The respective contribution of occupational and behavioural factors to social disparities in all-cause mortality has been studied very seldom. The objective of this study was to evaluate the role of occupational and behavioural factors in explaining social inequalities in premature and total mortality in the French working population. The study population consisted of a sample of 2189 and 1929 French working men and women, who responded to a self-administered questionnaire in mid-1996, and were followed up until the end of 2008. Mortality was derived from register-based information and linked to the baseline data. Socioeconomic status was measured using occupation. Occupational factors included biomechanical and physical exposures, temporary contract, psychological demands, and social support, and behavioural factors, smoking, alcohol abuse, and body mass index. Significant social differences were observed for premature and total mortality. Occupational factors reduced the hazard ratios of mortality for manual workers compared to managers/professionals by 72% and 41%, from 1.88 (95% CI: 1.17–3.01) to 1.25 (95% CI: 0.74–2.12) for premature mortality, and from 1.71 (95% CI: 1.18–2.47) to 1.42 (95% CI: 0.95–2.13) for total mortality. The biggest contributions were found for biomechanical and physical exposures, and job insecurity. The role of behavioural factors was very low. Occupational factors played a substantial role in explaining social disparities in mortality, especially for premature mortality and men. Improving working conditions amongst the lowest social groups may help to reduce social inequalities in mortality.

In a group of 46,000 North-American Adventist women aged 40 and above, we investigated the relationships between body mass index (BMI, kg/m2) at age 20 and the proportion of women who reported at least one miscarriage, periods with irregular menstruation or failing to become pregnant even if trying for more than one straight year. Approximately 31, 14 and 17 %, respectively, reported the three different problems related to reproduction. Positive age- and marital status adjusted relationships were found between BMI at age 20 and periods with irregular menstruation or failing to become pregnant even if trying for more than 1 year, but not with the risk of miscarriages. Women with BMI ≥ 32.5 kg/m2 when aged 20 had approximately 2.0 (95 % CI: 1.6, 2.4) and 1.5 (95 % CI: 1.3, 1.9) higher odds for irregular periods or failing to get pregnant, respectively, than women with BMI in the 20–24.9 kg/m2 bracket. These relationships were consistently found in a number of strata of the population, including the large proportion of the women who never had smoked or never used alcohol. Underweight (BMI < 18.5 kg/m2) when aged 20 marginally (approximately 15 %) increased the risk of failing to get pregnant within a year. Thus, obesity at age 20 increases the risk of reporting some specific reproductive problems, but not the risk of miscarriages.

Electronic supplementary material

The online version of this article (doi:10.1007/s10654-012-9749-8) contains supplementary material, which is available to authorized users.

Many effect measures used in clinical trials are problematic because they are differentially understood by patients and physicians. The emergence of novel methods such as accelerated failure-time models and quantile regression has shifted the focus of effect measurement from probability measures to time-to-event measures. Such modeling techniques are rapidly evolving, but matching non-parametric descriptive measures are lacking. We propose such a measure, the delay of events, demonstrating treatment effect as a gain in event-free time. We believe this measure to be of value for shared clinical decision-making. The rationale behind the measure is given, and it is conceptually explained using the Kaplan–Meier estimate and the quantile regression framework. A formula for calculation of the delay of events is given. Hypothetical and empirical examples are used to demonstrate the measure. The measure is discussed in relation to other measures highlighting the time effects of preventive treatments. There is a need to further investigate the properties of the measure as well as its role in clinical decision-making.

Dyspnea is a predictor of mortality. The effects of dyspnea severity and changes in dyspnea status on all-cause and cause-specific mortality remain unclear. The Vlagtwedde/Vlaardingen study started in 1965 and subjects were re-examined every 3 years until 1989/1990. Vital status of all 8,465 subjects on December 31st, 2008 was assessed. Associations between mortality and dyspnea severity and changes in dyspnea status were investigated using Cox regression adjusted for gender, age, FEV1 %predicted, place of residence, smoking and BMI. After 43 years of follow-up, 2,883 (39 %) of 7,360 subjects examined for dyspnea severity had died, 1,386 (19 %) due to cardiovascular disease, 267 (4 %) due to chronic obstructive pulmonary disease (COPD). Subjects with moderate and severe dyspnea had increased all-cause and cardiovascular mortality [moderate: HR = 1.3 (95 % CI 1.2–1.5) and 1.4 (1.1–1.6), severe: 1.5 (1.1–2.0) and 1.9 (1.3–2.6) respectively] compared to asymptomatics. Severe dyspnea was significantly associated with COPD mortality [3.3 (2.0–5.2)]. Subjects who lost dyspnea had hazard ratios for all-cause and cause-specific mortality comparable to asymptomatics. Persistent dyspnea and dyspnea development were risk factors for all-cause, cardiovascular and COPD mortality [persistent: 2.0 (1.4–2.8), 1.9 (1.2–3.3) and 3.3 (1.2–8.9), development: 1.5 (1.2–1.8), 2.0 (1.5–2.6) and 3.8 (2.3–6.3) respectively]. Additionally, dyspnea effects on mortality were more pronounced in overweight/obese and older subjects and in subjects with better lung function. These results show that dyspnea is associated with mortality in a severity-dependent manner. Furthermore this study is the first showing that dyspnea remission normalizes mortality risk. Having or developing dyspnea is a risk factor for mortality.

Electronic supplementary material

The online version of this article (doi:10.1007/s10654-012-9736-0) contains supplementary material, which is available to authorized users.

Early television exposure has been associated with various health outcomes including childhood obesity. This paper describes associations between patterns of television viewing, on one hand, and diet, taste preference and weight status, on the other, in European preschoolers and schoolchildren. The IDEFICS baseline survey was conducted at examination centers in Italy, Estonia, Cyprus, Belgium, Sweden, Germany, Hungary, and Spain. 15,144 children aged 2–9 completed the basic protocol, including anthropometry and parental questionnaires on their diets and television habits. A subsample of 1,696 schoolchildren underwent further sensory testing for fat and sweet taste preferences. Three dichotomous indicators described: children’s habitual television exposure time; television viewing during meals; and having televisions in their bedrooms. Based on these variables we investigated television habits in relation to overweight (IOTF) and usual consumption of foods high in fat and sugar. A possible role of taste preference in the latter association was tested in the sensory subgroup. All television indicators were significantly associated with increased risk of overweight, with odds ratios ranging from 1.21 to 1.30, in fully adjusted models. Children’s propensities to consume high-fat and high-sugar foods were positively and, in most analyses, monotonically associated with high-risk television behaviors. The associations between television and diet propensities were not explained by preference for added fat or sugar in test foods. To summarize, in addition to being more overweight, children with high-risk television behaviors may, independent of objectively measured taste preferences for fat and sugar, passively overconsume higher-fat and particularly higher-sugar diets.

Benzene, a recognized occupational leukemogen in adults, has been hypothesized to also increase the risk of childhood leukemia. We carried out a population-based case–control study in a northern Italy community involving 83 cases with acute childhood leukemia diagnosed in the years 1998–2009 and 332 matched controls. We assessed residential exposure to benzene and to particulate matter ≤10 μm (PM10) from motorized traffic using geocoded residences and detailed emission and dispersion modeling. Exposure to benzene, and to a lesser extent to PM10, appeared to be independently associated with an excess leukemia risk. When we stratified the study population by age and by leukemia subtype, the relative risk associated with benzene exposure was higher among children aged less than 5 years, and despite small numbers this relation appeared to be considerably stronger for acute myeloid leukemia than for acute lymphoblastic leukemia. Overall, these findings suggest that exposure to low levels of benzene released from motorized traffic may increase the risk of childhood leukemia, and suggest a possible independent effect of PM10, although unmeasured confounding due to other pollutants cannot be ruled out.

Sexual dysfunction often features as an outcome variable in community health surveys and epidemiological surveys. Key design imperatives for measures included in large scale, population-based surveys are acceptability, brevity and relevance to diverse sexual lifestyles. None of the available measures of sexual dysfunction are entirely suited to this task. We developed a new measure of sexual function for the third British National Survey of Sexual Attitudes and Lifestyles (Natsal 3). Items for the measure were derived from qualitative work from patients and community members. The draft measure was developed and validated using a general population sample (internet panel survey (n = 1,262)) and a clinical sample (patients attending sexual problems clinics (n = 100). Confirmatory factor analysis established that a ‘general-specific model’ had the best fit and was equivalent between general population and clinical samples (Comparative Fit Index = 0.963 Tucker Lewis Index = 0.951; Root Mean Square Error of Approximation = 0.064). The 17-item Natsal-SF is positively associated with the Female Sexual Function Index-6 (B = 0.572) and Brief Sexual Function Questionnaire for men (B = 0.705); it can discriminate between clinical and general population groups (OR = 2.667); and it has good test–retest reliability (r = 0.72). The Natsal-SF provides an estimate of the level of sexual function in the last year. By including items on distress about sex and sexual relationships, and by being relevant to all regardless of sexual lifestyle, it addresses some of the gaps in current measurement design.

Understanding the association between asthma and socioeconomic position (SEP) is key to identify preventable exposures to prevent inequalities and lessen overall disease burden. We aim to assess the variation in asthma across SEP groups in a historical cohort before the rise in asthma prevalence. Male students participating in a health survey at Glasgow University from 1948 to 1968 (n = 11,274) completed medical history of bronchitis, asthma, hay fever, eczema/urticaria, and reported father’s occupation. A subsample responded to postal follow-up in adulthood (n = 4,101) that collected data on respiratory diseases, early life and adult SEP. Lower father’s occupational class was associated with higher odds of asthma only (asthma without eczema/urticaria or hay fever) (trend adjusted multinomial odds ratio (aMOR) = 1.23, 95 % CI 1.03–1.47) but with lower odds of asthma with atopy (asthma with eczema/urticaria or hay fever) (trend aMOR = 0.66, 95 % CI 0.52–0.83) and atopy alone (trend aMOR = 0.84, 95 % CI 0.75–0.93). Household amenities (<3), in early life was associated with higher odds of adult-onset asthma (onset > 30 years) (OR = 1.48, 95 % CI 1.07–2.05) though this association attenuated after adjusting for age. Adult SEP (household crowding, occupation, income and car ownership) was not associated with adult-onset asthma. Lower father’s occupational class in early life was associated with higher odds of asthma alone but lower odds of asthma with atopy in a cohort that preceded the 1960s rise in asthma prevalence. Different environmental exposures and/or disease awareness may explain this opposed socioeconomic patterning, but it is important to highlight that such patterning was already present before rises in the prevalence of asthma and atopy.

We assessed whether the previously observed relationship between socioeconomic status (SES) and short-term mortality (pre-hospital mortality and 28-day case-fatality) after a first acute myocardial infarction (AMI) in persons <75 years, are also observed in the elderly (i.e. ≥75 years), and whether these relationships vary by sex. A nationwide register based cohort study was conducted. Between January 1st 1998 and December 31st 2007, 76,351 first AMI patients were identified, of whom 60,498 (79.2 %) were hospitalized. Logistic regression analyses were performed to measure SES differences in pre-hospital mortality after a first AMI and 28-day case-fatality after a first AMI hospitalization. All analyses were stratified by sex and age group (<55, 55–64, 65–74, 75–84, ≥85), and adjusted for age, ethnic origin, marital status, and degree of urbanization. There was an inverse relation between SES and pre-hospital mortality in both sexes. There was also an inverse relation between SES and 28-day case-fatality after hospitalization, but only in men. Compared to elderly men with the highest SES, elderly men with the lowest SES had a higher pre-hospital mortality in both 75–84 year-olds (OR = 1.26; 95 % CI 1.09–1.47) and ≥85 year-olds (OR = 1.26; 1.00–1.58), and a higher 28-day case-fatality in both 75–84 year-olds (OR = 1.26; 1.06–1.50) and ≥85 year-olds (OR = 1.36; 0.99–1.85). Compared to elderly women with the highest SES, elderly women with the lowest SES had a higher pre-hospital mortality in ≥85 year-olds (OR = 1.20; 0.99–1.46). To conclude, in men there are SES inequalities in both pre-hospital mortality and case-fatality after a first AMI, in women these SES inequalities are only shown in pre-hospital mortality. The inequalities persist in the elderly (≥75 years of age). Clinicians and policymakers need to be more vigilant on the population with a low SES background, including the elderly.

In order to explore how the choice of different study designs could influence the risk estimates, a case–crossover and case–time–control study were carried out and their outcomes were compared with those of a traditional case–control study design that evaluated the association between the exposure to psychotropic medications and the risk of having a motor vehicle accident (MVA). A record-linkage database availing data for 3,786 cases and 18,089 controls during the period 2000–2007 was used. The study designs (i.e., case–crossover and case–time–control) were derived from published literature, and the following psychotropic medicines were examined: antipsychotics, anxiolytics, hypnotics and sedatives, and antidepressants, stratified in the two groups selective serotonin reuptake inhibitors (SSRIs) and other antidepressants. Moreover, in order to further investigate the effects of frequency of psychoactive medication exposure on the outcomes of the case–crossover analysis, the data were also stratified by the number of defined daily doses (DDDs) and days of medication use in the 12 months before the motor vehicle accident. Three-thousand seven-hundred fifty-two cases were included in this second part of the case–crossover analysis. The case–crossover design did not show any statistically significant association between psychotropic medication exposure and MVA risk [e.g., SSRIs—Adj. OR = 1.00 (95 % CI: 0.69–1.46); Anxiolytics—Adj. OR = 0.95 (95 % CI: 0.68–1.31)]. The case–time–control design only showed a borderline statistically significant increased traffic accident risk in SSRI users [Adj. OR = 1.16 (95 % CI: 1.01–1.34)]. With respect to the stratifications by the number of DDDs and days of medication use, the analyses showed no increased traffic accident risk associated with the exposure to the selected medication groups [e.g., SSRIs, <20 DDDs—Adj. OR = 0.65 (95 % CI: 0.11–3.87); SSRIs, 16–150 days—Adj. OR = 0.55 (95 % CI: 0.24–1.24)]. In contrast to the above-mentioned results, our recent case–control study found a statistically significant association between traffic accident risk and exposure to anxiolytics [Adj. OR = 1.54 (95 % CI: 1.11–2.15)], and SSRIs [Adj. OR = 2.03 (95 % CI: 1.31–3.14)]. Case–crossover and case–time–control analyses produced different results than those of our recent case–control study (i.e., case–crossover and case–time–control analyses did not show any statistically significant association whereas the case–control analysis showed an increased traffic accident risk in anxiolytic and SSRI users). These divergent results can probably be explained by the differences in the study designs. Given that the case–crossover design is only appropriate for short-term exposures and the case–time–control design is an elaboration of this latter, it can be concluded that, probably, these two approaches are not the most suitable ones to investigate the relation between MVA risk and psychotropic medications, which, on the contrary, are often use chronically.

Ethnic disparities in the prevalence of asthma symptoms in children have been described. We evaluated to what extent the association between ethnic background and respiratory symptoms during the first 2 years of life could be explained by the mediating effect of risk factors for respiratory morbidity. The Generation R Study is a multiethnic, population-based birth cohort study. Pre and postnatal risk factors for respiratory morbidity were prospectively assessed by questionnaires. Information about ethnicity was available for 5,684 infants. The associations between ethnic background and lower respiratory symptoms at 12 and 24 months were evaluated with log-binomial regression models. Relative risks and 95 % confidence intervals (RR [95 % CI]) were computed for Cape Verdean, Moroccan, Antillean, Surinamese and Turkish ethnicity with Dutch ethnicity as the reference category. We found an increased risk of lower respiratory symptoms at 24 months in Antillean infants (1.32 [95 % CI 1.12–1.57]) that was mediated by early postnatal exposures (pets keeping, siblings, breastfeeding, daycare attendance, smoke exposure). Turkish infants also had an increased risk of lower respiratory symptoms at 12 and 24 months (1.14 [95 % CI 1.02–1.27] and 1.21 [95 % CI 1.07–1.38], respectively), partly explained by previous morbidity (eczema, infections and upper respiratory symptoms). There were no differences for Cape Verdean, Moroccan or Surinamese, as compared to Dutch infants. Hence, ethnic background was associated with respiratory symptoms during the first 2 years of life and this association was largely explained by mediating effects of known pre and postnatal risk factors for respiratory morbidity.

The rapid and continuing progress in gene discovery for complex diseases is fuelling interest in the potential application of genetic risk models for clinical and public health practice.The number of studies assessing the predictive ability is steadily increasing, but they vary widely in completeness of reporting and apparent quality.Transparent reporting of the strengths and weaknesses of these studies is important to facilitate the accumulation of evidence on genetic risk prediction.A multidisciplinary workshop sponsored by the Human Genome Epidemiology Network developed a checklist of 25 items recommended for strengthening the reporting of Genetic RIsk Prediction Studies (GRIPS), building on the principles established by prior reporting guidelines.These recommendations aim to enhance the transparency, quality and completeness of study reporting, and thereby to improve the synthesis and application of information from multiple studies that might differ in design, conduct or analysis.

Open-angle glaucoma (OAG) is the commonest cause of irreversible blindness worldwide. Apart from an increased intraocular pressure (IOP), oxidative stress and an impaired ocular blood flow are supposed to contribute to OAG. The aim of this study was to determine whether the dietary intake of nutrients that either have anti-oxidative properties (carotenoids, vitamins, and flavonoids) or influence the blood flow (omega fatty acids and magnesium) is associated with incident OAG. We investigated this in a prospective population-based cohort, the Rotterdam Study. A total of 3502 participants aged 55 years and older for whom dietary data at baseline and ophthalmic data at baseline and follow-up were available and who did not have OAG at baseline were included. The ophthalmic examinations comprised measurements of the IOP and perimetry; dietary intake of nutrients was assessed by validated questionnaires and adjusted for energy intake. Cox proportional hazard regression analysis was applied to calculate hazard ratios of associations between the baseline intake of nutrients and incident OAG, adjusted for age, gender, IOP, IOP-lowering treatment, and body mass index. During an average follow-up of 9.7 years, 91 participants (2.6%) developed OAG. The hazard ratio for retinol equivalents (highest versus lowest tertile) was 0.45 (95% confidence interval 0.23–0.90), for vitamin B1 0.50 (0.25–0.98), and for magnesium 2.25 (1.16–4.38). The effects were stronger after the exclusion of participants taking supplements. Hence, a low intake of retinol equivalents and vitamin B1 (in line with hypothesis) and a high intake of magnesium (less unambiguous to interpret) appear to be associated with an increased risk of OAG.

Type 2 diabetes mellitus (T2DM) influences bone metabolism, but the relation of T2DM with bone mineral density (BMD) remains inconsistent across studies. The objective of this study was to perform a meta-analysis and meta-regression of the literature to estimate the difference in BMD (g/cm2) between diabetic and non-diabetic populations, and to investigate potential underlying mechanisms. A literature search was performed in PubMed and Ovid extracting data from articles prior to May 2010. Eligible studies were those where the association between T2DM and BMD measured by dual energy X-ray absorptiometry was evaluated using a cross-sectional, cohort or case–control design, including both healthy controls and subjects with T2DM. The analysis was done on 15 observational studies (3,437 diabetics and 19,139 controls). Meta-analysis showed that BMD in diabetics was significantly higher, with pooled mean differences of 0.04 (95% CI: 0.02, 0.05) at the femoral neck, 0.06 (95% CI: 0.04, 0.08) at the hip and 0.06 (95% CI: 0.04, 0.07) at the spine. The differences for forearm BMD were not significantly different between diabetics and non-diabetics. Sex-stratified analyses showed similar results in both genders. Substantial heterogeneity was found to originate from differences in study design and possibly diabetes definition. Also, by applying meta-regression we could establish that younger age, male gender, higher body mass index and higher HbA1C were positively associated with higher BMD levels in diabetic individuals. We conclude that individuals with T2DM from both genders have higher BMD levels, but that multiple factors influence BMD in individuals with T2DM.

Stroke incidence rates have decreased in developed countries over the past 40 years, but trends vary across populations. We investigated whether age-and-sex-specific stroke incidence rates and associated risk factors as well as preventive medication use have changed in Rotterdam in the Netherlands during the last two decades. The study was part of the Rotterdam Study, a large population-based cohort study among elderly people. Participants were 10,994 men and women aged 55–94 years who were stroke-free at baseline. Trends were calculated by comparing the 1990 subcohort (n = 7516; baseline 1990–1993) with the 2000 subcohort (n = 2883; baseline 2000–2001). Poisson regression was used to calculate incidence rates and incidence rate ratios in age-and-sex-specific strata. We further compared the prevalence of stroke risk factors and preventive medication use in the two subcohorts. In the 1990 subcohort 467 strokes occurred during 45,428 person years; in the 2000 subcohort 115 strokes occurred in 18,356 person years. Comparing the subcohorts, incidence rates decreased by 34% in men, but remained unchanged in women. Blood pressure levels increased between 1990 and 2000, whereas the proportion of current cigarette smokers decreased in men, but not in women. There was a strong increase in medication use for treatment of stroke risk factors across all age categories in both sexes. Our findings suggest that in Rotterdam between 1990 and 2008 stroke incidence rates have decreased in men but not in women.

Measures of quality of life (QoL) have been found to be predictors of mortality and morbidity; however, there is still limited understanding of the multifaceted nature of these measures and of potential correlates. Using two large populations from the UK and US, we aimed to evaluate and compare measured levels of QoL and the key factors correlated with these levels. Participants were 6,472 white subjects (1,829 women) from the Whitehall II Study (mean age 55.8 years) and 3,684 white subjects (1,903 women) from the Western New York Health Study (mean age 58.7 years). QoL was assessed in both using the physical and mental health component summaries of the short form-36 questionnaire (SF-36). Analysis of covariance was used to compare gender-specific mean scores for the two populations across several potential correlates (including socio-demographic, lifestyle and co-morbidity factors). Levels of reported physical QoL tended to be higher in the UK population (51.2 vs. 48.6) while mental QoL was higher in the US group (53.1 vs. 51.1). Age, sleep duration and depressive symptoms were the main factors correlated with both physical and mental QoL in both samples. Increasing age was associated with poorer physical health but higher mental health scores in both populations (P < 0.001). Sleep duration below 6 or above 8 h was associated with lower levels of QoL. Depressive symptoms were strongly associated with poorer mental health scores (P < 0.001) while higher BMI, lower physical activity levels and presence of cardiovascular disease were associated with poorer physical health in both samples and gender (P < 0.05). There were consistent findings for correlates of QoL in this cross-cultural comparison of two populations from the UK and US. Strongest associations were between lifestyle and co-morbidity factors and the physical health component of the SF-36 rather than the mental health component. This is a novel finding which warrants further consideration.

The prevalence of cardiovascular diseases is rising. Therefore, adequate risk prediction and identification of its determinants is increasingly important. The Rotterdam Study is a prospective population-based cohort study ongoing since 1990 in the city of Rotterdam, The Netherlands. One of the main targets of the Rotterdam Study is to identify the determinants and prognosis of cardiovascular diseases. Case finding in epidemiological studies is strongly depending on various sources of follow-up and clear outcome definitions. The sources used for collection of data in the Rotterdam Study are diverse and the definitions of outcomes in the Rotterdam Study have changed due to the introduction of novel diagnostics and therapeutic interventions. This article gives the methods for data collection and the up-to-date definitions of the cardiac outcomes based on international guidelines, including the recently adopted cardiovascular disease mortality definitions. In all, detailed description of cardiac outcome definitions enhances the possibility to make comparisons with other studies in the field of cardiovascular research and may increase the strength of collaborations.

Most previous studies of burnout have focused on work environmental stressors, while familial factors so far mainly have been overlooked. The aim of the study was to estimate the relative importance of genetic influences on burnout (measured with Pines Burnout Measure) in a sample of monozygotic (MZ) and dizygotic (DZ) Swedish twins. The study sample consisted of 20,286 individuals, born 1959–1986 from the Swedish twin registry who participated in the cross-sectional study of twin adults: genes and environment. Probandwise concordance rates (the risk for one twin to be affected given that his/her twin partner is affected by burnout) and within pair correlations were calculated for MZ and DZ same—and opposite sexed twin pairs. Heritability coefficients i.e. the proportion of the total variance attributable to genetic factors were calculated using standard biometrical model fitting procedures. The results showed that genetic factors explained 33% of the individual differences in burnout symptoms in women and men. Environmental factors explained a substantial part of the variation as well and are thus important to address in rehabilitation and prevention efforts to combat burnout.

Previous studies have suggested that asthma, like other common diseases, has at least part of its origin early in life. Low birth weight has been shown to be associated with increased risks of asthma, chronic obstructive airway disease, and impaired lung function in adults, and increased risks of respiratory symptoms in early childhood. The developmental plasticity hypothesis suggests that the associations between low birth weight and diseases in later life are explained by adaptation mechanisms in fetal life and infancy in response to various adverse exposures. Various pathways leading from adverse fetal and infant exposures to growth adaptations and respiratory health outcomes have been studied, including fetal and early infant growth patterns, maternal smoking and diet, children’s diet, respiratory tract infections and acetaminophen use, and genetic susceptibility. Still, the specific adverse exposures in fetal and early postnatal life leading to respiratory disease in adult life are not yet fully understood. Current studies suggest that both environmental and genetic factors in various periods of life, and their epigenetic mechanisms may underlie the complex associations of low birth weight with respiratory disease in later life. New well-designed epidemiological studies are needed to identify the specific underlying mechanisms. This review is focused on specific adverse fetal and infant growth patterns and exposures, genetic susceptibility, possible respiratory adaptations and perspectives for new studies.

To assess whether two inflammatory markers, C-reactive protein (CRP) and interleukin-6 (IL-6), and change in their concentrations over 12 years, are associated with lung function (FVC and FEV1) 12 years after baseline. Data are from over 1,500 participants free from self-reported respiratory problems in a large-scale prospective cohort study of white-collar male and female civil servants. CRP and IL-6 measured at baseline (1991–1993) and follow-up (2002–2004) and FVC and FEV1, measured at follow-up. Results adjusted for sociodemographic and anthropometric characteristics, health behaviours, biological factors, chronic conditions and medications, and corrected for short-term variability in CRP and IL-6 concentrations. Higher baseline levels of CRP and IL-6 were strongly associated with lower FVC and FEV1, independent of potential confounders. A 10% increase serum CRP from baseline to follow-up was associated with lower values of FVC and FEV1 at follow-up, 4.7 and 3.0 ml, respectively. The corresponding values for a 10% increase in IL-6 were 12.6 ml for FVC and 7.3 ml for FEV1. Systemic low-grade inflammation is associated with only slightly poorer pulmonary function in a population free from self-reported respiratory problems 12 years earlier. These data provide evidence linking inflammation to adverse outcomes beyond cardiovascular disease. Interventions targeting inflammation may prevent lung function impairment.

Aims

To evaluate midlife risk factors of developing type 2 diabetes mellitus (T2DM) in late life in a population-based study of older persons.

Methods

A cohort of 2251 persons, aged 65-96, participated in AGES-Reykjavik in 2002-2004; all attended the Reykjavik Study 26 years earlier, at the mean age of 50. Based on glucometabolic status in 2002-2004 the participants are divided into a normoglycemic control group (n=1695), an impaired fasting glucose (IFG) group (n=313) and T2DM group (n=243). Change in risk parameters from midlife is evaluated in these three groups.

Results

Since examined earlier 14.3% of men and 8.2% of women developed T2DM. A family history of diabetes was reported in 39.5% of T2DM compared to 19.3% in both IFG and normoglycemics. The T2DM and IFG groups currently have higher levels of fasting triglycerides, greater BMI and higher systolic blood pressure than normoglycemics and this difference was already apparent in midlife. In late life, two or more metabolic syndrome criteria are present in 60% of the T2DM groups compared to 25% in normoglycemic groups. T2DM with impaired cardiovascular health is more marked in women than men when compared with controls.

Conclusions

Family history and higher levels of BMI, TG and systolic blood pressure in midlife are associated with the development of T2DM in late life, suggesting risk can be evaluated long before onset. A continued rise in risk factors throughout life allows a scope for more aggressive measures in preventing or delaying development of T2DM and its effect on cardiovascular health.

Depression and cardiovascular disease (CVD) are closely associated, but the mechanisms underlying this connection are unclear. Regardless of the low cholesterol levels observed in depression, a small particle size of low-density lipoproteins (LDL), as well as elevated apolipoprotein B (ApoB) levels, are related to increased CVD risk, even when levels of LDL cholesterol are low. We examined the association between elevated depressive symptoms and compositional changes in serum LDL particles in a sample of 2456 middle-aged Finnish men. Depressive symptoms were assessed with the 18-item Human Population Laboratory Depression Scale, and the study population was divided into two groups (elevated depressive symptoms, n=269; non-depressed, n=2187). The levels of serum total cholesterol (TC), low-and high-density lipoprotein cholesterol (LDL-C, HDL-C), triglycerides (TG), and ApoB were determined. The LDL-C/ApoB ratio, a marker of compositional changes in LDL particle size, was calculated. The group with elevated depressive symptoms had lowered levels of serum TC (p=0.028) and LDL-C (p=0.008). No differences were observed in the LDL-C/ApoB ratio. The likelihood for belonging to the group with elevated depressive symptoms increased 10% for each 0.5 mmol/L decrease in the levels of TC (p=0.002) or LDL-C (p=0.001) in regression models adjusted for age, examination years, marital and socioeconomic status, energy expenditure, body mass index, CVD history, alcohol consumption, smoking, and the use of lipid-lowering, antidepressant and antipsychotic medications. Our findings suggest that greater small-particle LDL levels are not associated with depression, and are thus unlikely to underlie the association between cardiovascular risk and depression.