Sentences with phrase «hpa axis»

Evidence for a normal HPA axis response to psychosocial stress in patients remitted from depression

Satisfaction with the partner, on the other hand, may reduce the stress - related activation of the HPA axis [29].

However, one of the major proposed mechanisms to account for the relationship between prenatal psychosocial stress and the offspring's susceptibility to infections is the secretion of cortisol, which is regulated by the maternal HPA axis and the placenta [14,20].

Thus, the physiological mechanisms underlying the associations found in the present study may be linked to maternal HPA axis activation.

These data were used to classify whether children's HPA axis activity was attenuated.

Animal studies have shown that maternal HPA axis activation not only affects the maternal immune system but also the offspring's immune system [20,25,26].

Several studies based on the general population show that marital distress may activate the HPA axis and predict adverse effects on maternal immune function [13,27,28].

The CAR is a widely used and reliable measure for HPA axis activity [35].

Findings reveal that different profiles of HPA axis arousal and emotion regulation are associated with substance use and symptoms of psychopathology among adolescents.

Dr. Fisher's work on children in foster care and the child welfare system includes (a) basic research characterizing the effects of early stress on neurobiological systems such as the HPA axis and areas of the prefrontal cortex involved in executive functioning; (b) the development of preventive interventions, including the Treatment Foster Care of Oregon Program for Preschoolers (TFCO - P) and the Kids in Transition to School Program (KITS); and (c) the dissemination of evidence - based practice in community settings.

He takes you through attachment theory, the HPA axis, and executive control functions, all without losing his footing nor prompting glazing in the reader's eyes.»

Early care experiences and HPA axis regulation in children: A mechanism for later trauma vulnerability

Mitigating HPA axis dysregulation associated with placement changes in foster care.

Nevertheless, these observations are consistent with the notion that T cells will be informative not only on immune specific genes that are associated with the HPA axis but also on some genes that are also involved in brain function.

Normally, one would expect to see low cortisol levels prestress, an increase in response to stress, and a return to baseline during recovery, and so an elevated, flat cortisol trajectory suggests that the HPA axis may have lost some of its resiliency (10).

Disregulation in the HPA axis has been observed in people with Major Depressive Disorder, and has been increasingly linked to PDD.

Blunted cortisol levels, often termed hypocortisolism, are increasingly recognized as a biomarker of chronic stress and may result from downregulation of the HPA axis subsequent to chronic cortisol elevations.18 - 20 There are a few possible interpretations for the normalization of these diurnal rhythms observed with the intervention.

[12] The HPA axis is responsible for responding to stress and regulating levels of stress hormones.

In humans, the end product of the HPA axis is cortisol, a steroid hormone that follows a diurnal rhythm — increasing early in the morning, peaking approximately 30 minutes after waking, and declining throughout the day, reaching near - zero levels at night.14 This diurnal pattern is not present at birth but begins to emerge around 3 months of age15, 16 and is fully entrained to daylight cycles by age 2 years.17 Children experiencing social deprivation or maltreatment show departures from this typical profile of diurnal HPA activity, suggestive of chronic stress.

These results provide evidence that interventions can simultaneously impact caregiver stress and buffer children from the negative impacts of caregiver stress on HPA axis regulation.

This can be attributed tohigher levels of diurnal cortisol secretion and disturbances of HPA axis.

A harsh early environment was associated with an elevated flat cortisol trajectory across the stress tasks, suggesting that HPA axis functioning may have been compromised by recurring or chronic early life stress exposure.

Additionally, some studies with institutionalized children experiencing neglect and transitioning into nurturing homes through adoption show an initial normalization of diurnal cortisol slopes, 10 but other studies show that years later dysregulated cortisol patterns are present again when compared with nonadopted children.33 This raises the possibility that early adversity may have programming effects on the HPA axis that become apparent with time and development, similar to what has been observed in experimental studies in primates and rodents.34 The follow - up assessment in the present study is ideally suited for testing the possibility of long - lasting reversals in HPA functioning.

[12] The development of the placenta during pregnancy is partially responsible for the disregulation of the HPA axis; the hormones that cause placental development can increase the sensitivity of the pituitary to stress hormones.

This work in animals has stimulated studies with young children.6 - 12 Initial findings underscore the complexity of relations among context, development, behavior, and HPA axis function in young children.

A rich body of literature on HPA axis function provides some insights.

Specifically, in the absence of findings from a comparison group at low risk for antisocial behavior, our findings could alternatively be interpreted as suggesting either that the intervention produced compensatory but abnormally high elevations in cortisol levels before peer entry or that the intervention normalizes an already perturbed HPA axis.

Social rearing effects on HPA axis activity over early development and in response to stress in rhesus monkeys

An emerging body of literature24, 25 shows that a subgroup of chronically aggressive children exhibit marked difficulty processing social cues that signal the need to inhibit aggressive impulses.26 These findings have been attributed to reduced responding in specific neural architecture associated with stress responses and HPA axis regulation.

Alternatively, no direct relationship may exist between the changes in behavior and HPA axis activity, with the intervention producing effects on both behavioral and neuroendocrine regulation, both of which are unrelated.

Maternal presence reduces activation of the HPA axis and ANS in young rodents exposed to a stressor (51), and in humans, the presence of a supportive caregiver is associated with reduced HPA axis reactivity in young children (52).

Timing of placement and HPA axis and parasympathetic nervous system reactivity.

Together, these findings suggest that the absence of a caregiver might lead to chronic elevations in activity of the HPA axis and ANS in early childhood, which may ultimately lead to reduced responsiveness of these systems to the environment later in life.

We examined changes in ANS and HPA axis measures during three tasks: two social stressors [the Trier Social Stress Test (TSST), which includes preparation, speech, and math portions; and a peer evaluation task], and one nonsocial stressor (a frustration task).

In humans, both the HPA system and the autonomic nervous system show developmental changes in infancy, with the HPA axis becoming organized between 2 and 6 months of age and the autonomic nervous system demonstrating relative stability by 6 to 12 months of age.63 The HPA axis in particular has been shown to be highly responsive to child - caregiver interactions, with sensitive caregiving programming the HPA axis to become an effective physiological regulator of stress and insensitive caregiving promoting hyperreactive or hyporeactive HPA systems.17 Several animal models as well as human studies also support the connection between caregiver experiences in early postnatal life and alterations of autonomic nervous system balance.63 - 65 Furthermore, children who have a history of sensitive caregiving are more likely to demonstrate optimal affective and behavioral strategies for coping with stress.66, 67 Therefore, children with histories of supportive, sensitive caregiving in early development may be better able to self - regulate their physiological, affective, and behavioral responses to environmental stressors and, consequently, less likely to manifest disturbed HPA and autonomic reactivity that put them at risk for stress - related illnesses such as asthma.

We examined two neuroendocrine markers that reflect HPA axis functioning: cortisol and DHEA - S.

Intervention effects on both the PNS and HPA axis were evident for children placed before 24 months of age, suggesting the possible presence of a sensitive period during which stress response systems are most strongly influenced by environmental inputs.

Therefore, the HPA axis of Novel rats is similar to that of the handled rats or rats that received greater maternal care (4, 8, 17, 24, 25).

It is important to note that there is no question that in neonatal handling studies, mothers of handled pups provide greater amounts of care toward handled pups compared with nonhandled pups (8) and that pups receiving handling or greater maternal care showed changes in emotionality (24) and a cascade of changes within the HPA axis and related brain structures (38).

Maternal presence has a strong regulatory influence on the ANS and HPA axis in rodents and primates (11, 43), and insecure attachment is associated with elevated cortisol reactivity and vagal withdrawal in young children (44, 45).

We present comprehensive data on autonomic nervous system (ANS) and HPA axis reactivity from the Bucharest Early Intervention Project (BEIP), the only randomized controlled trial of foster care as an alternative to institutional rearing for abandoned children, to address each of these challenges.

It is critical to point out that the present findings do not imply that maternal behavior is inconsequential, nor do they imply that any direct stimulation of the pups is sufficient for HPA axis development in offspring.

A similar pattern of findings has been observed in some, but not all, studies of HPA axis development in nonhuman primates following early - life adversity.

A large body of literature has explored the contribution of maternal care in mediating the early stimulation effect on offspring's HPA axis development.

Some studies document hyperreactivity of the SNS and HPA axis following early - life adversity (15 ⇓ ⇓ ⇓ — 19) and others observe blunted HPA axis reactivity (20 ⇓ — 22) or discordance between SNS and HPA axis responses (23).

After establishing the presence of intervention and timing effects on ANS and HPA axis reactivity, we examined whether children exposed to institutional rearing differed from never institutionalized children (NIG).

Glucocorticoid regulation of inflammation and its functional correlates: from HPA axis to glucocorticoid receptor dysfunction.

Elevated sympathetic tone (i.e., lower resting PEP) was observed among children in the care - as - usual group (CAUG) relative to the foster care group (FCG) and never institutionalized group (NIG)(see Table S1 for all values of ANS measures and Table S2 for all HPA axis measures).

To the contrary, this seemingly contradictory set of findings that make up the current literature may be reconciled by considering the contribution of both a stress activation of pups» HPA axis and a maternal modulation of this stress response (39).

Cortisol is the most widely used marker of HPA axis activity in human studies, and DHEA - S appears to have protective effects against some of the negative downstream effects of glucocorticoids, including in the hippocampus (69).