ORCID Profile
0000-0002-2125-8081
Current Organisations
UiT The Arctic University of Norway
,
University Hospital of North Norway
,
Universitetssykehuset Nord-Norge
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Publisher: Springer Science and Business Media LLC
Date: 03-12-2009
DOI: 10.1007/S00198-009-1131-7
Abstract: In this longitudinal study of 5,286 persons, men with anemia had a 2.15 higher risk of non-vertebral fractures than men with high hemoglobin levels. Women with anemia had no increased fracture risk. Low hemoglobin levels are associated with several risk factors for fractures such as low physical function, impaired cognition, and low bone mass. The aim of this population-based, prospective study was to examine whether anemia predicts non-vertebral fractures. A total of 5,286 inhabitants from the municipality of Tromsø, Norway (2,511 men and 2,775 women), 55-74 years old at baseline, were followed for mean 8.3 years. Measurements of hemoglobin, mean corpuscular volume, height, weight, blood pressure, blood lipids, serum creatinine, and bone mineral density and questionnaire information concerning smoking and drinking habits, physical activity, prevalent diseases, and use of medication was collected before start of follow-up. Non-vertebral fractures were registered during follow-up. A total of 235 men and 641 women sustained a new non-vertebral fracture. One SD lower value of hemoglobin was associated with a 1.27 higher risk of fracture in men (p < 0.001, after multiple adjustments) and 1.08 (p = 0.07) in women. Men with anemia (hemoglobin levels <13 g/dL) had a 2.15 higher risk of non-vertebral fractures than men with high levels (15.2-18.8, g/dL) whereas women with anemia (hemoglobin levels <12 g/dL) had no increased fracture risk. Anemia is associated with non-vertebral fractures in men but not in women.
Publisher: MDPI AG
Date: 02-01-2019
DOI: 10.3390/NU11010074
Abstract: The aim of this study was to determine if increased mortality associated with low levels of serum 25-hydroxyvitamin D (25(OH)D) reflects a causal relationship by using a Mendelian randomisation (MR) approach with genetic variants in the vitamin D synthesis pathway. In idual participant data from three European cohorts were harmonized with standardization of 25(OH)D according to the Vitamin D Standardization Program. Most relevant single nucleotide polymorphisms of the genes CYP2R1 (rs12794714, rs10741657) and DHCR7/NADSYN1 (rs12785878, rs11234027), were combined in two allelic scores. Cox proportional hazards regression models were used with the ratio estimator and the delta method for calculating the hazards ratio (HR) and standard error of genetically determined 25(OH)D effect on all-cause mortality. We included 10,501 participants (50.1% females, 67.1±10.1 years) of whom 4003 died during a median follow-up of 10.4 years. The observed adjusted HR for all-cause mortality per decrease in 25(OH)D by 20 nmol/L was 1.20 (95% CI: 1.15–1.25). The HR per 20 nmol/L decrease in genetically determined 25(OH)D was 1.32 (95% CI: 0.80–2.24) and 1.35 (95% CI of 0.81 to 2.37) based on the two scores. In conclusion, the results of this MR study in a combined s le from three European cohort studies provide further support for a causal relationship between vitamin D deficiency and increased all-cause mortality. However, as the current study, even with ~10,000 participants, was underpowered for the study of the effect of the allele score on mortality, larger studies on genetics and mortality are needed to improve the precision.
Publisher: Wiley
Date: 18-09-2013
DOI: 10.1002/JBMR.1952
Abstract: The risk of subsequent fracture is increased after initial fractures however, proper understanding of its magnitude is lacking. This population-based study examines the subsequent fracture risk in women and men by age and type of initial incident fracture. All incident nonvertebral fractures between 1994 and 2009 were registered in 27,158 participants in the Tromsø Study, Norway. The analysis included 3108 subjects with an initial incident fracture after the age of 49 years. Subsequent fracture (n = 664) risk was expressed as rate ratios (RR) and absolute proportions irrespective of death. The rates of both initial and subsequent fractures increased with age, the latter with the steepest curve. Compared with initial incident fracture rate of 30.8 per 1000 in women and 12.9 per 1000 in men, the overall age-adjusted RR of subsequent fracture was 1.3 (95% CI, 1.2-1.5) in women, and 2.0 (95% CI, 1.6-2.4) in men. Although the RRs decreased with age, the absolute proportions of those with initial fracture who suffered a subsequent fracture increased with age from 9% to 30% in women and from 10% to 26% in men, between the age groups 50-59 to 80+ years. The type of subsequent fracture varied by age from mostly minor fractures in the youngest to hip or other major fractures in the oldest age groups, irrespective of type and severity of initial fracture. In women and men, 45% and 38% of the subsequent hip or other major fractures, respectively, were preceded by initial minor fractures. The risk of subsequent fracture is high in all age groups. At older age, severe subsequent fracture types follow both clinically severe and minor initial incident fractures. Any fragility fracture in the elderly reflects the need for specific osteoporosis management to reduce further fracture risk.
Publisher: Public Library of Science (PLoS)
Date: 25-09-2014
Publisher: Mary Ann Liebert Inc
Date: 02-2014
Abstract: High serum thyrotropin (TSH) levels predict cardiovascular disease (CVD). Recently several single nucleotide polymorphisms (SNPs) associated with TSH levels have been identified, one of them being the rs4704397 SNP in the phosphodiesterase 8B (PDE8B) gene. If the relation between thyroid function and CVD is causal, one could also expect rs4704397 genotypes to predict CVD and possibly health in general. DNA was prepared and genotyping performed for rs4704397 in subjects who participated in the fourth survey of the Tromsø Study in 1994-1995 and who were registered with the endpoints myocardial infarction (MI), type 2 diabetes (T2DM), cancer, or death, as well as a randomly selected control group. Similarly, genotyping was performed in subjects who had participated in clinical trials where serum TSH, free T4 (fT4), and free T3 (fT3) were measured. From the Tromsø Study, 8938 subjects without thyroid disease or thyroid medication were successfully genotyped for rs4704397. Among these, 2098 were registered with MI, 1025 with T2DM, 2748 with cancer, and 3592 had died. The minor homozygote genotype (A:A) had a median serum TSH level that was 0.29 mIU/L higher than in the major homozygote genotype (G:G). The A:A genotype had a significantly increased risk of MI as compared to the G:G genotype (1.14 [1.00-1.29], hazard ratio [confidence interval], Cox regression with adjustment for age, sex, and body mass index). No significant associations were seen with the other endpoints or CVD risk factors. Furthermore, subjects with the G:G genotype were significantly taller than subjects with the A:A genotype (mean difference 1.5 cm). In 584 subjects with serum TSH, fT4, and fT3 measurements, the subjects with the A:A genotype had significantly higher serum TSH and nonsignificantly lower serum fT3 (mean difference 0.15 pmol/L) levels than subjects with the G:G genotype. rs4704397 is associated with thyroid function, risk of MI, and body height. However, confirmation in other cohorts is needed before firm conclusions can be drawn.
Publisher: Public Library of Science (PLoS)
Date: 16-02-2017
Publisher: Springer Science and Business Media LLC
Date: 16-04-2015
Publisher: Oxford University Press (OUP)
Date: 07-2007
DOI: 10.1530/EJE-07-0032
Abstract: Objectives : As bone fragility is partly the result of sex hormone deficiency, we sought to determine whether circulating sex steroids or sex hormone-binding globulin (SHBG) predicts non-vertebral fractures. Methods : Forearm bone mineral density (BMD), total estradiol and testosterone, calculated free levels, and SHBG were measured in 1386 postmenopausal women and 1364 men aged 50–84 years at baseline in the Tromsø Study (1994–1995). Non-vertebral fractures were documented between 1994 and 2005. Results : During 8.4 years (range 0.01–10.4) of follow-up, 281 women and 105 men suffered non-vertebral fractures. For both sexes, fracture cases had lower BMD and higher SHBG, but sex steroids were not lower. Each standard deviation ( s.d .) increase in SHBG increased non-vertebral fracture risk in women (hazards ratio (HR) 1.17 95% confidence interval (CI) 1.03–1.33) and men (HR 1.26 95% CI 1.03–1.54). After further adjustment for BMD, the risk was not statistically significant in women (HR 1.09 95% CI 0.95–1.24) or men (HR 1.22 95% CI 0.99–1.49). Each s.d . decrease in BMD increased fracture risk in women (HR 1.36 95% CI 1.19–1.56) and men (HR 1.41 95% CI 1.15–1.73). Fracture rates were highest in participants with SHBG in the highest tertile and BMD in the lowest tertile and were 37.9 and 17.0 per 1000 person-years in women and men respectively. However, in both sexes the combination of BMD and SHBG was no better predictor of fracture risk than BMD alone. Sex steroids were not associated with fracture risk. Conclusions : Measurements of sex steroids or SHBG are unlikely to assist in decision making regarding fracture risk susceptibility.
Publisher: Springer Science and Business Media LLC
Date: 06-07-2007
DOI: 10.1007/S00223-007-9035-Z
Abstract: Bone loss during advancing age in women and men is partly the result of sex steroid deficiency. As the contribution of circulating sex steroids and sex hormone-binding globulin (SHBG) to bone loss remains uncertain, we sought to determine whether levels of sex steroids or SHBG predict change in bone mineral density (BMD) in women and men. A population-based study in the city of Tromsø of 6.5 years' duration (range 5.4-7.4) included 927 postmenopausal women aged 37-80 years and 894 men aged 25-80 years. Total estradiol and testosterone, calculated free levels, and SHBG were measured at baseline, and BMD change at the distal forearm was determined using BMD measurements in 1994-1995 and 2001. Bone loss was detected in postmenopausal women and men. Free estradiol and SHBG predicted age-adjusted bone loss in postmenopausal women, but only free estradiol was associated after further adjustment for body mass index and smoking in mixed models (P < 0.05). After same adjustment, only SHBG persisted as a significant independent predictor of bone loss in men (P < 0.001). However, only 1% of the variance in bone loss was accounted for by these measurements. We therefore conclude that the relations between sex steroids and bone loss are weak and measurements of sex steroids are unlikely to assist in clinical decision making.
Publisher: Public Library of Science (PLoS)
Date: 23-12-2015
Publisher: Public Library of Science (PLoS)
Date: 23-05-2012
Publisher: Public Library of Science (PLoS)
Date: 18-05-2015
Location: Norway
No related grants have been discovered for Ragnar Martin Joakimsen.