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.
To examine whether physical activity and adiposity modify the increased risk of cancer associated with diabetes.
We prospectively examined the association of diabetes and risk of cancer among 73,726 persons stratified by physical activity and body mass index (BMI). Adjusted hazard ratios (HRs) with 95% confidence intervals (CI) were estimated from Cox regression.
During a median follow-up of 22.0 years, 9572 people were diagnosed with incident cancer. There was no clear association between diabetes and cancer risk in those reporting high levels of physical activity (=2.0h per week) (HR 0.93; 95% CI: 0.70-1.24) or those with a normal weight (BMI
Adverse parental life-style habits are associated with offspring adiposity, but it is unclear how changes in these habits affect offspring adiposity. Thus, the aim of this study was to assess how parental change in body weight, smoking habits and levels of physical activity were associated with adiposity in their children.
The study population consisted of 3 681 adolescents and their parents from the Nord-Trøndelag-Health-Study (HUNT). The parents participated in the two first waves of HUNT (HUNT-1:1984-86, HUNT-2:1995-97), where information on anthropometry, smoking habits and physical activity were obtained. The adolescents participated in the Youth-Part of HUNT-2. We used logistic regression to calculate odds-ratios (ORs) for adolescent offspring overweight according to parental change in body-weight, smoking habits and physical activity, adjusting for these factors in both parents, as well as for socioeconomic status and adolescent age and sex.
Children of parents who changed weight from normal weight to overweight from HUNT-1 to HUNT-2 had higher OR for overweight in adolescence than children of parents who remained normal weight (mothers: 1.9 [95% CI: 1.4,2.5], fathers: 2.2 [95% CI: 1.5,3.0]). Children of mothers who reduced their weight from overweight to normal weight had no higher OR for overweight in adolescence than mothers who remained normal weight (OR: 1.0; 95% CI: 0.2, 4.7). Children of mothers who quit smoking (OR: 0.5; 95% CI: 0.3, 0.8) had lower OR for overweight in adolescence than children of mothers who persisted in smoking.
Healthy changes in parental life-style during childhood are associated with lower occurrence of offspring overweight in adolescence.
Multimorbidity is prevalent, and knowledge regarding its aetiology is limited. The general pathogenic impact of adverse life experiences, comprising a wide-ranging typology, is well documented and coherent with the concept allostatic overload (the long-term impact of stress on human physiology) and the notion embodiment (the conversion of sociocultural and environmental influences into physiological characteristics). Less is known about the medical relevance of subtle distress or unease. The study aim was to prospectively explore the associations between existential unease (coined as a meta-term for the included items) and multimorbidity.
Our data are derived from an unselected Norwegian population, the Nord-Trøndelag Health Study, phases 2 (1995-1997) and 3 (2006-2008), with a mean of 11 years follow-up.
The analysis includes 20 365 individuals aged 20-59 years who participated in both phases and was classified without multimorbidity (with 0-1 disease) at baseline.
From HUNT2, we selected 11 items indicating 'unease' in the realms of self-esteem, well-being, sense of coherence and social relationships. Poisson regressions were used to generate relative risk (RR) of developing multimorbidity, according to the respondents' ease/unease profile.
A total of 6277 (30.8%) participants developed multimorbidity. They were older, more likely to be women, smokers and with lower education. 10 of the 11 'unease' items were significantly related to the development of multimorbidity. The items 'poor self-rated health' and 'feeling dissatisfied with life' exhibited the highest RR, 1.55 and 1.44, respectively (95% CI 1.44 to 1.66 and 1.21 to 1.71). The prevalence of multimorbidity increased with the number of 'unease' factors, from 26.7% for no factor to 49.2% for 6 or more.
In this prospective study, 'existential unease' was associated with the development of multimorbidity in a dose-response manner. The finding indicates that existential unease increases people's vulnerability to disease, concordant with current literature regarding increased allostatic load.
Cites: Dev Psychol. 2006 Mar;42(2):381-9016569175
Cites: Stress. 2015 Jan;18(1):1-1025407297
Cites: J Epidemiol Community Health. 2005 May;59(5):350-515831681
Cites: Int J Equity Health. 2012 Aug 22;11:4822909009
To prospectively study the relation between TSH and risk of hip and forearm fractures.
A population-based cohort study.
In a substudy of the second survey of the Nord Trøndelag Health Study, Norway (HUNT2, 1995-97), linked with a hospital-based fracture registry, we investigated the relation between baseline TSH and risk of hip and/or forearm fractures.
A total of 16?610 women and 8595 men aged 40 years or more, without previous self-reported thyroid disease and hip or forearm fractures.
During 12.5 years follow-up, a total of 1870 women and 342 men experienced hip or forearm fractures. Overall, there was no relation between baseline TSH and fracture risk. However, there was weak evidence that women with TSH 3.5?mU/l had a slightly increased risk of hip fractures (hazard ratio (HR) 1.30, 95% CI 0.97-1.94 and HR 1.19, 95% CI 0.93-1.52) compared with the reference group with TSH of 1.5-2.4?mU/l. Supplementary analyses showed higher hip fracture risk in women with TSH >4.0?mU/l and negative thyroid peroxidase antibodies (TPOAb) compared with the reference group (HR 1.75, 95% CI 1.24-2.46).
We found no statistically significant relation between baseline TSH and subsequent fracture risk, but the data suggest a weak positive association with hip fracture risk among women with both low and high TSH. The latter association was confined to women with negative TPOAb status.
Mechanical joint stress imposed by high body mass index (BMI) is associated with increased risk of knee and hip osteoarthritis. This prospective study investigated the independent and joint association of BMI and physical exercise on risk of knee and hip osteoarthritis.
The study includes 15,191 women and 14,766 men in the Norwegian HUNT Study without pain or physical impairment at baseline. Occurrence of self-reported physician-diagnosed osteoarthritis was assessed at 11 years of follow-up.
BMI was positively related to risk of knee osteoarthritis (P(trend)0.34). Exercise intensity was not associated with risk of osteoarthritis in any BMI category; that is, obese persons reporting high-intensity exercise had an RR of 1.28 (95% CI 0.59 to 2.79) for severe osteoarthritis compared with inactive persons.
High BMI increases the risk of knee osteoarthritis and severe osteoarthritis. Physical exercise does not increase the risk of osteoarthritis at any level of BMI, suggesting that exercise could be encouraged also among individuals with excessive body mass, without concern for an increased risk of osteoarthritis.
Cardiorespiratory fitness is suggested to be an important marker of cardiovascular risk but is rarely evaluated in health care settings. In the present study, directly measured peak oxygen uptake (V·O 2peak) from a diverse population of 4637 healthy participants were used to develop and cross-validate a new nonexercise regression model of cardiorespiratory fitness for men and women.
Multivariable regression analysis was used to develop a nonexercise model of cardiorespiratory fitness for men and women separately with V·O 2peak as the outcome. In the final models, 2067 men (mean age = 48.8 yr) and 2193 women (mean age = 47.9 yr) were included, respectively. Cross-validation of the models was done by standard data splitting procedures with evaluation of constant error and total error of a model developed on one sample and cross-validated on another sample. Age, waist circumference, leisure time physical activity, and resting HR, successively, were the most potent predictors of V·O 2peak for both men and women. Together, 61% and 56% of variance in V·O 2peak, for men and women, respectively, were explained by the full models. SEE was 5.70 and 5.14 for the models including men and women, respectively.
The nonexercise regression model developed in the present study was fairly accurate in predicting V·O 2peak in this healthy population of men and women. The model might be generalized to other healthy populations and might be a valid tool for a rough assessment of cardiorespiratory fitness in an outpatient setting.
The main objectives of the current study was i) to prospectively examine if chronic musculoskeletal pain in parents is associated with risk of chronic musculoskeletal pain in their adult offspring, and ii) to assess if these parent-offspring associations are modified by offspring body mass index and leisure time physical activity. We used data on 4,742 adult offspring linked with their parents who participated in the population-based HUNT Study in Norway in 1995-97 and in 2006-08. Family relations were established through the national Family Registry. A Poisson regression model was used to estimate relative risk (RR) with 95% confidence interval (CI). In total, 1,674 offspring (35.3%) developed chronic musculoskeletal pain during the follow-up period of approximately 11 years. Both maternal (RR: 1.26, 95% CI: 1.03, 1.55) and paternal chronic musculoskeletal pain (RR: 1.29, 95% CI: 1.06, 1.57) was associated with increased risk of offspring chronic musculoskeletal pain. Compared to offspring of parents without chronic musculoskeletal pain, the adverse effect of parental pain was somewhat stronger among offspring who reported a low (RR: 1.82, 95% CI: 1.32, 2.52) versus high (RR: 1.32, 95% CI: 0.95, 1.84) level of leisure time physical activity. Offspring of parents with chronic musculoskeletal pain and who were classified as obese had more than twofold increased risk (RR: 2.33, 95% CI: 1.68, 3.24) of chronic musculoskeletal pain compared to normal weight offspring of parents without pain. In conclusion, parental chronic musculoskeletal pain is positively associated with risk of chronic musculoskeletal pain in their adult offspring. Maintenance of normal body weight may reduce the risk of chronic musculoskeletal pain in offspring of pain-afflicted parents.
Cites: Prev Med. 2005 Jul;41(1):260-715917020
Cites: Neurology. 2005 Aug 9;65(3):437-4316087910
Cites: Scand J Public Health. 2005;33(4):268-7516087489
How different Global Initiative for Chronic Obstructive Lung Disease (GOLD) classifications of chronic obstructive pulmonary disease (COPD) predict mortality is unclear.
To examine the association of spirometric GOLD grades and the new ABCD groups with mortality, and to compare their informativeness in relation to mortality.
We studied 1540 people with post-bronchodilator COPD who participated in the Norwegian Nord-Tr?ndelag Health Study 1995-1997 and were followed up on all-cause mortality until May 2012. The associations of spirometric GOLD grades and ABCD groups with mortality were estimated by sex specific adjusted HRs from Cox regression and standardised mortality ratios. To assess the informativeness of spirometric GOLD grades and ABCD groups at predicting mortality we used the difference in twice the log-likelihood of a Cox regression model with and without each COPD classification.
The distribution of participants was 28% in GOLD 1, 57% in GOLD 2, 13% in GOLD 3 and 2% in GOLD 4, in contrast to 61% in group A, 18% in group B, 12% in group C and 10% in group D. During a median of 14.6 years of follow-up, 837 people (54%) died. Mortality increased gradually from GOLD 1 to 4, while it was generally similar in groups A and B, and in groups C and D. Spirometric GOLD grades were substantially more informative than ABCD groups at predicting mortality.
Spirometric GOLD grades predicted mortality better than the new ABCD groups among people with COPD from a Norwegian general population.
This study aimed to investigate the prospective influence of multisite pain, depression, anxiety, self-rated health and pain-related disability on recovery from chronic low back pain (LBP).
The data is derived from the second (1995-1997) and third (2006-2008) wave of the Nord-Trøndelag Health Study (HUNT) in Norway.
The study population comprises 4484 women and 3039 men in the Norwegian HUNT Study who reported chronic LBP at baseline in 1995-1997.
The primary outcome was recovery from chronic LBP at the 11-year follow-up. Persons not reporting pain and/or stiffness for at least three consecutive months during the last year were defined as recovered. A Poisson regression model was used to estimate adjusted risk ratios (RRs) with 95% CIs.
At follow-up, 1822 (40.6%) women and 1578 (51.9%) men reported recovery from chronic LBP. The probability of recovery was inversely associated with number of pain sites (P-trend
Cites: Lancet. 2012 Dec 15;380(9859):2163-96 PMID 23245607
Cites: Spine (Phila Pa 1976). 2012 May 15;37(11):E668-77 PMID 22146287