Tuesday, May 23, 2017

FAO/WHO Conclusions

Below is the FAO/WHO conclusion...verbatim
Calcium is an essential nutrient that plays a vital role in neuromuscular function, many enzyme-mediated processes, blood clotting, and providing rigidity to the skeleton by virtue of its phosphate salts. Its non-structural roles require the strict maintenance of ionised calcium concentration in tissue fluids at the expense of the skeleton if necessary and it is therefore the skeleton which is at risk if the supply of calcium falls short of requirement.
Calcium requirements are essentially determined by the relationship between absorptive efficiency and excretory rate – excretion being through the bowel, kidneys, skin,hair, and nails. In adults, the rate of calcium absorption from the gastrointestinal tract needs to match the rate of all losses from the body if the skeleton is to be preserved; in children and adolescents, an extra input is needed to cover the requirements of skeletal growth.
Compared with that of other minerals, calcium economy is relatively inefficient. On most intakes, only about 25–30 percent of dietary calcium is effectively absorbed and obligatory calcium losses are relatively large. Absorbed calcium has to match these obligatory losses and the dietary intake has to be large enough to ensure this rate of absorption if skeletal damage is to be avoided. The system is subject to considerable inter-individual variation in both calcium absorption and excretion for reasons that are not fully understood but which include vitamin D status, sodium and protein intake, age, and menopausal status in women.
Although it needs to be emphasised that calcium deficiency and negative calcium balance must sooner or later lead to osteoporosis, this does not mean that all osteoporosis can be attributed to calcium deficiency. On the contrary, there may be more osteoporosis in the world from other causes. 
Nonetheless, it would probably be generally agreed that any form of osteoporosis must inevitably be aggravated by negative external calcium balance. Such negative balance – even for short periods – is prejudicial because it takes so much longer to rebuild bone than to destroy it. Bone that is lost, even during short periods of calcium deficiency, is only slowly replaced when adequate amounts of calcium become available.
In seeking to define advisable calcium intakes on the basis of physiologic studies and clinical observations, nutrition authorities have to rely largely on data from developed nations living at relatively high latitudes.
Although it is now possible to formulate recommendations that are appropriate to different stages in the life cycle of the populations of these nations, extrapolation from these figures to other cultures and nutritional environments can only be tentative and must rely on what is known of nutritional and environmental effects on calcium absorption and excretion. Nonetheless, we have made an attempt in this direction, knowing that our speculative calculations may be incorrect because of other variables not yet identified.
Bucher, H.C., Guyatt, G.H. & Cook, R.J. 1996. Effect of calcium supplementation on pregnancy-induced hypertension and preeclampsia. JAMA, 275:1113-17.

Garland, C.F., Garland, F.C. & Gorham, E.D. 1991. Can colon cancer incidence and death rates be reduced with calcium and vitamin D? Am. J. Clin. Nutr., 54(Suppl):193s- 201s.

McCarron, D.A. 1997. Role of adequate dietary calcium intake in the prevention and management of salt-sensitive hypertension. Am. J. Clin. Nutr., 65(Suppl): 712s-716s. 
No reference has been made in this account to the possible beneficial effects of calcium in the prevention or treatment of pre-eclampsia, colon cancer, or hypertension  and no attempt has been made to use these conditions as endpoints on which to base calcium intakes.
Joffe, G.M., Esterlitz, J.R., Levine, R.J., Clemens, J.D., Ewell, M.G., Siba, I.B.M. & Catalano, P.M. 1998. The relationship between abnormal glucose tolerance and hypertensive disorders of pregnancy in healthy nulliparous women. Calcium for Preeclampsia Prevention (CPEP) Study Group. Am. J. Obstet. Gynecol, 179:1032-1037.

Martinez, M.E. & Willett, W.C. 1998. Calcium, vitamin D, and colorectal cancer: a review of the epidemiologic evidence. Cancer Epidemiol. Biomarkers Prev., 7: 163-168.

Resnick, L.M. 1999. The role of dietary calcium in hypertension: a hierarchical overview. Am. J. Hypertens., 12: 99-112.

DerSimonian, R. & Levine, R.J. 1999. Resolving discrepancies between a metaanalysis and a subsequent large controlled trial. JAMA, 282: 664-670.

Mobarhan, S. 1999. Calcium and the colon: recent findings. Nutr. Revs., 57: 124-126.

McCarron, D.A. & Reusser, M.E. Finding consensus in the dietary calcium-blood pressure debate. J. Am. Coll. Nutr., 18(Suppl): 398S-405S.
In each of the above conditions, epidemiologic data suggested an association with calcium intake, and experimentation with increased calcium intakes has now been tried. In each case the results have been disappointing, inconclusive, or negative and have stirred controversy.
Because there is no clear consensus about optimal calcium intake for prevention or treatment of these conditions and also no clear mechanistic ideas on how dietary calcium intakes affect them, it is not possible to allow for the effect of health outcomes in these areas on our calcium recommendations.
However,although the anecdotal information and positive effects of calcium observed in these three conditions cannot influence our recommendations, they do suggest that generous calcium allowances may confer other benefits besides protecting the skeleton. Similarly, no reference has been made to the effects of physical activity, alcohol, smoking, or other known risk factors on bone status because the effects of these variables on calcium requirement are beyond the realm of simple calculation.

No comments:

Post a Comment