Early Life Stress

Early Life Stress

1. Inhibits the production of neurosteroids which play a large part into how well you handle stress later in life.

2. Prenatal maternal stress, compared to a low stress control condition, has been shown to affect the infant microbiota (beneficial bacteria) measured at 7, 14, 28, 80, and 110 days of age in infants, suggesting important effects of adverse early life experience on the gut microbiome.

3. In humans, early-life stress is associated with a preterm birth and a low birth weight, and can prime the neonate for further complications later in life that include psychiatric disorders, aged-related cognitive dysfunction, obesity, and hypertension.

4. Exposure of the developing fetus to excessive levels of stress hormones in the womb can cause mood disorders in later life.

Adverse environment in early life

An adverse environment in early life has been demonstrated to be one of the most important factors affecting long life health. In humans, early adverse experiences, such as abuse, neglect, or loss of a parent, have an impact on cardiometabolic risk profile and increase the risk of developing mental health disorders, including attention deficit/hyperactivity disorder, conduct disorders, anxiety, depression, suicide, drug abuse, and post traumatic stress disorder. Talge et al2 revealed a large body of research relating stress to health and found an attributable load of emotional/behavioral problems and language delay because of prenatal stress and/or anxiety in approximately 15% of subjects.

Animal studies have also suggested that exposure to stressors or steroids during early life alters the programming of neuroendocrine and neuroimmune systems. For example, maternal separation of rodent pups during the first 2 weeks of life has been shown to induce alterations in behavior and hypothalamic-pituitary-adrenal (HPA) axis reactivity to stress that persists throughout life.

The long-term effects of early life stress on vulnerability to neurological events, such as seizures or stroke, are well documented. These findings provide evidence that early life stress modifies the development of the HPA axis, brain function, and neurobehavior.

Early‐Life Stress: Neuroactive Steroids

Animal studies have amply demonstrated that stress exposure during pregnancy or in early postnatal life can adversely influence brain development and have long‐term ‘programming’ effects on future brain function and behavior. Furthermore, a growing body of evidence from human studies supports the hypothesis that some psychiatric disorders may have developmental origins.

Consequences of early‐life stress can cause: dysregulation of the hypothalamic‐pituitary‐adrenal (HPA) axis, heightened anxiety behavior and cognitive impairments.  Neuroactive steroids modulate neuronal activity and play a key role in neurodevelopment. Moreover they can negatively modulate activity of the HPA axis, exert anxiolytic actions and influence cognitive performance.

Thus, neuroactive steroids may provide a link between early‐life stress and the resultant adverse effects on the brain and behavior. An enhanced understanding of the influence of early‐life stress on brain neurosteroid systems could aid the identification of new targets for developing treatments for stress‐related conditions in humans.

The Quality of Family Life

The quality of family life influences the development of individual differences in vulnerability for affective illnesses. Victims of childhood physical or sexual abuse or parental neglect are at considerably greater risk for affective disorders. Epidemiological studies provide compelling support for the association between cumulative, adverse childhood experiences and the risk for depression. This association remains significant when adjusting for living with a mentally ill parent, thus removing the effects of a gene-environment correlation.

Moreover, there is commonly a dose-response relationship between the number of types of adversity associated and the magnitude of the risk for depression. Statistical modeling demonstrates mediation by multiple intermediate variables, potentially acting with different degrees of effects at varying life stages. These include personality (neuroticism), low self-esteem, conduct disorder, increased risk of adverse life events, low social support, and difficulties in interpersonal relationships.

The results of prospective, longitudinal studies confirm the link between abuse/neglect and depression. Moreover, childhood maltreatment also associates with an increased severity of illness, reduced treatment responsivity, and increased comorbidity.

Broader forms of familial dysfunction including persistent emotional and physical neglect, family conflict, cold, distant parent-child relationships, and conditions of harsh, inconsistent discipline compromise cognitive and emotional development and increase the risk for depression and anxiety disorders to a level comparable to that for abuse. Family life also serves as a source of resilience in the face of chronic stress.  Thus, warm, nurturing families tend to promote resistance to stress and to diminish vulnerability to stress-induced illness. The epidemiology of affective disorders reflects the profound influence of family life on neural development and mental health.

Early Social Environment

The relationship between the quality of the early social environment and health in adulthood appears to be, in part, mediated by the development of individual differences in neural systems that underlie the expression of behavioral and endocrine responses to stress.

Thus, physical and sexual abuse in early life increases endocrine and autonomic responses to stress in adulthood. Likewise, variations in parental care associate with individual differences in neuroendocrine and autonomic responses to stress in humans as well as emotional reactivity. Finally, there is considerable evidence in favor of the hypothesis that individual differences in stress reactivity predict the risk for depression

Thus, the influence of familial depressive illness is, in part at least, mediated by increased stress reactivity, enhancing the response of the individual to mild, regular stressors (ie, hassles). Individuals with early adverse experience appear to be sensitized to the depressive effects of acute stress in adulthood.

Maternal prenatal stress may influence a baby’s gut microbiota

We have all felt it – stress. Sometimes it is a powerful ally that helps us perform better in an exam or when giving a talk. But when it turns into a long-lasting partner, it can become a serious health problem that may even interfere with our ability to live a normal life. Furthermore, stress is a key issue in certain periods of our life, such as pregnancy.

A number of scientific studies have already linked stress in pregnant women to premature birth, low birth weight, some skin conditions, asthma and even anxiety and attention-deficit hyperactivity disorder (ADHD). However, the reasons underlying these associations remain elusive. So what if gut microbiota played a role?

A new study by researchers from the Behavioural Science Institute of Radboud University Nijmegen in the Netherlands, published in the journal Psychoneuroendocrinology, appears to shed some light on this link between stress in pregnant women and their babies’ microbiota.

According to the authors of the study, mothers who experience high and prolonged levels of stress during gestation are more likely to have infants with more probabilities of suffering intestinal problems and allergic reactions.

The scientists recruited 56 pregnant mothers and measured women’s levels of stress by asking them to complete a questionnaire and to provide a saliva sample in which they analysed the concentrations of cortisol (the so-called stress hormone) prior to delivery. The Dutch researchers subsequently examined the microbiota of the babies’ guts through stool samples collected from the age of 7 days up until 4 months after birth.

According to this team of experts, there is a correlation between highly stressed pregnant mothers and the composition of microbes in the newborns’ guts. These infants had a significantly higher relative abundance of Proteobacterial groups, known, in the author’s words, to contain pathogens (Escherichia, Serratia and Enterobacter), and lower quantities of lactic acid bacteria such as Lactobacillus, Lactococcus, Aerococcus and Bifidobacteria.

Altogether, experts consider this pattern to be related to a potentially increased level of inflammation. This aberrant colonization pattern was related to more maternally reported infant gastrointestinal symptoms and allergic reactions. They also saw that breastfeeding, which is known to promote the development of beneficial microbes in the intestine due to the prebiotic content of breast milk, was not enough to protect the baby from the negative effects of its mother’s stress.

Although it remains a theory, researchers speculate that the cortisol may be interfering with bile production, which could, in turn, influence gut bacteria. They also highlight this stress hormone may be able to pass through the placenta and increase cortisol levels in the foetus, thus affecting the development of the gastrointestinal tract.

According to the authors of the paper, the study has shown clear links between the mother’s stress during pregnancy and the baby’s gut microbiota development and health. For these Dutch experts, the results suggest there is a possible mechanism by which maternal prenatal stress influences the development of the foetus.

Nevertheless, the reasons behind this link are still unknown and require further research. Finally, researchers from Radboud University Nijmegen consider their findings may open up a potential way for bacterial interventions to improve health and development in babies born to stressed mothers. 

Maternal prenatal stress is associated with the infant intestinal microbiota. (*)