Childhood adversity impacts adult health












Children who experience chronic stressors are vulnerable to emotional and physical health problems during their entire life. An adverse early life environment can induce changes on behavioural and metabolic responses later in life. Childhood adversity has been linked to elevated rates of morbidity and mortality from a number of chronic diseases.

Physiological   and   biomolecular   studies   are   increasingly  establishing  how  childhood  exposure  to  chronic   stress   leads   to   changes   in   development   of   nervous,  endocrine,  and  immune  systems,  resulting  in  impaired  cognitive,  social,  and  emotional  functioning and  increased  chronic  physiological  damage called allostatic  load. The most compelling data come from studies of children raised in poverty or maltreated by their parents, who show heightened vulnerability to vascular disease, autoimmune disorders, and premature mortality. Adverse early experience persistently impacts on the individual’s responses to stress, which is marked by  an abnormal metabolism of thyroid hormones. Children with early adverse events not only develop psychiatric disorders (e.g. unipolar depression and substance abuse) but also show increased prevalence of metabolic syndrome, coronary heart disease, some cancers, and autoimmune conditions as Hashimoto thyroiditis later in life.


How does early adversity influences the anatomy and physiology of the developing child?


  • Childhood adversity is associated with subtle differences in multiple aspects of  neural,  cardiovascular,  neuroendocrine,  and immune functioning.
  • A neuro-immune network hypothesis 

inflammation, autoimmune disease















Childhood adversity effects on cortico-amygdala function persist into adulthood.Childhood adversity sensitizes cortico-amygdala neural circuitry. Physically abused youth develop vigilance for facial cues that connote anger Such children tend to carefully monitor their environment for danger and maintain alow threshold for judging situations as threatening.

Childhood adversity leaves an inflammatory residue. Children who experienced an early adverse event display higher levels of inflammatory biomarkers relative to control subjects, including C-reactive protein and interleukin-6.

Research has identified the anatomical basis of brain-to-immune signaling. Research shows that network traffic also flows the other direction, from immune to brain. Peripheral inflammation can spread to the brain through multiple mechanisms.

  • Immune dysregulation may be one potential pathway that explains this link

Hashimoto thyrodiitis, Hashimoto's













  • Another potential bidirectional pathway in the neuroimmune network involves the cortico-basal ganglia circuit, which supports reward processing. Early adversity affects development of the cortico-basal ganglia circuit and the reward-related behaviors it subserves.

The associations between inflammation and depression are especially strong in persons exposed to childhood adversity. Though, research shows that depression itself is not associated with inflammation. Researchers state that childhood maltreatment may modify the relationship between major depressive disorder and hippocampal volume reduction.

The association between childhood trauma and C-reactive protein (CRP), a biomarker of inflammation that may play a role in autoimmune diseases. After controlling for current stress, researchers reported that childhood maltreatment was associated with elevated CRP levels in adults 20 years later, suggesting that childhood maltreatment independently increases inflammation later in life.

Research on nervous, endocrine, and immune interactions has revealed that these systems are anatomically and functionally interconnected. Stressors, such as infections, toxins, and/or psychological trauma, stimulate the hypothalamic-pituitary-adrenal axis to release corticoid-releasing hormone(CRH), resulting in elevated systemic levels of corticosteroids, such as glucocorticoids. Acute stress initially may increase inflammation through acute-phase mediators like IL-1,IL-6, and CRP that are eventually downregulated by glucocorticoids thereby maintaining homeostasis. Chronic stress has the opposite effect and decreases glucocorticoid levels. An epidemiologic longitudinal study confirmed the link between childhood abuse and long-term changes in immune response. It shows that childhood abuse was associated with elevated CRP levels, white blood cell counts, and other markers of inflammation 20 years later.

Physiological and anatomical changes in the brains of individuals who have experienced childhood abuse have been documented. For example, conducted electroencephalograms to measure limbic irritability and found the percentage of clinically significant brain-wave abnormalities to be higher among individuals who had a history of early trauma versus those who did not experience early trauma. Furthermore, magnetic resonance imaging has revealed reductions in hippocampal volumes among severely sexually abused women, and reductions in the intracranial and cerebral volumes among maltreated children compared with non-abused individuals.

Although the effects cannot be defined to any specific area of the brain, it has been shown that the limbic system, which is responsible for emotional response, is adversely affected. Because ACEs rarely occur in isolation, the cumulative effect of multiple ACEs may have an even more powerful negative effect on a young child’s developing brain via repeated activation of the stress response. This repeated “dosing” of the developing central nervous system by adrenal catecholamines and corticosteroids may contribute to central nervous system- and endocrine-mediated differences in immune function that result in an increased risk for autoimmune disease as Hashimoto thyroiditis.

Individuals who were exposed to multiple ACE had greater IL-6 than participants with lesser ACE exposure. However, current resilience resources significantly moderated this effect. Among  individuals who reported multiple ACE, higher resilience resources were associated with lower IL-6 levels. Results from a cross-sectional study suggest that adulthood resilience resources may weaken the association between early life adversity and health outcomes later in life.

But do different types of childhood adversity have different effect on the cell-mediated immune function and does timing of the occurrence matter?

The answer is yes.

Those persons who have been first physically abused before age of 3-5 and/or sexually abused more than 10 times, have elevated Epstein-Bar Virus antibodies later in life. Thus, childhood adversity has a persistent influence on immune responses to latent infection in adulthood.

  • Chronic inflammation contributes to a wide range of human diseases, and environments in infancy and childhood are important determinants of inflammatory phenotypes. Chronic inflammation may be one mechanism through which sexual abuse may affect future risk of physical and psychological disorders. Study researched the patterns of DNA methylation (DNAm) in inflammatory genes in young adulthood would be predicted by early life nutritional, microbial, and psychosocial exposures previously associated with levels of inflammation. The results show that DNAm is a potentially important biological mechanism through which developmental environments shape inflammatory phenotypes across the life course. These results suggest that epigenetic mechanisms may partially explain how early environments have enduring effects on inflammation and inflammation-related diseases.

Thus, there is no question that early adverse events influence our health and make us more prone to develop autoimmune condition as Hashimoto’s later in life. Though there is hope. You can reprogram our immune system now by joining the only world wide online evidence-based program.

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