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Evidence from a rising number of epidemiological and neurobiological studies show that adverse childhood experience (ACE) such as abuse, neglect and related adverse experiences show long lasting impacts on brain function and physical health, resulting in a predisposition to physical and mental health disorders throughout their lives. Community surveys from Europe and worldwide show the great prevalence of physical (22.9%), mental (29.1%) and sexual (9.6%) abuse in addition to physical (16.4%) and emotional neglect (18.3%) (Sethi et al., 2013) within the general population. Individuals who accumulate ACE have been shown to be at a higher risk of mental and physical disorders throughout their lifespan due to the possible compromise of cognitive and affective brain function. These changes can be observed through functional and morphometric changes in key stress and emotional centers of the brain (amygdala, hippocampus) and may result in heightening or diminishing sensory responses to salient stimuli. The result of the prevalence of ACE and the associated mental and physical disorders may reduce the individual’s ability to integrate within society, such as by receiving inadequate education, unable to form lasting relationships, and unemployment, thus reducing the level of support and economic ability to provide sufficient nutrition and safe housing. Thus, self-propagating the effects of social extradition, developing mental and physical disorders in adulthood resultant of the effects of ACE. Within this essay, the effects of ACE upon the body and its implications on adult health will be explored, in addition to how social circumstance may also facilitate later life health implications via disruption to education and job prospects.

Structural and Functional Brain Alterations Resultant of Exposure to ACE

The introduction of ACE into early childhood induces the action of compensatory mechanisms to adapt to the possible trauma received. The three-hit concept of resilience and vulnerability acts as the central hypothesis to understand the evolutionary reasoning behind such plastic changes to the brain’s morphology, and how mismatch in the phenotypic outcome of the adaption and the ability to cope with environmental stimuli is thought to raise the risk of psychological and somatic disease (Gluckman et al., 2009). The three-hit model acts to understand the pathogenesis of ACE upon the developing brain by linking the interaction of genetic factors (Hit 1) with early life environmental factors (Hit 2), via altered endocrine regulation and epigenetic modification, and then exposing this programmed phenotype to later life environment (Hit 3) where these adaptions to early life trauma are mismatched, compromising mental functions, inducing possible psychiatric symptoms (Nederhoff et al., 2012). Certain exposure to ACE results in functional changes to sensory systems involved in the trauma experienced. Such examples include the reduced visual cortex and right lingual grey gyrus grey matter in young adults who were exposed to witnessing domestic violence at childhood (Tomoda et al., 2012) and the thinning of the somatosensory genital field and brain regions associated with self-awareness and self-evaluation in young adults who were exposed to childhood sexual and emotional abuse (Heim et al., 2013). The changes in brain functionality and the resultant desensitization can be seen as a possible compensatory mechanism which can accumulate over a period of time, inducing epigenetic changes via elevated glucocorticoid release from the HPA (hypothalamus-pituitary axis), regulating gene transcription resulting in behavioral and psychological adaptions.

The manifestation of such functional brain changes in the face of salient stimuli confers mirrored morphometric changes in the offended regions of the brain in response to the altered cortisol levels and epigenetic alterations. Especially effected areas include the hippocampus, amygdala, and the ACC (anterior cingulate cortex) of the stress regulatory circuits, which contain a high density of glucocorticoid receptors, increasing the vulnerability of these regions to the effects of glucocorticoids (cortisol) (Calem et al., 2017, Sapolsky, 2003). The amygdala, a region of the limbic system responsible for fear association, anxiety, and aggression, in response to stress stimulates an increase in volume to facilitate an increase in activity in response to stress induced by the ACE. This hyperactivation, facilitates a greater level of fear conditioning, where amygdala neurons during a period of emotional turmoil promotes synaptic plasticity increasing the individuals ability to recognize and anticipate harm for certain stimuli, which in an environment where physical and mental abuse alongside other ACE are present would be beneficial, but when applied to daily living these hyperaware fear responses may induce social anxiety, OCD, post-traumatic stress as well as borderline personality disorders. We can therefore observe a correlation between an increase in amygdala activation and the development of social phobia, which results in extensive implications regarding social integration.

Psychosocial and Somatic Alterations as a Result of ACE

In addition to the heightened awareness to threatening stimuli, the physical and chemical alterations to the brain can result in changes to the behavior of the individual in addition to inducing widespread somatic changes in body chemistry disturbing homeostatic mechanisms inducing disease. Resultant of altered cognitive and affective processing, those who have experience ACE tend to show heightened experiences of loneliness (Boyda et al., 2015), increased aggression and reduced social cognitive functioning inducing an increase in risk for depression and PTSD. The development of such mental health disorders shows a correlation with the type and time of the ACE, with evidence suggesting the advent of depression is more likely in those exposed to emotional trauma, whereas a higher odds ratio for drug abuse in later life can be seen in those who experience physical abuse (Norman et al., 2012). This association may hark back to the topological changes within the brain whereby the introduction of these salient stimuli induces compensatory mechanisms which become redundant once the stimuli is removed and thus the euphoria induced by narcotics may act to counteract these hypersensitive neural loops, and thus provide a more desirable and addictive affect in those who experience physical trauma. Additionally, the timing of the ACE within an individual’s life is shown to have implications on mental health symptoms in their adult life. Earlier exposure to ACE has been shown to increase the risk of depressive symptoms, whereas similar trauma after the age of 12 are more likely to experience symptoms of PTSD (Glod et al., 1996). Similarly, dissociative symptoms were associated with emotional abuse at a peak age of 13-14 years old, and risk of PTSD and suicidal thoughts show an increased risk of development in those who experience ACE between 3 and 5 years old (Kaplow et al., 2007). The patterning of the development of certain phycological conditions at certain years of age indicates moments of vulnerability within the brain’s development where a certain region is particularly plastic to external stimuli, thus showing that later life mental health disorders may have a basis in early trauma at a specific point in development. The penetrance of such psychological defects and the variation in severity of the presented symptoms may be a product of the severity of the ACE, as well as the genetic and epigenetic resilience of the individual. Emerging evidence suggests that genetic variants and adverse social interaction can interact (via epigenetic modification and resultant gene silencing mechanisms), and that the genotype of an individual may be a determinant in the risk and resilience to any later life psychopathology (Luoni et al., 2016). Thus, this highlights the possibility of induced resilience, where genetically high-risk individuals in a supportive environment can epigenetically promote resilience by silencing of risk associated genes (McCrory et al., 2012).

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Additionally, a wide range of chronic disorders such as obesity, diabetes, inflammatory bowel disease, Crohn’s disease, have been attributed to the increase in proinflammatory markers within ACE affected individuals (such as IL-6 and TNF-alpha). In addition, an enhanced perception of pain induced by a heightened sensory ability can result in long term chronicity of pain, especially that of the lower lumbar spine. It has been reported that an increased level of pro-inflammatory markers, most notably TNF-alpha and IL-6, during critical phases of development, resultant of high stress environments attributed to ACE, can augment the development of neurobiological systems relevant for IBD with the type and timing of the ACE being critical to the possible disfunctions, developed in later life (Baumeister et al., 2016). Subgroup analysis for differing categories of ACE (physical, sexual, or emotional abuse) has been shown to have a differential impact on the level of proinflammatory cytokines, inducing ACE specific inflammatory profiles which has the ability to potentiate autoimmune and chronic disease. Pain perception is also differentially altered, enhancing pressure pain sensitivity (Tesarz et al., 2015). Recent experimentation has shown that stress is able to sensitize nociceptive neurons within the ascending tracts of the spinal cords and that neural responses are accompanied by changes in pain-induced behavior. Models further suggest that social rejection (ACE) produces long lasting effects in sensitivity of pain and results in altered social behavior that persists into adulthood (Schneider et al., 2016). Furthermore, parent-child separation has been shown to be associated with alterations in reproductive traits, prenatal maternal distress, and labor pain with women who experienced childhood sexual abuse, finding pregnancy often more frightening than in controls. Additionally, the experience of ACE alongside a possible low socioeconomic status of the mother plays a role in predicting a low birth weight of the offspring (Smith et al., 2016). Looking to historical records of periods of socioeconomic depravity and the associated birthweight of those born during that period, the Dutch Hunger Winter (1944-1945), we can observe various patterns, where the state of food depravity the mother experiences during the pregnancy period has a role in determining the offspring’s weight at birth and in later life. It was elucidated that offspring whose mothers had a low caloric intake at the end of the pregnancy period, but not the start, had a lower-than-average birthweight, whereas offspring whose had mother with a high caloric intake during late pregnancy, but experienced starvation initially had a higher than birthweight. This ACE experienced by the offspring prenatally is thought to have an epigenetic effect on the child’s ability to gain weight with those initially starved epigenetically adapted to retain much of the dietary intake in food stores such as fat. This effect has continued implications on the individual into adult life where their body is predisposed to weight gain, and thus more susceptible to obesity, type 2 diabetes, and other chronic illnesses.

Influence of Socioeconomic Status on Later Life

Alongside the biochemical alterations which may determine adult health, the socioeconomic situation of a child and the network of support placed around the individual has great influence over the opportunities available for the child to obtain, which therefore determines future job prospects and living situations which have a great influence over the health of the individual. Link and Phelan’s idea of fundamental causality of later life disease explores how stopping damaging social conditions such as smoking only has a partial influence over the health of the individual, and that there is a great wealth of factors which arise from substandard early living which determines the derivation of such habits and future susceptibility to illness. For example, smoking appears to be much more common within areas of a low economic income with possible habit induction from environmental peer pressure, resultant of smoking being seen as a positive value within social relationships (Lewis et al., 2013). The idea of smoking seen as a bonding and social activity suggests both differences in values held between groups which are more or less affluent. Therefore, looking to the incidence of smoking, it is common to observe other habits which are unhealthy and contribute to a lower later life health, such as a reduced precedence placed on exercise or healthy eating (which may be resultant of reduced free time from socioeconomic hardship forcing longer work hours), suggesting how negative salient stimuli typically occur as a group, and therefore, elimination of an accumulation of ACE requires grassroot social change. Furthermore, early exposure to such environments, via possible effects of secondary smoking can have extensive effects on lung health later in life, as shown in one of my PfP sessions where a patient had severe COPD and respiratory distress even though they have never smoked a single cigarette, but during childhood they spend a substantial amount of time in their parents pub, which, due to a lack of air ventilation, resulted in local atmospheric accumulation of noxious chemicals, and thus the accumulation of damage to their lung tissue.

In addition, reduced quality of education for the child and their carers can have a substantial impact upon the future opportunities the child has available. Direct consequences of a poor education can predispose an individual to reduced opportunities regarding employment and their economic situation, which both has an effect on the stress the individual may experience throughout life (which increases the allostatic load promoting chronic disease), alongside directly altering the living situation of the individual such as the area in which they live: in terms of infrastructure quality, the particulate content of the surrounding air which may predispose an individual to later life chronic lung disease, and the local social habits which may be beneficial or act to hinder overall health. Additionally, the economic security enhanced by education provides time for more self-care regarding the ability to attend health appointments and create a healthier lifestyle which may be both unattainable economically and temporally for someone who is forced into working a greater number of hours a day. Such situations (as I observed during work experience at a local GP practice) can be aided by the by working with relevant services signposting the patient to receive aid in planning healthier meals and finding time to exercise, however due to a greater number of individuals in similar positions the selection criteria for certain support has become more stringent, resulting in a vast number of individuals not receiving adequate care. In addition, the educational standard of the child guardian can result in ineffective and possibly harmful parenting and care, which may increase the incidence of ACE towards the child and result in a lower quality of health due to possible malnutrition and lack of support received from the parent due to longer working hours. The effect of wealth on the health of a child in later life was studied by Costello et al. (2010), where in 1996 a casino was opened on an Indian reservation, resulting in an increase in annual income from $500 to $9000 for each family. A representative sample of children aged 9,11 or 13 years in 1993 were assessed for psychiatric and substance use disorders through till age 21 (2006), and a lower prevalence of psychopathology was detected in the children whose family received the income supplement compared to those who did not. This we can possibly attribute to the higher quality of food the children would receive, altering the effects of possible malnutrition, which have long lasting implications on health into adulthood, as well as a reduced employment burden placed upon the parent facilitating a greater ability to spend more time with the child and aid their education, as well as their well-being. Thus, reducing the incidence of emotional trauma and resultant neurological and somatic effects on their child in adult life.

With the recent outbreak of Covid-19 and its associated socioeconomic impacts, the education and nutrition provided by schools has been severed, and thus a reduced educational and nutritional quality will be experienced by a large group of children. A study by Marmot et al. (2021) discussed the impacts of Covid-19 on the early years of a child’s development and found that due to the reduced social contact provided by nursery services and full-time education, children are reaching physical, social, intellectual, and emotional goals at a later age, which are shown to be linked to poorer later life outcomes. Before the advent of the 1st pandemic 68% of parents with children aged 3-4 years were accessing educational or childcare services, with only 7% of parents accessing the same facilities during the lockdown period. This placed great importance on the home learning environment, and thus children who have families who are less economically stable and thus are unable to work from home, due to possible implications of the parents’ educational upbringing, may be unable to keep up the rate of development, compared to those in full time care or have parents who are more economically stable. This has had the reported effect of when children returned to education, some children returned less confident, more anxious, and less independent reverting back to the use of nappies. In addition, an increased time spent at home has resulted in an increase in mental health issues in those who have been exposed to greater violence at home, greater stress and on increase in the incidence of malnutrition in disadvantaged students, leading to lifelong somatic and psychological health issues.


Adverse childhood experiences have a vast effect on later life through manipulating neural and somatic pathways, predisposing the individual to later life disease, as well as manifesting its effects through reducing later life opportunity, placing the individual into unhealthy high stress circumstances, implicating an increase in allostatic load or directly influencing the actions of the individual in terms of diet and social factors, which may promote the development of chronic disease. Additionally, it is important to consider the fundamental causes predisposing adult life illness, and how the linkage of multiple differing negative effects can lead to the great accumulation of possible factors, inducing disease leading to a reduced outlook of health in later life with the incidence of exacerbating factors such as the Covid-19, further aiding the accumulation of these adverse life experiences. Overall, there is a great wealth of evidence describing the vast pathways where adverse experiences in early life can shape an individual’s mind, body, and social circumstance, accumulating to reduce their quality of health in adult life.

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