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Early-Life Stress and Adult Inflammation Essay


In the article, “Early-Life Stress and Adult Inflammation,” the authors provide a literature synopsis of the relationship between early-life stress and inflammation in adulthood. They also discuss how factors that include neuroendocrine, epigenetic, psychological, and autonomic responses to childhood experiences put children at risk of inflammation in adulthood. The article’s conclusion provides recommendations that urge health care practitioners and other stakeholders to implement programs that aim to reduce the prevalence of stress among children. Modern psychology is primarily founded on the fundamental assumption that stressful experiences hurt individuals’ mental health. Studies conducted in the field of health psychology have shown that stress experienced during childhood affects physical well-being immensely (Fagundes and Way 277). For instance, it increases the risk of the development of conditions such as diabetes, cancer, cardiovascular disease, and type 2 diabetes. This claim has been augmented by research in the field of psychoneuroimmunology.

Research studies conducted in the fields of biological and behavioral sciences have validated the argument that early-life stress impacts physical well-being negatively. In that regard, certain conditions that develop in adulthood can be attributed to stressful situations that are experienced during childhood. Inflammation is a normal mechanism elicited by the immune system to eliminate foreign invaders such as bacteria and viruses (Fagundes and Way 278). However, it affects optimal body functioning if it persists. High levels of inflammation are common occurrences in conditions such as osteoporosis, certain cancers, Alzheimer’s disease, and rheumatoid arthritis, and they are also predictors of mortality, life quality, and morbidity in adults. Psychologists have studied both chronic and severe life stressors in children to determine how they affect the proper functioning of the immune system. Examples of conditions linked to chronic inflammation include periodontal disease, osteoporosis, fatigue, rheumatoid arthritis, frailty, disability, cardiovascular disease, and type 2 diabetes.

Previous studies conducted on early stress and inflammation have focused on socioeconomic status and parental maltreatment as the major sources of stress. Children from low socioeconomic backgrounds, experience numerous conditions that expose them to chronic risk. Moreover, they are subjected to a high risk of malnutrition, poor health practices, unhealthy diets, and substance abuse. According to the article, approximately 30-50 percent of adults report that they experienced some type of mistreatment during childhood, including sexual, physical, and emotional abuse as well as emotional and physical neglect (Fagundes and Way 279). Children raised in stressful environments exhibit higher levels of inflammatory cytokine production in comparison to children raised in low-stress environments. The prevalence of inflammation markers starts in childhood and progresses into adulthood. The article provides the results of several studies that found out that childhood adversity exposes children to inflammatory activity. The risk of developing certain chronic conditions in adulthood is higher among individuals who grew up in stressful environments and unsupportive families.

Psychological pathways that potentiate inflammation function by upregulating the transcription of nuclear factor kappa-light-chain-enhancer of activated B cells. Critical factors in the development of inflammatory activity include the frequency of stressful events and the intensity of reactivity to adversity. Studies have shown that adults who experienced childhood abuse exhibit high reactivity to stress in their daily lives compared to those who did not experience abuse. Moreover, they are more likely to report frequent psychological stress. Experiments conducted in the laboratory showed high levels of plasma IL-6 in response to simulated stressful situations by individuals who experienced traumatic events in childhood (Fagundes and Way 282). The levels were low in individuals who did not experience traumatic events in childhood. Experiments conducted among depressed participants showed high levels of IL-6 plasma in reaction to stress.

Scientists have established a relationship between autonomic activity and childhood abuse. The fight or flight response elicited by stressful situations is accentuated by responses to adversity. The response suppresses parasympathetic activity and increases inflammation. In that regard, increased sympathetic activity and decreased parasympathetic activity due to maltreatment exposes children to the risk of inflammation in adulthood. Children with a background of abuse exhibit lower heart-rate variability than children who were not abused. Childhood abuse also alters the body’s immune response to cortisol. Another cause of inflammation in adulthood is epigenetic change, which involves the structural modification of DNA. Methylation is an example of an epigenetic change that involves the addition of a chemical group to DNA (Fagundes and Way 285). More research needs to be conducted because few studies on epigenetic change have been done. Future studies should focus on the identification of periods during development that epigenetic changes occur and the role played by inflammatory molecules in DNA modification processes such as methylation.

In conclusion, the authors recommended basic research for the identification of the most responsive periods and biological pathways for the efficacious implementation of interventions. Implementing interventions that help children who experience maltreatment is critical to enhancing their mental and physical health. Anti-inflammatory medications should be administered to adults who experienced abuse during childhood. Effective psychological remedies include cognitive behavioral therapy and relaxation exercises. Researchers should study the role of inflammatory biomarkers in aiding the implementation of the aforementioned interventions.

Work Cited

Fagundes, Christopher P, and Baldwin Way. “Early –Life Stress and Adult Inflammation.” Current Directions in Psychological Science, vol. 23, no. 4, 2014, pp. 277-283.

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IvyPanda. "Early-Life Stress and Adult Inflammation." November 23, 2020. https://ivypanda.com/essays/early-life-stress-and-adult-inflammation/.

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IvyPanda. 2020. "Early-Life Stress and Adult Inflammation." November 23, 2020. https://ivypanda.com/essays/early-life-stress-and-adult-inflammation/.

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IvyPanda. (2020) 'Early-Life Stress and Adult Inflammation'. 23 November.

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