Infants
Infants constitute a population at risk for vitamin D deficiency because of relatively large vitamin D needs brought about by their high rate of skeletal growth. At birth, infants have acquired in utero the vitamin D stores that must carry them through the first months of life. A recent survey of French neonates revealed that 64 percent had 25-OH-D values below 30 nmol/l, the lower limit of the normal range. Breast-fed infants are particularly at risk because of the low concentrations of vitamin D in human milk. This problem is further compounded in some infants fed human milk by a restriction in exposure to ultraviolet (UV) light for seasonal, latitudinal, cultural, or social reasons.
Infants born in the autumn months at extremes of latitude are particularly at risk because they spend the first 6 months of their life indoors and therefore have little opportunity to synthesise vitamin D in their skin during this period. Consequently, although vitamin D deficiency is rare in developed countries, sporadic cases of rickets are still being reported in many northern cities but almost always in infants fed human milk.
Infant formulas are supplemented with vitamin D at levels ranging from 40 international units (IUs) or 1 μg /418.4 kJ to 100 IU or 2.5 μg /418.4 kJ, that provide approximately between 6 μg and 15 μg of vitamin D, respectively. These amounts of dietary vitamin D are sufficient to prevent rickets.
Adolescents
Another period of rapid growth of the skeleton occurs at puberty and increases the need not for the vitamin D itself, but for the active form 1,25-(OH)2D. This need results from the increased conversion of 25-OH-D to 1,25-(OH)2D in adolescents. Furthermore, unlike infants, adolescents are usually outdoors and therefore usually are exposed to UV light sufficient for synthesising vitamin D for their needs. Excess production of vitamin D in the summer and early fall months is stored mainly in the adipose tissue and is available to sustain high growth rates in the winter months that follow. Insufficient vitamin D stores during these periods of increased growth can lead to vitamin D insufficiency.
Elderly
Over the past 20 years, clinical research studies of the basic biochemical machinery handling vitamin D have suggested an age-related decline in many key steps of vitamin D action including rate of skin synthesis, rate of hydroxylation leading to activation to the hormonal form, and response of target tissues (e.g., bone) as well as reduced skin exposure.
Not surprisingly a number of independent studies from around the world have shown that there appears to be vitamin D deficiency in a subset of the elderly population, as characterised by low blood levels of 25-OH-D coupled with elevations of plasma PTH and alkaline bone mass and increases the incidence of hip fractures. Although some of these studies may exaggerate the extent of the problem by focusing on institutionalised individuals or in-patients with decreased sun exposures, in general they have forced health professionals to re-address the intakes of this segment of society and look at potential solutions to correct the problem. Several groups have found that modest increases in vitamin D intakes (between 10 and 20 μg/day) reduce the rate of bone loss and the fracture rate.
These findings have led agencies and researchers to suggest an increase in recommended vitamin D intakes for the elderly from the suggested 2.5–5 μg /day to a value that is able to maintain normal 25-OH-D levels in the elderly, such as 10–15 μg/day. This vitamin D intake results in lower rates of bone loss and is suggested for the middle-aged (50–70 years) and old-aged (>70 years) populations. The increased requirements are justified mainly on the grounds of the reduction in skin synthesis of vitamin D, a linear reduction occurring in both men and women, that begins with the thinning of the skin at age 20 years.
Pregnancy and lactation
Elucidation of the changes in calciotropic hormones occurring during pregnancy and lactation has revealed a role for vitamin D in the former but probably not the latter. Even in pregnancy, the changes in vitamin D metabolism which occur, namely an increase in the maternal plasma levels of 1,25-(OH)2D due to a putative placental synthesis of the hormone, do not seem to impinge greatly on the maternal vitamin D requirements. The concern that modest vitamin D supplementation might be deleterious to the foetus is not justified. Furthermore, because transfer of vitamin D from mother to foetus is important for establishing the newborn’s growth rate, the goal of ensuring adequate vitamin D status with conventional prenatal vitamin D supplements probably should not be discouraged.
In lactating women there appears to be no direct role for vitamin D because increased calcium needs are regulated by PTH-related peptide, and recent studies have failed to show any change in vitamin D metabolites during lactation. As stated above, the vitamin D content of human milk is low. Consequently, there is no great drain on maternal vitamin D reserves either to regulate calcium homeostasis or to supply the need of human milk. Because human milk is a poor source of vitamin D, rare cases of nutritional rickets are still found, but these are almost always in breast-fed babies deprived of sunlight exposure.
Furthermore, there is little evidence that increasing calcium or vitamin D supplements to lactating mothers results in an increased transfer of calcium or vitamin D in milk. Thus, the current thinking, based on a clearer understanding of the role of vitamin D in lactation, is that there is little purpose in recommending additional vitamin D for lactating women. The goal for mothers who breast-feed their infants seems to be merely to ensure good nutrition and sunshine exposure in order to ensure normal vitamin D status during the perinatal period.
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