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Free access

Moira Strand Hutchinson, Guri Grimnes, Ragnar Martin Joakimsen, Yngve Figenschau and Rolf Jorde

Objective

Ecologic and observational studies have suggested an association between serum 25-hydroxyvitamin D (25(OH)D) levels and cardiovascular disease (CVD) risk factors, CVD mortality, and cancer mortality. Based on this, low serum 25(OH)D levels should be associated with higher all-cause mortality in a general population. This hypothesis was tested in the present study.

Design

The Tromsø study is a longitudinal population-based multipurpose study initiated in 1974 with focus on lifestyle-related diseases. Our data are based on the fourth Tromsø study carried out in 1994–1995.

Methods

Information about death and cause of death was registered by obtaining information from the National Directory of Residents and the Death Cause Registry. Serum 25(OH)D was measured in 7161 participants in the fourth Tromsø study. Results are presented for smokers (n=2410) and non-smokers (n=4751) separately as our immunoassay seems to overestimate 25(OH)D levels for smokers.

Results

During a mean 11.7 years of follow-up, 1359 (19.0%) participants died. In multivariate regression models, there was a significantly increased risk of all-cause mortality (hazard ratio (HR) 1.32, confidence interval (CI) 1.07–1.62) among non-smoking participants in the lowest 25(OH)D quartile when compared with participants in the highest quartile. Equivalent results for smokers were not significant (HR 1.06, CI 0.83–1.35).

Conclusions

Low serum 25(OH)D levels were associated with increased all-cause mortality for non-smokers, but the results did not reach statistical significance for smokers. However, low 25(OH)D levels are known to be associated with impaired general health, and randomized controlled studies are needed to address the question of causality.

Open access

Stina T Sollid, Moira Y S Hutchinson, Vivian Berg, Ole M Fuskevåg, Yngve Figenschau, Per M Thorsby and Rolf Jorde

Objective

To determine the relationship between serum total 25-hydroxyvitamin D (25(OH)D), directly measured free 25(OH)D and calculated free 25(OH)D with regard to vitamin D-binding protein (DBP) phenotypes, sex, BMI, age and season, and their interrelationship to vitamin D supplementation.

Design, patients and interventions

A randomized controlled trial with 20 000 IU of vitamin D3 per week or placebo for 12 months was designed. A total of 472 subjects, 236 in each of the intervention groups, were included in the analyses.

Main outcome measures

Baseline serum concentrations and increases in serum total 25(OH)D, directly measured free 25(OH)D, calculated free 25(OH)D and DBP.

Results

Serum total 25(OH)D and DBP concentrations were significantly lower in subjects with the phenotype Gc2/Gc2 compared to phenotypes with the Gc1S allele, and lower in males compared to females. When using directly measured free 25(OH)D, the differences related to DBP phenotypes and sexes were clearly diminished. All calculated free 25(OH)D concentrations were overestimated compared to the directly measured free 25(OH)D. Serum parathyroid hormone showed an inverse correlation with all vitamin D parameters analyzed. The increases after 12 months of vitamin D supplementation were not significantly different for any of the vitamin D parameters regardless of DBP phenotype, sex or age. Supplementation with vitamin D did not affect serum DBP.

Conclusion

Direct measurements of free 25(OH)D reduce the differences seen in total 25(OH)D between DBP phenotype groups and sexes, probably caused by differences in DBP concentrations. With conditions affecting serum DBP concentrations, direct measurements of free 25(OH)D should be considered.

Free access

Guri Grimnes, Bjørg Almaas, Anne Elise Eggen, Nina Emaus, Yngve Figenschau, Laila Arnesdatter Hopstock, Moira Strand Hutchinson, Paal Methlie, Albena Mihailova, Monica Sneve, Peter Torjesen, Tom Wilsgaard and Rolf Jorde

Objective

Because we found higher serum 25-hydroxyvitamin D (25(OH)D) levels among smokers than among non-smokers with analyses using an electrochemiluminescence immunoassay (ECLIA) from Roche, the purpose of the present study was to examine whether this difference between smokers and non-smokers was maintained using other serum 25(OH)D assays.

Design

A cross-sectional population-based study on 6932 participants from the Tromsø study, 1994–1995, and one validation study comparing six different serum 25(OH)D assays in 53 non-smokers and 54 smokers were performed.

Methods

The association between smoking, season and serum 25(OH)D as measured by ECLIA (Roche) was assessed in the population-based study using general linear models with multivariate adjustments. In the validation study, serum levels of 25(OH)D were analysed with liquid chromatography coupled with mass spectrometry assay from two different laboratories, RIA (DiaSorin), HPLC, RIA (IDS) and ECLIA (Roche). T-tests and linear mixed model analyses were performed to compare the serum 25(OH)D levels in smokers and non-smokers within and between the methods.

Results

In the population-based study, the serum levels of 25(OH)D using the ECLIA method were 51.9, 53.2 and 72.0 nmol/l in never, former and current smokers (P<0.01). In the validation study, the serum concentration of 25(OH)D was 10.3 nmol/l higher in smokers than in non-smokers (P<0.01) using the ECLIA (Roche), while non-significantly lower serum levels of 25(OH)D were found in smokers using the other five methods.

Conclusions

These two studies indicate that the ECLIA (Roche) overestimates serum 25(OH)D levels in smokers by unknown mechanisms. If confirmed, this might have clinical consequences, and the issue needs further exploration.

Free access

Guri Grimnes, Bjørg Almaas, Anne Elise Eggen, Nina Emaus, Yngve Figenschau, Laila Arnesdatter Hopstock, Moira Strand Hutchinson, Paal Methlie, Albena Mihailova, Monica Sneve, Peter Torjesen, Tom Wilsgaard and Rolf Jorde

The authors and the journal apologise for errors in the Introduction section of this paper published in the European Journal of Endocrinology 2010 vol 163 pp 339–348. Lines 11–14 of the Introduction section should read as follows:

This reflects the amount of vitamin D ingested from food (ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3)) and the amount of vitamin D produced in the skin during ultraviolet B (UVB) exposure (vitamin D3)

and not as published.