© 2003 by European Society of Cardiology
Copyright © 2003, European Society of Cardiology
Maternal and postnatal vitamin D ingestion influences rat aortic structure, function and elastin content
[Cardiovasc. Res. 2002;55:369–374]
Royal London Hospital, Department of Diabetes and Metabolic Medicine, 5th floor, Alex Wing, London E1 1BB, UK
* Tel.: +44-1243-811-230; fax: +44-1243-811-924
Received 16 October 2002; accepted 21 October 2002
The above mentioned paper [1] makes a valuable contribution to explaining the adverse effects that excessive exposure to dietary vitamin D are known to have on the developing vasculature of rodents, rabbits and probably also in man [2,3]. The authors suggest that the dosages used were not excessive, mean circulating levels of 25-OH vitamin D not rising above 103 mmol/l in any group and the mean levels in sows being 30 ng/ml. If the use of different units for these levels is not in error then the sows had mean levels of about 75 nmol/l, somewhere in the middle of levels reported from the three groups of offspring, rather levels matching those fed control chow. The daily intake of vitamin D reported per kilo body weight was, however, much higher than is usual in man. Firstly, in the Methods section, 2.1, animal model, 1. "Control group chow", the authors state that normal chow contained "vitamin D (1,25 dihydroxycalciferol) 3000 IU/kg". Since it is not usual to add activated vitamin D to chow nor is the dosage of calciferol usually reported in IU one assumes that it was in fact chole-or ergo-calciferol that was added (as stated for the supplemented chow preparations). Even then, since the authors calculate that the intake of vitamin D averaged "no more than 1000 IU/kg even in the high dose group" (i.e. per kg body weight as judged from the text; 3.1 Animal nutrition), this represents an intake of 1 IU per gram body weight and is equivalent to an intake of 70,000 IU/day in a 70 kg man for the high dose group and of 35,000 IU/day and 17,500 IU/day for the low dose and control chow groups respectively. Whilst rodents appear to tolerate such doses they would all, if correct, be unduly high doses in man in comparison to current recommended daily intakes for young adults (100 IU/day in the UK, rising to 200–400 IU/day in pregnancy and to 600–800 IU/day in older people) [4].
Whilst there was an epidemic of infantile hypercalcaemia in babies in the 1960s due to the use of different foodstuffs containing vitamin D at the same time (e.g. cod-liver oil and supplemented milk powders) in which abnormal large vessel calcification was reported [2], we now find that vitamin D deficiency has been recognised to be an increasing problem in the western world in many population groups including pregnant women. This deficiency appears to increase the risk and severity of many auto-immune and chronic inflammatory disorders (e.g. Type 1 diabetes, tuberculosis, leprosy, rheumatoid arthritis), to increase the risk of several types of cancer and to increase the risk of acute events in ischaemic heart disease, probably through the inflammatory components of the disease [5–8]. It is, therefore, important that people should not be put off recommended levels of daily intake of this vitamin and that optimal intakes should be determined for those whose exposure to UV light is restricted for whatever reason. It would, therefore, be helpful if these findings could be tested, using non-invasive methods for measuring arterial compliance, in children born to mothers whose vitamin D consumption in pregnancy has been documented. Collaborative work might be considered where reduced risks of Type 1 diabetes have been shown in children supplemented with vitamin D in infancy (at up to 2000 IU/day (which would be an unusually high dosage in the UK)) or born to mothers who had taken supplemental cod-liver oil, but not multivitamins, when pregnant [9,10].
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