Phytic acid in cereal grains causes calcium depletion

Date: Sun, 8 Jun 1997 14:55:35 +0100
Sender: Paleolithic Diet Symposium List
From: Staffan Lindeberg <Wikipedia>
Subject: Re: Cereal grains

Dean asked for references to the notion that phytic acid in cereal grains causes calcium depletion. In 1992 Professor Harold H. Sandsted, who is Interim Editor-in-Chief of the American Journal of Clinical Nutrition, the most important journal of nutrition, 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" and that, "in view of the [reviewed] data, it appears that some health promoters who suggest that U.S. adults should consume 30-35 g dietary fiber daily either have not done their homework or have simply ignored carefully done research on this topic" [1]. My own opinion is that authorities who advocate cereals in a prudent western diet largely do so for practical reasons [2].

So let's look do the homework. Whole meal cereals and other seeds have in their shells phytic acid which strongly binds to minerals like calcium, iron, zinc and magnesium to form insoluble salts, phytates [1, 3-7]. It is well known that whole meal cereals by this mechanism decrease the absorption of such minerals [1, 3-7]. There is apparently no adaptation to a habitual high intake of phytic acid [8] which is an important contributing cause of iron deficiency in third world countries and possibly in the western world [9]. It is also an important cause of mineral deficiency in vegetarians [10-12]. The most commonly studied minerals are bound to phytic acid possibly in the following decreasing order: calcium > iron > zinc > magnesium (Fredlund K, personal communication).

Mellanby found back in the 30s that young dogs got rickets when they were fed oatmeal [13]. He was made aware of the calcium-binding effect of phytate [14] and showed that phytate was the dietary factor responsible for inhibition of calcium absorption by oatmeal as well as the induction of rickets in dogs [15]. McCance and Widdowson found adverse effects of bread prepared from high-extraction wheat flour on retention of essential metals by humans [16]. They also showed that destruction of phytate improved retention of calcium [17]. Substantial evidence have later firmly established this negative impact of phytate [1, 3-7]. Not even rats seem to be fully adapted to graminivorous diets since phytate adversely affects mineral absorption in them as well [18].

In the archaeological record, rickets is rare or absent in preagricultural human skeletons, while the prevalence increases during medieval urbanization and then explodes during industrialism [19]. In the year 1900, an estimated 80-90 per cent of Northern European children were affected [20, 21]. This can hardly be explained only in terms of decreasing exposure to sunlight and descreased length of breast-feeding. An additional possible cause is a secular trend of increasing intake of phytate since cereal intake increased during the Middle Ages (Morell M, personal communication) and since old methods of reducing the phytate content such as malting, soaking, scalding, fermentation, germination and sourdough baking may have been lost during the agrarian revolution and industrialism by the emergence of large-scale cereal processing. The mentioned methods reduce the amount of phytic acid by use of phytases, enzymes which are also present in cereals [22-26]. These enzymes are easily destroyed during industrial cereal processing [27, 28].

It should be noted that dietary fiber alone has no impact on mineral absorption [5, 29] why a high intake of fiber from fruits and tubers can safely be recommended, at least from this point of view.

Best regards to all of you,

  1. Sandstead HH. Fiber, phytates, and mineral nutrition. Nutr Rev 1992; 50: 30-1.
  2. Walker ARP, Walker BF I. I. Fiber, phytic acid, and mineral metabolism. Nutr Rev 1992; 50: 246-7.
  3. 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: 59-96. vol 3).
  4. Harland BF. Dietary fibre and mineral bioavailability. Nutr Res Rev 1989; 2: 133-47.
  5. Rossander L, Sandberg A-S, Sandstr=F6m 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:
  6. 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.
  7. Morris ER. Phytate and dietary mineral bioavailability. In: Graf E, ed. Phytic acid: Chemistry and applications. Minneapolis: Pilatus Press, 1986: 57-76. vol 4).
  8. Brune M, Rossander L, Hallberg L. Iron absorption: no intestinal adaptation to a high-phytate diet. Am J Clin Nutr 1989; 49: 542-5.
  9. Hallberg L, Rossander L, Skanberg AB. Phytates and the inhibitory effect of bran on iron absorption in man. Am J Clin Nutr 1987; 45: 988-96.
  10. Harland BF, Smith SA, Howard MP, Ellis R, Smith JJ. Nutritional status and phytate:zinc and phytate x calcium:zinc dietary molar ratios of lacto-ovo vegetarian Trappist monks: 10 years later. J Am Diet Assoc 1988; 88: 1562-6.
  11. Ellis R, Kelsay JL, Reynolds RD, Morris ER, Moser PB, Frazier CW.
  12. Phytate:zinc and phytate X calcium:zinc millimolar ratios in self-selected diets of Americans, Asian Indians, and Nepalese. J Am Diet Assoc 1987; 87: 1043-7.
  13. Gibson RS. Content and bioavailability of trace elements in vegetarian diets. Am J Clin Nutr 1994; 59(5 Suppl): 1223S-1232S.
  14. Mellanby E. A story of nutrition research.Baltimore: Williams & Wilkins Co, 1950
  15. Bruce H, Callow R. Cereals and rickets. The role of inositolhexaphosphoric acid. Biochem J 1934; 28: 517-28.
  16. Harrison D, Mellanby E. Phytic acid and the rickets-producing action of cereals. Biochem J 1934; 28: 517-28.
  17. McCance R, Widdowsos E. Mineral metabolism of healthy adults on white and brown bread dietaries. j Physiol 1942; 101: 44-85.
  18. McCance R, Edgecombe C, Widdowson E. Mineral metabolism of dephytinized bread. J Physiol 1942; 101:
    Fairweather TS, Wright AJ. The effects of sugar-beet fibre and wheat bran on iron and zinc absorption in rats. Br J Nutr 1990; 64: 547-52.
  19. Stuart-Macadam PL. Nutritional deficiency diseases: a survey of scurvy, rickets, and iron-deficiency anemia. In: Is=E7an MY, Kennedy KAR, ed. Reconstruction of life from the human skeleton. New York: Wiley-Liss, 1989: 201-22.
  20. Gibbs D. Rickets and the crippled child: an historical perspective [see comments]. J R Soc Med 1994; 87: 729-32.
  21. Hernigou P. Historical overview of rickets, osteomalacia, and vitamin D. Rev Rhum Engl Ed 1995; 62: 261-70.
  22. Sandberg AS. The effect of food processing on phytate hydrolysis and availability of iron and zinc. Adv Exp Med Biol 1991; 289: 499-508.
  23. Svanberg U, Sandberg A-S. Improved iron availability in weaning foods using germination and fermentation. In: Southgate DAT, Johnson IT, =46enwick GR, ed. Nutrient Availability: Chemical and biological aspects. Cambridge: Cambridge University press, 1989: 179-81.
  24. Larsson M, Sandberg A-S. Phytate reduction in bread containing oat flour, oat bran or rye bran. J Cereal Sci 1991; 14: 141-9.
  25. Navert B, Sandstrom B, Cederblad A. Reduction of the phytate content of bran by leavening in bread and its effect on zinc absorption in man. Br J Nutr 1985; 53: 47-53.
  26. Caprez A, Fairweather TS. The effect of heat treatment and particle size of bran on mineral absorption in rats. Br J Nutr 1982; 48: 467-75.
  27. Sandberg A-S. Food processing influencing iron bioavailability. In: Hallberg L, Asp N-G, ed. Iron Nutrition in Health and Disease. London: John Libbey, 1996: 349-58.
  28. Sandstrom B. Food processing and trace element supply. In: Somogyi JC, Muller HR, ed. Nutritional Impact of Food Processing. Bibl Nutr Dieta. Basel: Karger, 1989: 165-72.
  29. Andersson H, Navert B, Bingham SA, Englyst HN, Cummings JH. The effects of breads containing similar amounts of phytate but different amounts of wheat bran on calcium, zinc and iron balance in man. Br J Nutr 1983; 50: 503-10.

Date: Sun, 8 Jun 1997 12:28:00 -0600
Sender: Paleolithic Diet Symposium List
From: Loren Cordain
Subject: Re: More on cereal grains & response to Sarah Mason

The following citations show that excessive whole cereal grain consumption (>50% of total calories) can cause or exacerbate rickets and/or osteomalacia in both animals and man: (I inclued the articles on zinc deficiency because it (zinc deficiency) has now been shown to retard skeletal growth (12).
  1. Robertson I et al. The role of cereals in the aetiology of nutritional rickets: the lesson of the Irish National Nutrition Survey 1943-8. Brit J Nutr 1981;45:17-22.
  2. Ewer TK. Rachitogenicity of green oats. Nature 1950;166:732-33.
  3. Sly MR. et al. Exacerbation of rickets and osteomalacia by maize: a study of bone histomorphometry and composition in young baboons. Calcif Tissue Int 1984;36:370-79.
  4. Ford JA et al. A possible relationship between high extraction cereal and rickets and osteomalacia. Advances in Exp Med & Biol 1977;81:353-62.
  5. Ford JA et al. Biochemical response of late rickets and osteomalacia to a chupatty free diet. Brit Med J 1972;ii:446-447.
  6. MacAuliffe T. et al. Variable rachitogenic effects of grain and alleviation by extraction or supplementation with vitamin D, fat and antibiotics. Poultry Science 1976;55:2142-47.
  7. Hidiroglou M et al. Effect of a single intramuscular dose of vitamin D on concentrations of liposoluble vitamins in the plasma of heifers winter-fed oat silage, grass silage or hay. Can J Anim Sci 1980; 60:311-18.
  8. Reinhold JG. High phytate content of rural Iranian bread: a possible cause of human zinc deficiency. Am J Clin Nutr 1971;24:1204-06.
  9. Halsted JA et al. Zinc deficiency in man, The Shiraz Experiment. Am J Med 1972;53:277-84.
  10. Sandstrom B et al. Zinc absorption in humans from meals based on rye, barley, oatmeat, triticale and whole wheat. J Nutr 1987;117:1898-1902.
  11. Dagnelie PC et al. High prevalence of rickets in infants on macrobiotic diets. Am J Clin Nutr 1990;51:202-08.
  12. Golub MS et al. Adolescent growth and maturation in zinc-deprived rhesus monkeys. Am J Clin Nutr 1996;64:274-82.

Clearly, present day and historical accounts of hunter-gatherers have shown that cereal grains have been included in the human diet. Sarah's reference list on this topic is comprehensive and outlines most of the better known citations. However, the point to be made here is that cereal grains rarely formed the bulk of the daily caloric intake throughout the year of any of these peoples, and that for virtually all of the rest of the studied hunter-gatherer populations, cereal grains were not consumed. Consequently, in view of optimal foraging theory, it seems likely that during the late paleolithic and before, when large mammals abounded, our ancestors would almost have never consumed the seeds of grass.

As has been suggested by John Yudkin almost 30 years ago, cereal grains are a relatively recent food for hominids and our physiologies are still adjusting and adapting to their presence. Clearly, no human can live on a diet composed entirely of cereal grains (for one thing they have no vitamin C). As I pointed out in my last posting, when cereal grain calories reach 50% or more of the daily caloric intake, humans suffer severe health consequences. One has to look no further than the severe pellagra epidemics of the late 19th century in America and the beri-beri scourges of South East Asian to confirm this. The present day incidence of hypo-gonadal dwarfism in Iran (8,9) lends further support to this notion.

Simoons classic work (Simoons FJ. Celiac disease as a geographic problem. In: Food, Nutrition & Evolution, DN Walcher & N Kretchmer (Eds). NY, Masson Pub, 1981, 179-199) on the incidence of celiac disease shows that the distribution of the HLA B8 haplotype of the human major histocompatibility complex (MHC) nicely follows the spread of farming from the mideast to northern europe. Because there is strong linkage disequalibrium between HLA B8 and the HLA genotypes which are associated with celiac disease, it indicates that those populations with the least exposure to cereal grains (wheat primarily) have the highest incidence of celiac disease. This genetic argument is perhaps the strongest evidence to support Yudkin's observation that humans are incompletely adapted to the consumption of cereal grains.

Thus, the genetic evidence for human disease (in this case, I have used celiac disease, however other models of autoimmune disease could have been used) is supported by the archeological evidence which in turn supports the clinical evidence. Thus, the extrapolation of paleo diets has provided important clues to human disease - clues which may have gone un-noticed without the conglomeration of data from many diverse fields (archaeology, nutrition, immunology, genetics, anthropology and geography). So, in the case of the celiac disease, we clearly are not putting the cart before the horse. For a celiac, a healthy diet is definitely cereal free - why is this so - perhaps now the evolutionary data is finally helping to solve this conundrum.

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