| 1. |
- Andersson, Anneli, 1992-, et al.
(författare)
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Attention-deficit/hyperactivity disorder and smoking habits in pregnant women
- 2020
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 15:6
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Tidskriftsartikel (refereegranskat)abstract
- Background: Attention-deficit/hyperactivity disorder (ADHD) has been associated with an increased risk of tobacco smoking, and more difficulties with smoking cessation compared to non-ADHD individuals. Women with ADHD may therefore show elevated rates of smoking during pregnancy.Aims: To examine the association between ADHD and smoking habits among pregnant women in Sweden and Norway.Methods: Women pregnant for the first time were identified in Sweden (n = 622,037), and Norway (n = 293,383), of which 1.2% (n = 7,444), and 1.7% (n = 4,951) were defined as having ADHD, respectively. Data on smoking habits were collected early and late in pregnancy.Results: In Sweden, ADHD was associated with an increased risk of smoking early in pregnancy, adjusted risk ratio (adjRR) 2.69 (95% confidence interval, 2.58-2.81), and late in pregnancy, adjRR 2.95 (2.80-3.10). Similar findings were observed in the Norwegian data, early in pregnancy, adjRR 2.31 (2.21-2.40), and late in pregnancy, adjRR 2.56 (2.42-2.70). Women with ADHD were more likely to continue smoking during pregnancy, compared to women without ADHD, both in Sweden adjRR 1.13 (1.10-1.17), and in Norway, adjRR 1.16 (1.12-1.20). Having a sibling diagnosed with ADHD was associated with an increased risk of smoking early and late in pregnancy, in both Sweden and Norway.Conclusions: Women with ADHD are considerably more likely to smoke early and late in (their first) pregnancy and are less likely to stop smoking between the two time points. Smoking, early and late in pregnancy, co-aggregates in families with ADHD. Smoking prevention and intervention programs should be targeted towards women with ADHD, specifically during their childbearing years, to ensure better mother and child outcomes.
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| 2. |
- Chen, Qi, et al.
(författare)
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Common psychiatric and metabolic comorbidity of adult attention-deficit/hyperactivity disorder : A population-based cross-sectional study
- 2018
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 13:9
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Tidskriftsartikel (refereegranskat)abstract
- Attention-deficit/hyperactivity disorder (ADHD) is often comorbid with other psychiatric conditions in adults. Yet, less is known about its relationship with common metabolic disorders and how sex and ageing affect the overall comorbidity patterns of adult ADHD. We aimed to examine associations of adult ADHD with several common psychiatric and metabolic conditions. Through the linkage of multiple Swedish national registers, 5,551,807 adults aged 18 to 64 years and living in Sweden on December 31, 2013 were identified and assessed for clinical diagnoses of adult ADHD, substance use disorder (SUD), depression, bipolar disorder, anxiety, type 2 diabetes mellitus (T2DM), and hypertension. Logistic regression models and regression standardization method were employed to obtain estimates of prevalence, prevalence difference (PD), and prevalence ratio (PR). All comorbid conditions of interest were more prevalent in adults with ADHD (3.90% to 44.65%) than in those without (0.72% to 4.89%), with the estimated PRs being over nine for psychiatric conditions (p < 0.001) and around two for metabolic conditions (p < 0.001). Sex differences in the prevalence of comorbidities were observed among adults with ADHD. Effect modification by sex was detected on the additive scale and/or multiplicative scale for the associations of adult ADHD with all comorbidities. ADHD remained associated with all comorbidities in older adults aged 50 to 64 when all conditions were assessed from age 50 onwards. The comorbidity patterns of adult ADHD underscore the severity and clinical complexity of the disorder. Clinicians should remain vigilant for a wide range of psychiatric and metabolic problems in ADHD affected adults of all ages and both sexes.
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| 3. |
- Hegvik, Tor-Arne, et al.
(författare)
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Familial co-aggregation of attention-deficit/hyperactivity disorder and autoimmune diseases : a cohort study based on Swedish population-wide registers
- 2022
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Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 51:3, s. 898-909
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) has been associated with several autoimmune diseases (AD), both within individuals and across relatives, implying common underlying genetic or environmental factors in line with studies indicating that immunological mechanisms are key to brain development. To further elucidate the relationship between ADHD and autoimmunity we performed a population-wide familial co-aggregation study.METHODS: We linked Swedish national registries, defined a birth cohort with their biological relatives and identified individuals diagnosed with ADHD and/or 13 ADs. The cohort included 5 178 225 individuals born between 1960 and 2010, of whom 118 927 (2.30%) had been diagnosed with ADHD. We then investigated the associations between ADHD and ADs within individuals and across relatives, with logistic regression and structural equation modelling.RESULTS: Within individuals, ADHD was associated with a diagnosis of any of the 13 investigated ADs (adjusted odds ratio (OR) =1.34, 95% confidence interval (CI) = 1.30-1.38) as well as several specific ADs. Familial co-aggregation was observed. For example, ADHD was associated with any of the 13 ADs in mothers (OR = 1.29, 95% CI = 1.26-1.32), fathers (OR = 1.14, 95% CI = 1.11-1.18), full siblings (OR = 1.19, 95% CI = 1.15-1.22), aunts (OR = 1.12, 95% CI = 1.10-1.15), uncles (OR = 1.07, 95% CI = 1.05-1.10) and cousins (OR = 1.04, 95% CI = 1.03-1.06). Still, the absolute risks of AD among those with ADHD were low. The genetic correlation between ADHD and a diagnosis of any of the investigated ADs was 0.13 (95% CI = 0.09-0.17) and the environmental correlation was 0.02 (95% CI = -0.03-0.06).CONCLUSIONS: We found that ADHD and ADs co-aggregate among biological relatives, indicating that the relationship between ADHD and autoimmune diseases may in part be explained by shared genetic risk factors. The patterns of familial co-aggregation of ADHD and ADs do not readily support a role of maternal immune activation in the aetiology of ADHD. The findings have implications for aetiological models of ADHD. However, screening for autoimmunity among individuals with ADHD is not warranted.
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| 4. |
- Hegvik, Tor-Arne, et al.
(författare)
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Labor epidural analgesia and subsequent risk of offspring autism spectrum disorder and attention-deficit/hyperactivity disorder : A cross-national cohort study of 4.5 million individuals and their siblings
- 2023
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Ingår i: American Journal of Obstetrics and Gynecology. - : Elsevier. - 0002-9378 .- 1097-6868. ; 228:2, s. 233.e1-233.e12
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: A recent study has suggested that labor epidural analgesia may be associated with increased rates of offspring autism spectrum disorder (ASD). Subsequent replication attempts have lacked sufficient power to confidently exclude the possibility of a small effect and the causal nature of this association remains unknown.OBJECTIVE: To investigate the extent to which exposure to labor epidural analgesia is associated with offspring ASD and attention-deficit/hyperactivity disorder (ADHD) following adjustments for unmeasured familial confounding.STUDY DESIGN: We identified 4,498,462 singletons and their parents using the Medical Birth Registers in Finland (cohorts born 1987-2005), Norway (1999-2015), and Sweden (1987-2011), linked with population and patient registries. These cohorts were followed from birth until they either had the outcomes of interest, emigrated, died, or reached the end of the follow-up (at mean ages 13.6-16.8 years), whichever occurred first. Cox regression models were used to estimate country-specific associations between labor epidural analgesia recorded at birth and outcomes (e.g., at least one secondary care diagnosis of ASD and ADHD or at least one dispensed prescription of medication used for the treatment of ADHD). The models were adjusted for sex, birth year, birth order, and unmeasured familial confounders via sibling-comparisons. Pooled estimates across all three countries were estimated using inverse variance weighted fixed-effects meta-analysis models.RESULTS: A total of 4,498,462 individuals (48.7% female) were included, 1,091,846 (24.3%) of which were exposed to labor epidural analgesia. Of these, 1.2% were diagnosed with ASD and 4.0% with ADHD. On the population level, pooled estimates showed that labor epidural analgesia was associated with increased risk of offspring ASD (adjusted hazard ratio, aHR=1.12; 95% CI: 1.10-1.14, absolute risks: 1.20% vs. 1.07%) and ADHD (aHR=1.20; 1.19-1.21; 3.95% vs. 3.32%). However, when comparing full-siblings who were differentially exposed to labor epidural analgesia, the associations were fully attenuated for both conditions, with narrow confidence intervals (aHRASD=0.98; 0.93-1.03; aHRADHD=0.99; 0.96-1.02).CONCLUSION: In this large cross-national study, we found no support for the hypothesis that exposure to labor epidural analgesia causes either offspring autism spectrum disorder or attention-deficit/hyperactivity disorder.
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| 5. |
- Hegvik, Tor-Arne, et al.
(författare)
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The familial co-aggregation of ADHD and cerebral palsy : a population-based cohort study
- 2019
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 49:6, s. 536-536
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Cerebral palsy (CP) is a chronic, non-progressive neurological disorder characterized by motor dysfunction believed to be due to disturbances to the developing brain. Several studies have reported that the symptoms of attention-deficit/hyperactivity disorder (ADHD) may be common among individuals with CP. Likewise, clinically diagnosed ADHD has been associated with CP, both within individuals and across siblings. However, it is unknown whether ADHD and CP co-aggregate within extended families, which would further support the presence of shared familial factors in the etiology of the two disorders. To further assess the relationship between ADHD and CP, we conducted a population-wide familial co-aggregation study.With the use of Swedish national registries we defined a birth cohort born 1960–2010, 5 178,255 individuals, and their biological relatives. We then identified individuals diagnosed with ADHD and/or CP and investigated the familial co-aggregation of ADHD and CP using logistic regression.ADHD was associated with CP within individuals, adjusted odds ratio (OR) = 2.10 (95% confidence interval: 1.94–2.27), and across relatives with ADHD being associated with CP in mothers, OR = 1.51 (1.20–1.93), fathers, OR = 1.82 (1.44–2.29), full siblings, OR = 1.28 (1.16–1.41), and cousins, OR = 1.11 (1.05–1.17).Our preliminary findings suggest that ADHD and CP share etiological factors, which may also include genetic factors. This may have consequences for our understanding of both ADHD and CP. Furthermore, shared etiological mechanisms underlying ADHD and CP may indicate that the psychological and pharmacological treatments of ADHD could have a role in the treatment of some of the impairments common among individuals with CP.
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| 6. |
- Li, Lin, 1989-, et al.
(författare)
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Attention-deficit/hyperactivity disorder symptoms and dietary habits in adulthood : A large population-based twin study in Sweden
- 2020
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Ingår i: American Journal of Medical Genetics Part B. - : John Wiley & Sons. - 1552-4841 .- 1552-485X. ; 183:8, s. 475-485
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Tidskriftsartikel (refereegranskat)abstract
- Associations between adult attention-deficit/hyperactivity disorder (ADHD) symptoms and dietary habits have not been well established and the underlying mechanisms remain unclear. We explored these associations using a Swedish population-based twin study with 17,999 individuals aged 20-47 years. We estimated correlations between inattention and hyperactivity/impulsivity with dietary habits and fitted twin models to determine the genetic and environmental contributions. Dietary habits were defined as (a) consumption of food groups, (b) consumption of food items rich in particular macronutrients, and (c) healthy and unhealthy dietary patterns. At the phenotypic level, inattention was positively correlated with seafood, high-fat, high-sugar, high-protein food consumptions, and unhealthy dietary pattern, with correlation coefficients ranging from 0.03 (95%CI: 0.01, 0.05) to 0.13 (95% CI: 0.11, 0.15). Inattention was negatively correlated with fruits, vegetables consumptions and healthy dietary pattern, with correlation coefficients ranging from -0.06 (95%CI: -0.08, -0.04) to -0.07 (95%CI: -0.09, -0.05). Hyperactivity/impulsivity and dietary habits showed similar but weaker patterns compared to inattention. All associations remained stable across age, sex and socioeconomic status. Nonshared environmental effects contributed substantially to the correlations of inattention (56-60%) and hyperactivity/impulsivity (63-80%) with dietary habits. The highest and lowest genetic correlations were between inattention and high-sugar food (rA = .16, 95% CI: 0.07, 0.25), and between hyperactivity/impulsivity and unhealthy dietary pattern (rA = .05, 95% CI: -0.05, 0.14), respectively. We found phenotypic and etiological overlap between ADHD and dietary habits, although these associations were weak. Our findings contribute to a better understanding of common etiological pathways between ADHD symptoms and various dietary habits.
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| 7. |
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| 8. |
- Li, Lin, 1989-, et al.
(författare)
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Genetic and environmental contributions to the association between ADHD symptoms and unhealthy dietary habits in adulthood : a large population-based twin study
- 2019
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 49:6, s. 511-512
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- ADHD may be associated with unhealthy dietary habits in children and adolescents. The link between diets and adult ADHD symptoms are not well established and the underlying genetic and environmental mechanisms remain unclear. Therefore, we firstly estimated associations between ADHD symptoms (inattention, hyperactivity or both) and three unhealthy dietary groups (unhealthy food, high-sugar food, and high-fat food), and also stratified based on age, sex, and socioeconomic status (SES). This was done using self-report data from a Swedish population-based twin study on ADHD symptoms and food frequency questionnaire in 17,999 twins, aged 20 to 47 years. Secondly, univariate and bivariate twin model-fitting anal-yses were conducted to determine the relative contribution of genetic and environmental factors to the observed associations. We have found that at the phenotypical level, ADHD total score were positively associated with unhealthy food (r = 0.11, 95% CI 0.09, 0.13), high-sugar food (r = 0.10, 95% CI 0.08, 0.12), and high-fat food (r = 0.11, 95% CI 0.09, 0.13). Similar association patterns were also found when analyzing separately the inattention and hyperactivity symptoms of the ADHD total score. All these associations remained stable across age, sex, and SES. Genetic and non-shared environmental effects accounted for similar proportions of the phenotypical correlations. The highest bivariate heritability was between ADHD total score and high-sugar food (h2 = 40%, 95% CI 7, 70). This study is the first to provide evidence for a genetic overlap between ADHD symptoms and unhealthy dietary habits. The remaining non-shared environmental effects also suggest an opportunity for treatments and interventions targets that focus on modifiable non-genetic risk factors.
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| 9. |
- Li, Lin, 1989-, et al.
(författare)
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Maternal pre-pregnancy overweight/obesity and the risk of attention-deficit/hyperactivity disorder in offspring : a systematic review, meta-analysis and quasi-experimental family-based study
- 2020
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Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 49:3, s. 857-875
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Forskningsöversikt (refereegranskat)abstract
- BACKGROUND: Previous studies are inconclusive concerning the association between maternal pre-pregnancy overweight/obesity and risk of attention-deficit/hyperactivity disorder (ADHD) in offspring. We therefore conducted a systematic review and meta-analysis to clarify this association. To address the variation in confounding adjustment between studies, especially inadequate adjustment of unmeasured familial confounding in most studies, we further performed cousin and sibling comparisons in a nationwide population-based cohort in Sweden.METHODS: We searched PubMed, Embase and PsycINFO during 1975-2018. We used random-effects models to calculate pooled risk ratios (RRs) with 95% confidence interval. In the population-based study, Cox proportional hazard models were used to calculate the unadjusted hazard ratios (HRs) and HRs adjusted for all confounders identified in previous studies. Stratified Cox models were applied to data on full cousins and full siblings to further control for unmeasured familial confounding.RESULTS: Eight cohorts with a total of 784 804 mother-child pairs were included in the meta-analysis. Maternal overweight [RRoverweight = 1.31 (1.25-1.38), I2 = 6.80%] and obesity [RRobesity = 1.92 (1.84-2.00), I2 = 0.00%] were both associated with an increased risk of ADHD in offspring. In the population-based cohort of 971 501 individuals born between 1992 and 2004, unadjusted Cox models revealed similar associations [HRoverweight = 1.30 (1.28-1.34), HRobesity = 1.92 (1.87-1.98)]. These associations gradually attenuated towards the null when adjusted for measured confounders [HRoverweight = 1.21 (1.19-1.25), HRobesity = 1.60 (1.55-1.65)], unmeasured factors shared by cousins [HRoverweight = 1.10 (0.98-1.23), HRobesity = 1.44 (1.22-1.70)] and unmeasured factors shared by siblings [HRoverweight = 1.01 (0.92-1.11), HRobesity = 1.10 (0.94-1.27)].CONCLUSION: Pre-pregnancy overweight/obesity is associated with an increased risk of ADHD in offspring. The observed association is largely due to unmeasured familial confounding.
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