In recent years, studies involving animal models, case reports, and some epidemiological studies have
indicated that an accumulation of vitamin A in the liver is linked to low bone mineral content, fracture risk, and hence
osteoporosis. While vitamin A in its physiological level acts as an inducer of bone matrix protein (osteocalcin) and matrix
GLA protein in the osteoblast cells (bone formation), excess reinoic acid (a metabolic product of vitamin A) supresses
osteoblastic activity and stimulates osteoclast formation (bone degradation). There also appear to have an antagonistic
or synergistic interactions between vitamins A and D, influencing bone metabolosm; such effects are dose related. These
effects could be of concern, especially for the older persons, because of the age-associated cumulation of vitamin A in the
liver. The vitamin A status in elderly population, however, has not been as well documented as in an earlier age. In effect,
the Food and Nutrition Board of National Academy's Institute of Medicine has not made any differenciation in it's
recommendation for the Dietary Reference Intake (DRI) of vitamin A between 14 years and >70 years old individuals.
This report will delineate the ageing differences in metabolic availability of vitamin A and that such differences are
independent of its intake. The report will also attempt to formulate a hypothesis that in old age, deficiency of vitamin A is
not a concern but its potential toxicity involving bone.