INTEGRATION
The primitive diet, the one to which human physiology has adapted over the millennia of evolution, was calcium dense, with a calcium content of 70 - 80 mg/IOO kcal (0.42 - 0.48 mmol/ kJ). At energy expenditure levels that prevailed until the very recent advent of private automobiles and other labour-saving devices, such a diet would have provided individuals of contemporary body size with total calcium intakes in the range of 50 - 75 mmol (2000 - 3000 mg)/d. Additionally, evolution provided mechanisms to tide us over transient periods of dietary calcium deficiency. Modern diets, based on the calcium-poor foods that served as the basis of the agricultural revolution, provide total calcium intakes far short of those to which our physiologies are adapted.
For this reason, the same modern diets cause us to call into constant play the compensatory mechanisms that, under primitive conditions, allowed us to function during what would usually have been transient periods of food shortage. Except for some decline in the size of the calcium reserve, a substantial fraction of contemporary humans appears to be able to do this perfectly well, without sustaining any apparently untoward consequences. But many cannot cope so well. For some, the decreased calcium reserve translates to increased bony fragility. Still others, better able to protect their skeletons, develop hypertension. Others, with a potential for colon carcinogenesis, increase that risk by virtue of absence of a natural protective factor in the food residue from their diets. For the various reasons reviewed in this chapter, skeletal maintenance must be judged as a necessary, but insufficient, functional endpoint for calcium nutrition. Instead, policymakers need to calculate in terms of total health, recognizing that different racial, ethnic, age, and gender groups may have different sensitivities to, or abilities to adjust to, low calcium intakes.
As already noted, the skeletal endpoint may not be the right functional indicator of calcium 'tional status in African-Americans, who are manifestly able to amass and maintain strong nes on low calcium intakes. In them, the hypertensive disorders would seem to provide a re relevant indicator, but current data do not allow very precise estimation of the intake ded to minimize the calcium deficiency component of these ,nonskeletal disorders. As noted lier, the rise in the calcium requirement for skeletal health in the elderly reflects mainly ecline in ability to adapt to a low intake. In that sense, ,the skeletal requirement in the -.u.erly may reflect the true requirement at all ages, i.e., the intakes for which no compensatory ;"ptive response is required.
McKane and associates showed substantial involution of the parathyroid glands in healthy elderly women given 60 mmol (2400 mg) calcium for 3 yr. This seemingly high intake did not mppress PTH to subnormal levels; instead, the usually high PTH levels of the elderly were educed to healthy young adult normal levels. The same study also showed restoration of :xme remodeling activity to young adult normal levels. PTH and bone remodeling rise with
ge, not because these components of the calcium economy fail to adapt, but because the external end organs of the controlloop-calcium absorption and renal calcium retentionbecome less and less responsive with age. Available data suggest that a calcium intake in the range of 37.5 mmol (1500 mg)/d to 60 mmol (2400 mg)/d may be optimal for all body systems. Lest such an intake be thought "heroic" or "pharmacologic," it is useful to recall that diets with such calcium contents exhibit a calcium nutrient density less than, or in the range of, those of our hominid ancestors, and substantially below those of diets we feed our laboratory animals, including chimpanzees and other primates.
