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1,25-dihydroxyvitamin D linked to poorer bone health in men
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Study researchers from the European Male Aging Study group recently reported that serum 1,25-dihydroxyvitamin D is associated with a higher bone turnover and poorer bone health in middle-aged and older European men.
Men aged 40 to 79 years (n=2,783) from population registries at eight European centers completed questionnaires regarding lifestyle and measurements of quantitative ultrasound (QUS) of the heel, in addition to assessments for height and weight.
Further measurements included: 1,25-(OH)2D, 25-(OH)D, parathyroid hormone (PTH), bone markers serum N-terminal propeptide of type 1 procollagen (P1NP) and cross links (beta-cTX). In two of the centers, DXA of the hip and lumbar spine was conducted.
After adjustments for age and center, data indicate that 1,25-(OH)2D was positively associated with 25-(OH)D but not with PTH. Conversely, 25-(OH)D was negatively associated with PTH. After further adjustments, researchers wrote that 1,25-(OH)2D was negatively associated with QUS and DXA parameters, but positively with beta-cTX. However, 1,25-(OH)2D was not correlated with P1NP.
Moreover, 25-(OH)D was positively associated with the QUS and DXA parameters but not related to either bone turnover marker, the researchers wrote. Patients with high 1,25-(OH)2D (upper tertile) and low 25-(OH)D (lower tertile) had the lowest QUS and DXA parameters and the highest beta-cTX levels, according to data.
“These results contribute to the understanding of the influence of 1,25-(OH)2D on bone health in middle-aged and elderly men,” the researchers wrote.
Disclosure: The researchers report no relevant financial disclosures.
Perspective
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Clifford Rosen, MD
I'm not very impressed by this study. Everything they say is true, but it doesn't tell us anything. However, they are correct when they conclude that patients with the highest 1,25-dihydroxyvitamin D (1,25[OH]D) and the lowest 25-hydroxyvitamin D (25[OH]D) had the lowest bone density and the highest bone turnover marker, because those are usually the patients who have low calcium intake or a low vitamin D intake. Therefore, they have secondary hypoparathyroidism; this is what we would predict. The parathyroid hormone (PTH) level increase stimulates 1-alpha-hydroxylase. Now, the patients have higher 1,25(OH)D levels and they're trying to promote increased calcium absorption in response to poor calcium intake; therefore they raise their PTH and that can cause bone loss. I don't think this is very surprisin, and I didn't find it very illustrative.
One thing that we're beginning to understand is that 25(OH)D and 1,25(OH)D are associated with each other. For example, if you give enough vitamin D you can increase 25(OH)D and you can also increase 1,25(OH)D, which has some implications when you're giving high dose vitamin D.
If you're replacing it with very high doses of vitamin D, your 25(OH)D goes up and that can lead to an increase in 1,25(OH)D. We know that in the patients who took high dose vitamin D in a previous study (Sanders, 2010); they had some increased risks for fractures when they were administered 500,000 units. There was a pulse effect. It was converted to 25(OH)D and also gets converted to 1,25(OH)D.
As they showed in this study, that conversion can lead to bone resorption and bone loss. I think the implications are more provocative in terms of understanding that if you give enough substrate, you can get active vitamin D produced in the kidney which may be detrimental in the long run.
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