"Late-onset" ADHD symptoms in young adulthood: Is this ADHD?
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ABSTRACT:
SUBMITTER: Riglin L
PROVIDER: S-EPMC7612898 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundAttention-deficit/hyperactivity disorder (ADHD) is associated with substance use disorders (SUD; alcohol and/or drug dependence) and nicotine dependence. This study aims to advance our knowledge about the association between SUD, nicotine dependence, and the course of ADHD (persistent versus remittent ADHD and late-onset ADHD).MethodsADHD, SUD, and nicotine dependence were longitudinally assessed (mean age at study entry 11.3?years, mean age at follow-up 21.1?years) using structured psychiatric interviews and multi-informant questionnaires in a subsample of the Dutch part of the International Multicenter ADHD Genetics study. Individuals with persistent ADHD (n?=?62), remittent ADHD (n?=?12), late-onset ADHD (n?=?18; age of onset after 12?years), unaffected siblings (n?=?50), and healthy controls (n?=?47) were assessed. Hazard ratios (HR) with 95% confidence intervals (CIs) were estimated by Cox regression and adjusted for clustered family data, gender, follow-up length, and current age.ResultsIndividuals with persistent ADHD were at significantly higher risk of development of SUD relative to healthy controls (HR?=?4.56, CI 1.17-17.81). In contrast, levels of SUD in those with remittent ADHD were not different from healthy controls (HR?=?1.00, CI .07-13.02). ADHD persisters had also higher prevalence rates of nicotine dependence (24.2%) than ADHD remitters (16.7%) and healthy controls (4.3%). A similar pattern was found in initially unaffected siblings who met ADHD criteria at follow-up ("late-onset" ADHD); they had also a higher prevalence of SUD (33%) compared to stable unaffected siblings (20%) and were at significantly increased risk of development of nicotine dependence compared to healthy controls (HR?=?13.04, CI 2.08-81.83).ConclusionsSUD and nicotine dependence are associated with a negative ADHD outcome. Results further emphasize the need for clinicians to comprehensively assess substance use when diagnosing ADHD in adolescents and adults.
| S-EPMC6307241 | biostudies-literature
Project description:Young-onset and late-onset Alzheimer's disease has different clinical presentations with late-onset presenting most often with memory deficits while young-onset often presents with a non-amnestic syndrome. However, it is unknown whether there are differences in presentation and progression of neuropsychiatric symptoms in young- versus late-onset Alzheimer's disease. We aimed to investigate differences in the prevalence and severity of neuropsychiatric symptoms in patients with young- and late-onset Alzheimer's disease longitudinally with and without accounting for the effect of medication usage. Sex differences were also considered in these patient groups. We included 126 young-onset and 505 late-onset Alzheimer's disease patients from National Alzheimer's Coordinating Center-Uniform Data Set (NACC-UDS) and Alzheimer's Disease Neuroimaging Initiative (ADNI). We investigated the prevalence and severity of neuropsychiatric symptoms using the Neuropsychiatric Inventory-Questionnaire over 4 visits with 1-year intervals, using a linear mixed-effects model. The prevalence of depression was significantly higher in young-onset than late-onset Alzheimer's disease over a 4-year interval when antidepressant usage was included in our analyses. Our findings suggest that neuropsychiatric symptom profiles of young- and late-onset Alzheimer's disease differ cross-sectionally but also display significant differences in progression.
| S-EPMC8050126 | biostudies-literature
Project description:We investigated whether girls experiencing early menarche have an increased risk of depression during young adulthood. This study used data collected in the Growing Up Today Study (N?=?9,039), an ongoing prospective cohort of the daughters of women enrolled in the Nurses' Health Study II. After excluding girls who were postmenarcheal at baseline in 1996, <20 or ?26 years old in 2007, or missing data on key covariates, the final sample size was 3,711. Self-reported age at menarche was collected annually. Depressive symptomatology was measured in 2007 using the 10-item Center for Epidemiologic Studies Depression (CES-D-10) score. Sixteen percent of girls (N?=?596) reported high levels of depressive symptoms (CES-D-10???14) in 2007. Neither early nor late menarche was associated with high depressive symptoms (for early vs. normative menarche, odds ratio (OR)?=?1.08, 95 % confidence interval (CI)?=?0.85-1.38; for late vs. normative menarche, OR?=?0.91, 95 % CI?=?0.70-1.18) or with differences in continuous CES-D-10 score in young adulthood. Although previous studies suggest that girls with early menarche suffer from an increased risk of adolescent depression, this does not appear to persist into young adulthood.
| S-EPMC4742523 | biostudies-literature
Project description:BACKGROUND:Attention-deficit hyperactivity disorder (ADHD) is associated with mental health problems and functional impairment across many domains. However, how the longitudinal course of ADHD affects later functioning remains unclear.AimsWe aimed to disentangle how ADHD developmental patterns are associated with young adult functioning. METHOD:The Environmental Risk (E-Risk) Longitudinal Twin Study is a population-based cohort of 2232 twins born in England and Wales in 1994-1995. We assessed ADHD in childhood at ages 5, 7, 10 and 12 years and in young adulthood at age 18 years. We examined three developmental patterns of ADHD from childhood to young adulthood - remitted, persistent and late-onset ADHD - and compared these groups with one another and with non-ADHD controls on functioning at age 18 years. We additionally tested whether group differences were attributable to childhood IQ, childhood conduct disorder or familial factors shared between twins. RESULTS:Compared with individuals without ADHD, those with remitted ADHD showed poorer physical health and socioeconomic outcomes in young adulthood. Individuals with persistent or late-onset ADHD showed poorer functioning across all domains, including mental health, substance misuse, psychosocial, physical health and socioeconomic outcomes. Overall, these associations were not explained by childhood IQ, childhood conduct disorder or shared familial factors. CONCLUSIONS:Long-term associations of childhood ADHD with adverse physical health and socioeconomic outcomes underscore the need for early intervention. Young adult ADHD showed stronger associations with poorer mental health, substance misuse and psychosocial outcomes, emphasising the importance of identifying and treating adults with ADHD.Declaration of interestNone.
| S-EPMC6098692 | biostudies-literature
Project description:BackgroundAdult ADHD has been assumed to be a continuation of childhood-onset ADHD. However, recent studies have identified individuals with ADHD in adulthood who have not had ADHD in childhood. Whether or not these individuals have a 'typical' neurodevelopmental profile is not clear.MethodsWe tested two explanations for the emergence of apparent late-onset ADHD symptomatology using the ALSPAC epidemiological cohort, by grouping individuals according to their scores on the Strengths and Difficulties Questionnaire (SDQ) hyperactivity subscale at ages 12 and 17 years. First, we tested whether some of those with apparent late-onset ADHD symptoms had been potentially misclassified on the basis of earlier SDQ hyperactivity scores (ages 7, 8 and 9 years) or of subthreshold symptoms at age 12 years. Second, we investigated the possibility that those with 'genuine' late-onset ADHD symptoms had a delayed manifestation of the same liability that underlies childhood-onset symptoms, by investigating whether they had a similar profile of neurodevelopmental impairments (in the domains of autistic symptomatology, language, reading, spelling, executive functioning and IQ) as those with typical childhood-onset ADHD.ResultsN = 56/75 (75%) of those with apparent late-onset ADHD had had high ADHD scores at least one point in childhood, suggesting that they may have been misclassified on the basis of their score at age 12 years. The remaining 19 individuals (25%) with genuine late-onset ADHD symptoms did not show a profile of neurodevelopmental impairment typically seen in ADHD, instead showing similar levels of autistic symptoms, language skills, executive functioning ability and IQ to those without ADHD symptoms. The only exceptions were that this group showed reading and spelling problems at age 9 years.ConclusionsOur work suggests that this small number of individuals with genuine late-onset symptoms may not be most appropriately considered as having a typical neurodevelopmental disorder.
| S-EPMC6175329 | biostudies-literature
Project description:BackgroundAdvanced stages of dementia are characterized by severe cognitive and physical impairment. It has not yet been investigated whether persons with young onset dementia (YOD) and late onset dementia (LOD) differ in advanced disease stages.ObjectivesTo compare quality of life (QoL) between persons with advanced YOD and LOD; to explore the determinants of QoL; to investigate whether YOD and LOD differ with regard to symptoms and care.MethodsThe study was performed in the context of EPYLOGE (IssuEs in Palliative care for persons in advanced and terminal stages of YOD and LOD in Germany). Persons with advanced dementia (PWAD) were assessed and caregivers were interviewed. QoL was measured with the proxy rating Quality of Life in Late Stage Dementia (QUALID) scale.Results93 persons with YOD and 98 with LOD were included. No significant differences in QoL were detected. Determinants of QoL were similar in YOD and LOD. Behavioral and psychological symptoms of dementia (BPSD), suffering and other distressing symptoms were associated with a lower QoL. In YOD but not in LOD antipsychotic treatment was associated with low QoL. The group of persons who were younger than 65 years at the time of the study visit experienced significantly more distressing symptoms than older PWAD.ConclusionOverall, persons with advanced YOD do not appear to be disadvantaged compared to old and oldest PWAD. Special attention, however, must be paid to the group of the very young persons who seem to be particularly vulnerable.
| S-EPMC8075393 | biostudies-literature
Project description:BACKGROUND:Among adults, depressive symptoms are associated with higher rates of cardiovascular disease; however, the evidence is mixed regarding the association between depressive symptoms and hypertension, especially among young adults. The deleterious effects of some antidepressant medications on blood pressure may contribute to mixed findings. METHODS:Adolescents enrolled in Add Health (N = 11,183) (1994-2008) completed an abbreviated Center for Epidemiologic Studies Depression Scale at three waves (mean ages, 16, 22, and 29). Antidepressant use was measured at age 22 and at age 29. Hypertension at age 29 was defined as measured systolic blood pressure of 140?mm Hg or greater, diastolic blood pressure of 90?mm Hg or greater, or staff-inventoried anti-hypertensive medication use. RESULTS:The prevalence of hypertension at age 29 was 20%. High depressive symptoms in adolescence or young adulthood were not associated with hypertension in young adulthood. Antidepressant use at age 29 was associated with increased prevalence of hypertension (prevalence ratio [PR], 1.4; 95% CI, 1.2, 1.7) and an interaction with sex was observed (PRMen, 1.6; 95% CI, 1.2, 2.0; PRWomen, 1.2; 95% CI, 0.89, 1.6; pinteraction = 0.0227). Selective serotonin reuptake inhibitor and non-selective serotonin reuptake inhibitor antidepressant use were associated with hypertension (PRSSRI, 1.3; 95% CI, 1.0, 1.6; PRnon-SSRI, 1.6; 95% CI, 1.2, 2.1). CONCLUSIONS:In this sample, antidepressant use, but not depressive symptoms, was associated with hypertension in young adulthood. Further research is recommended to examine joint and independent relationships between depression and antidepressant use and hypertension among young adults. See video abstract at, http://links.lww.com/EDE/B355.
| S-EPMC5980764 | biostudies-literature
Project description:Objective: Substantial individual variation exists in the age of onset and course of ADHD symptoms over development. We evaluated whether, within this variation, meaningful developmental subtypes can be defined. Method: Using growth mixture modeling in a community-based sample (N = 1,571), we analyzed ADHD symptom trajectories based on measures taken at ages 7, 8, 9, 10, 11, 13, and 15 years. We evaluated whether those showing developmental trajectories characterized by later onsets versus early onsets differed in terms of mental health and behavioral outcomes in late adolescence (age 17 years). Result: The late onset category was best conceptualized as a milder subtype than early onset. The former was, however, more similar in outcomes to the latter than to the unaffected category, suggesting that later onsets are still associated with impairment. Conclusion: Considering diagnoses for those affected by ADHD symptoms but who do not meet current age of onset criteria may be important for ensuring that they receive appropriate support.
| S-EPMC7611469 | biostudies-literature
Project description:OBJECTIVE:To examine changes in depressive symptoms as well as between- and within-person associations between depressive symptoms and Type 1 diabetes (T1D) management across the transition from late adolescence to emerging adulthood. METHOD:Beginning in the senior year of high school, 197 late adolescents with T1D (Mage = 17.77) reported on their student status and living situation, and completed self-report measures of depressive symptoms and adherence to the diabetes regimen, annually at 3 time points. Glycemic control was gathered from hemoglobin A1c (HbA1c) assay kits at the same time points. RESULTS:Results of multilevel models demonstrated high depressive symptoms at baseline, with significant increases in depressive symptoms across time when participants were not living in their parental home, but no change when living with parents. Participants with higher mean levels of depressive symptoms relative to peers (between-person association) had poorer adherence and glycemic control (i.e., higher HbA1c) on average. Within-person fluctuations in depressive symptoms were significantly associated with adherence: greater increases in depressive symptoms (relative to adolescents' own average) were associated with greater deteriorations in adherence. There was not a significant within-person effect of depressive symptoms on glycemic control. CONCLUSIONS:The transition from late adolescence to emerging adulthood is particularly challenging for those with T1D. The findings that individuals with greater depressive symptoms have poorer adherence and glycemic control relative to those with lower depressive symptoms, and that increases in depressive symptoms are associated with declines in adherence, highlight the importance of screening and monitoring depressive symptoms during this life transition. (PsycINFO Database Record
| S-EPMC6080212 | biostudies-literature
Project description:Previous studies in children with ADHD identified two partially separable familial factors underlying cognitive dysfunction, but evidence in adolescents and adults is lacking. Here, we investigate the etiological structure of cognitive-neurophysiological impairments in ADHD in adolescents and young adults.Factor analyses and multivariate familial models were run in 356 participants from ADHD and control sibling pairs aged 11 to 27 years on data on IQ, digit span forward (DSF) and backward (DSB), and cognitive-performance and event-related potential (ERP) measures from three cognitive tasks.Three familial factors (cF1-3), showing substantial familial overlap with ADHD, captured the familial covariation of ADHD with nine cognitive-ERP measures. cF1 loaded on IQ, mean reaction time (MRT), and reaction-time variability (RTV); cF2 on DSF and DSB; and cF3 on number of errors and ERPs of inhibition and error processing.These results identify three partially separable etiological pathways leading to cognitive-neurophysiological impairments in adolescent and adult ADHD.
| S-EPMC7116505 | biostudies-literature