Page 130 - Vitamin D and Cancer

6 Vitamin D: Cardiovascular Function and Disease 117

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1951 1956 1961 1966 1971 1976 1981 1986 1991 1996 2001 2006
Fig. 6.1 Number of PubMed publications by year (1950–2008): search terms “Vitamin D” and
“Cardiovascular Disease”

hypercalcemia cases in 1959 remained at the same level as before the reduction in
vitamin D and did not decrease until 1960–1961 [1]. Thus, a report by the American
Academy of Pediatrics in 1967 concluded that the hypothesis that vitamin D caused
infantile hypercalcemia was unproven [1].
Despite this official report, many researchers still held the opinion that vitamin D
was a cause of infantile hypercalcemia, and went further by linking the condition
to a rare congenital abnormality in infants characterized by supravalvular aortic
stenosis, an elfin facies, and severe mental retardation [2–5]. The basis for linking
the two conditions was the similarity in the vascular lesions between those observed
in supravalvular aortic stenosis and those produced by vitamin D intoxication [6].
Evidence thought confirmatory at the time came from animal studies in which
pregnant rabbits were given intramuscular vitamin D doses of up to 4.5 million IU/
day, and their offspring 250 IU/day, with the latter at autopsy found to have medial
degeneration, calcification, and necrosis of the aorta that was similar to the pathol-
ogy of the congenital anomaly in children [2, 7]; while high doses of vitamin D (up
to 770 IU/g over 10 days) were found to cause both aortic and cardiac lesions in
young rabbits [8]. In contrast, several case reports of infants with arterial calcifica-
tion concluded it was not caused by vitamin D [9–12], and that high doses of vita-
min D taken during pregnancy did not result in infantile hypercalcemia or arterial
lesions such as aortic stenosis [13, 14].
However, the prevailing opinion remained that vitamin D was a risk factor for
vascular damage and CV disease [3, 15, 16]. This was supported by the development