Association of subcortical grey-matter volumes with life-course-persistent antisocial behavior in a population-representative longitudinal birth cohort

2021 ◽  
Author(s):  
Christina Carlisi
Keyword(s):  
Life Course ◽  
Antisocial Behavior ◽  
Birth Cohort ◽  
Statistical Power ◽  
Grey Matter ◽  
Brain Structures ◽  
Subcortical Structures ◽  
Low Level ◽  
Life Course Persistent ◽  
The Life Course

Objective:Neuropsychological evidence supports the Developmental Taxonomy Theory of Antisocial Behavior, suggesting that abnormal brain development distinguishes life-course-persistent antisocial behavior from adolescence-limited antisocial behavior. Recent neuroimaging work confirmed that prospectively-measured life-course-persistent antisocial behavior is associated with differences in cortical brain structure. Whether this extends to subcortical brain structures remains uninvestigated. Methods:This study compared subcortical grey-matter volumes between individuals characterized by life-course-persistent, adolescence-limited or low-level antisocial behavior. Participants were members of the Dunedin Study, a population-based birth cohort of 1037 individuals born in New Zealand between 1972-1973 and followed to age 45. 672 Study members previously defined as exhibiting life-course-persistent, adolescence-limited, or low-level antisocial behavior based on repeated assessments from ages 7-26 were included. Grey-matter volumes of 10 subcortical structures were compared across groups. Results:The life-course-persistent group (N=80;59% male) had lower volume of amygdala, brain stem, cerebellum, hippocampus, pallidum, thalamus, and ventral diencephalon compared to the low-antisocial group (N=441;47% male). Differences between the life-course-persistent and the adolescence-limited group (N=151;54% male) were comparable in effect-size to differences between the life-course persistent and low-antisocial group, but were not statistically significant due to less statistical power. Grey-matter volumes in the adolescence-limited group were near the norm in this population-representative cohort and similar to volumes in the low-antisocial group. Conclusions:Although this study cannot establish causal links between brain volume and antisocial behavior, it constitutes new biological evidence that all people with antisocial behavior are not the same, supporting a need for greater developmental and diagnostic precision in clinical, forensic, and policy-based interventions.

scholarly journals Association of subcortical gray-matter volumes with life-course-persistent antisocial behavior in a population-representative longitudinal birth cohort

2021 ◽  
pp. 1-11
Author(s):  
Christina O. Carlisi ◽  
Terrie E. Moffitt ◽  
Annchen R. Knodt ◽  
HonaLee Harrington ◽  
Stephanie Langevin ◽  
...  
Keyword(s):  
Life Course ◽  
Antisocial Behavior ◽  
Gray Matter ◽  
Statistical Power ◽  
Brain Structures ◽  
Subcortical Structures ◽  
Life Course Persistent ◽  
Subcortical Brain Structures ◽  
Neuropsychological Evidence ◽  
Gray Matter Volumes

Abstract Neuropsychological evidence supports the developmental taxonomy theory of antisocial behavior, suggesting that abnormal brain development distinguishes life-course-persistent from adolescence-limited antisocial behavior. Recent neuroimaging work confirmed that prospectively-measured life-course-persistent antisocial behavior is associated with differences in cortical brain structure. Whether this extends to subcortical brain structures remains uninvestigated. This study compared subcortical gray-matter volumes between 672 members of the Dunedin Study previously defined as exhibiting life-course-persistent, adolescence-limited or low-level antisocial behavior based on repeated assessments at ages 7–26 years. Gray-matter volumes of 10 subcortical structures were compared across groups. The life-course-persistent group had lower volumes of amygdala, brain stem, cerebellum, hippocampus, pallidum, thalamus, and ventral diencephalon compared to the low-antisocial group. Differences between life-course-persistent and adolescence-limited individuals were comparable in effect size to differences between life-course-persistent and low-antisocial individuals, but were not statistically significant due to less statistical power. Gray-matter volumes in adolescence-limited individuals were near the norm in this population-representative cohort and similar to volumes in low-antisocial individuals. Although this study could not establish causal links between brain volume and antisocial behavior, it constitutes new biological evidence that all people with antisocial behavior are not the same, supporting a need for greater developmental and diagnostic precision in clinical, forensic, and policy-based interventions.

The Developmental Taxonomy

2018 ◽  
pp. 148-158
Author(s):  
Tara Renae McGee ◽  
Terrie E. Moffitt
Keyword(s):  
Gender Differences ◽  
Life Course ◽  
Antisocial Behavior ◽  
Early Onset ◽  
Adult Onset ◽  
Low Level ◽  
Developmental Taxonomy ◽  
Offending Behavior ◽  
Life Course Persistent ◽  
The Life Course

This chapter considers whether the peak in the age–crime curve is a function of active offenders committing more crime during adolescence or a function of more individuals actively offending in the peak years. It discusses the two main and most empirically tested typological groupings: the life-course persistent group and the adolescence limited group. The chapter then reviews the evidence on a theoretically interesting grouping: those who abstain from antisocial and offending behavior. It focuses on the debate regarding whether those who were originally thought to recover from early-onset antisocial behavior have childhood-limited antisocial behavior or exhibit low-level chronic antisocial behavior across the life course. Finally, the chapter discusses how the theory it introduces accounts for adult-onset offending and considers whether there are gender differences that need to be accounted for by the theory.

scholarly journals Recomposing persons: Scavenging and storytelling in a birth cohort archive

2021 ◽  
pp. 095269512199539
Author(s):  
Penny Tinkler ◽  
Resto Cruz ◽  
Laura Fenton
Keyword(s):  
Life Course ◽  
Cohort Studies ◽  
Birth Cohort ◽  
Quantitative Data ◽  
Population Level ◽  
Relational Embeddedness ◽  
The Life Course ◽  
Over Time

Birth cohort studies can be used not only to generate population-level quantitative data, but also to recompose persons. The crux is how we understand data and persons. Recomposition entails scavenging for various (including unrecognised) data. It foregrounds the perspective and subjectivity of survey participants, but without forgetting the partiality and incompleteness of the accounts that it may generate. Although interested in the singularity of individuals, it attends to the historical and relational embeddedness of personhood. It examines the multiple and complex temporalities that suffuse people’s lives, hence departing from linear notions of the life course. It implies involvement, as well as reflexivity, on the part of researchers. It embraces the heterogeneity and transformations over time of scientific archives and the interpretive possibilities, as well as incompleteness, of birth cohort studies data. Interested in the unfolding of lives over time, it also shines light on meaningful biographical moments.

Associations between life-course frailty and later-life heart size and function in the 1946 NSHD British birth cohort-an epidemiological study

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C.C Topriceanu ◽  
J.C Moon ◽  
R Hardy ◽  
A.D Hughes ◽  
N Chaturvedi ◽  
...  
Keyword(s):  
Life Course ◽  
Birth Cohort ◽  
Frailty Index ◽  
Later Life ◽  
Left Ventricular ◽  
Step Change ◽  
Deficit Accumulation ◽  
Heart Size ◽  
And Function ◽  
The Life Course

Abstract Background Cardiovascular diseases are an important component of the multi-morbidity syndrome which is associated with negative health outcomes resulting in a major societal economic burden. An objective way to assess multi-morbidity is to calculate a frailty index based on medical deficit accumulation. Late-life frailty has been validated to predict mortality, but little is known about the association between life-course frailty and cardiovascular health in later-life. Purpose To study the association between life-course frailty and later-life heart size and function using data from the world's longest running birth cohort with continuous follow-up. Methods A 45-deficit frailty index (FI) was calculated at 4 age-intervals across the life-course (0 to 16 years old, 19 to 44 years old, 45 to 54 years old and 60 to 64 years old) in participants from the UK 1946 Medical Research Council (MRC) National Survey of Heath and Development (NSHD) birth cohort. The life-course frailty indices (FI0_16, FI19_44, FI45_54 and FI60_64) reflect the cumulative medical deficits at the corresponding age-intervals. They were used to derive FImean and FIsum reflecting overall-life frailty. The step change in deficit accumulation between age-intervals was also calculated (FI2-1, FI3-1, FI4-1, FI3-2, FI4-2, FI4-3). Echocardiographic data at 60–64 years provided: E/e' ratio, ejection fraction (EF), myocardial contraction fraction index (MCFi) and left ventricular mass index (LVmassi). Generalized linear mixed models with gamma distribution and log link assessed the association between FIs and echo parameters after adjustment for sex, socio-economic position and body mass index. Results 1.805 NSHD participants were included (834 male). Accumulation of a single deficit had a significant impact (p<0.0001 to p<0.049) on LVmassi and MCFi in all the life-course FIs and overall FIs. LVmassi increased by 0.89% to 1.42% for the life-course FIs and by 0.36%/1.82% for FIsum and FImean respectively. MCFi decreased by 0.62% to 1.02% for the life-course FIs and by 0.33%/ 1.04%. for FIsum and FImean respectively. One accumulated deficit translated into higher multiplicative odds (13.2 for FI60-64, 2.1 for FI4-1, 75.4 for FI4-2 and 78.5 for FI4-3) of elevated filling pressure (defined as E/e' ratio >13, p<0.0.005 to p<0.02).A unit increase in frailty decreased LV EF (%) by 11%/12% for FI45-54 and FI60-64 respectively, by 10% to 12% for FI2-1, FI3-1, FI4-1 and FI4-2, and 4%/15% for FIsum and FImean respectively (p<0.0014 to p<0.044). Conclusion Frailty during the life-course, overall life-frailty and the step change in deficit accumulation is associated with later-life cardiac dysfunction. Frailty strain appears to have its greatest impact on pathological myocardial hypertrophy (high LVmassi and low MCFi) potentially paving the way to later-life systolic or diastolic dysfunction in susceptible individuals. Funding Acknowledgement Type of funding source: None

scholarly journals Longitudinal birth cohort study finds that life-course frailty associates with later-life heart size and function

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Constantin-Cristian Topriceanu ◽  
James C. Moon ◽  
Rebecca Hardy ◽  
Nishi Chaturvedi ◽  
Alun D. Hughes ◽  
...  
Keyword(s):  
Life Course ◽  
Birth Cohort ◽  
Left Ventricular ◽  
Step Change ◽  
Deficit Accumulation ◽  
Cardiac Phenotype ◽  
Time Period ◽  
Time Periods ◽  
The Life Course ◽  
Health Deficit

AbstractA frailty index (FI) counts health deficit accumulation. Besides traditional risk factors, it is unknown whether the health deficit burden is related to the appearance of cardiovascular disease. In order to answer this question, the same multidimensional FI looking at 45-health deficits was serially calculated per participant at 4 time periods (0–16, 19–44, 45–54 and 60–64 years) using data from the 1946 Medical Research Council (MRC) British National Survey of Health and Development (NSHD)—the world’s longest running longitudinal birth cohort with continuous follow-up. From these the mean and total FI for the life-course, and the step change in deficit accumulation from one time period to another was derived. Echocardiographic data at 60–64 years provided: ejection fraction (EF), left ventricular mass indexed to body surface area (LVmassi, BSA), myocardial contraction fraction indexed to BSA (MCFi) and E/e′. Generalized linear models assessed the association between FIs and echocardiographic parameters after adjustment for relevant covariates. 1375 participants were included. For each single new deficit accumulated at any one of the 4 time periods, LVmassi increased by 0.91–1.44% (p < 0.013), while MCFi decreased by 0.6–1.02% (p < 0.05). A unit increase in FI at age 45–54 and 60–64, decreased EF by 11–12% (p < 0.013). A single health deficit step change occurring between 60 and 64 years and one of the earlier time periods, translated into higher odds (2.1–78.5, p < 0.020) of elevated LV filling pressure. Thus, the accumulation of health deficits at any time period of the life-course associates with a maladaptive cardiac phenotype in older age, dominated by myocardial hypertrophy and poorer function.

scholarly journals Life-course burden of health deficits associates with later-life heart size and function in the 1946 British birth cohort

2020 ◽  
Author(s):  
Constantin-Cristian Topriceanu ◽  
James C Moon ◽  
Rebecca Hardy ◽  
Nishi Chaturvedi ◽  
Alun Hughes ◽  
...  
Keyword(s):  
Life Course ◽  
Birth Cohort ◽  
Later Life ◽  
Myocardial Contraction ◽  
Left Ventricular ◽  
Heart Size ◽  
Time Periods ◽  
And Function ◽  
The Life Course ◽  
Myocardial Contraction Fraction

Aim: To study the association between the life course accumulation of health deficits and later life heart size and function using data from the 1946 National Survey of Heath and Development (NSHD) British birth cohort, the longest running birth cohort with continuous follow up in the world. Methods and Results: A multidimensional health deficit index (DI) looking at 45 health deficits was serially calculated at 4 time periods of the life course in NSHD participants (0 to 16, 19 to 44, 45 to 54 and 60 to 64 years), and from these the mean and total DI for the life course was derived (DImean, DIsum). The step change in deficit accumulation from one time period to another was also calculated. Echocardiographic data at 60-64 years provided: ejection fraction (EF), left ventricular mass indexed to body surface area (LVmassi, BSA), myocardial contraction fraction indexed to BSA (MCFi) and E/e. Generalized linear models assessed the association between DIs and echocardiographic parameters after adjustment for sex, socioeconomic position and body mass index. 1,375 NSHD participants were included (46.47% male). For each single new deficit accumulated at any one of the 4 time periods of the life course, LVmassi increased by 0.91 to 1.44% (p<0.013), while MCFi decreased by 0.6 to 1.02% (p<0.05 except at 45 to 54 years). One unit increase in DI at age 45 to 54 and 60 to 64 decreased LV EF by 11 to 12% (p<0.013). A single deficit step change occurring between 60-64 years and one of the earlier time periods, translated into significantly higher odds (2.1 to 78.5, p<0.020) of elevated LV filling pressure defined as E/e>13. Conclusion: The accumulation of health deficits at any time period of the life course associates with a maladaptive cardiac phenotype in older age, dominated by myocardial hypertrophy and poorer function. The burden of health deficits appears to strain the myocardium potentially leading to future cardiac dysfunction. Keywords: frailty; cardiovascular disease; ejection fraction; left ventricular mass index; myocardial contraction fraction; E/e.

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