•The aggregated effect size of early adversity on CRP is very small, z = .07.•The aggregated effect size of early adversity on IL-6 is very small, z = .17.•More studies looking at TNF-α are ...needed.•More studies using in vitro assays of immune cells are needed.
This study provides a comprehensive review of the published research on the association between early life adversity and markers of inflammation in children and adolescents. We conducted a systematic review of the published literature on the association between early life adversity and markers of inflammation in pediatric populations. To date, 27 studies have been published in this area representing a wide range of global populations and diverse methods of which nearly half were prospective, longitudinal studies. Of these 27, only 12 studies shared an inflammatory outcome with 4 or more other studies; 9 for CRP, and 6 for IL-6. The association between early life adversity and both CRP, z = .07 .04, .10, and IL-6, z = .17 −.07, .42, were small and only significant for CRP although comparable in magnitude to the effects observed in adult samples. Descriptively, the association between early life adversity and CRP appeared to be stronger in studies conducted in infants and adolescents compared with middle childhood. There was minimal evidence of publication bias for studies measuring CRP, but evidence of publication bias for studies using IL-6. Eight studies have looked at the association between early life adversity and stimulated inflammatory cytokines in vitro, and both the methods and results of these studies were mixed; the majority observed exaggerated production of inflammatory cytokines despite mixed methodological approaches that make comparisons across studies difficult. In summary, the evidence supporting an association between early life adversity and inflammation in pediatric samples is limited so far by the number of studies and their heterogeneous methodological approaches. More research that is grounded in a developmental framework and informed by the complexity of the innate immune system is needed in this area.
•Exogenously-induced inflammation leads to expression of 3 features of depression.•They are neural reactivity to negative stimuli, reward processing, somatic symptoms.•Little evidence for the role of ...inflammation in cognitive control was observed.•Effects of inflammation on behavior depend on the timing and dose of the stimulus.
A wealth of evidence has implicated inflammation in the development of depression. Yet, the heterogeneous nature of depression has impeded efforts to understand, prevent, and treat the disease. The purpose of this integrative review is to summarize the connections between inflammation and established core features of depression that exhibit more homogeneity than the syndrome itself: exaggerated reactivity to negative information, altered reward processing, decreased cognitive control, and somatic syndrome. For each core feature, we first provide a brief overview of its relevance to depression and neurobiological underpinnings, and then review evidence investigating a potential role of inflammation. We focus primarily on findings from experimental paradigms of exogenously-induced inflammation. We conclude that inflammation likely plays a role in exaggerated reactivity to negative information, altered reward reactivity, and somatic symptoms. There is less evidence supporting an effect of inflammation on cognitive control as assessed by standard neuropsychological measures. Finally, we discuss implications for future research and recommendationsfor how to test the role of inflammation in the pathogenesis of heterogeneous psychiatric disorders.
The COVID-19 pandemic and efforts to slow the spread of disease have particularly affected the lives of adolescents. Many studies have recently identified the risks to adolescent mental health posed ...by the COVID-19 pandemic, yet few have identified the markers of resilience to the events and concerns associated with the pandemic's lived experience. This study examined the moderating role of psychosocial resources in the association between the tangible and emotional experiences of the COVID-19 pandemic and symptoms of common psychiatric problems during adolescence (depression, anxiety, proactive and reactive aggression, and sleep problems).
Participants were adolescents in the United States who were oversampled for early life adversity before the COVID-19 pandemic. The psychosocial resources assessed were humor styles, emotion regulation, social support, optimism, and purpose in life, which have previously been identified as protective in the acute aftermath of stressful events.
Greater COVID-19 impact was associated with more anxiety, depressive symptoms, sleep disturbance, and proactive aggression. COVID-19 impact and psychiatric symptoms were unrelated among youth reporting high self-enhancing humor and cognitive reappraisal.
Adolescents high in humor and cognitive reappraisal may be protected against the mental health correlates of the COVID-19 pandemic and other prolonged stressors. Importantly, these factors are known to be modifiable through behavioral interventions. Attention to their effectiveness in prevention and intervention studies is needed as the pandemic continues to exert its impact on individuals and society.
Research conducted over the past several decades has revolutionized our understanding of the role of the immune system in neural and psychological development and function across the life span. Our ...goal in this review is to introduce this dynamic area of research to a psychological audience and highlight its relevance for clinical psychology. We begin by introducing the basic physiology of immune-to-brain signaling and the neuroimmune network, focusing on inflammation. Drawing from preclinical and clinical research, we then examine effects of immune activation on key psychological domains, including positive and negative valence systems, social processes, cognition, and arousal (fatigue, sleep), as well as links with psychological disorders (depression, posttraumatic stress disorder, anxiety, schizophrenia). We also consider psychosocial stress as a critical modulator of neuroimmune activity and focus on early life adversity. Finally, we highlight psychosocial and mind-body interventions that influence the immune system and may promote neuroimmune resilience.
The brain and immune system are intricately connected, and perturbations in one system have direct effects on the other. This review focuses on these dynamic psychoneuroimmune interactions and their ...implications for mental and physical health in the context of the COVID-19 pandemic. In particular, we describe how psychological states influence antiviral immunity and the vaccine response, and how immune changes triggered by COVID (either via infection with SARS-CoV-2 or associated stressors) can influence the brain with effects on cognition, emotion, and behavior. We consider negative psychological states, which have been the primary focus of psychological research in the context of COVID-19 (and psychoneuroimmunology more generally). We also consider positive psychological states, including positive affect and eudaimonic well-being, given increasing evidence for their importance as modulators of immunity. We finish with a discussion of interventions that may be effective in improving immune function, the neuro-immune axis, and ultimately, mental and physical health.
•There are dynamic bi-directional interactions between the brain and immune system.•Both negative and positive psychological states influence antiviral immunity.•Immune activation leads to behavioral changes relevant for long-haul COVID.•Psychosocial interventions can enhance both mental health and immune function.
Highlights • We characterized the relationship between trauma subtypes to HPA-axis functioning. • We examined three common indices of HPA-axis functioning. • Non-intentional trauma predicted elevated ...cortisol at bedtime. • Physical abuse was associated with faster reactivity to acute stress. • Emotional abuse predicted delayed recovery of cortisol following acute stress.
•Higher CRP predicts greater SAD symptom improvement during VR exposure therapy.•CRP, SAD symptoms, and subjective distress all decline during VR exposure therapy.•However, declines in CRP and SAD ...symptoms are not associated within-persons.
Social anxiety disorder (SAD) places a profound burden on public health and individual wellbeing. Systemic inflammation may be important to the onset and maintenance of SAD, and anti-inflammatory treatments have shown promise in relieving symptoms of SAD. In the present study, we conducted secondary analyses on data from a randomized clinical trial to determine whether C-reactive protein (CRP) concentrations and social anxiety symptoms decreased over the course of virtual reality exposure therapy, and whether changes in social anxiety symptoms as a function of treatment varied as a function of CRP.
Adult participants (N = 78) with a diagnosis of SAD (59 % female) were randomized to receive exposure therapy alone, or exposure therapy supplemented with scopolamine. Social anxiety symptoms, salivary CRP, and subjective units of distress were measured across three exposure therapy sessions, at a post-treatment extinction retest, and at a 1-month follow-up.
CRP decreased over the course of treatment, b = −0.03 (SE = 0.01), p =.02 95 %CI −0.06, −0.004, as did all social anxiety symptom domains and subjective distress. Higher CRP was associated with greater decreases from pre-treatment to 1-month follow-up in fear, b = −0.45 (SE = 0.15), p =.004 95 %CI −0.74, −0.15, and avoidance, b = −0.62 (SE = 0.19), p =.002 95 %CI −1.01, −0.23, and in-session subjective distress from pre-treatment to post-treatment, b = −0.42 (SE = 0.21), p =.05 95 %CI −0.83, −0.001. However, declines in CRP were not correlated with declines in fear, r = −0.07, p =.61, or avoidance, r = −0.10, p =.49, within-persons.
Virtual reality exposure therapy may be associated with an improvement in systemic inflammation in patients with severe SAD. Pre-treatment CRP may also be of value in predicting which patients stand to benefit the most from this treatment.
•Exposure therapy was less effective for individuals with high in-session cortisol.•Inhibition of autonomic activation during exposure sessions did not alter the link between cortisol and symptom ...change.•A more sensitive, pre-treatment measure of individual differences in glucocorticoid regulation is needed.
The purpose of this study was to explore whether individual differences in glucocorticoid concentrations were associated with symptom improvement following exposure therapy for patients with social anxiety disorder. To do this, 60 participants with social anxiety disorder completed a randomized-controlled trial of exposure therapy, where participants were randomized to receive scopolamine-augmentation or placebo during their 7 exposure sessions. Scopolamine is an antimuscarinic which blocks the effects of acetylcholine and reduces autonomic arousal. During sessions 1, 4, 7, and during the post-treatment extinction assessment, participants provided up to 16 saliva samples (4 in each session). Pre-treatment, post-treatment, and at 1-month follow-up, participants completed the Liebowitz Social Anxiety Scale to monitor change in fear and avoidance symptoms. Elevated endogenous in-session cortisol during exposure sessions was associated with less symptom improvement from pre- to post-treatment and at 1-month follow-up. The association between elevated endogenous in-session cortisol and attenuated symptom change was not moderated by scopolamine treatment condition. Individuals with social anxiety disorder who have elevated neuroendocrine signaling may under-benefit from exposure therapy. This is the first study, to our knowledge, to examine whether endogenous in-session cortisol concentrations predict symptom changes following exposure therapy for the treatment of social anxiety disorder. More investigation of non-invasive and reliable biological markers that explain variability in responses to effective treatments are needed.
Inflammation has been shown to predict depression, but sensitivity to inflammation varies across individuals. Experimental studies administering potent pro-inflammatory agents have begun to ...characterize this sensitivity. However, risk factors for inflammation-associated depression in naturalistic contexts have not been determined. The present study examined key psychological and behavioral risk factors (state anxiety, perceived stress, negative affect, disturbed sleep, and childhood adversity) as potential moderators of the relationship between inflammation and depressive symptoms in a prospective longitudinal study of breast cancer survivors. Women with early stage breast cancer were recruited after completing primary cancer treatment (n
= 161). Depressive symptoms, inflammatory markers (CRP, IL-6, and sTNF-RII), and key risk factors were assessed post treatment (T1), at 6 and 12-month follow-ups (T2 and T3), and during a final follow-up (TF) 3-6 years after T1; childhood adversity was measured only at T3. Inflammatory markers were combined into a single inflammatory index prior to analyses. Women who reported higher levels of state anxiety, perceived stress, negative affect, and/or sleep disturbance at T1 (post-treatment) exhibited higher depressive symptoms at times when inflammation was higher than typical (interaction βs ranged from .06 to .08; all ps < .014). Results demonstrate the relevance of these risk factors for understanding inflammation-associated depression in a clinical context and could inform targeted strategies for prevention and treatment among at-risk populations.
•We examined the impact of Facebook use, personality, and sex on depressive symptoms.•We found no direct link between Facebook use and depressive symptoms.•Facebook use among high neuroticism females ...predicted lower depressive symptoms.
The popularity of social networking sites, such as Facebook, has increased rapidly over the past decade, especially among youth. Consequently, the impact of Facebook use on mental health problems (e.g., depressive symptomatology) has become a recent area of concern. Yet, evidence for such a link has been mixed and factors that contribute to heterogeneity of findings have not been identified. In this study, we examined whether the association between Facebook use and depressive symptoms is moderated by individual factors (i.e., personality and sex). To this end, we measured Facebook use, depressive symptoms, and personality domains (i.e., extroversion and neuroticism) among 237 young adults. No direct association was found between Facebook use and depressive symptoms. However, for females with high neuroticism, more frequent Facebook use was associated with lower depressive symptoms. Our findings suggest a complex relationship between Facebook use and depressive symptomatology that appears to vary by sex and personality. Facebook use may be protective against depressive symptoms for female users with high levels of neuroticism, while Facebook use may be unrelated to depressive symptoms among males.
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