Not all vitamin D = dietary vitamin D

[Guest guest]

hi All, Not all vitamin D = dietary vitamin D. See the attached.

Cheers, Al.

Alan Pater, Ph.D.; Faculty of Medicine; Memorial University; St. 's, NL

A1B 3V6 Canada; Tel. No.: (709) 777-6488; Fax No.: (709) 777-7010; email:

apater@...

Cardiovascular Research

Volume 56, Issue 2, November 2002, Pages 323-324

Vitamin D ingestion and changes to rat aorta

Reinhold Vieth

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, 4 and 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 and 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 and 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 and 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.

References

1. P. Norman, I. Moss, M. Sian, M. Gosling and J. , Maternal and

postnatal vitamin D ingestion influences rat aortic structure, function and

elastin content. Cardiovasc Res 55 (2002), pp. 369–374.

2. J.T. Mortensen, P. Brinck and L. Binderup , Toxicity of vitamin D

analogues in rats fed diets with standard or low calcium contents.

Pharmacol Toxicol 72 (1993), pp. 124–127.

3. R.M. Shepard and H.F. DeLuca , Plasma concentrations of vitamin D3 and

its metabolites in the rat as influenced by vitamin D3 or 25-hydroxyvitamin

D3 intakes. Arch Biochem Biophys 202 (1980), pp. 43–53.

4. R. Vieth and S. Milojevic , Moderate vitamin D3 supplementation lowers

serum 1,25-dihydroxy-vitamin D3 in rats. Nutr Res 15 5 (1995), pp. 725–731.

5. R. Vieth, S. Milojevic and V. Peltekova , Improved cholecalciferol

nutrition in rats is noncalcemic, suppresses parathyroid hormone and

increases responsiveness to 1,25-dihydroxycholecalciferol. J Nutr 130

(2000), pp. 578–584.

6. J. Moon, B. Bandy and A.J. on , Hypothesis: etiology of

atherosclerosis and osteoporosis: are imbalances in the calciferol

endocrine system implicated?. J Am Coll Nutr 11 (1992), pp. 567–583.

7. R.P. Holmes and F.A. Kummerow , The relationship of adequate and

excessive intake of vitamin D to health and disease. J Am Coll Nutr 2

(1983), pp. 173–199.

8. D. Fraser , The relation between infantile hypercalcemia and vitamin D:

public health implications in North America. Pediatrics 40 (1967), pp.

1050–1061.

9. S.G. Rostand , Ultraviolet light may contribute to geographic and racial

blood pressure differences. Hypertension 30 (1997), pp. 150–156.

10. R. Krause, M. Buhring, W. Hopfenmuller, M.F. Holick and A.M. Sharma ,

Ultraviolet B and blood pressure. Lancet 352 (1998), pp. 709–710.

11. R. Vieth , Vitamin D supplementation, 25-hydroxyvitamin D

concentrations, and safety. Am J Clin Nutr 69 (1999), pp. 842–856.

12. R. Vieth and D. Fraser , Vitamin D insufficiency: no recommended

dietary allowance exists for this nutrient. CMAJ 166 (2002), pp. 1541–1542.