Young adults who faced extreme deprivation have lower IQ and increased ADHD symptoms

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Researchers from King’s College London have shown that the brains of young adult Romanian adoptees who were institutionalised as children are around 8.6% smaller than the brains of English adoptees who have not suffered this form of deprivation.

According to the research, the longer the time the Romanian adoptees spent in the institutions, the smaller the total brain volume, with each additional month of deprivation associated with a 0.27% reduction in total brain volume.

Deprivation related changes in brain volume were associated with lower IQ and more symptoms of attention deficit hyperactivity disorder (ADHD).

Published in Proceedings of the National Academy of Sciences (PNAS), the study analysed the MRI brain scans of 67 young adults, aged 23-28 years, who were exposed to severely depriving conditions in Romanian institutions under the Communist regime and subsequently adopted into nurturing families in the UK. They were compared to the MRI brain scans of 21 English adoptees aged 23-26 years who had not suffered this institutional deprivation.

MRI scans were conducted at the Centre for Neuroimaging Sciences at King’s College London, as part of the Medical Research Council (MRC) funded English and Romanian Adoptees Brain Imaging Study (ERABIS).

This is part of the larger ERA project that has collected information from Romanian and English adoptees over time including measures of mental health and cognitive performance.

This is the first time research has examined the impacts of severe early childhood deprivation on the brain structure of young adults.

Statistical analysis showed that, in this group of young Romanian adults, those changes in brain volume that were related to deprivation were also associated with lower IQ and more ADHD symptoms.

This implies that changes in brain structure could play a mediating role between the experience of deprivation and levels of cognitive performance and mental health.

The research investigated other possible factors that could have influenced the results but found the results were unaffected by level of nutrition, physical growth and genetic predisposition for smaller brains.

The principle investigator of the study, Professor Edmund Sonuga-Barke from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN), King’s College London said: ‘The English and Romanian Adoptees (ERA) study addresses one of the most fundamental questions in developmental psychology and psychiatry – how does early experience shape individual development?

It’s essential to recognise that these young people have nearly always received great care in loving adoptive families since they left the institutions.

However, despite a lot of positive experiences and achievements there remain some deep-seated effects of deprivation on these young adults.’

First author, Dr Nuria Mackes from the IoPPN said: ‘Previous research on the English and Romanian Adoptees (ERA) study has suggested that the emergence and persistence of low IQ and a high level of ADHD symptoms involves structural changes in the brain but, until now, we have not been able to provide direct evidence of this.

Showing these very profound effects of early deprivation on brain size and then showing that this difference is associated with low IQ and greater ADHD symptoms provides some of the most compelling evidence of the neuro-biological basis of these problems following deprivation.’

The study also investigated where these changes were occurring in the brain and what localised features contributed to the differences.

In comparison to the UK adoptees, the young Romanian adults who had suffered deprivation as children had markedly smaller right inferior frontal regions of the brain both in terms of volume and surface area.

In contrast the right inferior temporal lobe was larger in volume and surface area and thickness for the Romanian young adults and this was associated with lower levels of ADHD symptoms.

This implies that this increase in volume and surface area in this region may play a compensatory role in preventing development of ADHD symptoms. In the right medial prefrontal region, the longer the duration of deprivation, the larger the volume and surface area.

The research investigated other possible factors that could have influenced the results but found the results were unaffected by level of nutrition, physical growth and genetic predisposition for smaller brains.

The neuroimaging lead for the study, Professor Mitul Mehta from the IoPPN said: ‘We found structural differences between the two groups in three regions of the brain.

These regions are linked to functions such as organisation, motivation, integration of information and memory. It’s interesting to see the right inferior temporal lobe is in fact larger in the Romanian young adults and that this was related to fewer ADHD symptoms, suggesting that the brain can adapt to reduce the negative effects of deprivation.

This may explain why some individuals appear less affected than others by deprivation. We believe this is the first time that research has shown such compelling evidence of compensatory effects around deprivation.’

The Romanian young adults in the study had entered into institutions in the first few weeks of life, where they were often malnourished with minimal social contact and little stimulation. The time spent in institutions before adoption into families in the UK varied between 3 and 41 months.

Reflecting on the implications of the study Professor Sonuga-Barke said: ‘By investigating the long term impact of deprivation our research highlights the need for a life-span perspective on the provision of any help and support, especially during the transition to adulthood.

More speculatively the evidence of neural compensation in the inferior temporal lobe provides encouragement to look for ways that might help the brain adjust to deprivation and to improve outcomes. For example, it would be interesting to see if targeting this area directly through cognitive training might reduce ADHD symptoms.’

Funding: The research was published in Proceedings of the National Academy of Sciences and funded by Medical Research Council, Economic and Social Research Council and NIHR Maudsley Biomedical Research Centre.


Early childhood deprivation is associated with higher rates of neurodevelopmental and mental disorders in adulthood. The impact of childhood deprivation on the adult brain and the extent to which structural changes underpin these effects are currently unknown.

To investigate these questions, we utilized MRI data collected from young adults who were exposed to severe deprivation in early childhood in the Romanian orphanages of the Ceaușescu era and then, subsequently adopted by UK families; 67 Romanian adoptees (with between 3 and 41 mo of deprivation) were compared with 21 nondeprived UK adoptees. Romanian adoptees had substantially smaller total brain volumes (TBVs) than nondeprived adoptees (8.6% reduction), and TBV was strongly negatively associated with deprivation duration.

This effect persisted after covarying for potential environmental and genetic confounds. In whole-brain analyses, deprived adoptees showed lower right inferior frontal surface area and volume but greater right inferior temporal lobe thickness, surface area, and volume than the nondeprived adoptees. Right medial prefrontal volume and surface area were positively associated with deprivation duration.

No deprivation-related effects were observed in limbic regions. Global reductions in TBV statistically mediated the observed relationship between institutionalization and both lower intelligence quotient (IQ) and higher levels of attention deficit/hyperactivity disorder symptoms.

The deprivation-related increase in right inferior temporal volume seemed to be compensatory, as it was associated with lower levels of attention deficit/hyperactivity disorder symptoms. We provide compelling evidence that time-limited severe deprivation in the first years of life is related to alterations in adult brain structure, despite extended enrichment in adoptive homes in the intervening years.

Neuroplasticity, the brain’s inherent ability to dynamically adapt and change in response to environmental influences, supports normal learning and development. It also promotes recovery of function following injury and insult (1).

At the same time, it may leave the human brain vulnerable to the negative effects of adverse psychosocial experiences, such as maltreatment (2). This might be especially true during early childhood, which is characterized by rapid and dynamic changes in brain structure and function (3) that have been hypothesized to increase malleability to environmental influences (4).

Animal experiments support this hypothesis and suggest that the amygdala, hippocampus, and prefrontal cortex are particularly vulnerable to the effects of early life stress (4), perhaps because of their protracted development and close links to the hypothalamus–pituitary–adrenal axis (5).

It is challenging to interpret findings from human early maltreatment studies, which cannot experimentally manipulate exposure to adversity for obvious ethical reasons. This is because design limitations restrict the ability to assign a causal role to such exposures (6).

For instance, in many observational studies, maltreated individuals remain with their families—often the perpetrators—making it difficult to isolate early from later adverse exposures (7). Even in cases where children escape maltreatment by parents through adoption or fostering, effects of maltreatment are genetically confounded: environmental exposures, correlated brain alterations, and associated psychopathology may all be driven by common genetic risk factors passed from parent to child (6).

In addition, the majority of findings are based on retrospective reports of maltreatment that show limited agreement with prospectively assessed maltreatment (8). Recruiting participants on the basis of retrospective reports may also lead to an oversampling of individuals with psychopathology (910). This makes it difficult to isolate the effects of early adversity on the brain from the effects of later adversity or the brain-based manifestations of genetic risk or subsequent psychopathology (11).

While only studies in which deprivation is experimentally manipulated can definitively establish a causal link between adversity and outcomes, prospective longitudinal studies of adopted children exposed to deprivation for a time-limited period in early childhood within nonfamilial institutions rather than biological families offer the best opportunity to disentangle the effects of early adverse environmental exposures on brain development from such confounding factors.

Inference about the causal role of exposure to adversity is strengthened further if children enter the institutions very early in life and the switch from deprived to nurturing adoptive rearing environment is abrupt, precisely timed, and not determined by underlying risk within the child but rather, by historical circumstances (6).

The large-scale international adoption of the children discovered living in the brutally depriving Romanian orphanages at the time of the fall of the Ceaușescu regime represents an example of such a natural experiment.

To date, most studies of this cohort have focused on cognitive and mental health outcomes rather than brain development—concluding that extended deprivation is associated with increased rates of neurodevelopmental and mental disorders, which are often severe and persistent in nature (1213).

In the English and Romanian Adoptees (ERA) study, adoptees entered the institutions in the first few weeks of life and then, spent between 2 wk and 43 mo living there before being adopted into families in the United Kingdom that provided mostly nurturing environments. Thus, adoption constituted a radical and sudden improvement in circumstances when compared with the appalling conditions experienced in the institutions.

In the institutions, children were frequently malnourished and had minimal social contact, with insufficient caregiving and very little cognitive stimulation due to a lack of toys and confinement to cots (14). The ERA study included a comparison group of nondeprived adoptees from the host country placed before 6 mo of age to isolate the effects of deprivation from adoption per se.

The sample was also stratified by duration of deprivation, thereby allowing a test of the effects of deprivation “dose” to further clarify the meaning of the link between deprivation and brain outcomes (14). Initial reports documented a devastating and pervasive initial effect of deprivation on cognitive and social development for most children. This was followed by subsequent rapid recovery up to the age of 6 y (14).

Despite this, many individuals who spent an extended period (i.e., >6 mo) in the institutions subsequently displayed a distinctive and highly impairing combination of increased symptom rates of neurodevelopmental disorders, including attention deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and disinhibited social engagement (DSE; a pattern of indiscriminate friendliness toward strangers and lack of selectivity in attachment-related behaviors [15]), which has persisted in many individuals through to young adulthood (1216). In contrast, the marked cognitive impairments seen in childhood have gradually remitted over time such that, by adulthood, most adoptees are within the normal range (12).

Here, we harness the strengths of the ERA study design to provide evidence of a specific association between exposure to deprivation limited to early childhood and altered brain structure in young adulthood. We asked if early deprivation was associated with alterations in the adult brain in terms of both global volume and regional structural metrics.

The handful of studies that have examined the links between institutional deprivation and brain structure in childhood and adolescence are consistent in finding reduced total gray and white matter volumes (1722).

Results are, however, inconsistent with regard to the loci of regional effects of deprivation, perhaps because of problems with reproducibility of findings from studies using small samples combined with the different developmental stages of the assessments. There is some evidence for alterations in volumes in the prefrontal cortex (19), amygdala, and hippocampus (1822) as well as cortical thinning in prefrontal, parietal, and temporal regions (23).

Nevertheless, there have not been any systematic investigations that assess multiple morphometric measures simultaneously to test whether deprivation-related alterations in volume reflect changes in cortical thickness, surface area, or gyrification. Furthermore, none of the above studies have investigated the impact of severe deprivation on brain structure in adulthood (the mean age of the oldest sample studied to date was 16 y [18]).

In this study, we used a comprehensive whole-brain analysis strategy to first examine whether early institutional deprivation is associated with alterations in total brain volume (TBV) in young adulthood. We did this by comparing Romanian adoptees with nondeprived UK adoptees and also, by investigating associations with deprivation duration. We also tested whether any changes persisted after covarying for the potential confounders of adult body height, birth weight, and subnutrition.

In an exploratory analysis, we examined the potential role of genetic confounders by testing whether polygenic scores for intracranial volume accounted for the effects of deprivation duration. Statistically taking account of these confounding factors is especially important in order to control for the possibility that later adoption (thus, extended deprivation) is linked to genetic or environmental risk (perhaps because of selection factors determining which children were adopted early vs. late) rather than deprivation exposure per se.

The links between deprivation and localized changes in cortical volume, surface area, thickness, and gyrification and subcortical volumes were then explored, controlling for TBV. Based on previous studies in institutionalized children, we predicted a deprivation-related reduction in TBV and hypothesized that this effect would persist after controlling for available information on genetic and environmental confounds.

Above and beyond such effects, regionally specific effects on cortical (prefrontal, parietal, and temporal lobes) and subcortical (limbic) areas were predicted. As cortical surface area is relatively less established at birth compared with cortical thickness and gyrification (2425), we predicted that it would be more vulnerable than the other measures to deprivation-related effects.

Our second question was if global and regional deprivation-related brain alterations statistically mediate adult neurodevelopmental and cognitive outcomes. A previous study based on the Bucharest Early Intervention Project sample reported that cortical thinning in frontal, parietal, and temporal cortices mediated the effects of institutional deprivation on inattentive symptoms in childhood (23).

However, other studies have reported brain structural differences following early maltreatment in the absence of psychopathology (26). This has led researchers to propose that maltreatment-related brain alterations might in some cases represent compensatory changes, which promote resilience from psychopathology, rather than increased risk for disorders (26). This hypothesis has rarely been tested in humans (27).

Given the passage of time and the wide range of postdeprivation experience since exposure, we predicted that early deprivation would be associated with adult brain structure in heterogeneous ways—some would manifest as structural markers of disorder risk (i.e., mediating poor outcomes of deprivation), and some would manifest as compensatory processes (i.e., mediating positive outcomes despite deprivation).

Based on prior findings from nondeprived populations, we predicted that deprivation-related reductions in TBV would be related to low IQ (28) and higher levels of ADHD symptoms (29). Over and above this, we made the general prediction that brain regions implicated in neurodevelopmental outcomes in nondeprived samples would also be implicated in deprivation-related outcomes. For example, we hypothesized that ADHD symptoms in this sample would be linked to structural alterations within the prefrontal and temporal cortices, similar to those observed in nondeprivation-related variants of ADHD (30).


Source:
King’s College London
Media Contacts:
Louise Pratt – King’s College London

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