To understand why children exposed to adverse psychosocial experiences are at elevated risk for age-related disease, such as cardiovascular disease, by testing whether adverse childhood experiences predict enduring abnormalities in stress-sensitive biological systems, namely, the nervous, immune, and endocrine/metabolic systems.
A 32-year prospective longitudinal study of a representative birth cohort.
A total of 1037 members of the Dunedin Multidisciplinary Health and Development Study.
During their first decade of life, study members were assessed for exposure to 3 adverse psychosocial experiences: socioeconomic disadvantage, maltreatment, and social isolation.
Main Outcome Measures
At age 32 years, study members were assessed for the presence of 3 age-related-disease risks: major depression, high inflammation levels (high-sensitivity C-reactive protein level >3 mg/L), and the clustering of metabolic risk biomarkers (overweight, high blood pressure, high total cholesterol, low high-density lipoprotein cholesterol, high glycated hemoglobin, and low maximum oxygen consumption levels.
Children exposed to adverse psychosocial experiences were at elevated risk of depression, high inflammation levels, and clustering of metabolic risk markers. Children who had experienced socioeconomic disadvantage (incidence rate ratio, 1.89; 95% confidence interval, 1.36–2.62), maltreatment (1.81; 1.38–2.38), or social isolation (1.87; 1.38–2.51) had elevated age-related-disease risks in adulthood. The effects of adverse childhood experiences on age-related-disease risks in adulthood were nonredundant, cumulative, and independent of the influence of established developmental and concurrent risk factors.
Children exposed to adverse psychosocial experiences have enduring emotional, immune, and metabolic abnormalities that contribute to explaining their elevated risk for age-related disease. The promotion of healthy psychosocial experiences for children is a necessary and potentially cost-effective target for the prevention of age-related disease.
Using data from the large, 30-year prospective Dunedin cohort study, we examined whether preexisting individual differences in childhood temperament predicted adulthood disordered gambling (a diagnosis covering the full continuum of gambling-related problems). A 90-min observational assessment at age 3 was used to categorize children into five temperament groups, including one primarily characterized by behavioral and emotional undercontrol. The children with undercontrolled temperament at 3 years of age were more than twice as likely to evidence disordered gambling at ages 21 and 32 than were children who were well-adjusted at age 3. These associations could not be explained by differences in childhood IQ or family socioeconomic status. Cleanly demonstrating the temporal relation between behavioral undercontrol and adult disordered gambling is an important step toward building more developmentally sensitive theories of disordered gambling and may put researchers in a better position to begin considering potential routes to disordered-gambling prevention through enhancing self-control and emotional regulation.
disordered gambling; undercontrol; personality; temperament; prediction; psychopathology; self-control; personality
Premorbid cognitive deficits in schizophrenia are well documented and have been interpreted as supporting a neurodevelopmental etiological model. The authors investigated the following three unresolved questions about premorbid cognitive deficits: What is their developmental course? Do all premorbid cognitive deficits follow the same course? Are premorbid cognitive deficits specific to schizophrenia or shared by other psychiatric disorders?
Participants were members of a representative cohort of 1,037 males and females born between 1972 and 1973 in Dunedin, New Zealand. Cohort members underwent follow-up evaluations at specific intervals from age 3 to 32 years, with a 96% retention rate. Cognitive development was analyzed and compared in children who later developed schizophrenia or recurrent depression as well as in healthy comparison subjects.
Children who developed adult schizophrenia exhibited developmental deficits (i.e., static cognitive impairments that emerge early and remain stable) on tests indexing verbal and visual knowledge acquisition, reasoning, and conceptualization. In addition, these children exhibited developmental lags (i.e., growth that is slower relative to healthy comparison subjects) on tests indexing processing speed, attention, visual-spatial problem solving ability, and working memory. These two premorbid cognitive patterns were not observed in children who later developed recurrent depression.
These findings suggest that the origins of schizophrenia include two interrelated developmental processes evident from childhood to early adolescence (ages 7–13 years). Children who will grow up to develop adult schizophrenia enter primary school struggling with verbal reasoning and lag further behind their peers in working memory, attention, and processing speed as they get older.
To test how genomic loci identified in genome-wide association studies influence the development of obesity.
A 38-year prospective longitudinal study of a representative birth cohort.
The Dunedin Multidisciplinary Health and Development Study, Dunedin, New Zealand.
One thousand thirty-seven male and female study members.
We assessed genetic risk with a multilocus genetic risk score. The genetic risk score was composed of single-nucleotide polymorphisms identified in genome-wide association studies of obesity-related phenotypes. We assessed family history from parent body mass index data collected when study members were 11 years of age.
Main Outcome Measures
Body mass index growth curves, developmental phenotypes of obesity, and adult obesity outcomes were defined from anthropometric assessments at birth and at 12 subsequent in-person interviews through 38 years of age.
Individuals with higher genetic risk scores were more likely to be chronically obese in adulthood. Genetic risk first manifested as rapid growth during early childhood. Genetic risk was unrelated to birth weight. After birth, children at higher genetic risk gained weight more rapidly and reached adiposity rebound earlier and at a higher body mass index. In turn, these developmental phenotypes predicted adult obesity, mediating about half the genetic effect on adult obesity risk. Genetic associations with growth and obesity risk were independent of family history, indicating that the genetic risk score could provide novel information to clinicians.
Genetic variation linked with obesity risk operates, in part, through accelerating growth in the early childhood years after birth. Etiological research and prevention strategies should target early childhood to address the obesity epidemic.
To determine whether parental periodontal disease history is a risk factor for periodontal disease in adult offspring.
Proband periodontal examination (combined attachment loss (CAL) at age 32, and incidence of CAL from ages 26–32) and interview data were collected during the age-32 assessments in the Dunedin Study. Parental data were also collected. The sample was divided into two familial-risk groups for periodontal disease (high- and low-risk) based on parents’ self-reported periodontal disease.
Periodontal risk analysis involved 625 proband-parent(s) groups. After controlling for confounding factors, the high-familial-risk periodontal group was more likely to have 1+ sites with 4+mm CAL (RR 1.45; 95% CI 1.11–1.88), 2+ sites with 4+mm CAL (RR 1.45; 95% CI 1.03–2.05), 1+ sites with 5+mm CAL (RR 1.60; 95% CI 1.02–2.50) and 1+ sites with 3+mm incident CAL (RR 1.64; 95% CI 1.01–2.66) than the low-familial-risk group. Predictive validity was enhanced when information was available from both parents.
Parents with poor periodontal health tend to have offspring with poor periodontal health. Family/parental history of oral health is a valid representation of the shared genetic and environmental factors that contribute to an individual’s periodontal status, and may help predict patient prognosis and preventive treatment need.
periodontal; intergenerational; risk; family history
A parental/family history of poor oral health may influence the oral-health-related quality of life (OHRQOL) of adults.
To determine whether the oral health of mothers of young children can predict the OHRQOL of those same children when they reach adulthood.
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.
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.
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.
oral health; oral health-related quality of life: OHIP-14; intergenerational; risk; family history
Impaired lung function is associated with systemic inflammation and is a risk factor for cardiovascular disease in older adults. It is unknown when these associations emerge and to what extent they are mediated by smoking, chronic airways disease, and/or established atherosclerosis. We explored the association between the forced expiratory volume in one second (FEV1) and the systemic inflammatory marker C‐reactive protein (CRP) in young adults.
Associations between spirometric lung function and blood CRP were assessed in a population based birth cohort of approximately 1000 New Zealanders at ages 26 and 32 years. Analyses adjusted for height and sex to account for differences in predicted lung function and excluded pregnant women.
There were significant inverse associations between FEV1 and CRP at both ages. Similar results were found for the forced vital capacity. These associations were similar in men and women and were independent of smoking, asthma, and body mass index.
Reduced lung function is associated with systemic inflammation in young adults. This association is not related to smoking, asthma, or obesity. The reasons for the association are unexplained, but the findings indicate that the association between lower lung function and increased inflammation predates the development of either chronic lung disease or clinically significant atherosclerosis. The association between poor lung function and cardiovascular disease may be mediated by an inflammatory mechanism.
inflammation; C‐reactive protein; spirometry; cohort studies
The association between depression and inflammation is inconsistent across research samples.
This study tested the hypothesis that a history of childhood maltreatment could identify a subgroup of depressed individuals with elevated inflammation levels, thus helping to explain previous inconsistencies.
Prospective longitudinal cohort study.
A representative birth cohort of 1,000 individuals was followed to age 32 years as part of the Dunedin Multidisciplinary Health and Development Study. Study members were assessed for history of childhood maltreatment and current depression.
MAIN OUTCOME MEASURES
Inflammation was assessed by a clinically-relevant categorical measure of high-sensitivity C-reactive protein (hsCRP >3mg/L), and a dimensional inflammation factor indexing the shared variance of continuous measures of hsCRP, fibrinogen, and white blood cells.
Although depression was associated with high hsCRP (RR=1.45; 95%CI=1.06;1.99), this association was significantly attenuated and no longer significant when the effect of childhood maltreatment was taken into account. Individuals with current depression and childhood maltreatment history were more likely to show high hsCRP levels than controls (N=27; RR=2.07; 95%CI=1.23;3.47). In contrast, individuals with current depression only showed a non-significant elevation in risk (N=109; RR=1.40; 95%CI=0.97;2.01). Results generalized to the inflammation factor. The elevated inflammation levels in depressed+maltreated individuals were not explained by correlated risk factors, such as depression recurrence, low socioeconomic status in childhood or adulthood, poor health, or smoking.
A history of childhood maltreatment contributes to the co-occurrence of depression and inflammation. Information about experiences of childhood maltreatment may help to identify depressed individuals with elevated inflammation levels and thus cardiovascular disease risk.
Existing neuropsychological studies of obsessive–compulsive disorder
(OCD) are cross-sectional and do not provide evidence of whether deficits are
trait-related (antecedent and independent of symptomatology) or state-related
(a consequence, dependent on symptomatology).
To investigate whether there are premorbid neuropsychological deficits
associated with adult OCD.
Longitudinal data were collected from participants of the Dunedin
Multidisciplinary Health and Developmental study. Neuropsychological data
collected at age 13 were linked with age 32 diagnosis of OCD.
The group who had OCD at age 32 differed significantly from the control
group with no OCD on their performance at age 13 on neuropsychological tests
of visuospatial, visuoconstructive and visuomotor skills, controlling for
gender and socioeconomic status, but did not differ on tests of general IQ or
verbal ability. Performance of the group with OCD on tests of executive
functioning was mixed.
Individuals with OCD have premorbid impairment in visuospatial abilities
and some forms of executive functioning, consistent with biological models of
Although concurrent influences on adolescent physical activity are well documented, longitudinal studies offer additional insights about early life antecedents of participation. The aim of this study was to examine associations between childhood and contemporaneous factors and patterns of physical activity participation during adolescence.
Physical activity participation at ages 15 and 18 was assessed among members of the Dunedin Multidisciplinary Health and Development Study cohort using the interview-based Minnesota Leisure Time Physical Activity Questionnaire. Logistic regression was used to examine associations between childhood factors (socioeconomic status, family ‘active-recreation’ orientation, home activities, motor ability, intelligence and psychiatric disorder), contemporaneous factors (parental health, BMI, predicted VO2max, general health, television viewing, smoking and alcohol use) and ‘Persistent Inactivity’, ‘Declining Participation’ or ‘Persistent Activity’ during adolescence.
In multivariate models, Persistent Inactivity during adolescence was associated with lower childhood family active-recreation orientation, and poorer cardiorespiratory fitness and general health during adolescence. Declining participation was more likely among those who reported fewer activities at home during childhood. Persistent Activity was associated with better cardiorespiratory fitness and watched less television during adolescence.
This study found that childhood and contemporaneous factors were associated with Persistent Inactivity, Persistent Activity and Declining Participation during adolescence. The findings highlight several factors from the family and home environment of potential importance in early intervention programs to support adolescent participation in physical activity.
Tobacco smoking is a recognized behavioral risk factor for periodontal disease (through its systemic effects), and cannabis smoking may contribute in a similar way.
To determine whether cannabis smoking is a risk factor for periodontal disease.
Design and Setting
Prospective cohort study of the general population, with cannabis use determined at ages 18, 21, 26, and 32 years and dental examinations conducted at ages 26 and 32 years. The most recent data collection (at age 32 years) was completed in June 2005.
A complete birth cohort born in 1972 and 1973 in Dunedin, New Zealand, and assessed periodically (with a 96% follow-up rate of the 1015 participants who survived to age 32 years). Complete data for this analysis were available from 903 participants (comprising 89.0% of the surviving birth cohort).
Main Outcome Measure
Periodontal disease status at age 32 years (and changes from ages 26 to 32 years) determined from periodontal combined attachment loss (CAL) measured at 3 sites per tooth.
Three cannabis exposure groups were determined: no exposure (293 individuals, or 32.3%), some exposure (428; 47.4%), and high exposure (182; 20.2%). At age 32 years, 265 participants (29.3%) had 1 or more sites with 4 mm or greater CAL, and 111 participants (12.3%) had 1 or more sites with 5 mm or greater CAL. Incident attachment loss between the ages of 26 and 32 years in the none, some, and high cannabis exposure groups was 6.5%, 11.2%, and 23.6%, respectively. After controlling for tobacco smoking (measured in pack-years), sex, irregular use of dental services, and dental plaque, the relative risk estimates for the highest cannabis exposure group were as follows: 1.6 (95% confidence interval [CI], 1.2–2.2) for having 1 or more sites with 4 mm or greater CAL; 3.1 (95% CI, 1.5–6.4) for having 1 or more sites with 5 mm or greater CAL; and 2.2 (95% CI, 1.2–3.9) for having incident attachment loss (in comparison with those who had never smoked cannabis). Tobacco smoking was strongly associated with periodontal disease experience, but there was no interaction between cannabis use and tobacco smoking in predicting the condition’s occurrence.
Cannabis smoking may be a risk factor for periodontal disease that is independent of the use of tobacco.
Cognitive reserve has been proposed as important in the etiology of neuropsychiatric disorders. However, tests of the association between premorbid IQ and adult mental disorders other than schizophrenia have been limited and inconclusive. The authors tested the hypothesis that low childhood IQ is associated with increased risk and severity of adult mental disorders.
Participants were members of a representative 1972-1973 birth cohort of 1,037 males and females in Dunedin, New Zealand, who were followed up to age 32 with 96% retention. WISC-R IQ was assessed at ages 7, 9, and 11. Research diagnoses of DSM mental disorders were made at ages 18, 21, 26, and 32.
Lower childhood IQ was associated with increased risk of developing schizophrenia spectrum disorder, adult depression, and adult anxiety. Lower childhood IQ was also associated with greater comorbidity and with persistence of depression; the association with persistence of generalized anxiety disorder was nearly significant. Higher childhood IQ predicted increased risk of adult mania.
Lower cognitive reserve, as reflected by childhood IQ, is an antecedent of several common psychiatric disorders and also predicts persistence and comorbidity. Thus, many patients who seek mental health treatment may have lower cognitive ability; this should be considered in prevention and treatment planning.
Concern is building about high rates of schizophrenia in large cities, and among immigrants, cannabis users, and traumatized individuals, some of which likely reflects the causal influence of environmental exposures. This, in combination with very slow progress in the area of molecular genetics, has generated interest in more complicated models of schizophrenia etiology that explicitly posit gene-environment interactions (EU-GEI. European Network of Schizophrenia Networks for the Study of Gene Environment Interactions. Schizophrenia aetiology: do gene-environment interactions hold the key? [published online ahead of print April 25, 2008] Schizophr Res; S0920-9964(08) 00170–9). Although findings of epidemiological gene-environment interaction (G × E) studies are suggestive of widespread gene-environment interactions in the etiology of schizophrenia, numerous challenges remain. For example, attempts to identify gene-environment interactions cannot be equated with molecular genetic studies with a few putative environmental variables “thrown in”: G × E is a multidisciplinary exercise involving epidemiology, psychology, psychiatry, neuroscience, neuroimaging, pharmacology, biostatistics, and genetics. Epidemiological G × E studies using indirect measures of genetic risk in genetically sensitive designs have the advantage that they are able to model the net, albeit nonspecific, genetic load. In studies using direct molecular measures of genetic variation, a hypothesis-driven approach postulating synergistic effects between genes and environment impacting on a final common pathway, such as “sensitization” of mesolimbic dopamine neurotransmission, while simplistic, may provide initial focus and protection against the numerous false-positive and false-negative results that these investigations engender. Experimental ecogenetic approaches with randomized assignment may help to overcome some of the limitations of observational studies and allow for the additional elucidation of underlying mechanisms using a combination of functional enviromics and functional genomics.
epidemiology; psychosis; schizophrenia; genetics; gene-environment interaction; gene-environment correlation
Clinical and epidemiologic studies have established that posttraumatic stress disorder (PTSD) is highly comorbid with other mental disorders. However, such studies have largely relied on adults' retrospective reports to ascertain comorbidity. The authors examined the developmental mental health histories of adults with PTSD using data on mental disorders assessed across the first 3 decades of life among members of the longitudinal Dunedin Multidisciplinary Health and Development Study; 100% of those diagnosed with past-year PTSD and 93.5% of those with lifetime PTSD at age 26 had met criteria for another mental disorder between ages 11 and 21. Most other mental disorders had first onsets by age 15. Of new cases of PTSD arising between ages 26 and 32, 96% had a prior mental disorder and 77% had been diagnosed by age 15. These data suggest PTSD almost always develops in the context of other mental disorders. Research on the etiology of PTSD may benefit from taking lifetime developmental patterns of comorbidity into consideration. Juvenile mental-disorder histories may help indicate which individuals are most likely to develop PTSD in populations at high risk of trauma exposure.
posttraumatic stress disorder; trauma; comorbidity; birth cohort; epidemiology
This study investigates what risk factors contribute to an excess risk of poor adult health among children who experienced socioeconomic (SES) disadvantage. Data come from 1,037 children born in Dunedin, New Zealand, in 1972–1973, followed from birth up to age 32. Childhood SES was measured at multiple points between birth and age 15 years. Risk factors included a familial liability to poor health, childhood/adolescent health risks, low childhood IQ, exposure to childhood maltreatment, and adult socioeconomic status. Adult health outcomes at age 32 were major depressive disorder, anxiety disorders, tobacco dependence, alcohol or drug dependence, and cardiovascular risk status. Results showed that low childhood SES was associated with an increased risk of substance dependence and poor physical health in adulthood (sex-adjusted Risk Ratios: tobacco dependence: 2.27, 95% Confidence Interval: 1.41, 3.65; alcohol or drug dependence; 2.11, 95% Confidence Interval: 1.16, 3.84; cardiovascular risk status: 2.55, 95% Confidence Interval: 1.46, 4.46). Together the risk factors studied here accounted for 55–67 percent of poor health outcomes among adults exposed to low SES as children. No single risk factor emerged as the prime explanation, suggesting that the processes mediating the link between childhood low SES and adult poor health are multifactorial.
Adolescent; Adolescent Development; Adult; Alcoholism; epidemiology; Cardiovascular Diseases; epidemiology; Child; Child Development; Child; Preschool; Cohort Studies; Confidence Intervals; Female; Health Status; Humans; Infant; Intelligence Tests; statistics & numerical data; Longitudinal Studies; Male; Mental Disorders; epidemiology; Mental Health; New Zealand; epidemiology; Poverty; Risk Assessment; Risk Factors; Socioeconomic Factors; Substance-Related Disorders; epidemiology; Tobacco Use Disorder; epidemiology
To describe oral health-related quality of life (OHRQoL) among New Zealand adults and assess the relationship between clinical measures of oral health status and a well-established OHRQoL measure, controlling for sex, socioeconomic status (SES) and use of dental services.
A birth cohort of 924 dentate adults (participants in the Dunedin Multidisciplinary Health and Development Study) was systematically examined for dental caries, tooth loss, and periodontal attachment loss (CAL) at age 32 years. OHRQoL was measured using the 14-item Oral Health Impact Profile questionnaire (OHIP-14). The questionnaire also collected data on each study member’s occupation, self-rated oral health and reasons for seeing a dental care provider. SES was determined from each individual’s occupation at age 32 years.
The mean total OHIP-14 score was 8.0 (SD 8.1); 23.4% of the cohort reported one or more OHIP problems ‘fairly often’ or ‘very often’. When the prevalence of impacts ‘fairly/very often’ was modeled using logistic regression, having untreated caries, two or more sites with CAL of 4+ mm and 1 or more teeth missing by age 32 years remained significantly associated with OHRQoL, after adjusting for sex and ‘episodic’ dental care. Multivariate analysis using Poisson regression determined that being in the low SES group was also associated with the mean number of impacts (extent) and the rated severity of impacts.
OHIP-14 scores were significantly associated with clinical oral health status indicators, independently of sex and socioeconomic inequalities in oral health. The prevalence of impacts (23.4%) in the cohort was significantly greater than age- and sex-standardized estimates from Australia (18.2%) and the UK (15.9%).
adult; dental caries; oral health; Oral Health Impact Profile; periodontal diseases; prevalence; quality of life; tooth loss
Information is lacking on the natural history of periodontitis through the third and fourth decades of life.
Periodontal examinations were conducted at 26 and 32 years of age in a longstanding prospective study of a birth cohort born in Dunedin, New Zealand, in 1972 and 1973. At each age, gingival recession (GR) and probing depth (PD) were recorded at three sites per tooth using a diagonal half-mouth design (measurements were made in all four quadrants at 32 years of age, but longitudinal comparisons were made using only the half-mouth data).
A total of 882 individuals were examined at both ages. The mean number of measured sites fell between 26 and 32 years of age. The overall prevalence of one or more sites with ≥4 mm combined attachment loss (CAL) rose from 18.6% to 21.8%, whereas there were greater increases in the proportion with two or more sites with ≥4 mm CAL (from 8.0% to 12.6%) and one or more sites with ≥5 mm CAL (from 3.6% to 8.0%). The extent and severity of CAL also increased. A total of 403 individuals (45.7%) had an increase in CAL ≥2 mm at one or more sites, whereas 110 (12.5%) had a CAL increase ≥3 mm at one or more sites. Seen in ~4% of sites, negative GR (i.e., gingival enlargement) had a substantial effect on PD-based estimates. An increase in PD ≥2 mm at one or more sites was experienced by 345 individuals (39.1%), whereas 88 people (10.0%) had an increase in PD ≥3 mm at one or more sites. The greatest mean attachment loss was experienced at disto-lingual sites on molars, and most manifested as PD increases. Notable increases in GR were seen with lower incisors and canines.
Periodontal loss of attachment continues among a sizable proportion of people from the third to the fourth decade of life; however, contrary to patterns in older adults, changes in the PD component are greater than the changes in the recession component. Incident attachment loss is most frequently observed at proximal sites on posterior teeth.
Adults; cohort study; incidence; periodontal attachment loss
Childhood factors have been associated with increased risk of developing post-traumatic stress disorder (PTSD). Previous studies assessed only a limited number of childhood factors retrospectively. We examined the association between childhood neurodevelopmental, temperamental, behavioral and family environmental characteristics assessed before age 11 years and the development of PTSD up to age 32 years in a birth cohort.
Members of a 1972–73 New Zealand birth cohort (n=1037) who were assessed at ages 26 and 32 years for PTSD as defined by DSM-IV.
We identified two sets of childhood risk factors. The first set of risk factors was associated both with increased risk of trauma exposure and with PTSD assessed at age 26. These included childhood externalizing characteristics and family environmental stressors, specifically maternal distress and loss of a parent. The second set of risk factors affected risk for PTSD only and included low IQ and chronic environmental adversity. The effect of cumulative childhood factors on risk of PTSD at age 26 was substantial; over 58% of cohort members in the highest risk quartile for three developmental factors had PTSD as compared to only 25% of those not at high risk on any factors. Low IQ at age 5, antisocial behavior, and poverty before age 11 continued to predict PTSD related to traumatic events that occurred between the ages of 26 and 32.
Developmental capacities and conditions of early childhood may increase both risk of trauma exposure and the risk that individuals will respond adversely to traumatic exposures. Rather than being solely a response to trauma, PTSD may have developmental origins.
Smoking is recognized as the primary behavioural risk factor for periodontal attachment loss (AL), but confirmatory data from prospective cohort studies are scarce.
To quantify the association between cigarette smoking patterns and AL by age 32.
Periodontal examinations were conducted at ages 26 and 32 in a longstanding prospective study of a birth cohort born in Dunedin (New Zealand) in 1972/1973. Longitudinal categorization of smoking exposure was undertaken using data collected at ages 15, 18, 21, 26 and 32.
Complete data were available for 810 individuals of whom 48.9% had ever smoked (31.5% were current smokers). Compared with never-smokers, long-term smokers (and other age-32 smokers) had very high odds ratios (ORs of 7.1 and 5.7, respectively) for having 1 +sites with 5 +mm AL, and were more likely to be incident cases after age 26 (ORs of 5.2 and 3.2, respectively). Two-thirds of new cases after age 26 were attributable to smoking. There were no significant differences in periodontal health between never-smokers and those who had quit smoking after age 26.
Current and long-term smoking in young adults is detrimental to periodontal health, but smoking cessation may be associated with a relatively rapid improvement in the periodontium.
cohort study; periodontal disease; smoking; tobacco
To describe the prevalence and associations of xerostomia among adults in their early thirties, with particular attention to medication exposure as a putative risk factor.
Material and Methods
The prevalence and associations of xerostomia were investigated among 32-year-old participants in a long-standing prospective cohort study. Some 950 individuals were assessed at ages 26 and 32 years, with medications being recorded on both occasions.
The prevalence of xerostomia was 10.0% (with no apparent gender difference), and was significantly higher among those taking antidepressants (odds ratio =4.7), iron supplements (OR =4.1) or narcotic analgesics (OR =2.4). Those taking antidepressants at both ages 26 and 32 years had 22 times the odds of reporting xerostomia.
Xerostomia may be a problem for a sizeable minority of young adults.
Longitudinal studies; medications; Xerostomia
Rates of depression have been rising, as have rates of work stress. We tested the influence of work stress on diagnosed depression and anxiety in young working adults.
Participants are enrolled in the Dunedin Study, a 1972–73 longitudinal birth cohort assessed most recently in 2004–2005, at age 32 (n=972, 96% of 1,015 cohort members still alive). Work stress (psychological job demands, work decision latitude, low work social support, physical work demands) was ascertained by interview. Major depression and generalized anxiety disorder were ascertained using the Diagnostic Interview Schedule and diagnosed according to DSM-IV criteria.
Participants exposed to high psychological job demands (excessive workload, extreme time pressures) had a twofold risk of major depression or generalized anxiety disorder compared to those with low job demands (Relative Risks adjusting for all work characteristics: women: 1.90 (95% Cl 1.22–2.98); men: 2.00 (95% Cl 1.13–3.56). Analyses ruled out the possibility that the association between work stress and disorder resulted from study members’ socioeconomic position, a personality tendency to report negatively, or a history of psychiatric disorder prior to labor-market entry. Prospective longitudinal analyses showed that high-demand jobs were associated with the onset of new depression and anxiety disorder in individuals without any pre-job history of diagnosis or treatment for either disorder.
Work stress appears to precipitate diagnosable depression and anxiety in previously-healthy young workers. Helping workers cope with work stress or reducing work stress levels could prevent the occurrence of clinically-significant depression and anxiety.
Several studies have reported an association between asthma and gastro-oesophageal reflux, but it is unclear which condition develops first. The role of obesity in mediating this association is also unclear. We explored the associations between respiratory symptoms, lung function, and gastro-oesophageal reflux symptoms in a birth cohort of approximately 1000 individuals.
Information on respiratory symptoms, asthma, atopy, lung function and airway responsiveness was obtained at multiple assessments from childhood to adulthood in an unselected birth cohort of 1037 individuals followed to age 26. Symptoms of gastro-oesophageal reflux and irritable bowel syndrome were recorded at age 26.
Heartburn and acid regurgitation symptoms that were at least "moderately bothersome" at age 26 were significantly associated with asthma (odds ratio = 3.2; 95% confidence interval = 1.6–6.4), wheeze (OR = 3.5; 95% CI = 1.7–7.2), and nocturnal cough (OR = 4.3; 95% CI = 2.1–8.7) independently of body mass index. In women reflux symptoms were also associated with airflow obstruction and a bronchodilator response to salbutamol. Persistent wheezing since childhood, persistence of asthma since teenage years, and airway hyperresponsiveness since age 11 were associated with a significantly increased risk of heartburn and acid regurgitation at age 26. There was no association between irritable bowel syndrome and respiratory symptoms.
Reflux symptoms are associated with respiratory symptoms in young adults independently of body mass index. The mechanism of these associations remains unclear.
Recent research has suggested that chronic dry mouth affects the day-to-day lives of older people living in institutions. The condition has usually been considered to be a feature of old age, but recent work by our team produced the somewhat surprising finding that 10% of people in their early thirties are affected. This raises the issue of whether dry mouth is a trivial condition or a more substantial threat to quality of life among younger people. The objective of this study was to examine the association between xerostomia and oral-health-related quality of life among young adults while controlling for clinical oral health status and other potential confounding factors.
Cross-sectional analysis of data from a longstanding prospective observational study of a Dunedin (New Zealand) birth cohort: clinical dental examinations and questionnaires were used at age 32. The main measures were xerostomia (the subjective feeling of dry mouth, measured with a single question) and oral-health-related quality of life (OHRQoL) measured using the short-form Oral Health Impact Profile (OHIP-14).
Of the 923 participants (48.9% female), one in ten were categorised as 'xerostomic', with no apparent gender difference. There was a strong association between xerostomia and OHRQoL (across all OHIP-14 domains) which persisted after multivariate analysis to control for clinical characteristics, gender, smoking status and personality characteristics (negative emotionality and positive emotionality).
Xerostomia is not a trivial condition; it appears to have marked and consistent effects on sufferers' day-to-day lives.
The UK government is considering reclassifying cannabis because of concerns about links with mental health problems. What does the evidence show?