Based on the landmark study “Adverse Childhood Experience Study” (and/or other studies), discuss the empirical evidence regarding the effects of childhood abuse and neglect on adult mental and physical health. Research has shown that certain health problems increase with the amount of ACEs (Adverse Childhood Experiences) the individual reports. Continuous stress arising from ACEs, causes neurobiological changes in the brain, resulting in impairment of the normal development of multiple brain structures and functions that are associated with a range of mental and physical health problems.
In addition to this other maladaptive behaviours that arise from abuse may also contribute to behaviours that exacerbate or precipitate the health problems to be discussed (Anda et al, 2006). Consistent stress results in dysregulation of the Hypothalamic Pituitary and Adrenal axis (HPA axis) and related systems having adverse effects on the brain. The inhibitory mechanism that allows cortisol levels return back to normal does not develop properly. Having a low stress threshold and high stress levels from a young age generates diminished resilience in overcoming stressful situations in later life.
CRF (corticotrophin releasing factor) is released during the stress response and influences many of the brain systems that are related to the health issues found in ACE sufferers (Anda et al, 2006 :Chartier 2007). Victims of ACE have been found to have an increased risk of developing anxiety disorders as CRH regulates anxiogenic and anxiolytic pathways (Anda et al, 2006 ) Dysregualtion of the HPA is linked to having low serotonin and high dopamine levels: this combination results in hyper-vigilance, and contributes to anxiety disorders.
Overactive limbic system are also thought to contribute to anxiety disorders as they regulate emotions and the fear response (Hulme,2011). Decreased levels of serotonin in prefrontal cortex are thought to affect executive function and judgement which may explain why ACE sufferer are prone to maladaptive coping behaviours such as somatization, substance abuse, self-harm, suicidal behaviours (Kendler, Kuhn, Vittum, Prescott & Riley, 2005) While these also arise from parental practices, they have a physiological basis.
Development of affective disorders (i. e. depression and anxiety) can be attributed to chronic stress contributing to the dysregulation of serotonin, a known cause of depression and related mood disorders. Expectedly persons who experienced four or more categories of ACE, compared to those who had experienced none, had 4-to 12-fold increased health risks for alcoholism, drug abuse, depression, and suicide attempts; a 2- to 4-fold increase in smoking (Edwards, Anda, Fellitti & Dube, 2004).
Several brain abnormalities contribute to increased incidence of substance abuse and their related health risks in ACE sufferers. Animal studies have found that early life stressors lead to increased levels on norepinephrine in the brain (Anda et al , 2006). As alcohol and heroin are known to decrease activity in the locus coerulus and hence norepinephrine, those who have experienced ACE are more likely to use these substances as a relief from the PTSD like symptoms that norepinephrine causes (Bremner & Vermetten, 2001: Anda et al , 200).
High HPA activity during childhood and denial of developmentally appropriate experience results in general hindrances on brain development and thus learning capacity. ACE sufferers have decreased myelination and neuronal activity, synaptic connectivity, smaller hypothalamus and corpus callosum contributing to sub -optimal learning and further developmental outcomes (Perry and Pollard, 1998). Abnormally high levels of dopamine that arise from high cortisol levels coupled with a decrease in hypothalamic volume has been thought to contribute to difficulties with learning, memory and attention (Kendall-Tackett, 2003).
Dopamine regulates reward systems associated with forming habits and sustaining attention. These abnormalities plus inconsistent discipline may be involved in development of ADD and CD in childhood that lead often persist into adulthood (Lupien, McEwen, Gunnar, & Heim, 2009). Cortisol works with adrenaline to create memories of emotional events, but has been thought to be involved in other memory mechanisms.
Cortisol inhibits memory retrieval of already stored information (deQuervian, Roozendaal, MCGaugh, 1998) therefore adults with elevated cortisol levels in their saliva have been found to have decreased performance on tasks of language, executive function and verbal memory and learning in comparison to controls (Lee et al 2007, p. 41). Deficits in verbal declarative memory were found in women who suffered sexual abuse as children (Hulme, 2011). Another consequence of HPA dysregulation is deficits of oxytocin. On an emotional level, oxytocin regulates pair bonding and social attachment.
Unsurprisingly low oxytocin levels contribute to difficulties in finding and maintaining social and sexual satisfaction (Hulme, 2011). High scores on ACE questionnaires reported difficulty in forming long term attachments, resulting in increased risks of having multiple sexual partners, early sexual intercourse, divorce , contracting HIV and other STIs and perpetrating intimate partner violence (IPV) (Edwards, Anda, Fellitti & Dube, 2004). On a physical level low oxytocin levels have been linked to ischaemic heart diseases.
The stress response has profound effects on vasodilation and cardiac inotropism and therefore increased incidence of ischaemic heart disease has been found in ACE. Other vasodilation problems such as chronic migraines, and chronic pain conditions occur in ACEs (Anda et al, 2006: Bremner & Vermetten, 2001)
On a more general level stress causes inhibition of the immune system, and this leads to problems with immune system such as asthma, increased infection and reduced recovery time and even early onset of arthritis. Springer, Shridan, Kuo & Carnes, 2007) CRF is known to be involved in appetite suppression and metabolism regulation-obesity and eating disorders are more common amongst people with HPA dysregulation (Miller, 2010). However, studies correlating the incidence of disease to ACE have their limitations. For instance, there may have been an over-emphasis on clinical samples. They may also have been subject to response biases.
In the cases of studies having low response rates, the severely traumatized participants may not have chosen to participate leading to underestimation of effects. However, overestimation may have occurred just as easily as less severely traumatized participants may not have participated as the issues were not important to them, or may have not counted themselves as abused at all and hence not participated, leading to inaccurate findings with poor generalisability (Walker et al 1999). Child abuse is rarely unaccompanied by potential confounding events which could play a greater role.
For instance a deprived intellectual environment, having lack of role models to base coping mechanisms on, poor parenting style, sub-optimal attachment style, maternal depression, copying maladaptive beliefs or behavior patterns of family members, head injuries resulting from abuse, do all contribute to the development of mental illness or poor physical health (Miller, 2010). Overall the victim of ACE’s experiences themselves as being inadequate in many dimensions. Current rhetoric should place more emphasis on evidence about ACEs and biological predispositions for illnesses as well as exhibiting the a tendency for high risk behaviours.
With cross-sectional study designs it is difficult to determine which factors have a direct causal relationship, more longitudinal or experimental research designs are needed for additional direct evidence (Anda et al,2006).
References
- Anda, R. F. , Felitti, V. J. , Bremner, J. D. , Walker, J. D. , Whitfield, C. , Perry, B. D. , Giles, W. H. (2006). The enduring effects of abuse and related adverse experiences in childhood: A convergence of evidence from neurobiology and epidemiology. European Archives of Psychiatry and Clinical Neuroscience, 256(3), 174-186
- Bremner, J. D. , & Vermetten, E. (2001). Stress and development: Behavioral and biological consequences. Development and Psychopathology, 13(3), 473-489.
- Chartier, M. J. ,(2007)The relationship between childhood abuse, adult physical health and health care utilization. Dissertation Abstracts International: Section B: The Sciences and Engineering, , 240-240 de Quervain DJ, Roozendaal B, McGaugh JL ( 1998). “Stress and glucocorticoids impair retrieval of long-term spatial memory”. Nature 394 (6695): 787–90.
- Edwards, V. J. , Anda, R. F. , Felitti, V. J. , & Dube, S. R. (2004). Adverse childhood experiences and health-related quality of life as an adult. (pp. 81-94).
- Washington, DC, US: American Psychological Association, Washington, DC Hulme, P. A. (2011). Childhood sexual abuse, HPA axis regulation, and mental health: An integrative review. Western Journal of Nursing Research, 33(8), 1069-1097
- Kendler, K. S. , Kuhn, J. W. , Vittum, J. , Prescott, C. A. , & Riley, B. (2005). The interaction of stressful life events and a serotonin transporter polymorphism in the prediction of episodes of major depression. Archives of General Psychiatry,62(5), 529-535.
