259 research outputs found

    Does maternal oral health predict child oral health-related quality of life in adulthood?

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    <p>Abstract</p> <p>Background</p> <p>A parental/family history of poor oral health may influence the oral-health-related quality of life (OHRQOL) of adults.</p> <p>Objectives</p> <p>To determine whether the oral health of mothers of young children can predict the OHRQOL of those same children when they reach adulthood.</p> <p>Methods</p> <p>Oral examination and interview data from the Dunedin Study's age-32 assessment, as well as maternal self-rated oral health data from the age-5 assessment were used. The main outcome measure was study members' short-form Oral Health Impact Profile (OHIP-14) at age 32. Analyses involved 827 individuals (81.5% of the surviving cohort) dentally examined at both ages, who also completed the OHIP-14 questionnaire at age 32, and whose mothers were interviewed at the age-5 assessment.</p> <p>Results</p> <p>There was a consistent gradient of relative risk across the categories of maternal self-rated oral health status at the age-5 assessment for having one or more impacts in the overall OHIP-14 scale, whereby risk was greatest among the study members whose mothers rated their oral health as "poor/edentulous", and lowest among those with an "excellent/fairly good" rating. In addition, there was a gradient in the age-32 mean OHIP-14 score, and in the mean number of OHIP-14 impacts at age 32 across the categories of maternal self-rated oral health status. The higher risk of having one or more impacts in the psychological discomfort subscale, when mother rated her oral health as "poor/edentulous", was statistically significant.</p> <p>Conclusions</p> <p>These data suggest that maternal self-rated oral health when a child is young has a bearing on that child's OHRQOL almost three decades later. The adult offspring of mothers with poor self-rated oral health had poorer OHRQOL outcomes, particularly in the psychological discomfort subscale.</p

    Cigarette smoking and periodontal disease among 32-year-olds: a prospective study of a representative birth cohort

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    Smoking is recognized as the primary behavioural risk factor for periodontal attachment loss (AL), but confirmatory data from prospective cohort studies are scarce

    Juvenile Mental Health Histories of Adults with Anxiety Disorders

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    OBJECTIVE: Information about the psychiatric histories of adults with anxiety disorders was examined to further inform nosology and etiological/ preventive efforts. METHOD: The authors used data from a prospective longitudinal study of a representative birth cohort (N=1,037) from ages 11 to 32 years, making psychiatric diagnoses according to DSM criteria. For adults with anxiety disorders at 32 years, follow-back analyses ascertained first diagnosis of anxiety and other juvenile disorders. RESULTS: Of adults with each type of anxiety disorder, approximately half had been diagnosed with a psychiatric disorder (one-third with an anxiety disorder) by age 15. The juvenile histories of psychiatric problems for adults with different types of anxiety disorders were largely nonspecific, partially reflecting comorbidity at 32 years. Histories of anxiety and depression were most common. There was also specificity. For example, adults with panic disorder did not have histories of juvenile disorders, whereas those with other anxiety disorders did. Adults with posttraumatic stress disorder had histories of conduct disorder, whereas those with other anxiety disorders did not. Adults with specific phobia had histories of juvenile phobias but not other anxiety disorders. CONCLUSIONS: Strong comorbidity between different anxiety disorders and lack of specificity in developmental histories of adults with anxiety disorders supports a hierarchical approach to classification, with a broad class of anxiety disorders having individual disorders within it. The early first diagnosis of psychiatric difficulties in individuals with anxiety disorders suggests the need to target research examining the etiology of anxiety disorders and prevention early in life

    Enduring mental health: Prevalence and prediction.

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    We review epidemiological evidence indicating that most people will develop a diagnosable mental disorder, suggesting that only a minority experience enduring mental health. This minority has received little empirical study, leaving the prevalence and predictors of enduring mental health unknown. We turn to the population-representative Dunedin cohort, followed from birth to midlife, to compare people never-diagnosed with mental disorder (N = 171; 17% prevalence) to those diagnosed at 1–2 study waves, the cohort mode (N = 409). Surprisingly, compared to this modal group, never-diagnosed Study members were not born into unusually well-to-do families, nor did their enduring mental health follow markedly sound physical health, or unusually high intelligence. Instead, they tended to have an advantageous temperament/personality style, and negligible family history of mental disorder. As adults, they report superior educational and occupational attainment, greater life satisfaction, and higher-quality relationships. Our findings draw attention to “enduring mental health” as a revealing psychological phenotype and suggest it deserves further study

    Life satisfaction and mental health problems (18 to 35 years)

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    Background: Previous research has found that mental health is strongly associated with life satisfaction. In this study we examine associations between mental health problems and life satisfaction in a birth cohort studied from 18 to 35 years. Method: Data were gathered during the Christchurch Health and Development Study, which is a longitudinal study of a birth cohort of 1265 children, born in Christchurch, New Zealand, in 1977. Assessments of psychiatric disorder (major depression, anxiety disorder, suicidality, alcohol dependence and illicit substance dependence) using DSM diagnostic criteria and life satisfaction were obtained at 18, 21, 25, 30 and 35 years. Results: Significant associations (p < 0.01) were found between repeated measures of life satisfaction and the psychiatric disorders major depression, anxiety disorder, suicidality, alcohol dependence and substance dependence. After adjustment for non-observed sources of confounding by fixed effects, statistically significant associations (p < 0.05) remained between life satisfaction and major depression, anxiety disorder, suicidality and substance dependence. Overall, those reporting three or more mental health disorders had mean life satisfaction scores that were nearly 0.60 standard deviations below those without mental health problems. A structural equation model examined the direction of causation between life satisfaction and mental health problems. Statistically significant (p < 0.05) reciprocal associations were found between life satisfaction and mental health problems.Conclusions: After adjustment for confounding, robust and reciprocal associations were found between mental health problems and life satisfaction. Overall, this study showed evidence that life satisfaction influences mental disorder, and that mental disorder influences life satisfaction

    Brain-age in midlife is associated with accelerated biological aging and cognitive decline in a longitudinal birth-cohort

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    An individual’s brainAGE is the difference between chronological age and age predicted from machine-learning models of brain-imaging data. BrainAGE has been proposed as a biomarker of age-related deterioration of the brain. Having an older brainAGE has been linked to Alzheimer’s, dementia and mortality. However, these findings are largely based on cross-sectional associations which can confuse age differences with cohort differences. To illuminate the validity of brainAGE as a biomarker of accelerated brain aging, a study is needed of a large cohort all born in the same year who nevertheless vary on brainAGE. In the Dunedin Study, a population-representative 1972–73 birth cohort, we measured brainAGE at age 45 years, as well as the pace of biological aging and cognitive decline in longitudinal data from childhood to midlife (N=869). In this cohort, all chronological age 45 years, brainAGE was measured reliably (ICC=.81) and ranged from 24 to 72 years. Those with older midlife brainAGEs tended to have poorer cognitive function in both adulthood and childhood, as well as impaired brain health at age 3. Furthermore, those with older brainAGEs had an accelerated pace of biological aging, older facial appearance and early signs of cognitive decline from childhood to midlife. These findings help to validate brainAGE as a potential surrogate biomarker for midlife intervention studies that seek to measure dementia-prevention efforts in midlife. However, the findings also caution against the assumption that brainAGE scores represent only age-related deterioration of the brain as they may also index central nervous system variation present since childhood

    Associations between life-course-persistent antisocial behaviour and brain structure in a population-representative longitudinal birth cohort

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    BACKGROUND Studies with behavioural and neuropsychological tests have supported the developmental taxonomy theory of antisocial behaviour, which specifies abnormal brain development as a fundamental aspect of life-course-persistent antisocial behaviour, but no study has characterised features of brain structure associated with life-course-persistent versus adolescence-limited trajectories, as defined by prospective data. We aimed to determine whether life-course-persistent antisocial behaviour is associated with neurocognitive abnormalities by testing the hypothesis that it is also associated with brain structure abnormalities. METHODS We used structural MRI data collected at 45 years of age from participants in the Dunedin Study, a population-representative longitudinal birth cohort of 1037 individuals born between April 1, 1972, and March 31, 1973, in Dunedin, New Zealand, who were resident in the province and who participated in the first assessment at 3 years of age. Participants underwent MRI, and mean global cortical surface area and cortical thickness were extracted for each participant. Participants had been previously subtyped as exhibiting life-course-persistent, adolescence-limited, or no history of persistent antisocial behaviour (ie, a low trajectory group) based on informant-reported and self-reported conduct problems from the ages of 7 years to 26 years. Study personnel who processed the MRI images were masked to antisocial group membership. We used linear estimated ordinary least squares regressions to compare each antisocial trajectory group (life-course persistent and adolescence limited) with the low trajectory group to examine whether antisocial behaviour was related to abnormalities in mean global surface area and mean cortical thickness. Next, we used parcel-wise linear regressions to identify antisocial trajectory group differences in surface area and cortical thickness. All results were controlled for sex and false discovery rate corrected. FINDINGS Data from 672 participants were analysed, and 80 (12%) were classified as having life-course-persistent antisocial behaviour, 151 (23%) as having adolescence-limited antisocial behaviour, and 441 (66%) as having low antisocial behaviour. Individuals on the life-course-persistent trajectory had a smaller mean surface area (standardised β=–0·18 [95% CI −0·24 to −0·11]; p<0·0001) and lower mean cortical thickness (standardised β=–0·10 [95% CI −0·19 to −0·02]; p=0·020) than did those in the low group. Compared with the low group, the life-course-persistent group had reduced surface area in 282 of 360 anatomically defined parcels and thinner cortex in 11 of 360 parcels encompassing circumscribed frontal and temporal regions associated with executive function, affect regulation, and motivation. Widespread differences in brain surface morphometry were not observed for the adolescence-limited group compared with either non-antisocial behaviour or life-course-persistent groups. INTERPRETATION These analyses provide initial evidence that differences in brain surface morphometry are associated with life-course-persistent, but not adolescence-limited, antisocial behaviour. As such, the analyses are consistent with the developmental taxonomy theory of antisocial behaviour and highlight the importance of using prospective longitudinal data to define different patterns of antisocial behaviour development. FUNDING US National Institute on Aging, Health Research Council of New Zealand, New Zealand Ministry of Business, Innovation and Employment, UK Medical Research Council, Avielle Foundation, and Wellcome Trust
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