose to a maximum of 184 lbs. To manage his weight, Stefansson tried cutting down on calorie intake for some years but only lost five pounds. He also had noticed that he was developing a stiffness in one knee. This gradually worsened and, by the time he was 75, Stefansson also had increasing soreness in both his hip and shoulder joints. Eventually, in 1955, he decided to revert to the 'Stone Age' all fat-meat diet he had used on his Arctic explorations. It worked; not only did he lose his excess weight, the diet cured his arthritis. Stefansson's wife, Evelyn' remarked:[43]
'As his knee stiffened, he began to go up and down stairs one step at a time. One day, some months after the start of our meat diet, he found to his surprise that he could use both legs with equal facility in climbing the stairs. Astonished, he proceeded down. When he had reached the foot of the stairs, without pain or stiffness, he shouted for me to come and see.'
Stefansson, himself, says:
'I did indeed shout for Evelyn, because I had just discovered something that I had not forecast to her because I had not foreseen it. The recovery of not only my stiff right knee but of all my joints, blessedly including my typing fingers, had been "magical."'
Stefansson lived on his 'Stone Age diet' until his death in 1962 at the age of 83, with no further problems with his joints.
Rickets and Osteomalacia
Rickets is a disease of children in which the bones do not harden and are malformed. It is caused by a deficiency of calcium and vitamin D. Rickets was once so common in England that it was called 'The English Disease'. That diet could be a factor was shown by studies in the 1930s which showed that young dogs got rickets when they were fed oatmeal.[44] It was determined that the phytate in cereals bound calcium,[45] and that the phytate was the dietary factor responsible for inhibition of calcium absorption by oatmeal as well as the induction of rickets in dogs.[46] Similar adverse effects were observed in humans eating wholemeal and other bran-rich breads.[47] These studies also showed removing the phytate improved calcium retention. Substantial evidence has since firmly established this negative impact of cereals.
In the archaeological record, rickets is rare or absent in pre-agricultural human skeletons. Its prevalence increased during medieval urbanisation and it really took off during industrialisation.[48] By the beginning of the Twentieth Century, estimates suggested that as many as eighty to ninety percent of children throughout Northern Europe were affected with rickets.[49] It is unlikely that this was caused by decreased exposure to sunlight. More likely causes were firstly a trend of increasing cereal intake during the Middle Ages which increased phytate intake as well, and secondly the introduction of large-scale cereal processing and the industrialisation of bread making in which processes such as malting, soaking, scalding, fermentation, germination and sourdough baking, which had previously reduced the phytate content, were abolished to speed up bread manufacture and reduce costs. All the methods mentioned reduce the amount of phytic acid by use of phytases: enzymes which are also present in cereal.[50] These enzymes are easily destroyed during industrial cereal processing.[51]
With better nutrition in the 1930s rickets was relegated to the past — it was thought. However, since the advent of 'healthy eating' rickets is returning.[52]
Osteomalacia is the adult counterpart to rickets. In this disease bones soften due to both insufficient vitamin D because women don't go into the sun or cover themselves up, and to insufficient calcium in their diet. This disease leads to a progressive decalcification of the bones, often causing bone pain. If not treated soon enough, the condition may be irreversible. Osteomalacia is most common in women of childbearing age in whom calcium is lost during pregnancy. Thus it is particularly important to avoid a diet high in wholemeal cereals, bran and soya at this time.
Colon cancer
Apart from its role in bones, calcium plays an important role in the processes that keep normal body cells normal. Imbalances in these processes can have such adverse consequences as acute disruption leading to rapid cell death, and start other processes which may lead to cancer. Several studies have shown that increases in dietary calcium may protect against cancer of the colon.[53] From this it seems logical that if calcium is not available because of the amount of bran in the diet, the risk of such cancer may be increased.
Alzheimer's disease
Patients with Alzheimer's disease (senile dementia) have been found to have abnormal amounts of aluminium in their brains. But, as aluminium was known not to pass the blood/brain barrier, scientists couldn't understand how this happened. In the 1980s, tests on the people of Guam and parts of New Guinea and Japan, who get the disease at a much younger age, linked it to a lack of calcium. It was suggested that the lack of calcium caused a hormonal imbalance which allowed the aluminium to penetrate the brain.[54]
Infant brain damage
Infants can suffer a similar brain damage if fed soya based baby milk. Soya milk has a high phytate content which, as we have seen, inhibits the absorption of some minerals, one of which is zinc. Not only does zinc play a very important part in the developing brain, it is believed that a zinc deficiency caused by soya and other products which contain phytate enhances the uptake and deposition of aluminium in the milk.[55]
Iron deficiency anaemia
If there is a large intake of 'anti-nutrients' such as phytate, dietary fibre and tannins, which impair the absorption of iron,[56] and a low intake of flesh foods (another result of the diet-heart recommendations), there is a real risk of iron deficiency anaemia. And sub-optimal iron intakes were already being found in Britain, USA, Canada and South Africa.[57]
Other conditions
Depression, anorexia, low birth weight, slow growth, mental retardation, and amenorrhoea are also associated with deficiencies of zinc and the first five of these are also associated with a deficiency of iron.[58] There is an apparent relation between dietary fibre and reproductive function in women. It affects the onset of menstruation and retards uterine growth.[59] Later it is associated with menstrual dysfunction.[60]
Men only
Professor David Southgate is a world-renowned expert on dietary fibre. He concludes that the effects of excessive intakes of dietary fibre on calcium, iron and zinc absorption would be particularly undesirable for infants, children and young adolescents, and recommends that dietary fibre intakes in those groups should be separated from those for the general adult population and given on a body-weight basis.[61] To them should be added pregnant women and post-menopausal women whose mineral needs are greater and who should also be protected from excessive consumption of fibre.
The advice given by dieticians, nutritionists and doctors appears to include no warnings concerning age, sex or body weight. Indeed, the impression given by them all is that we should all eat as much fibre as we can tolerate. The British Medical Association in its publication The Slimmers' Guide, even recommended bran as a good source of calcium![62] Not unnaturally, the makers of All-bran and similar breakfast cereals, and wholemeal breads bombard us via television advertisements stressing the goodness contained in their products by virtue of the high bran content. Yet the only members of the population who may eat these in any quantity with relative impunity are adult men.
Conclusion
Dr Moynahan warned that 'Any substantial return to a high-fibre diet may lead to a reversal to the situation that obtained a century ago'. As any doctor today can testify, it has.
Dr Moynahan continued: 'Apparently, therefore, the amount of fibre must be strictly limited or the cereals fortified not only with calcium but also with iron and zinc as well, if this is to be avoided'. This means that it may not be a good idea to eat wholemeal bread because, while white bread must have added calcium, the law does not require it of wholemeal bread.
It would appear, therefore, that although a modest increase of vegetable fibre would probably not have any significant adverse effects, provided that there were adequate amounts of proteins, minerals, etc, in the diet, any advice must be given in such a way as to prevent the excessive intake of phytate associated with bran. Incidentally, I read somewhere that as a breaker of teeth, granary bread is second only to a punch in the mouth.
One truly healthy aspect of a low-carb way of eating is that it generally means cutting down on cereals such as bread and pasta. This has the advantage that reduction of cereals also reduces the amount of phytic acid consumed, without you having to do anything else. Many people give up bread altogether. This isn't necessary but, if you do eat bread, make it white bread. Although white bread will have lost some of its nutritional value, on balance it may be healthier than wholemeal bread because of the lack of phytates — and it does have that added calcium.
There may be a limit under which bran may not be harmful — but we have no ready way to know what that limit is. Therefore, it is much safer for you to avoid bran than to try to gauge what your safe limit might be. If you feel the need for fibre, there is an easier way: Get your fibre from green leafy vegetables and don't eat bran, wholemeal bread and unfermented soya.
References
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[2]. Kelsay J L. A review of research on effect of fibre intake on man. Am J Clin Nutr 1978; (31): 142.
[3]. Sandstead HH. Fiber, phytates, and mineral nutrition. Nutr Rev 1992; 50: 30-1.
[4]. Spivey Fox MR, Tao S-H. Antinutritive effects of phytate and other phosphorylated derivatives. In: Hathcock JN, ed. Nutritional Toxicology. New York: Academic Press, 1989: vol 3; 59-96.; Harland BF. Dietary fibre and mineral bioavailability. Nutr Res Rev 1989; 2: 133-47.; Rossander L, Sandberg AS, Sandström B. The influence of dietary fibre on mineral absorption and utilisation. In: Schweizer TF, Edwards CA, ed. Dietary fibre — a component of food. Nutritional function in health and disease. London: 1992.; Sandberg AS, Hasselblad C, Hasselblad K, Hulten L. The effect of wheat bran on the absorption of minerals in the small intestine. Br J Nutr 1982; 48: 185-91.; Morris ER. Phytate and dietary mineral bioavailability. In: Graf E, ed. Phytic acid: Chemistry and applications. Minneapolis: Pilatus Press, 1986: vol 4, 57-76.
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[10]. Kelsay J L. Op cit.
[11]. Stevens J, et al. Effect of psyllium gum and wheat bran on spontaneous energy intake. Am J Clin Nutr 1987; 46: 812.
[12]. Balasubraminian R, et al. Effect of wheat bran on bowel function and fecal calcium in older adults. J Am Coll Nutr. 1987; 6(3): 199.
[13]. Hallfisch J, et al. Mineral balances of men and women consuming high fibre diets with complex or simple carbohydrate. J Nutr. 1987; 117(2): 403.
[14]. Kesaniemi Y A, Tarpila S, Miettinen T A. Low vs high dietary fiber and serum, biliary, and fecal lipids in middle-aged men. Am J Clin Nutr 1990; 51: 1007.
[15]. Fractured neck of femur: prevention and management. A report of the Royal College of Physicians, London. 1989.
[16]. 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.
[17]. Susan Love, MD. Dr Susan Love's Hormone Book. Random House, New York, 1997, p. 85.
[18]. Frost H. The pathomechanics of osteoporosis. Clin Orthop 1985; 200: 198-225.
[19]. Susan Love, op. cit., p 77.
[20]. Consensus Development Conference. Prophylaxis and treatment of osteoporosis. Conference Report. Am J Med 1991: 107-110.
[21]. Susan Brown, PhD. Better Bones, Better Body. Keats Publishing, Connecticut, USA, 1996, p.38.
[22]. Susan Brown, op cit.
[23]. Fehily A M. Dietary determinants of bone mass and fracture risk: a review. J Hum Nutr and Diet 1989; 2: 299.
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[25]. 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. Amer J Clin Nutr; 1995, 62:621-32; Spencer, Osis, and Kramer, Do protein and phosphorus cause calcium loss? J Nutr 1988;118:657-60; Farnsworth E, Luscombe ND, Noakes M, et al. Effect of a high-protein, energy-restricted diet on body composition, glycemic control, and lipid concentrations in overweight and obese hyperinsulinemic men and women. Am J Clin Nutr 2003; 78: 31-39
[26]. Cooper C, et al. Dietary protein and bone mass in women. Calcif Tiss. Int 1996; 58:320-5.
[27]. 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
[28]. 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
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