N05018: The importance of meat consumption in regulating vitamin D metabolism and preventing metabolic bone disease
Wednesday 6 August 2003
This research project aims to assess whether the consumption of meat provides protection against certain bone diseases and investigate vitamin D status and bone health in humans of different ethnic backgrounds.
Background
Vitamin D deficiency, whether at the clinical level (true deficiency, associated with osteomalacia and rickets) or sub-clinical level (vitamin D insufficiency, associated with osteoporosis), is a major challenge to bone health especially in the elderly and some Asian immigrants. Vitamin D is unique in that a dietary source is only essential if the physiological supply, via synthesis in the skin after ultraviolet radiation (UVR) or sunlight exposure, is not met. Declining levels of calcium and poor vitamin D status in the diets of the elderly may lead to secondary hyperparathyroidism (i.e. raised serum levels of parathyroid hormone, PTH) and it is now recognised that this is detrimental to cortical bone, which accounts for 80% of the bony skeleton, and leads to an increase in fractures, especially of long bones. Epidemiological evidence, principally obtained from the British Asian community in Glasgow by Dunnigan's group, has shown that consumption of meat and meat products provides substantial protection against privational rickets and osteomalacia. The omnivore British diet appears to provide complete protection against privational rickets at low levels of UVR. It seems likely that this state of affairs is due to the relatively high intakes of meat and meat products that characterise this diet. However, the effects of eating meat on protection against vitamin D insufficiency are less well established. The principle aims of this project were:
- to assess vitamin D status and bone health according to the ethnicity of subjects
- to test the epidemiological evidence that the consumption of meat and meat products provides substantial protection against privational rickets and osteomalacia
- to examine whether or not diet affects the rate of metabolism of a given dose of vitamin D
The results of the study are used to explain how the omnivore diet is protective to the skeleton and will provide advice on nutrition for healthy bones.
Research Approach
Experimental evidence was gathered first by establishing the baseline measures of bone health, including bone mineral density (BMD) and serum biochemistry. The meat content of the diets was assessed by dietary surveys. The effect of diet on vitamin D metabolism was then studied in two ways. Firstly, single large oral doses of vitamin D2 were given to Asian and white women between the ages of 20 and 65 years, from Manchester and Glasgow. The major circulating hepatic metabolite, 25-hydroxyvitamin D2, (25OHD2), and the biologically active renal metabolite 1,25-dihydroxyvitamin D2 (1,25D2) were assayed in serum. Measurement of BMD permitted an assessment of any link between meat intake and risk factors for osteoporosis. Secondly, the plateau level of serum 25OHD2 was studied in white women taking 400iu vitamin D2 per day (the recommended daily allowance (RDA)).
Extended information was provided through a link with the Cambridge EPOS/EPIC study, and enabled us to produce data on vitamin D status, diet and bone health in over 600 “young elderly” (66-79 y) women.
Results and findings
Key findings
1. Asian women had lower vitamin D status and lower bone mineral density than Caucasian women, irrespective of diet.
This observation needs further investigation. The question of why 'westernized' Asian women, who had similar sunlight exposure to their white counterparts, still had a low vitamin D status remains unanswered.
2. Bone mineral density was lower in vegetarian women, both in Caucasians and Asians, than in those who consumed some meat in their diet.
3. The absence of meat in the diet was the only dietary factor related to the lower bone mineral density of vegetarians. There was no apparent relationship between the quantity of meat eaten and the bone mineral density or vitamin D status.
4. 'Young elderly' omnivorous women living in a rural environment had, in general, good indices of bone health, especially vitamin D nutritional status, although BMD was significantly and negatively related to age.
We conclude that meat consumption does have a protective effect on bone mineral density and vitamin D status.
5. Supplementation of Asian or white women with a single large oral dose of 50,000 international units of vitamin D2 did not reveal any quantitative differences in the metabolism of vitamin D related to diet or ethnicity (as determined by serum 25OHD concentration and measurement of area under the dose response curve). Similarly, there was no difference in the plateau level reached in the white vegetarian and omnivore women taking 400 international units per day for four weeks.
We conclude that meat is not having a significant effect on vitamin D turnover. The mechanism by which meat is having its protective effect needs further investigation.
6. Contrary to the presumed effect of current recommendations for vitamin D intake, a daily oral dose of 400 international units of vitamin D2 for one month did not raise the concentration of 25OHD in serum to values that indicated adequate vitamin D status (>15 nanograms per millilitre).
These results should be considered by COMA that recommends a daily intake of 400 international units for people not exposed to sunlight.
7. From the 25OHD levels in serum and from the changes in those levels in response to dosing with 400 international units it is hypothesised that meat contributes a bio-equivalent effect of 100–170 international units (2.5–4.25 micrograms) of vitamin D to the diet of meat-eating women in the study. This exceeds the current estimates of the bio-effective vitamin D content of meat.
Current estimates depend mainly on assuming a five times greater potency for 25OHD compared with vitamin D. This assumption, based on a rat intestinal calcium absorption model may need to be revised if the current analysis is confirmed. Further investigation is needed to confirm the validity of this hypothesis.
Contact: Dr Alison Tedstone
Tel: 020 7276 8929
Email: alison.tedstone@foodstandards.gsi.gov.uk
