 Can Vitamins Save Over $20 Billion in Hospital Costs?
Substantial evidence indicates that intakes greater than the recommended dietary allowances (RDAs) for various vitamins may be necessary to provide protection against disease. Also, in reducing the risk of disease, vitamin supplements may significantly decrease the utilization of healthcare services and associated expenditures. According to the American Institute for Cancer Research, approximately 1/3 of all cancer deaths are caused by an inappropriate diet.
There is substantial evidence that high intake of carotenoids and vitamin C may decrease the risk of various cancers. Evidence for the role of folate and vitamin E deficiency and cancer is less substantial, although vitamin E may possibly decrease the risk of lung and cervical cancers.
A deficiency in vitamin D is associated with increased parathyroid hormone secretion, increased bone turnover, osteoporosis and mild osteomalacia and an increased risk of hip and other fractures. Although vitamin D deficiency is often detected in the general population, its prevalence has only recently been studied in a hospitalized population. In 290 consecutive patients admitted to a general medical ward, 164 (57%) were found to have vitamin D deficiency; 25 (8.6%) had severe hypovitaminosis and 99 (34.1%) had moderate hypovitaminosis.
Watson determined that low 1,25-vitamin D levels were inversely related with the extent of atherosclerotic calcification in 173 patients with moderate and high risk for coronary heart disease (CHD), indicating that vascular calcification may be a systemic derangement of calcium metabolism.
It has been confirmed in a number of studies that elevated homocysteine concentrations are associated with increased risk of CHD. Folic acid, vitamin B6, and B12 are cofactors in the metabolism of homocysteine and are all effective in reducing homocysteine levels.
Following methionine loading (a precursor of homocysteine), B6 supplementation resulted in a 22.1% reduction of homocysteine levels and folic acid/B12 resulted in a 26.2% decrease.
Rimm et al found a significant inverse relationship between dietary intakes of folate and B6 with morbidity and mortality from CHD.
Mildly elevated homocysteine concentrations were reduced by 30% in subjects who received folate/B6/B12 supplementation, by 32% in those who received B vitamins plus antioxidants (C, alpha-tocopherol, and beta-carotene), and a non-significant increase of 5.1% was noted in patients receiving only antioxidants.
In a recent study, subjects with CHD were given breakfast cereals containing three different amounts of folic acid, in addition to B6 and B12. Plasma folate increased and plasma homocysteine decreased in relation to the folic acid content of the cereal.
A recent report by the Institute of Medicine stated that all adults, not just women of childbearing age, should consume 400mcg folate per day. In addition, although Americans and Canadians consume adequate amounts of vitamin B12, 10-30% of older adults have lost the ability to absorb adequate amounts of this vitamin; therefore, it is recommended that individuals over 50 take vitamin supplements or utilize fortified foods.
Bendich et al developed a method for translating published risk reduction estimates based on vitamin intake into estimates of potential savings due to avoidable U.S. hospitalizations. It was determined that annual hospital charges for birth defects, low-birth-weight premature births, and CHD could be reduced by 40%, 60%, and 38%, respectively, if there were daily use of folic acid and zinc- containing multiple vitamins by all women of childbearing age and daily vitamin E supplementation by both men and women over 50. Projected savings in hospital charges were calculated to be nearly $20 billion.
If clinical trials confirm data suggesting these and other conditions can be ameliorated with other vitamins or mineral supplementation, healthcare savings could be significantly greater.
American Institute for Cancer Research, 1997
Thomas MK. N Engl J Med 1998;338:777-83
Watson KE. Circulation 1997;96:1755-60
Welch GN. N Engl J Med 1998;338:1042-50 Bostom AG. Ann Intern Med 1997;127:1089-92 Rimm EB. JAMA 1998;279:359-64
Woodside JV. Am J Clin Nutr 1998;67:858-66
Malinow MR. N Engl J Med 1998;338:1009-1015 Institute of Medicine. http://www2.nas.edu/iom
|
