Daniel W. Belsky

A gradient of childhood self-control predicts health, wealth, and public safety

Policy-makers are considering large-scale programs aimed at self-control to improve citizens’ health and wealth and reduce crime. Experimental and economic studies suggest such programs could reap benefits. Yet, is self-control important for the health, wealth, and public safety of the population? Following a cohort of 1,000 children from birth to the age of 32 y, we show that childhood self-control predicts physical health, substance dependence, personal finances, and criminal offending outcomes, following a gradient of self-control. Effects of childrens self-control could be disentangled from their intelligence and social class as well as from mistakes they made as adolescents. In another cohort of 500 sibling-pairs, the sibling with lower self-control had poorer outcomes, despite shared family background. Interventions addressing self-control might reduce a panoply of societal costs, save taxpayers money, and promote prosperity.

The p Factor: One General Psychopathology Factor in the Structure of Psychiatric Disorders?

Mental disorders traditionally have been viewed as distinct, episodic, and categorical conditions. This view has been challenged by evidence that many disorders are sequentially comorbid, recurrent/chronic, and exist on a continuum. Using the Dunedin Multidisciplinary Health and Development Study, we examined the structure of psychopathology, taking into account dimensionality, persistence, co-occurrence, and sequential comorbidity of mental disorders across 20 years, from adolescence to midlife. Psychiatric disorders were initially explained by three higher-order factors (Internalizing, Externalizing, and Thought Disorder) but explained even better with one General Psychopathology dimension. We have called this dimension the p factor because it conceptually parallels a familiar dimension in psychological science: the g factor of general intelligence. Higher p scores are associated with more life impairment, greater familiality, worse developmental histories, and more compromised early-life brain function. The p factor explains why it is challenging to find causes, consequences, biomarkers, and treatments with specificity to individual mental disorders. Transdiagnostic approaches may improve research.

Is Adult ADHD a Childhood-Onset Neurodevelopmental Disorder? Evidence From a Four-Decade Longitudinal Cohort Study

OBJECTIVE Despite a prevailing assumption that adult ADHD is a childhood-onset neurodevelopmental disorder, no prospective longitudinal study has described the childhoods of the adult ADHD population. The authors report follow-back analyses of ADHD cases diagnosed in adulthood, alongside follow-forward analyses of ADHD cases diagnosed in childhood, in one cohort. METHOD Participants belonged to a representative birth cohort of 1,037 individuals born in Dunedin, New Zealand, in 1972 and 1973 and followed to age 38, with 95% retention. Symptoms of ADHD, associated clinical features, comorbid disorders, neuropsychological deficits, genome-wide association study-derived polygenic risk, and life impairment indicators were assessed. Data sources were participants, parents, teachers, informants, neuropsychological test results, and administrative records. Adult ADHD diagnoses used DSM-5 criteria, apart from onset age and cross-setting corroboration, which were study outcome measures. RESULTS As expected, childhood ADHD had a prevalence of 6% (predominantly male) and was associated with childhood comorbid disorders, neurocognitive deficits, polygenic risk, and residual adult life impairment. Also as expected, adult ADHD had a prevalence of 3% (gender balanced) and was associated with adult substance dependence, adult life impairment, and treatment contact. Unexpectedly, the childhood ADHD and adult ADHD groups comprised virtually nonoverlapping sets; 90% of adult ADHD cases lacked a history of childhood ADHD. Also unexpectedly, the adult ADHD group did not show tested neuropsychological deficits in childhood or adulthood, nor did they show polygenic risk for childhood ADHD. CONCLUSIONS The findings raise the possibility that adults presenting with the ADHD symptom picture may not have a childhood-onset neurodevelopmental disorder. If this finding is replicated, then the disorders place in the classification system must be reconsidered, and research must investigate the etiology of adult ADHD.

Quantification of biological aging in young adults

Significance The global population is aging, driving up age-related disease morbidity. Antiaging interventions are needed to reduce the burden of disease and protect population productivity. Young people are the most attractive targets for therapies to extend healthspan (because it is still possible to prevent disease in the young). However, there is skepticism about whether aging processes can be detected in young adults who do not yet have chronic diseases. Our findings indicate that aging processes can be quantified in people still young enough for prevention of age-related disease, opening a new door for antiaging therapies. The science of healthspan extension may be focused on the wrong end of the lifespan; rather than only studying old humans, geroscience should also study the young. Antiaging therapies show promise in model organism research. Translation to humans is needed to address the challenges of an aging global population. Interventions to slow human aging will need to be applied to still-young individuals. However, most human aging research examines older adults, many with chronic disease. As a result, little is known about aging in young humans. We studied aging in 954 young humans, the Dunedin Study birth cohort, tracking multiple biomarkers across three time points spanning their third and fourth decades of life. We developed and validated two methods by which aging can be measured in young adults, one cross-sectional and one longitudinal. Our longitudinal measure allows quantification of the pace of coordinated physiological deterioration across multiple organ systems (e.g., pulmonary, periodontal, cardiovascular, renal, hepatic, and immune function). We applied these methods to assess biological aging in young humans who had not yet developed age-related diseases. Young individuals of the same chronological age varied in their “biological aging” (declining integrity of multiple organ systems). Already, before midlife, individuals who were aging more rapidly were less physically able, showed cognitive decline and brain aging, self-reported worse health, and looked older. Measured biological aging in young adults can be used to identify causes of aging and evaluate rejuvenation therapies.

Bullying victimisation and risk of self harm in early adolescence: longitudinal cohort study.

Objectives To test whether frequent bullying victimisation in childhood increases the likelihood of self harming in early adolescence, and to identify which bullied children are at highest risk of self harm. Design The Environmental Risk (E-Risk) longitudinal study of a nationally representative UK cohort of 1116 twin pairs born in 1994-95 (2232 children). Setting England and Wales, United Kingdom. Participants Children assessed at 5, 7, 10, and 12 years of age. Main outcome measures Relative risks of children’s self harming behaviour in the six months before their 12th birthday. Results Self harm data were available for 2141 children. Among children aged 12 who had self harmed (2.9%; n=62), more than half were victims of frequent bullying (56%; n=35). Exposure to frequent bullying predicted higher rates of self harm even after children’s pre-morbid emotional and behavioural problems, low IQ, and family environmental risks were taken into account (bullying victimisation reported by mother: adjusted relative risk 1.92, 95% confidence interval 1.18 to 3.12; bullying victimisation reported by child: 2.44, 1.36 to 4.40). Victimised twins were more likely to self harm than were their non-victimised twin sibling (bullying victimisation reported by mother: 13/162 v 3/162, ratio=4.3, 95% confidence interval 1.3 to 14.0; bullying victimisation reported by child: 12/144 v 7/144, ratio=1.7, 0.71 to 4.1). Compared with bullied children who did not self harm, bullied children who self harmed were distinguished by a family history of attempted/completed suicide, concurrent mental health problems, and a history of physical maltreatment by an adult. Conclusions Prevention of non-suicidal self injury in young adolescents should focus on helping bullied children to cope more appropriately with their distress. Programmes should target children who have additional mental health problems, have a family history of attempted/completed suicide, or have been maltreated by an adult.

Etiological features of borderline personality related characteristics in a birth cohort of 12-year-old children

It has been reported that borderline personality related characteristics can be observed in children, and that these characteristics are associated with increased risk for the development of borderline personality disorder. It is not clear whether borderline personality related characteristics in children share etiological features with adult borderline personality disorder. We investigated the etiology of borderline personality related characteristics in a longitudinal cohort study of 1,116 pairs of same-sex twins followed from birth through age 12 years. Borderline personality related characteristics measured at age 12 years were highly heritable, were more common in children who had exhibited poor cognitive function, impulsivity, and more behavioral and emotional problems at age 5 years, and co-occurred with symptoms of conduct disorder, depression, anxiety, and psychosis. Exposure to harsh treatment in the family environment through age 10 years predicted borderline personality related characteristics at age 12 years. This association showed evidence of environmental mediation and was stronger among children with a family history of psychiatric illness, consistent with diathesis-stress models of borderline etiology. Results indicate that borderline personality related characteristics in children share etiological features with borderline personality disorder in adults and suggest that inherited and environmental risk factors make independent and interactive contributions to borderline etiology.

Polygenic Risk, Rapid Childhood Growth, and the Development of Obesity: Evidence From a 4-Decade Longitudinal Study

OBJECTIVE To test how genomic loci identified in genome-wide association studies influence the development of obesity. DESIGN A 38-year prospective longitudinal study of a representative birth cohort. SETTING The Dunedin Multidisciplinary Health and Development Study, Dunedin, New Zealand. PARTICIPANTS One thousand thirty-seven male and female study members. MAIN EXPOSURES 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. RESULTS 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. CONCLUSIONS 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.

Polygenic Risk and the Developmental Progression to Heavy, Persistent Smoking and Nicotine Dependence Evidence From a 4-Decade Longitudinal Study

IMPORTANCE Genome-wide hypothesis-free discovery methods have identified loci that are associated with heavy smoking in adulthood. Research is needed to understand developmental processes that link newly discovered genetic risks with adult heavy smoking. OBJECTIVE To test how genetic risks discovered in genome-wide association studies of adult smoking influence the developmental progression of smoking behavior from initiation through conversion to daily smoking, progression to heavy smoking, nicotine dependence, and struggles with cessation. DESIGN A 38-year, prospective, longitudinal study of a representative birth cohort. SETTING The Dunedin Multidisciplinary Health and Development Study of New Zealand. PARTICIPANTS The study included 1037 male and female participants. EXPOSURE We assessed genetic risk with a multilocus genetic risk score. The genetic risk score was composed of single-nucleotide polymorphisms identified in 3 meta-analyses of genome-wide association studies of smoking quantity phenotypes. MAIN OUTCOMES AND MEASURES Smoking initiation, conversion to daily smoking, progression to heavy smoking, nicotine dependence (Fagerström Test of Nicotine Dependence), and cessation difficulties were evaluated at 8 assessments spanning the ages of 11 to 38 years. RESULTS 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 2 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. CONCLUSIONS AND RELEVANCE 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.

Longitudinal rates of postoperative adverse outcomes after glaucoma surgery among medicare beneficiaries 1994 to 2005.

PURPOSE To determine longitudinal rates of postoperative adverse outcomes after incisional glaucoma surgery in a nationally representative longitudinal sample. DESIGN Retrospective, longitudinal cohort analysis. PARTICIPANTS Medicare beneficiaries >or=68 years who underwent a primary trabeculectomy (PT), trabeculectomy with scarring (TS), or glaucoma drainage device (GDD) implantation from 1994 to 2003 with follow-up through 2005. INTERVENTION Primary trabeculectomy, TS, and GDD were identified from International Classification of Diseases (ICD-9-CM) and Current Procedural Terminology (CPT) procedure codes. Change in rates of postoperative adverse outcomes associated with these 3 surgical interventions was analyzed by cumulative incidence rates and Cox proportional hazards model regression; regression analysis controlled for prior adverse outcome measures (3-year run-up) and demographic variables. MAIN OUTCOME MEASURES First-, second-, and sixth-year cumulative rates and probability of experiencing serious adverse outcomes (retinal detachment, endophthalmitis, suprachoroidal hemorrhage), less serious adverse outcomes (choroidal detachment, corneal edema, hypotony), and receipt of additional glaucoma surgery were identified through Medicare claims for each treatment group. RESULTS At the 1-year follow-up, rates of severe adverse outcomes were higher among beneficiaries in the GDD group (2.0%) relative to the PT (0.6%) and TS groups (1.3%). Controlling for prior adverse outcomes to the surgery and demographic factors in Cox proportional analysis, differences were often reduced, but generally remained statistically and clinically significant. Rates of severe outcomes, less severe outcomes, corneal edema, and low vision/blindness were higher for persons undergoing GDD than PT or TS. However, rates of reoperation were higher for TS than GDD. CONCLUSIONS The risk for adverse outcomes was higher in GDD than in PT surgery or TS, controlling for a number of important case mix and demographic factors.

Childhood forecasting of a small segment of the population with large economic burden.

Policymakers are interested in early-years interventions to ameliorate childhood risks. They hope for improved adult outcomes in the long run that bring a return on investment. The size of the return that can be expected partly depends on how strongly childhood risks forecast adult outcomes, but there is disagreement about whether childhood determines adulthood. We integrated multiple nationwide administrative databases and electronic medical records with the four-decade-long Dunedin birth cohort study to test child-to-adult prediction in a different way, using a population-segmentation approach. A segment comprising 22% of the cohort accounted for 36% of the cohort’s injury insurance claims; 40% of excess obese kilograms; 54% of cigarettes smoked; 57% of hospital nights; 66% of welfare benefits; 77% of fatherless child-rearing; 78% of prescription fills; and 81% of criminal convictions. Childhood risks, including poor brain health at three years of age, predicted this segment with large effect sizes. Early-years interventions that are effective for this population segment could yield very large returns on investment.