© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Vitamin D ingestion and changes to rat aorta
Department of Laboratory Medicine and Pathobiology, Mount Sinai Hospital, 600 University Ave., and Department of Medicine, University of Toronto, Toronto, Ontario, Canada M5G 1X5
* Tel.: +1-416-586-5920; fax: +1-416-586-8628. rvieth{at}mtsinai.on.ca
Received 14 August 2002; accepted 26 August 2002
The recent paper by Norman et al. [1] raises alarming issues about the effect of ‘vitamin D’ in rats. Several points warrant comment or clarification from the authors.
The methods section specifies that 1,25(OH)2D was the form of ‘vitamin D’ added to the rat diets [1], and this was further supported by their reference to Mortensen et al. [2], a paper that had nothing to do with vitamin D nutrition, but instead dealt with analogs of 1,25(OH)2D. I point out that earlier rat studies, involving similar amounts of the true nutrient form of vitamin D3 (cholecalciferol) have never produced hypercalcemia [3–5]. Thus, it appears that Norman et al. [1] have confused the more potent, vitamin D-derived hormone, 1,25(OH)2D, with the true nutrient, cholecalciferol (i.e. vitamin D3).
I agree with the 25(OH)D levels reported by Norman et al. [1]. However, their results under the heading ‘animal nutrition’ show that there was more going on experimentally than simply variation in vitamin D supply. How else could one explain why a four-fold higher dietary vitamin D content was associated with only a two-fold increase in vitamin D consumption by the pregnant and lactating female rats? This translates to a 50% reduction in the amount of diet consumed by mother rats receiving the highest amount of vitamin D. Furthermore, the offspring rats fed the diet with the highest amount of vitamin D were significantly heavier than the control animals, an effect we have never seen in rats given similar, modest increases in vitamin D3 [4,5]. In any other situation, a dietary manipulation that cuts food consumption by half suggests a higher caloric density or some other difference.
Norman et al. [1] pointed out that the clinical implications of their findings are not clear, and that in man the reduction in elastic lamellae associated with vitamin D ingestion in their rats may actually be protective against supraventricular aortic stenosis. Nonetheless, they went on to express a one-sided, alarmist perspective when discussing the plausibility of their observations. They cited only relatively old literature [6,7] that contended ‘consumption of vitamin D in most Western countries has probably been excessive’. The ‘epidemic’ of infantile hypercalcemia in the 1940s that they refer to has never been confirmed as being due to food fortification with vitamin D [8]. The physiological range for 25(OH)D in humans extends to beyond 200 nmol/l (80 ng/ml), and high levels are associated with lower blood pressure [9,10] and prevention of a variety of diseases [11]. Far from vitamin D intakes being excessive, many studies have shown that adult intakes this nutrient are inadequate [12].
I agree that the work of Norman et al. [1] merits further research, but when it comes to vitamin D, readers must be aware of two points. Firstly, there is a big difference between nutrition and use of the hormone made from vitamin D, 1,25(OH)2D. Secondly, modern adults are not consuming physiologically meaningful amounts of vitamin D through foods or vitamin pills.
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- Norman P., Moss I., Sian M., Gosling M., Powell J. Maternal and postnatal vitamin D ingestion influences rat aortic structure, function and elastin content. Cardiovasc Res (2002) 55:369–374.
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[Abstract/Free Full Text] - Vieth R., Fraser D. Vitamin D insufficiency: no recommended dietary allowance exists for this nutrient. CMAJ (2002) 166:1541–1542.
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