Sarah M. Lyle

Psychological distress has been associated with dampened antibody production following vaccination. Questions remain, however, about whether psychological distress influences vaccine response uniformly across the lifespan, and whether changes in distress result in changes in antibody production across the same period.
Participants (N = 148; Mage = 32.2 years, SD = 19.7, range = 12–80 years) took part in consecutive vaccine studies during the 2017–2018 and 2018–2019 influenza seasons. Each influenza season, they reported on their depressive symptoms, provided blood samples, and received the standard influenza vaccine. Participants then provided a second blood sample one month later. Antibody titers were examined pre- and post-vaccination.
Analyses examined both within-season and across-season effects of depressive symptoms, age, and their interaction on vaccine response. Within-season analyses revealed that age predicted antibody response during both seasons (2017–2018 and 2018–2019). Neither depressive symptoms nor the interaction with age were associated with antibody response to vaccination within either season. Across the two seasons, age significantly moderated the association between change in depressive symptoms and change in antibody production. For people who were 48 or older, increases in depressive symptoms across the two seasons were associated with a less robust response to the vaccine in the second season relative to the first season. For people younger than 48, changes in depressive symptoms were not significantly related to changes in antibody production.
These findings highlight the important role of mental health for older adults’ vaccine response, which could have clinical relevance for protection against disease.

Parental knowledge attenuates delinquency in adolescence and may be particularly effective in low-resourced environments. Moreover, parenting behaviors in one generation may influence subsequent generations' psychosocial adjustment. In this pilot study with data spanning three generations, we explored whether the first generation's (G1; n = 48) parental knowledge throughout the second generation's (G2; n = 48) adolescence was associated with the third generation's (G3; n = 60) psychosocial adjustment outcomes. Further, we examined potential mediators and moderators of the links between G1 parental knowledge and G3 outcomes. G1 parental knowledge predicted lower G3 depressive symptoms, anxiety, risky behaviors, and poor self-control. Although mechanisms remain unclear given non-significant mediation models, socioeconomic hardship moderated the association between G1 parental knowledge and G3 anxiety.

Low socioeconomic status (SES) is a risk factor for poor outcomes across development. Recent evidence suggests that, although psychosocial resilience among youth living in low-SES households is common, such expressions of resilience may not extend to physical health. Questions remain about when these diverging mental and physical health trajectories emerge. The current study hypothesized that skin-deep resilience - a pattern wherein socioeconomic disadvantage is linked to better mental health but worse physical health for individuals with John Henryism high-effort coping - is already present in childhood. Analyses focus on 165 Black and Latinx children (M  = 11.5) who were free of chronic disease and able to complete study procedures. Guardians provided information about their SES. Children reported on their John Henryism high-effort coping behaviors. They also provided reports of their depressed and anxious mood, which were combined into a composite of internalizing symptoms. Children's cardiometabolic risk was captured as a composite reflecting high levels of systolic or diastolic blood pressure, waist circumference, HbA1c, triglycerides, and low high-density lipoprotein cholesterol. Among youth who reported using John Henryism high-effort coping, SES risk was unrelated to internalizing symptoms and was positively associated with cardiometabolic risk. In contrast, for youth who did not engage in high-effort coping, SES risk was positively associated with internalizing symptoms and was unrelated to cardiometabolic risk. For youth with high-effort coping tendencies, socioeconomic disadvantage is linked to cardiometabolic risk. Public health efforts to support at-risk youth must consider both mental and physical health consequences associated with striving in challenging contexts.

The purpose of this study was to explore how both ongoing emotional distress and the experience of a targeted rejection over the past 6 months are associated with adolescents' antibody response to influenza virus vaccination. We predicted that experiencing a targeted rejection would amplify the hypothesized negative association between emotional distress and antibody response after vaccination.
Adolescent participants (N = 148) completed two study visits (mean [standard deviation] days between visits = 27.4 [1.8]). At the first visit, they provided blood samples, were administered the seasonal (2018-2019) quadrivalent influenza vaccine (Fluzone, Sanofi Pasteur), completed questionnaires, and participated in a semistructured interview. At the second visit, they provided another blood sample. Hemagglutination-inhibition assays were conducted to determine prevaccination and postvaccination antibody titers. Targeted rejection experiences were coded from adolescents' interviews.
The emotional distress by targeted rejection interaction predicted antibody response to the two A strains and the composite of all vaccine strains (b values = -0.451 to -0.843, p values < .05), but not the two B strains. Results suggested that, among adolescents who experienced a targeted rejection over the past 6 months, emotional distress was negatively associated with vaccine response (however, this finding did not reach statistical significance). Conversely, among adolescents who did not experience a targeted rejection, emotional distress was positively associated with vaccine response (b = 0.173, p = .032).
The current study highlights the importance of evaluating both acute life events and ongoing distress as they relate to adaptive immune functioning in adolescence.

Objective: Neighborhood risk in childhood is associated with poor health across the life span. However, many people who are reared in risky neighborhoods remain healthy in adulthood. In the context of high-risk neighborhoods, parenting practices that are controlling might promote better physical health outcomes later in life. The current study used a viral challenge paradigm to examine whether parental control throughout childhood moderated the association between recalled neighborhood risk and cytokine-mediated cold susceptibility.
Methods: A sample of 209 healthy adults completed questionnaires to assess recalled neighborhood risk and parental control over the first 15 years of life, were exposed to a common cold virus, and were quarantined for 6 days. Researchers assessed nasal proinflammatory cytokine production and objective markers of illness. Participants were diagnosed with a clinical cold if they met the infection and objective illness criteria.
Results: A significant Neighborhood Risk by Parental Control interaction emerged to predict proinflammatory cytokine production. Furthermore, parental control moderated the cytokine-mediated association between neighborhood risk and cold diagnosis (index = -0.073, 95% confidence interval [CI] = -0.170 to -0.016), likelihood of infection (index = -0.071, 95% CI = -0.172 to -0.015), and meeting the objective symptom criteria (index = -0.074, 95% CI = -0.195 to -0.005). Specifically, there was a negative association between neighborhood risk and objective cold diagnosis and infection status at higher levels of parental control, but a nonsignificant association at lower levels of parental control.
Conclusions: Findings suggest that the degree towhich recalled neighborhood risk is related to adult health varies as a function of parental control throughout childhood.

The human gut microbiome can influence health through the brain-gut-microbiome axis. Growing evidence suggests that the gut microbiome can influence sleep quality. Previous studies that have examined sleep deprivation and the human gut microbiome have yielded conflicting results. A recent study found that sleep deprivation leads to changes in gut microbiome composition while a different study found that sleep deprivation does not lead to changes in gut microbiome. Accordingly, the relationship between sleep physiology and the gut microbiome remains unclear. To address this uncertainty, we used actigraphy to quantify sleep measures coupled with gut microbiome sampling to determine how the gut microbiome correlates with various measures of sleep physiology. We measured immune system biomarkers and carried out a neurobehavioral assessment as these variables might modify the relationship between sleep and gut microbiome composition. We found that total microbiome diversity was positively correlated with increased sleep efficiency and total sleep time, and was negatively correlated with wake after sleep onset. We found positive correlations between total microbiome diversity and interleukin-6, a cytokine previously noted for its effects on sleep. Analysis of microbiome composition revealed that within phyla richness of Bacteroidetes and Firmicutes were positively correlated with sleep efficiency, interleukin-6 concentrations and abstract thinking. Finally, we found that several taxa (Lachnospiraceae, Corynebacterium, and Blautia) were negatively correlated with sleep measures. Our findings initiate linkages between gut microbiome composition, sleep physiology, the immune system and cognition. They may lead to mechanisms to improve sleep through the manipulation of the gut microbiome.

We tested the extent to which the catechol-O-methyltransferase (COMT) Val158Met polymorphism is associated with affective state and evening cortisol levels. We limited our study to women as previous research suggests that the link between COMT genotype and psychological health is entangled by sex differences.
The participants were assessed on measures of anxiety, mood disturbance, depressive symptomatology, and perceived stress. We also evaluated participants on a quality of life measures that included two emotion domains and two physical domains (physical health and environment).
We found that under normal (nonstress) conditions, the COMT A allele (Met carriers, higher dopamine) associates with healthier affect and lower afternoon cortisol levels in women. These effects were limited to affective measures and not to physical or environmental quality of life.
These findings help to shed light on the complex nature of COMT and emotion, and suggest that both sex and task condition (stress vs. nonstress) should be considered when examining the relationship between COMT genotype and emotion.

Clarifying the mechanisms that underlie stress-induced alterations of learning and memory may lend important insight into susceptibility factors governing the development of stress-related psychological disorders, such as post-traumatic stress disorder (PTSD). Previous work has shown that carriers of the ADRA2B Glu301-Glu303 deletion variant exhibit enhanced emotional memory, greater amygdala responses to emotional stimuli and greater intrusiveness of traumatic memories. We speculated that carriers of this deletion variant might also be more vulnerable to stress-induced enhancements of long-term memory, which would implicate the variant as a possible susceptibility factor for traumatic memory formation. One hundred and twenty participants (72 males, 48 females) submerged their hand in ice cold (stress) or warm (no stress) water for 3min. Immediately afterwards, they studied a list of 42 words varying in emotional valence and arousal and then completed an immediate free recall test. Twenty-four hours later, participants’ memory for the word list was examined via free recall and recognition assessments. Stressed participants exhibiting greater heart rate responses to the stressor had enhanced recall on the 24-h assessment. Importantly, this enhancement was independent of the emotional nature of the learned information. In contrast to previous work, we did not observe a general enhancement of memory for emotional information in ADRA2B deletion carriers. However, stressed female ADRA2B deletion carriers, particularly those exhibiting greater heart rate responses to the stressor, did demonstrate greater recognition memory than all other groups. Collectively, these findings implicate autonomic mechanisms in the pre-learning stress-induced enhancement of long-term memory and suggest that the ADRA2B deletion variant may selectively predict stress effects on memory in females. Such findings lend important insight into the physiological mechanisms underlying stress effects on learning and their sex-dependent nature.

► We tested the effects of brief stress given 30min before learning on 24-h memory. ► Stress had no significant effect on short-term memory. ► Cortisol Responders exhibited impaired recognition of neutral words. ► Male cortisol Responders exhibited impaired 24-h recall and recognition. ► Female cortisol Non-Responders exhibited impaired 24-h recognition.
We have examined the influence of sex and the perceived emotional nature of learned information on pre-learning stress-induced alterations of long-term memory. Participants submerged their dominant hand in ice cold (stress) or warm (no stress) water for 3min. Thirty minutes later, they studied 30 words, rated the words for their levels of emotional valence and arousal and were then given an immediate free recall test. Twenty-four hours later, participants’ memory for the word list was assessed via delayed free recall and recognition assessments. The resulting memory data were analyzed after categorizing the studied words (i.e., distributing them to “positive-arousing”, “positive-non-arousing”, “negative-arousing”, etc. categories) according to participants’ valence and arousal ratings of the words. The results revealed that participants exhibiting a robust cortisol response to stress exhibited significantly impaired recognition memory for neutral words. More interestingly, however, males displaying a robust cortisol response to stress demonstrated significantly impaired recall, overall, and a marginally significant impairment of overall recognition memory, while females exhibiting a blunted cortisol response to stress demonstrated a marginally significant impairment of overall recognition memory. These findings support the notion that a brief stressor that is temporally separated from learning can exert deleterious effects on long-term memory. However, they also suggest that such effects depend on the sex of the organism, the emotional salience of the learned information and the degree to which stress increases corticosteroid levels.