Our goal was to examine the association between parent-rated sleep problems during childhood and neuropsychological functioning during adolescence.
PARTICIPANTS AND METHODS
Longitudinal prospective data on an entire birth cohort from Dunedin, New Zealand, were obtained. One thousand thirty-seven children were enrolled in the study (52% male). Parents reported on sleep problems when the study members were 5, 7, and 9 years of age. Neuropsychological functioning was assessed by using 7 tests when the participants were 13 years of age.
After adjusting for gender and socioeconomic status, persistent sleep problems during childhood predicted scores on 2 neuropsychological tests: the copy score of the Rey-Osterrieth Complex Figure Test and 2 measures of performance on the Halstead Trail Making Test. These results were substantively replicated when sleep was assessed at the 5- and 9-year (but not 7-year) assessments separately.
Sleep problems during childhood may be associated with certain aspects of neuropsychological functioning during adolescence. This adds to the growing body of literature suggesting that childhood sleep problems may be a risk indicator of later difficulties.
sleep; neuropsychological; longitudinal; prospective
It is unclear how many people in the community have obsessions and compulsions and associated levels of interference. It is also unknown what variables predict help-seeking for these symptoms, whether they are developmentally stable, and whether they increase the risk of mental disorders.
The authors analyzed data from the prospective longitudinal Dunedin study of an unselected birth cohort. The presence of obsessions and compulsions and mental disorders was assessed using the Diagnostic Interview Schedule (DIS) at ages 11, 26, and 32. Data on interference and help-seeking were obtained at ages 26 and 32.
Obsessions and compulsions were frequent in individuals with mental disorders other than obsessive-compulsive disorder (OCD) and among people without mental disorders. Even in the latter group, these symptoms caused significant interference. The presence of anxiety/depression and of obsessions (particularly aggressive and shameful thoughts), but not compulsions, was associated with help-seeking. Harm/checking was the most prevalent symptom dimension. Symptom dimensions were temporally stable and associated with increased comorbidity. Obsessive-compulsive symptoms at age 11 predicted a high risk of an adult OCD diagnosis as well as elevated adult symptom dimensions.
Obsessions and compulsions are common in the adult population, have their roots in childhood, and are associated with interference, risk for disorders, and help-seeking. Subclinical obsessions and compulsions should be taken into account in research, intervention, and DSM-V.
Research into social inequalities in health has tended to focus on low socioeconomic status in adulthood. We aimed to test the hypothesis that children’s experience of socioeconomic disadvantage is associated with a wide range of health risk factors and outcomes in adult life.
We studied an unselected cohort of 1000 children (born in New Zealand during 1972–73) who had been assessed at birth and ages 3, 5, 7, 9, 11, 13, and 15 years. At age 26 years, we assessed these individuals for health outcomes including body-mass index, waist:hip ratio, blood pressure, cardiorespiratory fitness, dental caries, plaque scores, gingival bleeding, periodontal disease, major depression, and tobacco and alcohol dependence, and tested for associations between these variables and childhood and adult socioeconomic status.
Compared with those from high socioeconomic status backgrounds, children who grew up in low socioeconomic status families had poorer cardiovascular health. Significant differences were also found on all dental health measures, with a threefold increase in adult periodontal disease (31·1% vs 11·9%) and caries level (32·2% vs 9·9%) in low versus high childhood socioeconomic status groups. Substance abuse resulting in clinical dependence was related in a similar way to childhood socioeconomic status (eg, 21·5% vs 12·1% for adult alcohol dependence). The longitudinal associations could not be attributed to life-course continuity of low socioeconomic status, and upward mobility did not mitigate or reverse the adverse effects of low childhood socioeconomic status on adult health.
Protecting children against the effects of socioeconomic adversity could reduce the burden of disease experienced by adults. These findings provide strong impetus for policy makers, practitioners, and researchers to direct energy and resources towards childhood as a way of improving population health.
The objective of the study was to examine the link between anxiety and allergies to establish whether it reflects a psychobiological reality or a possible methodological bias. A cohort of 1,037 children enrolled in the study. Anxiety disorders were assessed between 11 and 21 years. Anxious personality was assessed at 18 years. Allergies were examined at 21 years by (a) self reports, (b) skin pricks, and (c) serum total immunoglobulin E (IgE). Self-reported allergies were predicted by recurrent anxiety disorders (OR [95% CI]=1.56 [1.06–2.30], p=.023) and self-reports of anxious personality (OR [95% CI]=1.67 [1.17–2.37], p=.004): Objectively verified allergies were not. These results suggest that the link between anxiety and allergies may reflect a methodological artifact rather than a psychobiological reality.
Genetic and environmental factors shape life-long vulnerability to depression, but most gene–environment interaction (G×E) research has focused on cross-sectional assessments rather than life-course phenotypes. This study tests the hypothesis that the G×E involving the length polymorphism in the serotonin-transporter-gene-linked-promoter-region (5-HTTLPR) and childhood maltreatment is specific to depression that runs a persistent course in adulthood.
The hypothesis is tested in two cohorts. Men and women in the Dunedin Study (N=847), New Zealand, followed to age 32 years with 96% retention and women in the E-Risk Study (N=930), England, followed to age 40 years with 96% retention. Diagnoses of past-year major depressive episode were established at four separate assessments. Depression diagnosed on two or more occasions was considered persistent.
In both cohorts, statistical tests of gene–environment interactions showed positive results for persistent depression but not single-episode depression. Individuals with two short 5-HTTLPR alleles and childhood maltreatment had elevated risk of persistent but not single-episode depression.
Some cases of recurrent depression may have been misclassified as single-episode due to non-contiguous assessment windows, but this would have a conservative effect on the findings. Chronic and recurrent depression could not be reliably distinguished due to non-contiguous periods of assessment. Therefore, the term persistent depression is used to describe either chronic or recurrent course.
The specific effect on persistent depression increases the significance of this G×E for public health. Research that does not distinguish persistent course may underestimate G×E effects and account for some replication failures in G×E research.
Depression; Persistent course; Gene–environment interactions; Serotonin transporter; Childhood maltreatment
If family history is associated with clinical features that are thought to index seriousness of disorder, this could inform clinicians predicting patients’ prognosis and researchers selecting cases for genetic studies. Although tests of associations between family history and clinical features are numerous for depression, such tests are relatively lacking for other disorders.
To test the hypothesis that family history is associated with 4 clinical indexes of disorder (recurrence, impairment, service use, and age at onset) in relation to 4 psychiatric disorders (major depressive episode, anxiety disorder, alcohol dependence, and drug dependence).
Prospective longitudinal cohort study.
A total of 981 members of the 1972 to 1973 Dunedin Study birth cohort (96% retention).
Main Outcome Measures
For each disorder, family history scores were calculated as the proportion of affected family members from data on 3 generations of the participants’ families. Data collected prospectively at the study’s repeated assessments (ages 11–32 years) were used to assess recurrence, impairment, and age at onset; data collected by means of a life history calendar at age 32 years were used to assess service use.
Family history was associated with the presence of all 4 disorder types. In addition, family history was associated with a more recurrent course for all 4 disorders (but not significantly for women with depression), worse impairment, and greater service use. Family history was not associated with younger age at onset for any disorder.
Associations between family history of a disorder and clinical features of that disorder in probands showed consistent direction of effects across depression, anxiety disorder, alcohol dependence, and drug dependence. For these disorder types, family history is useful for determining patients’ clinical prognosis and for selecting cases for genetic studies.
We investigated age-26 personality characteristics and age-32 oral health in a prospective study of a complete birth cohort born in Dunedin, New Zealand. Personality was measured using the Multidimensional Personality Questionnaire (MPQ). Oral health was measured using the short-form Oral Health Impact Profile (OHIP-14), a global measure, and dental examinations. Personality profiles were constructed for 916 individuals (50.8% men) using standardized MPQ scores, and multivariate analyses examined their association with oral health. Those reporting 1+ OHIP-14 impacts had higher Negative Emotionality scores (and lower Constraint and Positive Emotionality MPQ superfactor scores) than those who did not. After controlling for gender, clinical status, and the other two MPQ superfactors, those scoring higher on Negative Emotionality had a greater risk of reporting 1+ OHIP-14 impacts, as well as 3+ OHIP-14 impacts and worse-than-average oral health. They also had a greater risk of having lost at least one tooth from caries and of having 3+ decayed surfaces. Personality characteristics appear to shape self-reports of oral health. Personality is also a risk factor for clinical disease status, at least with respect to dental caries and its sequelae. Because the attitudes and values tapped into by personality tests can be altered by brief cognitive interventions, those might be useful in preventive dentistry.
cohort studies; oral health; personality; psychology; social
A previous study reported a gene × environment interaction in which a haplotype in the corticotropin-releasing hormone receptor 1 gene (CRHR1) was associated with protection against adult depressive symptoms in individuals who were maltreated as children (as assessed by the Childhood Trauma Questionnaire [CTQ]).
To replicate the interaction between childhood maltreatment and a TAT haplotype formed by rs7209436, rs110402, and rs242924 in CRHR1, predicting adult depression.
Two prospective longitudinal cohort studies.
England and New Zealand.
Participants in the first sample were women in the E-Risk Study (N= 1116), followed up to age 40 years with 96% retention. Participants in the second sample were men and women in the Dunedin Study (N= 1037), followed up to age 32 years with 96% retention.
Main Outcome Measure
Research diagnoses of pastyear and recurrent major depressive disorder.
In the E-Risk Study, the TAT haplotype was associated with a significant protective effect. In this effect, women who reported childhood maltreatment on the CTQ were protected against depression. In the Dunedin Study, which used a different type of measure of maltreatment, this finding was not replicated.
A haplotype in CRHR1 has been suggested to exert a protective effect against adult depression among research participants who reported maltreatment on the CTQ, a measure that elicits emotional memories. This suggests the hypothesis that CRHR1’s protective effect may relate to its function in the consolidation of memories of emotionally arousing experiences.
In vitro studies have shown that p53 mediates a protective response against DNA damage by causing either cell-cycle arrest and DNA repair, or apoptosis. These responses have not yet been demonstrated in humans. A common source of DNA damage in humans is cigarette smoke, which should activate p53 repair mechanisms. The level of p53 is regulated by HDM2, which targets p53 for degradation. The G-allele of a polymorphism in intron 1 of HDM2 (rs2279744:G/T) results in higher HDM2 levels, and should be associated with a reduced p53 response and hence more DNA damage and corresponding tissue destruction. Similarly, the alleles of a polymorphism (rs1042522) in TP53 that encode arginine (G-allele) or proline (C-allele) at codon 72 cause increased pro-apoptotic (G-allele) or cell-cycle arrest activities (C-allele), respectively, and may moderate p53's ability to prevent DNA damage. To test these hypotheses we examined lung function in relation to cumulative history of smoking in a population-based cohort. The G-alleles in HDM2 and TP53 were found to be associated with accelerated smoking-related decline in lung function. These data support the hypothesis that p53 protects from DNA damage in humans and provides a potential explanation for variation in lung function impairment amongst smokers.
Exposure to alcohol and illicit drugs during early adolescence has been associated with poor outcomes in adulthood. However, many adolescents with exposure to these substances also have a history of conduct problems, which raises the question of whether early exposure to alcohol and drugs leads to poor outcomes only for those adolescents who are already at risk. In a 30-year prospective study, we tested whether there was evidence that early substance exposure can be a causal factor for adolescents’ future lives. After propensity-score matching, early-exposed adolescents remained at an increased risk for a number of poor outcomes. Approximately 50% of adolescents exposed to alcohol and illicit drugs prior to age 15 had no conduct-problem history, yet were still at an increased risk for adult substance dependence, herpes infection, early pregnancy, and crime. Efforts to reduce or delay early substance exposure may prevent a wide range of adult health problems and should not be restricted to adolescents who are already at risk.
The effects of the oral health status of one generation on that of the next within families are unclear.
To determine whether parental oral health history is a risk factor for oral disease.
Oral examination and interview data were collected during the age-32 assessments in the Dunedin Study. Parental data were also collected on this occasion. The sample was divided into two familial-risk groups for caries/tooth loss (high risk and low risk) based on parents’ self-reported history of tooth loss at the age-32 assessment interview.
Main outcome measures
Probands’ dental caries and tooth loss status at age 32, together with lifelong dental caries trajectory (age 5–32).
Caries/tooth-loss risk analysis was conducted for 640 proband-parents groups. Referent groups were the low-familial-risk groups. After controlling for confounding factors (sex, episodic use of dental services, socio-economic status and plaque trajectory), the prevalence ratio (PR) for having lost 1+ teeth by age 32 for the high-familial-risk group was 1.41 (95% confidence interval [CI] 1.05, 1.88) and the rate ratio for DMFS at age 32 was 1.41 (95% CI 1.24, 1.60). In the high-familial-risk group, the PR of following a high caries trajectory was 2.05 (95% CI 1.37, 3.06). Associations were strongest when information was available about both parents’ oral health. Nonetheless, when information was available for one parent only, associations were significant for some proband outcomes.
People with poor oral health tend to have parents with poor oral health. Family/parental history of oral health is a valid representation of the intricacies of the shared genetic and environmental factors that contribute to an individual’s oral health status. Associations were strongest when data from both parents can be obtained.
oral health; family history; intergenerational; risk
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