Rationale: Asthma is prospectively associated with
age-related chronic diseases and mortality, suggesting the hypothesis that asthma may
relate to a general, multisystem phenotype of accelerated aging.
Objectives: To test whether chronic asthma is associated with a proposed
biomarker of accelerated aging, leukocyte telomere length.
Methods: Asthma was ascertained prospectively in the Dunedin
Multidisciplinary Health and Development Study cohort (n = 1,037) at nine
in-person assessments spanning ages 9–38 years. Leukocyte telomere length was
measured at ages 26 and 38 years. Asthma was classified as life-course-persistent,
childhood-onset not meeting criteria for persistence, and adolescent/adult-onset. We
tested associations between asthma and leukocyte telomere length using regression
models. We tested for confounding of asthma-leukocyte telomere length associations
using covariate adjustment. We tested serum C-reactive protein and white blood cell
counts as potential mediators of asthma-leukocyte telomere length associations.
Measurements and Main Results: Study members with life-course-persistent
asthma had shorter leukocyte telomere length as compared with sex- and age-matched
peers with no reported asthma. In contrast, leukocyte telomere length in study
members with childhood-onset and adolescent/adult-onset asthma was not different from
leukocyte telomere length in peers with no reported asthma. Adjustment for life
histories of obesity and smoking did not change results. Study members with
life-course-persistent asthma had elevated blood eosinophil counts. Blood eosinophil
count mediated 29% of the life-course-persistent asthma-leukocyte telomere length
Conclusions: Life-course-persistent asthma is related to a proposed
biomarker of accelerated aging, possibly via systemic eosinophilic inflammation. Life
histories of asthma can inform studies of aging.
asthma; telomere; aging; longitudinal; developmental phenotype
Despite widespread belief that neuropsychological decline is a cardinal feature of the progression from the premorbid to the chronic form of schizophrenia, few longitudinal studies have examined change in neuropsychological functioning from before to after the onset of schizophrenia. We addressed the following unresolved questions: Is neuropsychological decline generalized versus confined to particular mental functions? Is neuropsychological decline unique to schizophrenia? Do individuals with schizophrenia also have cognitive problems in everyday life?
Participants were members of a representative cohort of 1,037 individuals born in Dunedin, New Zealand between 1972-73 and followed prospectively to age 38, with 95% retention. Assessment of IQ and other specific neuropsychological functions was conducted at ages 7-13, before the onset of schizophrenia, and again at age 38. Informants also reported on cognitive problems at age 38.
Individuals with schizophrenia showed decline in IQ as well as a range of different mental functions, particularly those tapping processing speed, learning, executive functioning, and motor functioning. There was little evidence of decline in verbal abilities or delayed memory, however, and the developmental progression of deficits in schizophrenia differed across mental functions. Processing speed deficits increased gradually from childhood to beyond the early teen years, whereas verbal deficits emerged early but remained static through midlife. Neuropsychological decline was specific to schizophrenia, as no evidence of decline was apparent among individuals with persistent depression, children with mild cognitive impairment, individuals matched on childhood risk factors for schizophrenia, and psychiatrically healthy individuals. Informants also reported cognitive problems for individuals diagnosed with schizophrenia.
There is substantial neuropsychological decline in schizophrenia from the premorbid to post-onset period, but the extent and developmental progression of decline varies across mental functions. Findings suggest that different pathophysiological mechanisms might underlie deficits in different mental functions.
Retinal and cerebral microvessels are structurally and functionally
homologous, but, unlike cerebral microvessels, retinal microvessels can be
noninvasively measured in vivo via retinal imaging. Here we
test the hypothesis that individuals with schizophrenia show microvascular
abnormality and evaluate the utility of retinal imaging as a tool for future
Participants were members of the Dunedin Study, a
population-representative cohort followed from birth with 95%
retention. Study members underwent retinal imaging at age 38 years. We
assessed retinal arteriolar and venular caliber for all members of the
cohort, including individuals who developed schizophrenia.
Study members who developed schizophrenia were distinguished by wider
retinal venules, suggesting microvascular abnormality reflective of
insufficient brain oxygen supply. Analyses that controlled for confounding
health conditions suggested that wider retinal venules are not simply an
artifact of co-occurring health problems in schizophrenia patients. Wider
venules were also associated with a dimensional measure of adult psychosis
symptoms and with psychosis symptoms reported in childhood.
Findings provide initial support for the hypothesis that individuals
with schizophrenia show microvascular abnormality. Moreover, results suggest
that the same vascular mechanisms underlie subthreshold symptoms and
clinical disorder and that these associations may begin early in life. These
findings highlight the promise of retinal imaging as a tool for
understanding the pathogenesis of schizophrenia.
Cross-sectional studies have found that obesity is associated with low intellectual ability and neuroimaging abnormalities in adolescence and adulthood. Some have interpreted these associations to suggest that obesity causes intellectual decline in the first half of the life course. We analyzed data from a prospective longitudinal study to test whether becoming obese was associated with intellectual decline from childhood to midlife. We used data from the ongoing Dunedin Multidisciplinary Health and Development Study, a population-representative birth cohort study of 1,037 children in New Zealand who were followed prospectively from birth (1972–1973) through their fourth decade of life with a 95% retention rate. Intelligence quotient (IQ) was measured in childhood and adulthood. Anthropometric measurements were taken at birth and at 12 subsequent in-person assessments. As expected, cohort members who became obese had lower adulthood IQ scores. However, obese cohort members exhibited no excess decline in IQ. Instead, these cohort members had lower IQ scores since childhood. This pattern remained consistent when we accounted for children's birth weights and growth during the first years of life, as well as for childhood-onset obesity. Lower IQ scores among children who later developed obesity were present as early as 3 years of age. We observed no evidence that obesity contributed to a decline in IQ, even among obese individuals who displayed evidence of the metabolic syndrome and/or elevated systemic inflammation.
cognitive aging; intellectual decline; intelligence quotient; IQ decline; life course; longitudinal study; metabolic syndrome; obesity
We examine prospectively the influence of two separate but potentially interrelated factors in the etiology of posttraumatic stress disorder (PTSD): childhood maltreatment as conferring a susceptibility to the PTSD-response to adult trauma and juvenile disorders as precursors of adult PTSD.
The Dunedin Multidisciplinary Health and Development Study is a birth cohort (n=1037) from the general population of New Zealand's South Island, with multiple assessments up to age 38. DSM-IV PTSD was assessed among participants exposed to trauma at ages 26–38. Complete data were available on 928 participants.
Severe maltreatment in the first decade of life, experienced by 8.5% of the sample, was associated significantly with the risk of PTSD among those exposed to adult trauma (odds ratio, (OR)=2.64, 95% CI: 1.16, 6.01), compared to no maltreatment. Moderate maltreatment, experienced by 27.2 %, was not associated significantly with that risk (OR=1.55, 95% CI: 0.85, 2.85). However, the two estimates did not differ significantly from one another. Juvenile disorders (ages 11–15), experienced by 35% of the sample, independent of childhood maltreatment, was associated significantly with the risk of PTSD-response to adult trauma (OR=2.35, 95% CI: 1.32, 4.18).
Severe maltreatment was associated with risk of PTSD-response to adult trauma, compared to no maltreatment, and juvenile disorders, independent of earlier maltreatment, was associated with that risk. The role of moderate maltreatment remained unresolved. Larger longitudinal studies are needed to assess the impact of moderate maltreatment, experienced by the majority of adult trauma victims with history of maltreatment.
The purpose of the present study was to identify child and adult correlates that differentiate (a) individuals with persistent alcohol dependence from individuals with developmentally-limited alcohol dependence and (b) individuals with adult-onset alcohol dependence from individuals who never diagnose. Participants are 1,037 members of the Dunedin longitudinal study, a birth cohort followed prospectively from birth until age 32. Past-year DSM-IV alcohol dependence diagnoses were ascertained with structured diagnostic interviews at ages 18, 21, 26, and 32. Individuals were classified as developmentally-limited, persistent, or adult-onset subtypes based on their time-ordered pattern of diagnoses. The persistent subtype generally exhibited the worst scores on all correlates, including family psychiatric history, adolescent and adult externalizing and internalizing problems, adolescent and adult substance use, adult quality of life, and coping strategies. The prospective predictors that distinguished them from the developmentally-limited subtype involved family liability, adolescent negative affectivity, daily alcohol use, and frequent marijuana use. Furthermore, young people who developed the persistent subtype of alcohol dependence were distinguished from the developmentally-limited subtype by an inability to reduce drinking and by continued use despite problems, already by age 18. The adult-onset group members were virtually indistinguishable from ordinary cohort members as children or adolescents, but, in adulthood, adult-onset cases were distinguished by problems with depression, substance use, stress, and strategies for coping with stress. Information about age-of-onset and developmental course is fundamental for identifying subtypes of alcohol dependence. Subtype-specific etiologies point to targeted prevention and intervention efforts based on characteristics of each subtype.
Alcohol; subtypes; development; longitudinal
Quantifying diagnostic transitions across development is needed to estimate the long-term burden of mental illness. This study estimated patterns of diagnostic transitions from childhood to adolescence and from adolescence to early adulthood.
Patterns of diagnostic transitions were estimated using data from three prospective, longitudinal studies involving close to 20,000 observations of 3,722 participants followed across multiple developmental periods covering ages 9 to 30. Common DSM psychiatric disorders were assessed in childhood (ages 9 to 12; two samples), adolescence (ages 13 to 18; three samples), and early adulthood (ages 19 to age 32; three samples) with structured psychiatric interviews and questionnaires.
Having a disorder at an early period was associated with at least a 3-fold increase in odds for having a disorder at a later period. Homotypic and heterotypic transitions were observed for every disorder category. The strongest evidence of continuity was seen for behavioral disorders (particularly ADHD) with less evidence for emotional disorders such as depression and anxiety. Limited evidence was found in adjusted models for behavioral disorders predicting later emotional disorders. Adult substance disorders were preceded by behavioral disorders, but not anxiety or depression.
Having a disorder in childhood or adolescence is a potent risk factor for a range of psychiatric problems later in development. These findings provide further support for prevention and early life intervention efforts and suggest that treatment at younger ages, while justified in its own right, may also have potential to reduce the risk for disorders later in development.
Epidemiology; Longitudinal; Depression; Anxiety; Behavioral disorders; Comorbidity
Why do more intelligent people live healthier and longer lives? One possibility is that intelligence tests assess health of the brain, but psychological science has lacked technology to evaluate this hypothesis. Digital retinal imaging, a new non-invasive method to visualize microcirculation in the eye, may reflect vascular conditions in the brain. We studied the association between retinal vessel caliber and neuropsychological functioning in the representative Dunedin birth cohort. Wider venular caliber was associated with poorer neuropsychological functioning at midlife, independent of potentially confounding factors. This association was not limited to any specific test domain, and extended to informant-reports of cognitive difficulties in everyday life. Moreover, wider venular caliber was associated with lower childhood IQ tested 25 years earlier. The finding indicates that retinal venular caliber may be an indicator of neuropsychological health years before dementing diseases’ onset, and suggests digital retinal imaging as an investigative tool for psychological science.
To test how genomic loci identified in genome-wide association studies (GWAS) influence the developmental progression of smoking behavior.
A 38-year prospective longitudinal study of a representative birth-cohort.
The Dunedin Multidisciplinary Health and Development Study, New Zealand.
N=1037 male and female study members.
We assessed genetic risk with a multi-locus genetic risk score (GRS). The GRS was composed of single-nucleotide polymorphisms identified in three meta-analyses of GWAS of smoking quantity phenotypes.
Smoking initiation, conversion to daily smoking, progression to heavy smoking, nicotine dependence (Fagerstrom Test of Nicotine Dependence), and cessation difficulties were evaluated at eight assessments spanning ages 11-38 years.
Genetic risk score was unrelated to smoking initiation. However, individuals at higher genetic risk were more likely to convert to daily smoking as teenagers, progressed more rapidly from smoking initiation to heavy smoking, persisted longer in smoking heavily, developed nicotine dependence more frequently, were more reliant on smoking to cope with stress, and were more likely to fail in their cessation attempts. Further analysis revealed that two adolescent developmental phenotypes—early conversion to daily smoking and rapid progression to heavy smoking--mediated associations between the genetic risk score and mature phenotypes of persistent heavy smoking, nicotine dependence, and cessation failure. The genetic risk score predicted smoking risk over and above family history.
Initiatives that disrupt the developmental progression of smoking behavior among adolescents may mitigate genetic risks for developing adult smoking problems. Future genetic research may maximize discovery potential by focusing on smoking behavior soon after smoking initiation and by studying young smokers.
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