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Journal of the American College of Nutrition, Vol. 20, No. 4, 269-270 (2001)
Published by the American College of Nutrition


Editorial

Controversy over Dietary Phosphorus

John J.B. Anderson, PhD, FACN and Sanford C. Garner, PhD

Department of Nutrition
University of North Carolina
Chapel Hill, North Carolina

The perspective presented by Leonard Sax in his Commentary, "The Institute of Medicine’s ‘Dietary Reference Intake’ for Phosphorus: A Critical Perspective," provides persuasive evidence that the Institute of Medicine (IOM) may have given less attention to a potentially important adverse effect of high phosphorus intake accompanied by low calcium consumption, primarily resulting from poor food choices, than it deserves [1]. The issues raised by the author point clearly to the need for further human research on the long-term influence of a high-phosphorus, low-calcium dietary pattern on the stimulation of parathyroid hormone and the eventual reduction of bone mass and density. At the current state of our knowledge base, it seems inappropriate to denigrate the IOM committee for its cursory examination of the high phosphorus issue [2], but rather it seems wiser to argue persuasively with NIH and other granting agencies to provide the appropriate funding to settle this perplexing question. A few points need to be elaborated on that make the argument of the author plausible, but a few cautionary comments are also in order.

First, several animal model studies using mice, rats and dogs and a couple of well-designed human investigations, though short-term, support the concept that a high-phosphorus, low-calcium diet with a ratio of approximately 4 P:1 Ca (or worse) elevates serum parathyroid concentrations in a chronic fashion [35]. In the animal models, bone losses were extensive, but in the human investigations the study designs were too brief to expect to see any adverse skeletal effects [67]. A few observational human reports, largely based on cross-sectional data, suggest that the high phosphorus content of the US diet may be responsible for fractures in pre-adolescents and adolescents [89]. Unfortunately, the designs of these two studies have many limitations.

Secondly, the author comes down hard on the IOM committee regarding its uncritical acceptance of published reports in support of its position that a high-phosphorus, low-calcium diet is not harmful to the skeleton, yet he does the same thing in giving carte blanche to the findings of published reports that favor his contention that adverse effects do result from such a diet [1]. Sometimes our biases get in the way of our own logic!

Finally, the author makes a most acceptable recommendation at the conclusion of his report that further experimental investigation is necessary on this issue to sort out the facts from the fictions. One approach would be a prospective controlled trial of a sufficient number of older adults with appropriate checks and safeguards in place so that the investigation could be terminated if any identified adverse effects of such a diet were scientifically confirmed at some time into the study, especially if bone measurements showed, say at six months, a statistically significant decline from baseline.

A forthcoming publication on phosphorus makes essentially the same point on the need for better data, but it also suggests that we need to assess better the hidden use of phosphate salts in foods because of their widespread use by the foods industry and by cola-type beverage producers [10]. Because of this latter concern about the high use of phosphates in food/beverage applications, federal regulatory agencies also need to enter into this issue. What we all really want is the truth of the matter on phosphorus, however it comes out.

In summary, the current attack on the IOM report should stimulate both debate and controversy that hopefully will lead to further research on this conundrum.

REFERENCES

  1. Sax L: The Institute of Medicine’s "Dietary Reference Intake" for phosphorus: a critical perspective. J Am Coll Nutr 20: 271–278, 2001.[Abstract/Free Full Text]
  2. Institute of Medicine (IOM), Food and Nutrition Board: "Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride." Washington, DC: National Academy Press, 1997.
  3. Shah BG, Krishnaro GVG, Draper HH: The relationship of Ca and P nutrition during adult life and osteoporosis in aged mice. J Nutr 92: 30–42, 1967.
  4. Clark I: Importance of dietary Ca:PO4 ratios on skeletal Ca, Mg, and PO4 metabolism. Am J Physiol 217: 865–870, 1969.[Free Full Text]
  5. Krook L, Lutwak L, Henrikson P, Kallfelz F, Hirsh C, Romanu B, Belanger LF, Marier JR, Sheffy BE: Reversibility of nutritional osteoporosis: physicochemical data on bones from an experimental study in dogs. J Nutr 101: 233–246, 1971.
  6. Calvo MS, Kumar R, Heath H: Persistently elevated parathyroid hormone secretion and action in young women after four weeks of ingesting high phosphorus, low calcium diets. J Clin Endocrinol Metab 70: 1334–1340, 1990.[Abstract]
  7. Barger-Lux MJ, Heaney RP: Effects of calcium restriction on metabolic characteristics of premenopausal women. J Clin Endocrinol Metab 76: 103–107, 1993.[Abstract]
  8. Wyshak G: Teenaged girls, carbonated beverage consumption, and bone fractures. Arch Pediatr Adolesc Med 154: 610–613, 2000.[Abstract/Free Full Text]
  9. Wyshak G, Frisch RE: Carbonated beverages, dietary calcium, the dietary/calcium ratio, and bone fractures in girls and boys. J Adolesc Health 15: 210–215, 1994.[Medline]
  10. Anderson JJB, Sell ML, Garner SC, Calvo MS: Phosphorus. In Russell R, Bowman B (eds): "Present Knowledge in Nutrition," 8th ed. Washington, DC: ILSI Press, 2001 [in press].




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