|Year : 2019 | Volume
| Issue : 2 | Page : 79-81
Poverty and its effect on neurobiology – What do we know?
Avinash De Sousa
Department of Psychiatry, Lokmanya Tilak Municipal Medical College, Mumbai, Maharashtra, India
|Date of Web Publication||18-Dec-2019|
Dr. Avinash De Sousa
Carmel, 18, St. Francis Road, Off SV Road, Santacruz West, Mumbai - 400 054, Maharashtra
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
De Sousa A. Poverty and its effect on neurobiology – What do we know?. Ann Indian Psychiatry 2019;3:79-81
Poverty is a common phenomenon in India with around 3% of its population living below the poverty line in 2019. We as psychiatrists have always studied the interplay of developmental factors and their role in the genesis of psychopathology and their effects on psychosocial and brain development. This field of study has been labeled as developmental psychopathology and has been the backbone of clinical assessment in a child and adult psychiatry. The recent trends in neurobiology research are now looking at the interplay of social factors and their effects on the developmental neurobiology and in turn on the genesis of psychiatric disorders. The contemporary neuroscience has studied the influence of poverty on cognitive, emotional, and stress regulation systems and looked at how these contextual factors associated with lack of food, shelter, education, and health-care influence neural development. Various factors in brain development such as the analysis of neural plasticity and regulation of cognition, emotion, and stress have been studied with mixed results.
The effects of poverty need to be studied at different levels and different stages of development with the aim of uncovering the mechanisms through which these influences exert their impact and how these influences are or are not modified by interventions. It would be also worthwhile to know critical periods in brain development where such factors have their greatest impact and whether appropriate timing of interventions could be constituted.
Poverty is a phenomenon which is multidimensional, relational, and dynamic. It has many definitions which sciences such as economy, sociology, political science, epidemiology, and anthropology have given it in the last two centuries. There are some approaches to poverty that have been found to be common across studied namely (a) as a material condition in which needs, pattern of deprivations, and limited access to resources are main components; (b) as an economic circumstance where standards of living, inequality, and economic position are the main components; and (c) as a social circumstance where lack of basic security, exclusion, dependency, and social class are the most preferred components. The criteria to define poverty have always been economical in nature when it comes to inclusion in studies. Medically, the above approach considers several indicators of basic needs and rights such as (a) health (i.e., nutrition, infant mortality); (b) education (i.e., years of education, school enrollment); and (c) standard of living (i.e., cooking fuel, sanitation, water, electricity, floor, and goods). Most of the studies on poverty and its effect on neurocognitive development were researched using three main measures namely income, parental education, and occupation.
There are multiple risk factors entwined in poverty that affect the brain and neurocognitive development. These factors include prenatal and maternal health (i.e., nutrition, exposure to environmental toxins, drugs, and stressors), perinatal health (i.e., premature births and low birth weight), quality of early attachment and parental bonds, stressors at home and school, parenting styles, early cognitive stimulation, and parent mental health. There are also compounding factors such as the presence of developmental disorders, family financial stress, and access to social security, health-care facilities, and community resources. Family, social, and cultural expectations about child development and natural disasters leading to trauma also play a role in countries like India.
The evidence suggests that the influence of poverty on cognitive development is a function of the accumulation of risk factors, the co-occurrence of adversities, the individual's susceptibility to family and social environments, the duration of exposure to deprivations and all this being coupled to the biological predisposition in the form of genetic and epigenetic mechanisms at play. All these factors influence neural and brain development in many ways and across many developmental pathways.
It has been shown that growing up in poverty can affect brain development, and many studies have demonstrated that circumstances of poverty and chronic stress disrupt brain development. Studies from war-torn and impoverished countries such as Afghanistan and Iran have shown that children suffer from irreversible brain damage arising out of malnutrition and poor nutrition in the first 2 years of life has permanent effects on brain growth and development. The United Nations Children's Fund report mentions that children are more vulnerable to poverty than other age groups. They experience poverty differently than adults as their personal and affective needs vary at different ages and stages of development. These critical periods in child development coupled with poverty affect time-sensitive processes of development and maturation thereby implying that the outcomes of child poverty on the brain are profound, long-lasting, and irreversible.
A study in 2015 showed that the influence of childhood poverty is on both brain structure and cognitive performance. It demonstrated in short that poverty does shrink the brains from birth. It also mentioned that it is in the first 3 years of life that the human brain grows more than at any other stage. This is coupled with the highest synaptic density and the bran being 80% of the adult size at 3 years assists in learning occurring more easily than at any other time. During this short but unique period, children need adequate attention, stimuli, and interactions that allow them to develop their greatest potential at the cognitive and noncognitive levels. Some deficit in appropriate stimuli during early childhood can be compensated for later, but the cost is so high that the damage to the brain is often irreversible.
The study of poverty and its effect on neurobiology is indeed a complex one. It is important to study the analysis of causality in this area carefully and to avoid communicating correlational evidence as if it were causal because positive correlational studies do not translate into cause and effect relationships. We need longitudinal studies that involve different levels of organization and multiple mediation analysis that would allow (a) the identification of differential effects of the accumulation and/or combination of several types of adversities during development; (b) explain how different types of adversities modulate the efficiency of distinct neural networks; and (c) these studies must help us identify periods of vulnerability and greater sensitivity to different types of adverse experiences.
In a longitudinal analysis of 77 children participating in the National Institutes of Health magnetic resonance imaging (MRI) study of normal brain development, it was noted in children seen between the early postnatal period and age of 4 years that those in low-income or poor families were found to have total gray matter volumes that were nearly half a standard deviation smaller than their financially better-off counterparts. These reductions were particularly large in the frontal and parietal regions associated with executive function abilities. The analysis indicated that the associations are developmental, with reduced growth trajectories for total, frontal, and parietal gray matter volumes that were most pronounced for children in poverty. Similar findings were seen in a longitudinal analysis of 145 children followed longitudinally from preschool and who underwent MRI when they were approximately 10 years old. In this analysis, household income-to-need was positively related to gray and white matter volumes; the quality of parenting that children received in early childhood and the number of stressful life events experienced were found to mediate some of the effects of income on the volume of the hippocampus.
The mechanisms that link children's exposure to poverty-related adversity and brain development include the presence of chronic stressors such as household chaos, conflict among family members and other trauma that alter physiological responses to stress, leading to potentially damaging effects of stress-related hormones on the developing brain that in turn affects a range of negative cognitive, emotional, and behavioral sequelae. Poverty and poverty-related stressors have been argued and shown to program the physiological response to stress in ways that alter neuroendocrine activity and neural activity, thereby influencing the course of brain development and function.
A number of studies have shown that serum cortisol levels and stress markers are elevated in children when poverty is present. The effects of poverty on the stress response partly underlie the effects of poverty on the development of executive functions and the regulations of emotions and attention. These effects are consistent with animal models and indicate that cortisol influences the development of brain structures and neural circuitry that are important not only in regulating the hypothalamo-pituitary-adrenal (HPA) response to stress but also for executive function abilities.
Effects of early stress on development have been demonstrated most clearly in the hypothalamic–pituitary–adrenal (HPA) axis component of the stress response system. The HPA axis is characterized by a cascade of activity in which stimulation of the amygdala initiates the release of corticotropin-releasing hormone (CRH) from the paraventricular nucleus of the hypothalamus leading to the secretion of adrenocorticotropic hormone from the pituitary and resulting release of the glucocorticoid hormone cortisol (corticosterone in rodents) from the adrenals. Circulating glucocorticoid then feeds back on the HPA system to inhibit CRH and the resulting production of cortisol. In addition to fast and slow effects of stress on brain function, glucocorticoids affect brain structure through epigenetic processes. Levels of circulating cortisol/corticosterone affect processes in the cell nucleus and influence DNA transcription and gene expression. Interactions among the components of stress physiology are intricate, and more research is needed on how they are related to one another developmentally.
Researchers have noted that a single intervention involving one policy area (e.g. center-based early education and universal prekindergarten) can significantly reduce poverty's negative sequelae when delivered with levels of high quality. Classic early intervention studies have indicated initial effects on general mental ability with long-term effects on academic achievement and a number of indicators of health and well-being. While neuroscientific methods have been of great value in highlighting the brain-based benefits of reading interventions with older children, we are aware of only one early education study that has directly examined treatment-related effects of a preschool intervention targeting self-regulation on brain development using neuroimaging methods.
The effects of poverty on neurobiology and brain development are far-fetched and too complex to be encompassed in this editorial. Poverty affects the brain, and it is important that this area be studied further as working toward the reduction of poverty can in turn help brain development and prevent the deleterious effects if poverty in brain development.
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