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Background: In Norway, 6000 patients were operated on due to hip fracture in 2016. Hip fracture results in increased suffering and often in a dramatic change in an older person's life. The experience of suffering in patients with hip fracture, or nursing staff's perception of it in the preoperative period, is sparsely studied. The perspective of the study was based on caring sciences., Aim: The aim of this study was to gain a deeper understanding of subjective experiences of suffering among elderly hip-fracture patients during the preoperative period, seen from the patients' and nurses' perspective., Methodological Approach: A Q-methodological approach was used. Forty statements (Q-sample), based on interviews and theory, were ranked in a forced-choice distribution curve from 'mostly agree' to 'mostly disagree', followed by postinterviews. Nine patients and five nurses participated. A by-person factor analysis in the form of principal component analysis with varimax and hand rotation was conducted., Results: Three factors, also called viewpoints, emerged as follows: (i) 'Feeling safe through presence, trust and hope'; (ii) 'Feeling safe occurs when the patient is seen, met and informed'; and (iii) 'Feeling alone and angry at oneself'. A polarisation between participants occurred, since the youngest patients (median age 73), the oldest patients (median age 90) and the nurses were represented in each specific factor., Conclusion: There exist differences between how the nursing staff, the youngest and the oldest elderly patients experienced the preoperative period and what can enhance or alleviate their suffering. Where the youngest elderly communicated safety through trust and relatives' presence, the oldest elderly communicated insecurity in relation to staff and experienced severe pain and loneliness. Nursing staff and one patient emphasised the importance of seeing the patient in the first meeting to establish a feeling of security., (© 2019 Nordic College of Caring Science.)

Background and Purpose: Headache has been associated with various lifestyle and psychosocial factors, one of which is smoking. The aim of the present study was to investigate whether the association between smoking intensity and headache is likely to be causal., Method: A total of 58 316 participants from the Nord-Trøndelag Health (HUNT) study with information on headache status were genotyped for the rs1051730 C>T single-nucleotide polymorphism (SNP). The SNP was used as an instrument for smoking intensity in a Mendelian randomization analysis. The association between rs1051730 T alleles and headache was estimated by odds ratios with 95% confidence intervals. Additionally, the association between the SNP and migraine or non-migrainous headache versus no headache was investigated. All analyses were adjusted for age and sex., Results: There was no strong evidence that the rs1051730 T allele was associated with headache in ever smokers (odds ratio 0.99, 95% confidence interval 0.95-1.02). Similarly, there was no association between the rs1051730 T allele and migraine or non-migrainous headache versus no headache., Conclusion: The findings from this study do not support that there is a strong causal relationship between smoking intensity and any type of headache. Larger Mendelian randomization studies are required to examine whether higher smoking quantity can lead to a moderate increase in the risk of headache subtypes., (© 2018 EAN.)

We aimed to investigate potential causal associations between serum 25-hydroxyvitamin D (25(OH)D) levels and incidence of lung cancer overall and histologic types.We performed a Mendelian randomisation analysis using a prospective cohort study in Norway, including 54 580 individuals and 676 incident lung cancer cases. A 25(OH)D allele score was generated based on the vitamin D-increasing alleles rs2282679, rs12785878 and rs10741657. Hazard ratios with 95% confidence intervals for incidence of lung cancer and histologic types were estimated in relation to the allele score. The inverse-variance weighted method using summarised data of individual single nucleotide polymorphisms was applied to calculate the Mendelian randomisation estimates.The allele score accounted for 3.4% of the variation in serum 25(OH)D levels. There was no association between the allele score and lung cancer incidence overall, with HR 0.99 (95% CI 0.93-1.06) per allele score. A 25 nmol·L -1 increase in genetically determined 25(OH)D level was not associated with the incidence of lung cancer overall (Mendelian randomisation estimate HR 0.96, 95% CI 0.54-1.69) or any histologic type.Mendelian randomisation analysis did not suggest a causal association between 25(OH)D levels and risk of lung cancer overall or histologic types in this population-based cohort study., Competing Interests: Conflict of interest: Y-Q. Sun reports grants from the Norwegian Cancer Society (project ID 5769155-2015), during the conduct of the study. B.M. Brumpton reports grants from the Liaison Committee for education, research and innovation in Central Norway, during the conduct of the study., (Copyright ©ERS 2018.)

Previous prospective studies have shown inconsistent associations between serum 25-hydroxyvitamin D [25(OH)D] level and lung cancer incidence. The aim of the present study was to explore the associations of serum 25(OH)D levels with incidence of lung cancer overall and different histologic types. We performed a population-based prospective case-cohort study including 696 incident lung cancer cases and 5804 individuals in a subcohort who participated in the second survey of the Nord-Trøndelag Health Study in Norway. Cox proportional hazards regression models counting for the case-cohort design were used to estimate hazard ratios (HRs) with 95% confidence interval (CIs) for lung cancer overall or histologic types in relation to serum 25(OH)D levels. Compared with the fourth season-specific quartile of 25(OH)D (median 68.0 nmol/L), lower 25(OH)D levels were not associated with the incidence of overall, small or squamous cell lung cancer. However, the risk of adenocarcinoma was lower in the second and third quartiles (median 39.9 and 51.5 nmol/L) compared with the fourth quartile, with HRs of 0.63 (95% CI 0.41-0.98) and 0.58 (0.38-0.88), respectively. The associations of lower levels of 25(OH)D with a reduced risk of adenocarcinoma were only observed in the overweight/obese subjects [HRs for second and third quartiles: 0.40 (0.22-0.72) and 0.50 (0.27-0.92)] but not in the normal weight subjects [HRs: 0.95 (0.52-1.75) and 0.60 (0.32-1.10)]. Serum 25(OH)D levels were not associated with the risk of lung cancer in general. The observation that lower 25(OH)D levels were associated with a lower risk of adenocarcinoma should be interpreted with caution.

Background: Tobacco smoking has been associated with cardiovascular risk factors including adverse serum lipid levels, central obesity and higher resting heart rate, but lower blood pressure and body mass index (BMI). We used a Mendelian randomization approach to study whether these associations may be causal. If smoking affects cardiovascular risk factors then rs1051730 T alleles, predictors of increased smoking quantity, should be associated with cardiovascular risk factors among smokers, but not among never smokers., Methods: Among 56,625 participants of a population-based study, we estimated associations of rs1051730 T alleles with cardiovascular risk factors and examined whether the associations differed by smoking status., Results: Rs1051730 T alleles were associated with lower BMI and waist and hip circumferences and higher resting heart rate and estimated glomerular filtration rate (eGFR), and the associations were strongest among current smokers (P interaction 5×10(-9) to 0.01). Rs1051730 T alleles were associated with lower systolic blood pressure and pulse pressure and higher HDL cholesterol concentrations, but these associations did not robustly differ by smoking status. There were no convincing associations of rs1051730 T alleles with waist-hip ratio, diastolic blood pressure and non-fasting serum concentrations of non-HDL cholesterol, triglycerides, glucose and C-reactive protein., Conclusions: This Mendelian randomization analysis provides evidence that smoking may cause lower BMI and waist and hip circumferences and higher resting heart rate and eGFR. The findings further suggest that smoking is not a major determinant of waist-hip ratio or adverse blood pressure, serum lipid or glucose levels., (© The Author 2014; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Blood lipid levels are heritable, treatable risk factors for cardiovascular disease. We systematically assessed genome-wide coding variation to identify new genes influencing lipid traits, fine map known lipid loci and evaluate whether low-frequency variants with large effects exist for these traits. Using an exome array, we genotyped 80,137 coding variants in 5,643 Norwegians. We followed up 18 variants in 4,666 Norwegians and identified ten loci with coding variants associated with a lipid trait (P < 5 × 10(-8)). One variant in TM6SF2 (encoding p.Glu167Lys), residing in a known genome-wide association study locus for lipid traits, influences total cholesterol levels and is associated with myocardial infarction. Transient TM6SF2 overexpression or knockdown of Tm6sf2 in mice alters serum lipid profiles, consistent with the association observed in humans, identifying TM6SF2 as a functional gene within a locus previously known as NCAN-CILP2-PBX4 or 19p13. This study demonstrates that systematic assessment of coding variation can quickly point to a candidate causal gene.

This article discusses dignity from a Q-methodological study among patients at a psychiatric hospital. The aim of this study is to gain a deeper understanding of the subjective experiences of patients in a psychiatric hospital with respect to dignity. A Q-sample of 51 statements was developed. A total of 15 participants ranked these statements from those they most agreed with to those they most disagreed with. Post-interviews were also conducted. Principal Component Factor Analysis and varimax rotation followed by hand rotation produced the clearest results. Four different viewpoints emerged: being met as equal human being, experience of dignity despite suffering, suffering due to inferior feelings and suffering and fighting for one's own dignity. There seem to be variations in those with dignity-promoting experiences in Viewpoint 1 and to some extent in Viewpoint 2, to those with dignity-inhibiting experiences in Viewpoints 3 and 4.

Genetic studies have shown an association between single-nucleotide polymorphisms on chromosome 15q25 and smoking-related traits and diseases, such as quantity of smoking, lung cancer and chronic obstructive pulmonary disease (COPD). A discussion has centred on the variants and their effects being directly disease related or indirect via nicotine addiction. To address these discrepancies, we genotyped the single-nucleotide polymorphism rs16969968 in the CHRNA5/A3/B4 gene cluster at chromosome 15q25, in 56 307 individuals from a large homogenous population-based cohort, the North Trøndelag Health Study (HUNT) in Norway. The variant was examined in relation to four different outcomes: lung cancer, loss of lung function equivalent to that of COPD, smoking behaviour and the use of smokeless tobacco (snus). Novel associations were found between rs16969968 and the motivational factor for starting to use snus, and the quantity of snus used. Our results also confirm and extend previous findings for associations between rs16969968 and lung cancer, loss of lung function equivalent to that of COPD, and smoking quantity. Our data suggest a role for rs16969968 in nicotine addiction, and the novel association with snus strengthens this observation.

Background: Cigarette smoking is strongly associated with mental illness but the causal direction of the association is uncertain. We investigated the causal relationship between smoking and symptoms of anxiety and depression in the Norwegian HUNT study using the rs1051730 single nucleotide polymorphism (SNP) variant located in the nicotine acetylcholine receptor gene cluster on chromosome 15 as an instrumental variable for smoking phenotypes. Among smokers, this SNP is robustly associated with smoking quantity and nicotine dependence. Method In total, 53 601 participants were genotyped for the rs1051730 SNP and provided information on smoking habits and symptoms of anxiety and depression using the Hospital Anxiety and Depression Scale (HADS)., Results: Self-reported smoking was positively associated with the prevalence of both anxiety and depression, and the measured polymorphism was positively associated with being a current smoker and the number of cigarettes smoked in current smokers. In the sample as a whole, risk of anxiety increased with each affected T allele [odds ratio (OR) 1.06, 95% confidence interval (CI) 1.02-1.09, p = 0.002] but there was no association with depression (p = 0.31). However, we found no clear association of the polymorphism with either anxiety (OR 1.03, 95% CI 0.97-1.09, p = 0.34) or depression (OR 1.02, 95% CI 0.95-1.09, p = 0.62) among smokers., Conclusions: As there was no association of the smoking-related rs1051730 SNP with anxiety and depression among smokers, the results suggest that smoking is not a cause of anxiety and depression.

The etiology of preeclampsia is complex, with susceptibility being attributable to multiple environmental factors and a large genetic component. Although many candidate genes for preeclampsia have been suggested and studied, the specific causative genes still remain to be identified. Catechol-O-methyltransferase (COMT) is an enzyme involved in catecholamine and estrogen degradation and has recently been ascribed a role in development of preeclampsia. In the present study, we have examined the COMT gene by genotyping the functional Val108/158Met polymorphism (rs4680) and an additional single-nucleotide polymorphism, rs6269, predicting COMT activity haplotypes in a large Norwegian case/control cohort (n(cases)= 1135, n(controls)= 2262). A low COMT activity haplotype is associated with recurrent preeclampsia in our cohort. This may support the role of redox-regulated signaling and oxidative stress in preeclampsia pathogenesis as suggested by recent studies in a genetic mouse model. The COMT gene might be a genetic risk factor shared between preeclampsia and cardiovascular diseases.

Objective: Previous studies have indicated that the latent autoimmune diabetes in adults (LADA) phenotype is heterogeneous and that LADA patients share features of type 1 and type 2 diabetes in various proportions. We tested for association of known type 1 and type 2 diabetes susceptibility genes in LADA subjects and analyzed relationships to a marker of autoimmune activity (titers of anti-GAD) and a phenotypic risk factor of type 2 diabetes (BMI)., Research Design and Methods: Data were assembled from the Nord-Trøndelag Health Study (HUNT) study, which comprises the adult population of an entire county in Norway. We genotyped 60 single nucleotide polymorphisms (SNPs) known to be associated with type 1 or type 2 diabetes, including 14 tag SNPs used for HLA haplotyping in 120 type 1 diabetic, 126 LADA, and 1,090 type 2 diabetic patients and 1,503 age- and sex-matched nondiabetic subjects., Results: The majority of the strongly associated HLA haplotypes for type 1 diabetes were significantly associated with LADA in general, but mainly with high anti-GAD LADA patients. Two distinct HLA haplotypes were associated only with LADA and mainly in low anti-GAD LADA patients. There were no associations of non-HLA type 1 diabetes loci with LADA. Of type 2 diabetes-associated genes, the CC/CT genotypes of rs7961581 (TSPAN8) and the obesity-linked AA/AC genotypes of rs8050136 (FTO) were associated with LADA in general, but mainly in low anti-GAD LADA patients (P = 0.004 and P = 0.004, respectively)., Conclusions: Genetic heterogeneity in LADA is linked to various degrees of autoimmune activity and may be partly distinct from both type 1 and type 2 diabetes.

Purpose: The aim of this prospective study was to evaluate the impact of codon 158 polymorphism at the catechol-O-methyltransferase (COMT) gene on prescription of antipsychotic medication in a general population., Methods: The sample comprised 2623 non-diabetic individuals who participated in the Nord-Trøndelag Health Study (HUNT) in the period 1995-97 and who were alive 1 January 2004. The subjects were followed up with respect to prescription of antipsychotic medication based on data obtained from the Norwegian prescription database., Results: Among the group of 76 individuals who had been prescribed antipsychotic medication the distribution did not differ between genotypes and alleles when compared to a control group. For 47 individuals with at least three prescriptions a correlation between median total defined daily doses (DDDs) and genotype groups was found (Spearman's rho, -0.40, p = 0.01), being highest for the Met/Met genotype (250), intermediate for the Met/Val genotype (126) and lowest for the Val/Val genotype (47) (p = 0.03)., Conclusion: In this population-based cohort of 2623 adults, the Val158Met polymorphism at the COMT gene had no major impact on number of individuals who had been prescribed antipsychotic medication. However, linkage to the prescription database may in an indirect way indicate an association between the COMT Val158Met polymorphism and treatment response or dose requirements of antipsychotic medication.

Background: The catechol-O-methyltransferase (COMT) gene contains a functional polymorphism, Val158Met. A few studies on animals have shown a relationship between the COMT gene and BP, but whether this exists in human beings is unclear. The aim of this study was to evaluate the relationship between codon 158 COMT gene polymorphism and BP in a population-based cohort., Methods: In the 1995-97 Nord-Trøndelag Health Study (HUNT), the association between Val/Met polymorphism at the COMT gene and BP was evaluated in a group of 2966 nondiabetic individuals., Results: Among the 2591 individuals without current use of antihypertensive drugs, systolic BP > or =140 mm Hg was more likely among persons with Val/Val genotype compared with the other genotypes (44.8% v 39.1%, P = .02). In the multivariate analysis the prevalence odds ratio for having the Val/Val genotype was 1.63 (95% CI = 1.18 to 2.24) among individuals with systolic BP > or =160 mm Hg compared with those with systolic BP <140 mm Hg. Val/Val genotype was also more likely (OR = 1.30, 95% CI = 1.04 to 1.63) among individuals with hypertension (as defined by use of antihypertensive medication, systolic BP > or =140 mm Hg, or diastolic BP > or =90 mm Hg) than among those with normal BP., Conclusions: Based on the study findings, the Val/Val genotype appears to be associated with a higher prevalence of increased systolic BP compared with the Met/Met or Met/Val genotypes at the COMTgene.

The catechol-O-methyltransferase (COMT) gene contains a functional polymorphism, Val158Met, that has been found to influence human pain perception, and one study has found that migraine was less likely among those with the Val/Val polymorphism. In the 1995-97 Nord-Trøndelag Health (HUNT) Study, the association between the Val158Met polymorphism and headache was evaluated in a random sample of 2451 individuals. No association between Val158Met polymorphism and migraine was found. Among women, a lower prevalence of non-migrainous headache was found among individuals with the Val/Val genotype than among those with other genotypes (26.2% vs. 33.6%, p = 0.04). That non-migrainous headache was less likely among women with the Val/Val genotype may be an incidental finding, but should be investigated in further studies.