Workplace health promotion to facilitate physical activity among office workers in Sweden.

Office workers spend most of their working time being sedentary, contributing to a sedentary lifestyle that increases the risk of developing disease and disability. A gradual decline in cardiorespiratory fitness among adults, along with increased rate of non-communicable diseases across developed countries, makes the workplace an important opportunity for promoting healthy behaviors. This study aimed to investigate: how office companies in Sweden organize and provide workplace health promotion services related to physical activity; the companies' vision for providing workplace health promotion; and potential facilitators and barriers. Nine informants from eight companies participated in the study, and both qualitative and quantitative data were collected by semi-structured interviews. Informants were selected through purposive sampling in collaboration with eight companies in the office market, including companies that own and develop office buildings, shared workspaces, interior design, sustainable solutions, or consult on issues related to the office sector. The framework method was used to analyze the data in a flexible and systematic way. The results showed that workplace health promotion is implemented to maintain employee health, productivity, and employee branding. Also, a significant number of financial resources, organizational support and office space are devoted to workplace health promotion. Convenience and easy access to storage and fitness facilities are key facilitators. In conclusion, this study highlights the importance of employees' engagement in developing and improving workplace health promotion and addressing work-life balance constraints that hinder a healthy lifestyle. Removing barriers on an organizational level may improve the usage of workplace health promotion related to physical activity among office employees.

The outdoor office: a pilot study of environmental qualities, experiences of office workers, and work-related well-being.

Outdoor office work is an emerging aspect of the concept of 'new ways of working', but only sparse data are available about the environmental qualities of the outdoor office space, experiences of office workers, and work-related well-being of outdoor office work. Here, we present an exploratory pilot study on well-being and outdoor office work in a public urban space. An outdoor office was set up in the courtyard of a university campus, and the participants (n = 16) conducted office work outdoors for 30 min and thereafter participated in an eye-tracking session for 11-15 min (n = 8) and subsequently filled out surveys (n = 16). The eye tracker allowed the discovery of natural and built elements in the outdoor environment that caught the participants' visual attention, whereas the surveys assessed aspects of their subjective experiences of the outdoor office space (its visual and spatial qualities) and the work there. The results are presented as network graphs where correlations are shown regarding different aspects of office work outdoors. The results indicate that outdoor office work in a public urban space may promote work-related well-being in terms of positive outdoor office space experiences. Based on the findings, a preliminary set of outdoor office qualities is proposed. Those qualities relate to the legibility and imageability of the outdoor office space, its focal points, and depth/spaciousness, in addition to attributes of usability and environmental richness, including if the outdoor office space affords natural contact and supports activities, in addition to social and individual interactions and relations.

Active Commuting and Healthy Behavior among Adolescents in Neighborhoods with Varying Socioeconomic Status: The NESLA Study.

(1) Background: The World Health Organization recommends active commuting as a source of physical activity. Active commuting is determined by various factors, including the socioeconomic status (SES) of families and neighborhoods, distance to schools, perceived neighborhood safety, lifestyles and availability of walkways and biking paths. This study aimed to assess factors associated with modes of transportation to and from school among adolescents aged 16-19 living in a middle-sized city in Sweden. (2) Method: Three hundred and fourteen students, of whom 55% were females, from schools in the city of Västerås participated in the study. Printed as well as web-based self-administered questionnaires were used to collect the data. (3) Results: Adolescents living in high SES neighborhoods were 80% more likely to bike or walk to school (OR = 1.80; CI: 1.01, 3.20) than adolescents living in low SES neighborhoods. Furthermore, active commuting was associated with higher consumption of fruits and vegetables (OR = 1.77; CI: 1.05, 2.97) and less consumption of junk foods (OR = 0.43; CI: 0.26, 0.71), as compared to passive commuting. (4) Conclusions: Active commuting is a cost-effective and sustainable source of regular physical activity and should be encouraged at a societal level.

Age-of-onset information helps identify 76 genetic variants associated with allergic disease.

Risk factors that contribute to inter-individual differences in the age-of-onset of allergic diseases are poorly understood. The aim of this study was to identify genetic risk variants associated with the age at which symptoms of allergic disease first develop, considering information from asthma, hay fever and eczema. Self-reported age-of-onset information was available for 117,130 genotyped individuals of European ancestry from the UK Biobank study. For each individual, we identified the earliest age at which asthma, hay fever and/or eczema was first diagnosed and performed a genome-wide association study (GWAS) of this combined age-of-onset phenotype. We identified 50 variants with a significant independent association (P<3x10-8) with age-of-onset. Forty-five variants had comparable effects on the onset of the three individual diseases and 38 were also associated with allergic disease case-control status in an independent study (n = 222,484). We observed a strong negative genetic correlation between age-of-onset and case-control status of allergic disease (rg = -0.63, P = 4.5x10-61), indicating that cases with early disease onset have a greater burden of allergy risk alleles than those with late disease onset. Subsequently, a multivariate GWAS of age-of-onset and case-control status identified a further 26 associations that were missed by the univariate analyses of age-of-onset or case-control status only. Collectively, of the 76 variants identified, 18 represent novel associations for allergic disease. We identified 81 likely target genes of the 76 associated variants based on information from expression quantitative trait loci (eQTL) and non-synonymous variants, of which we highlight ADAM15, FOSL2, TRIM8, BMPR2, CD200R1, PRKCQ, NOD2, SMAD4, ABCA7 and UBE2L3. Our results support the notion that early and late onset allergic disease have partly distinct genetic architectures, potentially explaining known differences in pathophysiology between individuals.

Eleven loci with new reproducible genetic associations with allergic disease risk.

BACKGROUND: A recent genome-wide association study (GWAS) identified 99 loci that contain genetic risk variants shared between asthma, hay fever, and eczema. Many more risk loci shared between these common allergic diseases remain to be discovered, which could point to new therapeutic opportunities. OBJECTIVE: We sought to identify novel risk loci shared between asthma, hay fever, and eczema by applying a gene-based test of association to results from a published GWAS that included data from 360,838 subjects. METHODS: We used approximate conditional analysis to adjust the results from the published GWAS for the effects of the top risk variants identified in that study. We then analyzed the adjusted GWAS results with the EUGENE gene-based approach, which combines evidence for association with disease risk across regulatory variants identified in different tissues. Novel gene-based associations were followed up in an independent sample of 233,898 subjects from the UK Biobank study. RESULTS: Of the 19,432 genes tested, 30 had a significant gene-based association at a Bonferroni-corrected P value of 2.5 × 10-6. Of these, 20 were also significantly associated (P < .05/30 = .0016) with disease risk in the replication sample, including 19 that were located in 11 loci not reported to contain allergy risk variants in previous GWASs. Among these were 9 genes with a known function that is directly relevant to allergic disease: FOSL2, VPRBP, IPCEF1, PRR5L, NCF4, APOBR, IL27, ATXN2L, and LAT. For 4 genes (eg, ATXN2L), a genetically determined decrease in gene expression was associated with decreased allergy risk, and therefore drugs that inhibit gene expression or function are predicted to ameliorate disease symptoms. The opposite directional effect was observed for 14 genes, including IL27, a cytokine known to suppress TH2 responses. CONCLUSION: Using a gene-based approach, we identified 11 risk loci for allergic disease that were not reported in previous GWASs. Functional studies that investigate the contribution of the 19 associated genes to the pathophysiology of allergic disease and assess their therapeutic potential are warranted.

Bidirectional relationship between eating disorders and autoimmune diseases.

BACKGROUND: Immune system dysfunction may be associated with eating disorders (ED) and could have implications for detection, risk assessment, and treatment of both autoimmune diseases and EDs. However, questions regarding the nature of the relationship between these two disease entities remain. We evaluated the strength of associations for the bidirectional relationships between EDs and autoimmune diseases. METHODS: In this nationwide population-based study, Swedish registers were linked to establish a cohort of more than 2.5 million individuals born in Sweden between January 1, 1979 and December 31, 2005 and followed up until December 2013. Cox proportional hazard regression models were used to investigate: (a) subsequent risk of EDs in individuals with autoimmune diseases; and (b) subsequent risk of autoimmune diseases in individuals with EDs. RESULTS: We observed a strong, bidirectional relationship between the two illness classes indicating that diagnosis in one illness class increased the risk of the other. In women, the diagnoses of autoimmune disease increased subsequent hazards of anorexia nervosa (AN), bulimia nervosa (BN), and other eating disorders (OED). Similarly, AN, BN, and OED increased subsequent hazards of autoimmune diseases.Gastrointestinal-related autoimmune diseases such as, celiac disease and Crohn's disease showed a bidirectional relationship with AN and OED. Psoriasis showed a bidirectional relationship with OED. The previous occurence of type 1 diabetes increased the risk for AN, BN, and OED. In men, we did not observe a bidirectional pattern, but prior autoimmune arthritis increased the risk for OED. CONCLUSIONS: The interactions between EDs and autoimmune diseases support the previously reported associations. The bidirectional risk pattern observed in women suggests either a shared mechanism or a third mediating variable contributing to the association of these illnesses.

Occupational stress and risk for Parkinson's disease: A nationwide cohort study.

BACKGROUND: Stress has been suggested as a contributing factor in the etiology of Parkinson's Disease (PD), but epidemiological evidence is sparse. OBJECTIVE: The objective of this study was to explore the association between occupational stress according to the job demands-control model and the risk for PD. METHODS: We conducted a population-based cohort study with 2,544,748 Swedes born 1920 to 1950 who had an occupation reported in the population and housing censuses in 1980 or, if missing, in 1970. Job demands and control were measured using a job-exposure matrix. Incident PD cases were identified using Swedish national health registers from 1987 to 2010. Data were analyzed with Cox regression with age as the underlying time scale, adjusting for sex, education, and chronic obstructive pulmonary disease as a proxy for smoking. RESULTS: During a mean follow-up time of 21.3 years, 21,544 incident PD cases were identified. High demands were associated with increased PD risk among men, most evident in men with high education. High control was associated with increased PD risk among the low educated. This association was more pronounced in women. High-strain jobs (high demands and low control) was only associated with increased PDrisk among men with high education, whereas active jobs (high demands and high control) were associated with increased PD risk among men with low education. INTERPRETATION: High job demands appear to increase PD risk in men, especially in men with high education, whereas high job control increases PD risk among low educated, more strongly in women. © 2018 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

Strong impact on plasma protein profiles by precentrifugation delay but not by repeated freeze-thaw cycles, as analyzed using multiplex proximity extension assays.

Background A number of factors regarding blood collection, handling and storage may affect sample quality. The purpose of this study was to assess the impact on plasma protein profiles by delayed centrifugation and plasma separation and multiple freeze-thaw cycles. Methods Blood samples drawn from 16 healthy individuals were collected into ethylenediaminetetraacetic acid tubes and kept either at 4 °C or 22 °C for 1-36 h prior to centrifugation. Plasma samples prepared 1 h after venipuncture were also subjected to two to eight cycles of freezing at -80 °C and thawing at 22 °C. Multiplex proximity extension assay, an antibody-based protein assay, was used to investigate the influence on plasma proteins. Results Up to 36 h delay before blood centrifugation resulted in significant increases of 16 and 40 out of 139 detectable proteins in samples kept at 4 °C or 22 °C, respectively. Some increases became noticeable after 8 h delay at 4 °C but already after 1 h at 22 °C. For samples stored at 4 °C, epidermal growth factor (EGF), NF-kappa-B essential modulator, SRC, interleukin 16 and CD6 increased the most, whereas the five most significantly increased proteins after storage at 22 °C were CD40 antigen ligand (CD40-L), EGF, platelet-derived growth factor subunit B, C-X-C motif chemokine ligand 5 and matrix metallopeptidase 1 (MMP1). Only matrix metallopeptidase 7 (MMP7) decreased significantly over time and only after storage at 22 °C. No protein levels were found to be significantly affected by up to eight freeze-thaw cycles. Conclusions Plasma should be prepared from blood after a limited precentrifugation delay at a refrigerated temperature. By contrast, the influence by several freeze-thaw cycles on detectable protein levels in plasma was negligible.

Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology.

Asthma, hay fever (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals, partly because of a shared genetic origin. To identify shared risk variants, we performed a genome-wide association study (GWAS; n = 360,838) of a broad allergic disease phenotype that considers the presence of any one of these three diseases. We identified 136 independent risk variants (P < 3 × 10-8), including 73 not previously reported, which implicate 132 nearby genes in allergic disease pathophysiology. Disease-specific effects were detected for only six variants, confirming that most represent shared risk factors. Tissue-specific heritability and biological process enrichment analyses suggest that shared risk variants influence lymphocyte-mediated immunity. Six target genes provide an opportunity for drug repositioning, while for 36 genes CpG methylation was found to influence transcription independently of genetic effects. Asthma, hay fever and eczema partly coexist because they share many genetic risk variants that dysregulate the expression of immune-related genes.

Adherence to dietary recommendations for Swedish adults across categories of greenhouse gas emissions from food.

OBJECTIVE: To explore associations between diet-related greenhouse gas emissions (GHGE), nutrient intakes and adherence to the Nordic Nutrition Recommendations among Swedish adults. DESIGN: Diet was assessed by 4d food records in the Swedish National Dietary Survey. GHGE was estimated by linking all foods to carbon dioxide equivalents, using data from life cycle assessment studies. Participants were categorized into quartiles of energy-adjusted GHGE and differences between GHGE groups regarding nutrient intakes and adherence to nutrient recommendations were explored. SETTING: Sweden. SUBJECTS: Women (n 840) and men (n 627) aged 18-80 years. RESULTS: Differences in nutrient intakes and adherence to nutrient recommendations between GHGE groups were generally small. The dietary intake of participants with the lowest emissions was more in line with recommendations regarding protein, carbohydrates, dietary fibre and vitamin D, but further from recommendations regarding added sugar, compared with the highest GHGE group. The overall adherence to recommendations was found to be better among participants with lower emissions compared with higher emissions. Among women, 27 % in the lowest GHGE group adhered to at least twenty-three recommendations compared with only 12 % in the highest emission group. For men, the corresponding figures were 17 and 10 %, respectively. CONCLUSIONS: The study compared nutrient intakes as well as adherence to dietary recommendations for diets with different levels of GHGE from a national dietary survey. We found that participants with low-emission diets, despite higher intake of added sugar, adhered to a larger number of dietary recommendations than those with high emissions.

Exploring the Causal Pathway From Telomere Length to Coronary Heart Disease: A Network Mendelian Randomization Study.

RATIONALE: Observational studies have found shorter leukocyte telomere length (TL) to be a risk factor for coronary heart disease (CHD), and recently the association was suggested to be causal. However, the relationship between TL and common metabolic risk factors for CHD is not well understood. Whether these risk factors could explain pathways from TL to CHD warrants further attention. OBJECTIVE: To examine whether metabolic risk factors for CHD mediate the causal pathway from short TL to increased risk of CHD using a network Mendelian randomization design. METHODS AND RESULTS: Summary statistics from several genome-wide association studies were used in a 2-sample Mendelian randomization study design. Network Mendelian randomization analysis-an approach using genetic variants as the instrumental variables for both the exposure and mediator to infer causality-was performed to examine the causal association between telomeres and CHD and metabolic risk factors. Summary statistics from the ENGAGE Telomere Consortium were used (n=37 684) as a TL genetic instrument, CARDIoGRAMplusC4D Consortium data were used (case=22 233 and control=64 762) for CHD, and other consortia data were used for metabolic traits (fasting insulin, triglyceride, total cholesterol, low-density lipoprotein cholesterol, fasting glucose, diabetes mellitus, glycohemoglobin, body mass index, waist circumference, and waist:hip ratio). One-unit increase of genetically determined TL was associated with -0.07 (95% confidence interval, -0.01 to -0.12; P=0.01) lower log-transformed fasting insulin (pmol/L) and 21% lower odds (95% confidence interval, 3-35; P=0.02) of CHD. Higher genetically determined log-transformed fasting insulin level was associated with higher CHD risk (odds ratio, 1.86; 95% confidence interval, 1.01-3.41; P=0.04). CONCLUSIONS: Overall, our findings support a role of insulin as a mediator on the causal pathway from shorter telomeres to CHD pathogenesis.

Is a diet low in greenhouse gas emissions a nutritious diet? - Analyses of self-selected diets in the LifeGene study.

BACKGROUND: Climate change is an urgent global issue and the food sector is a major contributor to greenhouse gas emissions (GHGE). Here we study if a diet low in GHGE could be a nutritious diet compared to the Nordic Nutrition Recommendations (NNR). METHODS: The environmental impact of foods from Life Cycle Assessment (LCA) data was linked to a food frequency questionnaire (FFQ) filled out by 5,364 participants in the Swedish LifeGene study. Thereafter, we calculated the daily emission of CO2 equivalents (CO2e) as well as the intake of selected nutrients associated with vegetables, fruits, meat and dairy products. The CO2e was divided into quartiles were quartile 1 corresponds to a diet generating the lowest CO2e, and quartile 4 corresponds to a diet with the highest CO2e. RESULTS: The overall diet-related emission was 4.7 kg CO2e/day and person, corresponding to 1.7 ton CO2e/year. In general, there were only small differences in nutrient intake between groups of varying levels of CO2e, regardless if the intake was analyzed as absolute intake, energy percent or as nutrient density. Moreover, adherence to NNR was high for the group with the lowest CO2e, except for saturated fat where the intake was higher than recommended for all CO2e groups. On the other hand, only the group with the lowest CO2e fulfilled recommended intake of fiber. However, none of the CO2e groups reached the recommended intake of folate and vitamin D. CONCLUSIONS: Here we show that a self-selected diet low in CO2e provides comparable intake of nutrients as a diet high in in CO2e.

Vagotomy and Parkinson disease: A Swedish register-based matched-cohort study.

OBJECTIVE: To examine whether vagotomy decreases the risk of Parkinson disease (PD). METHODS: Using data from nationwide Swedish registers, we conducted a matched-cohort study of 9,430 vagotomized patients (3,445 truncal and 5,978 selective) identified between 1970 and 2010 and 377,200 reference individuals from the general population individually matched to vagotomized patients by sex and year of birth with a 40:1 ratio. Participants were followed up from the date of vagotomy until PD diagnosis, death, emigration out of Sweden, or December 31, 2010, whichever occurred first. Vagotomy and PD were identified from the Swedish Patient Register. We estimated hazard ratios (HRs) with 95% confidence intervals (CIs) using Cox models stratified by matching variables, adjusting for country of birth, chronic obstructive pulmonary disease, diabetes mellitus, vascular diseases, rheumatologic disease, osteoarthritis, and comorbidity index. RESULTS: A total of 4,930 cases of incident PD were identified during 7.3 million person-years of follow-up. PD incidence (per 100,000 person-years) was 61.8 among vagotomized patients (80.4 for truncal and 55.1 for selective) and 67.5 among reference individuals. Overall, vagotomy was not associated with PD risk (HR 0.96, 95% CI 0.78-1.17). However, there was a suggestion of lower risk among patients with truncal vagotomy (HR 0.78, 95% CI 0.55-1.09), which may be driven by truncal vagotomy at least 5 years before PD diagnosis (HR 0.59, 95% CI 0.37-0.93). Selective vagotomy was not related to PD risk in any analyses. CONCLUSIONS: Although overall vagotomy was not associated the risk of PD, we found suggestive evidence for a potential protective effect of truncal, but not selective, vagotomy against PD development.

Broad HIV-1 inhibition in vitro by vaccine-elicited CD8(+) T cells in African adults.

We are developing a pan-clade HIV-1 T-cell vaccine HIVconsv, which could complement Env vaccines for prophylaxis and be a key to HIV cure. Our strategy focuses vaccine-elicited effector T-cells on functionally and structurally conserved regions (not full-length proteins and not only epitopes) of the HIV-1 proteome, which are common to most global variants and which, if mutated, cause a replicative fitness loss. Our first clinical trial in low risk HIV-1-negative adults in Oxford demonstrated the principle that naturally mostly subdominant epitopes, when taken out of the context of full-length proteins/virus and delivered by potent regimens involving combinations of simian adenovirus and poxvirus modified vaccinia virus Ankara, can induce robust CD8(+) T cells of broad specificities and functions capable of inhibiting in vitro HIV-1 replication. Here and for the first time, we tested this strategy in low risk HIV-1-negative adults in Africa. We showed that the vaccines were well tolerated and induced high frequencies of broadly HIVconsv-specific plurifunctional T cells, which inhibited in vitro viruses from four major clades A, B, C, and D. Because sub-Saharan Africa is globally the region most affected by HIV-1/AIDS, trial HIV-CORE 004 represents an important stage in the path toward efficacy evaluation of this highly rational and promising vaccine strategy.

Early-Life Factors and Risk of Parkinson's Disease: A Register-Based Cohort Study.

Parkinson's disease (PD) may take decades to develop and early life exposures such as infection may be important. However, few epidemiological studies have evaluated early life risk factors in relation to PD risk. We therefore examined such associations in a prospective analysis of 3 545 612 individuals born in Sweden between 1932 and 1970 without PD on January 1, 2002. Incident PD cases were identified using the Swedish Patient Register during 2002-2010. Information on sibship size, number of older and younger siblings, multiple births, parental age, birth month and season was obtained from the Swedish Multi-Generation Register. Monthly data on national burden of influenza-like illness during 1932-1970 were obtained from the Swedish Public Health Agency. Hazard ratios with 95% confidence intervals (CI) were estimated using Cox proportional hazards regression. During the follow-up, 8779 incident PD cases were identified. As expected, older age, male sex, parental occupation as farmers, and family history of PD were associated with higher PD risk. Overall, early life factors, including flu burden in the year of birth, were not associated with PD risk, although we did find a lower PD risk among participants with older siblings than those without (HR = 0.93, 95%CI: 0.89, 0.98). Our study therefore provided little support for important etiological contributions of early life factors to the PD risk late in life. The finding of a lower PD risk among individuals with older siblings will need confirmation and further investigation.

Body mass index in relation to serum prostate-specific antigen levels and prostate cancer risk.

High Body mass index (BMI) has been directly associated with risk of aggressive or fatal prostate cancer. One possible explanation may be an effect of BMI on serum levels of prostate-specific antigen (PSA). To study the association between BMI and serum PSA as well as prostate cancer risk, a large cohort of men without prostate cancer at baseline was followed prospectively for prostate cancer diagnoses until 2015. Serum PSA and BMI were assessed among 15,827 men at baseline in 2010-2012. During follow-up, 735 men were diagnosed with prostate cancer with 282 (38.4%) classified as high-grade cancers. Multivariable linear regression models and natural cubic linear regression splines were fitted for analyses of BMI and log-PSA. For risk analysis, Cox proportional hazards regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) and natural cubic Cox regression splines producing standardized cancer-free probabilities were fitted. Results showed that baseline Serum PSA decreased by 1.6% (95% CI: -2.1 to -1.1) with every one unit increase in BMI. Statistically significant decreases of 3.7, 11.7 and 32.3% were seen for increasing BMI-categories of 25 < 30, 30 < 35 and ≥35 kg/m(2), respectively, compared to the reference (18.5 < 25 kg/m(2)). No statistically significant associations were seen between BMI and prostate cancer risk although results were indicative of a positive association to incidence rates of high-grade disease and an inverse association to incidence of low-grade disease. However, findings regarding risk are limited by the short follow-up time. In conclusion, BMI was inversely associated to PSA-levels. BMI should be taken into consideration when referring men to a prostate biopsy based on serum PSA-levels.

Relative immaturity and ADHD: findings from nationwide registers, parent- and self-reports.

BACKGROUND: We addressed if immaturity relative to peers reflected in birth month increases the likelihood of ADHD diagnosis and treatment. METHODS: We linked nationwide Patient and Prescribed Drug Registers and used prospective cohort and nested case-control designs to study 6-69 year-old individuals in Sweden from July 2005 to December 2009 (Cohort 1). Cohort 1 included 56,263 individuals diagnosed with ADHD or ever used prescribed ADHD-specific medication. Complementary population-representative cohorts provided DSM-IV ADHD symptom ratings; parent-reported for 10,760 9-year-old twins born 1995-2000 from the CATSS study (Cohort 2) and self-reported for 6,970 adult twins age 20-47 years born 1959-1970 from the STAGE study (Cohort 3). We calculated odds ratios (OR:s) for ADHD across age for individuals born in November/December compared to January/February (Cohort 1). ADHD symptoms in Cohorts 2 and 3 were studied as a function of calendar birth month. RESULTS: ADHD diagnoses and medication treatment were both significantly more common in individuals born in November/December versus January/February; peaking at ages 6 (OR: 1.8; 95% CI: 1.5-2.2) and 7 years (OR: 1.6; 95% CI: 1.3-1.8) in the Patient and Prescribed Drug Registers, respectively. We found no corresponding differences in parent- or self-reported ADHD symptoms by calendar birth month. CONCLUSION: Relative immaturity compared to class mates might contribute to ADHD diagnosis and pharmacotherapy despite absence of parallel findings in reported ADHD symptom loads by relative immaturity. Increased clinical awareness of this phenomenon may be warranted to decrease risk for imprecise diagnostics and treatment. We speculate that flexibility regarding age at school start according to individual maturity could reduce developmentally inappropriate demands on children and improve the precision of ADHD diagnostic practice and pharmacological treatment.