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Sleep Habits and Susceptibility to Upper Respiratory Illness: the Moderating Role of Subjective Socioeconomic Status
Abstract
Background:
Sleep is a predictor of infectious illness that may depend on one's socioeconomic status (SES).
Purpose:
This study aimed to investigate the moderating effects of objective and subjective SES on sleep-clinical cold risk link and test whether nasal inflammation serves as a plausible biological pathway.
Methods:
This study combined data (n = 732) from three viral challenge studies. Measures of self-reported sleep and objective and subjective measures of SES were obtained. Participants were quarantined and administrated rhinovirus (RV) or influenza virus and monitored over 5 (RV) or 6 (influenza) days for the development of a cold. Symptom severity, including mucus production and nasal clearance time, and levels of nasal cytokines (interleukin (IL)-6 and IL-1β) were measured prior to administration and each day during the quarantined period.
Results:
Subjective SES, but not objective SES, moderated associations between shorter sleep duration and increased likelihood of a clinical cold. Compared to ≥8-hour sleepers, ≤6-hour sleepers with low subjective SES were at increased risk for developing a cold (OR = 2.57, 95% CI 1.10-6.02). There was no association between sleep duration and colds in high subjective SES participants. Among infected individuals who reported low subjective SES, shorter sleep duration was associated with greater mucus production. There was no evidence that markers of nasal inflammation mediated the link between sleep duration and cold susceptibility among those reporting low subjective SES.
Conclusion:
Subjective SES may reflect an important social factor for understanding vulnerability to and protection against infectious illness among short sleepers.
... Studies on sleep and URTI occurrence have conflicting results. Viral challenge studies showed that short sleep and sleep disturbance are associated with increased URTIs (10)(11)(12), yet a study in Sweden found that sleep duration and quality were not associated with increased URTIs (13). We therefore aimed to bring together the entirety of the clinical evidence in the first systematic review of sleep and URTIs. ...
... Citation searching gave one extra study. Title and abstract screening removed 3392 studies, full-text review excluded 45 studies, resulting in 11 eligible studies (10-13,21-27), with nine included in the meta-analysis (10)(11)(12)(13)(23)(24)(25)(26)(27). Two eligible studies (21,22) were not included in the meta-analysis, as they did not report sufficient quantitative information. ...
... Two eligible studies (21,22) were not included in the meta-analysis, as they did not report sufficient quantitative information. One study (15) included in the meta-analysis presented pooled data from three similar studies from the same research group: Prather 2017a was referred to as 'The Pittsburgh Cold Study 2' (PCS2), Prather 2017b as 'The Pittsburgh Cold Study 3' (PCS3) and Prather 2017c as 'The Pittsburgh Mind-Body Center Study' (PMBC) in the Prather 2017 paper (11). Prather 2015 (10) and Cohen 2009 (12) report on the same participants as in Prather 2017b and Prather 2017c, respectively. ...
Background
Upper respiratory tract infections (URTIs) are common, mostly self-limiting, but result in inappropriate antibiotic prescriptions. Poor sleep is cited as a factor predisposing to URTIs, but the evidence is unclear.
Objective
To systematically review whether sleep duration and quality influence the frequency and duration of URTIs.
Methods
Three databases and bibliographies of included papers were searched for studies assessing associations between sleep duration or quality and URTIs. We performed dual title and abstract selection, discussed full-text exclusion decisions and completed 50% of data extraction in duplicate. The Newcastle–Ottawa Quality Assessment Scale assessed study quality and we estimated odds ratios (ORs) using random effects meta-analysis.
Results
Searches identified 5146 papers. Eleven met inclusion criteria, with nine included in meta-analyses: four good, two fair and five poor for risk of bias. Compared to study defined ‘normal’ sleep duration, shorter sleep was associated with increased URTIs (OR: 1.30, 95% confidence interval [CI]: 1.19–1.42, I2: 11%, P < 0.001) and longer sleep was not significantly associated (OR: 1.11 95% CI: 0.99–1.23, I2: 0%, P = 0.070). Sensitivity analyses using a 7- to 9-hour baseline found that sleeping shorter than 7–9 hours was associated with increased URTIs (OR: 1.31, 95% CI: 1.22–1.41, I2: 0%, P < 0.001). Sleeping longer than 7–9 hours was non-significantly associated with increased URTIs (OR: 1.15, 95% CI: 1.00–1.33, I2: 0%, P = 0.050, respectively). We were unable to pool sleep quality studies. No studies reported on sleep duration and URTI severity or duration.
Conclusions
Reduced sleep, particularly shorter than 7–9 hours, is associated with increased URTIs. Strategies improving sleep should be explored to prevent URTIs.
... Objective SES and subjective social status sometimes influence sleep and immune functioning differently. Subjective social status, but not objective SES, is associated with cold susceptibility [18] and also influences the relationship between sleep duration and cold severityamong infected individuals who reported low subjective social status, short sleep duration was associated with more mucus production [19]. The relationship between persistent sleep problems and immunological health may differ between low and high objective SES and/or subjective social status during bereavement. ...
... Still, education was a stronger moderator than subjective social status. These findings differ from previous work by Prather et al. [19]; they found that only subjective social status, not education, moderated the association between sleep duration and cold susceptibility among older adults. Several studies report that, relative to objective indicators of SES, subjective social status more strongly predicts physiological health outcomes like cold susceptibility [18], respiratory illness [16], and resting heart rate [15]. ...
... The effect of subjective social status on health may be less pronounced than objective SES in high SES samples. In studies that found that subjective social status had a stronger effect than objective SES, the socioeconomic range was wider and less skewed toward higher SES [15,18,19]. Compared to the sample in Prather et al. [19], subjects from the current sample on average, were more educated (3þ years) and reported higher rankings of subjective social status (3þ). ...
Widow(er)s experience significant sleep disruption that may dysregulate immune functioning. This longitudinal study aimed to determine 1) whether changes in sleep quality were associated with changes in pro-inflammatory cytokine production during the first six months of bereavement and 2) whether these relationships depended on objective socioeconomic status (SES) and/or subjective social status. One hundred and six bereaved spouses (M = 68.49 years, SD = 9.35, 69 females) completed the following assessments at approximately three months post-death and six-month post-death: a venous blood draw and self-report questionnaires on sleep quality (Pittsburgh Sleep Quality Index), SES (MacArthur Sociodemographic Questionnaire), health, and demographic information. T-cell stimulated pro-inflammatory cytokines were assessed, including IL-6, TNF-α, IFN-γ, IL-17A, and IL-2. Worsening sleep quality was associated with increased levels of pro-inflammatory activity even after adjusting for confounding variables. The present study also identified SES as an important factor for understanding health following spousal bereavement: individuals with low SES were more susceptible to sleep-related changes in immune function. Compared to more educated widow(er)s, less educated widow(er)s showed greater increases and decreases in inflammation when sleep quality worsened or improved, respectively, over time. Findings provide evidence for a biobehavioral pathway linking bereavement to disease risk, highlight SES disparities in late adulthood, and identify individuals who may require tailored interventions to offset SES-related burden that impedes adaptive grief recovery.
... 62,63 Thus, individuals with high subjective socioeconomic status are less vulnerable to stressful events and deal with them better. 64,65 For instance, women's appearance concerns entice them to make impulsive purchases of appearance-enhancing products that would align their body image with culturally prescribed attractiveness, particularly in eastern cultures emphasizing interdependence. 31,66 Individuals with high socioeconomic status, on the other hand, value their own preferences and choices more than conforming to societally based beauty standards due to their financial and psychological resources; 67 hence, their high subjective socioeconomic position may buffer the detrimental effect of social appearance anxiety on self-control and impulsive buying of fashionable outfits. ...
... One possible explanation can be the buffering and protective effect of subjective socioeconomic status. 64,94 This may be because high subjective socioeconomic status can provide individuals with psychological resources such as social capital to help them better deal with stressful events and negative emotions. 62,63 Meanwhile, young females can feel less bound to obey socially prescribed beauty norms due to their high subjective socioeconomic status, 31,67 thus buffering the negative effect of social appearance anxiety. ...
Purpose
With the rise of social media, an increasing number of young females have focused more attention on their body image, leading to social appearance anxiety. Thus, the current study aimed to investigate a moderated mediation model of social appearance anxiety and online impulse purchases of fashionable outfits through self-control moderated by subjective socioeconomic status during the pandemic.
Methods
A total of 1651 female college students (Age = 17–24, Mage = 19.30, SD = 1.14) with more than one month of closed-off management experience completed self-report questionnaires concerning social appearance anxiety, self-control, online impulse purchases of fashionable outfits, and subjective socioeconomic status.
Results
After controlling for the potential influence of coronavirus stress, the results indicated that social appearance anxiety was positively related to online impulse purchases of fashionable outfits among female college students during the pandemic, mediated by self-control. Furthermore, subjective socioeconomic status moderated the indirect link between social appearance anxiety and the online impulse purchase of fashionable outfits. Specifically, subjective socioeconomic status buffers the negative effect of social appearance anxiety on self-control and the risk effect of low self-control on the online impulse purchases of fashionable outfits.
Implications
The current study deepens the research on the relationship between social appearance anxiety and online impulse purchases during pandemic periods; meanwhile, it provides evidence for preventing excessive online impulse purchases of fashionable outfits among young females.
... those with higher levels of disadvantage) at baseline were more likely to develop symptomatic illness, independent of traditional markers of social disadvantage [29]. In a follow-up study, SSS was found to be a key moderator of the impact of sleep duration on common cold infection [30]. Thompson et al. further tested this finding in a sample of health care workers and demonstrated, consistent with our results, that low SSS at baseline was associated with increased rates of ARI [31]. ...
... These changes could result in increased biologic vulnerability to infections both in the short-term and the long-term. The studies by Cohen et al. on SSS seem to point to the plausibility of the biologic vulnerability hypothesis given the prospective nature of the studies and the uniform exposure of the viral challenge [29,30]. We did not collect data on asymptomatic or subclinical infections and therefore could not explicitly replicate their findings in a real-world scenario. ...
Social patterning of infectious diseases is increasingly recognised. Previous studies of social determinants of acute respiratory illness (ARI) have found that highly educated and lower income families experience more illnesses. Subjective social status (SSS) has also been linked to symptomatic ARI, but the association may be confounded by household composition. We examined SSS and ARI in the Household Influenza Vaccine Evaluation (HIVE) Study in 2014–2015. We used SSS as a marker of social disadvantage and created a workplace disadvantage score for working adults. We examined the association between these measures and ARI incidence using mixed-effects Poisson regression models with random intercepts to account for household clustering. In univariate analyses, mean ARI was higher among children <5 years old ( P < 0.001), and females ( P = 0.004) at the individual level. At the household level, mean ARI was higher for households with at least one child <5 years than for those without ( P = 0.002). In adjusted models, individuals in the lowest tertile of SSS had borderline significantly higher rates of ARI than those in the highest tertile (incidence rate ratio (IRR) 1.34, 95% confidence interval (CI) 0.98–1.92). Households in the lowest tertile of SSS had significantly higher ARI incidence in household-level models (IRR 1.46, 95% CI 1.05–2.03). We observed no association between workplace disadvantage and ARI. We detected an increase in the incidence of ARI for households with low SSS compared with those with high SSS, suggesting that socio-economic position has a meaningful impact on ARI incidence.
... The spatial distribution of SD within a population is influenced by sociodemographic variables like age, sex, profession and comorbidities 17,18 . Socioeconomic status (SES), and thus living conditions, lifestyle habits, stress, physical and mental health and aging 14,16,[19][20][21][22] can all influence the development and progression of SD. The variations in SES within the population correspond to variations in the level of access to different conditions and resources favorable to health [22][23][24] . ...
... Socioeconomic status (SES), and thus living conditions, lifestyle habits, stress, physical and mental health and aging 14,16,[19][20][21][22] can all influence the development and progression of SD. The variations in SES within the population correspond to variations in the level of access to different conditions and resources favorable to health [22][23][24] . While SES is an important determinant of health, its role in the development and maintenance of SD is not well studied. ...
Influence of socioeconomic status-stress induced on sleep quality: a systematic review. Preprints 2018 SUMMARY Sleep disorders (SD) have a complex aetiology, and socioeconomic status (SES) as determined by social class, household income, ethnicity and education plays an important role in their development. As SD are associated with cognitive impairment and mood disorders, they in turn impact SES. Socioeconomic status also influences allostatic load caused by chronic accumulation of stress throughout life. Environmental and psychological stressors have a direct effect on SD, and they are modulated by SES, in combination with comorbidities like obesity and cardiovascular disease. This review explores the recent theories about the influence of SES on the development of SD in the general population, whether or not occurring with comorbidities, and also focusses on the interplay between socioeconomic status, circadian rhythms, aging and clinical outcomes like metabolic diseases and cancer.
... However, we did not find evidence of this pathway, as parental home ownership and NA reactivity did not interact to predict nasal proinflammatory cytokine production (online supplemental materials). Similarly, local nasal inflammation did not explain the association between shorter sleep duration and symptoms of illness among low SES individuals in one previous study (Prather et al., 2017). ...
Objetivo: La desventaja socioeconómica durante la niñez y la adolescencia se asocia con un mayor riesgo de sufrir muchos problemas de salud física, incluyendo enfermedades infecciosas, a lo largo de la vida. Una mayor reactividad afectiva negativa (NA, por sus siglas en inglés) ha mostrado vínculos similares con un mayor riesgo de afecciones de salud física y patrones alterados de funcionamiento biológico asociados con la infección respiratoria aguda como desventaja socioeconómica; sin embargo, no se han examinado sus efectos interactivos sobre los resultados de salud física. Por lo tanto, el presente estudio examinó si la reactividad de NA acentuaba el vínculo entre la desventaja socioeconómica temprana y la susceptibilidad al resfriado común. Método: Los participantes fueron 212 adultos (42% mujeres, entre 18–55 años de edad) que completaron medidas de NSE (SES, por sus siglas en inglés) (posesión de hogar parental) infantil y posteriormente estuvieron expuestos a un virus que causa el resfriado común. Luego, los participantes permanecieron en cuarentena durante cinco días, durante los cuales se evaluaron múltiples indicadores de infección viral y enfermedad clínica. Antes y después de la cuarentena, los participantes completaron una tarea de estrés de laboratorio para evaluar la reactividad de NA. Resultados: La relación entre la posesión de la vivienda de los padres y el diagnóstico clínico de resfriado en la edad adulta fue moderada por la reactividad de NA (b = −0.11, p = .018), de modo que menos años de posesión de la vivienda de los padres se asociaron con mayores probabilidades de desarrollar un resfriado únicamente entre los adultos que tenían una mayor reactividad de NA (OR = 0.89, CI del 95% [0.82, 0.96]), pero no entre aquellos que tenían una menor reactividad de NA (OR = 1.01, CI del 95% [0.94, 1.09]). Conclusiones: Estos hallazgos sugieren que la forma en que los individuos reaccionan negativamente a factores estresantes posteriores puede exacerbar el impacto del SES infantil en la susceptibilidad a las infecciones agudas. Estos resultados pueden ayudar a informar los esfuerzos de prevención e intervención para los jóvenes desfavorecidos.
... The prevalence varies according to factors such as sex, age, socioeconomic status and circadian preference-evening types are reported to be more susceptible (2,7). There is emerging evidence, both from controlled laboratory and epidemiological observational studies, that sleep disturbances and short sleep duration increase the risk of infection (8)(9)(10)(11)(12)(13)(14)(15)(16)(17). The underlying mechanisms behind this association are unclear and is further complicated by the bidirectional relationship between the two (1). ...
Objectives
There is emerging evidence that sleep problems and short sleep duration increase the risk of infection. We aimed to assess whether chronic insomnia disorder, chronic sleep problems, sleep duration and circadian preference based on self-report were associated with risk of infections and antibiotic use among patients visiting their general practitioner (GP).
Methods
We conducted a cross-sectional study of 1,848 unselected patients in Norway visiting their GP during 2020.The patients completed a one-page questionnaire while waiting for the consultation, that included the validated Bergen Insomnia Scale (BIS), questions on self-assessed sleep problem, sleep duration and circadian preference and whether they have had any infections or used antibiotics in the last 3 months. Relative risks (RR) were estimated using modified Poisson regression models.
Results
The risk of infection was 27% (95% CI RR 1.11–1.46) and 44% higher (95% CI 1.12–1.84) in patients sleeping < 6 h and >9 h, respectively, compared to those sleeping 7–8 h. The risk was also increased in patients with chronic insomnia disorder or a chronic sleep problem. For antibiotic use, the risk was higher for patients sleeping < 6 h, and for those with chronic insomnia disorder or a chronic sleep problem.
Conclusions
Among patients visiting their GP, short sleep duration, chronic insomnia and chronic sleep problem based on self-report were associated with higher prevalence of infection and antibiotic use. These findings support the notion of a strong association between sleep and infection.
... Data from a meta-analysis supported these initial findings that insomnia symptoms were associated with higher levels of IL-6 and CRP [42]. This is also consistent with other research suggesting that short sleep duration increases susceptibility to respiratory infections [26,27]. Put differently, these data support the notion that our immune system produces an inflammatory response to the insomnia itself (or the shortened sleep associated with insomnia). ...
Objective
/Background: The goal of the present study was to assess the prevalence and incidence of insomnia in the United States during the COVID-19 pandemic, and whether, among those that contracted COVID-19, insomnia predicted worse outcomes (e.g., symptoms of greater frequency, duration, or severity).
Methods
A nationwide sample of 2980 adults living in the United States were surveyed online at two points during the COVID-19 pandemic (T1 = April–June 2020; T2 = January–March 2021). Insomnia symptoms were assessed at both time points using the Insomnia Severity Index (ISI). The T2 survey also asked questions regarding COVID-19 testing and symptoms.
Results
The prevalence of insomnia (defined as ISI ≥15) was 15% at T1 and 13% at T2. The incidence rate of insomnia (i.e., new cases from T1 to T2) was 5.6%. Participants with insomnia were not more likely to contract COVID-19 relative to those participants without insomnia. Among those participants in our sample that contracted the virus during the study interval (n = 149), there were no significant group differences in COVID-19 symptom outcomes, with one exception, participants with insomnia were more likely to report a longer symptom duration (insomnia = 24.8 sick days, no insomnia = 16.1 sick days).
Conclusions
The present study suggests the prevalence of insomnia in the U.S. population remained high during the COVID-19 pandemic. The data also support that insomnia may be related to experiencing more chronic COVID-19 symptoms. These findings have more general implications for the role of sleep and insomnia on immune functioning.
... The sample population comprised of young male and female infantry recruits, primarily Caucasian and of lower socioeconomic status (SES) 57 , limiting the generalizability of these findings. Whether these findings are generalizable to other populations where sleep restriction is commonplace such as workers rising early for long commutes 58 and new parents 59 warrants investigation, particularly as low SES has been associated with increased vulnerability to URTI amongst short sleepers 60 . Nevertheless, civilians embarking on a military training course affords a unique opportunity to examine the association between sleep restriction, PSQ and URTI in a healthy, pre-screened population under standardized conditions. ...
Study Objectives
Prospectively examine the association between sleep restriction, perceived sleep quality (PSQ) and upper respiratory tract infection (URTI).
Methods
In 1,318 military recruits (68% males) self-reported sleep was assessed at the beginning and end of a 12-week training course. Sleep restriction was defined as an individualized reduction in sleep duration of ≥2 hours/night compared with civilian life. URTIs were retrieved from medical records.
Results
On commencing training, approximately half of recruits were sleep restricted (52%; 2.1 ± 1.6 h); despite the sleep debt, 58% of recruits with sleep restriction reported good PSQ. Regression adjusted for covariates showed that recruits commencing training with sleep restriction were more likely to suffer URTI during the course (OR = 2.93, 95% CI 1.29–6.69, P = 0.011). Moderation analysis showed this finding was driven by poor PSQ (B = -1.12, SE 0.50, P = 0.023), as no significant association between sleep restriction and URTI was observed in recruits reporting good PSQ, despite a similar magnitude of sleep restriction during training. Associations remained in the population completing training, accounting for loss to follow-up. Recruits reporting poor PSQ when healthy at the start and end of training were more susceptible to URTI (OR = 3.16, 95% CI 1.31–7.61, P = 0.010, vs good PSQ).
Conclusion
Good perceived sleep quality was associated with protection against the raised risk of respiratory infection during sleep restriction. Studies should determine whether improvements in sleep quality arising from behavioral sleep interventions translate to reduced respiratory infection during sleep restriction.
... In addition, participants were, in general, highly educated and fairly affluent. As such, the types of emotions and daily events that people experience differ considerably across different levels of socioeconomic status (Grzywacz et al., 2004;Prather et al., 2017;Surachman et al., 2019), which could have constrained this sample. Additionally, we used single item measures of positive and negative affect in the morning diaries which limited our ability to distinguish activated from deactivated states. ...
Sleep is an important process that can influence and be influenced by daily events and emotions. We examined the bidirectional relationships between sleep, daily events, and emotions with a daily diary method completed by 181 mothers (M age = 41.91, SD = 5.06). They answered morning and evening questionnaires for 1 week at three different points in time separated by nine months each, 21 days in total. Measures of sleep quality and emotional experiences each morning were assessed, and they reported on their best and worst experience of the day, peak emotional responses to these events, and affect in the evening. Sleep behavior, including total sleep time and sleep efficiency, was objectively quantified using wrist actigraphy. Multilevel modeling analyses showed that longer sleep duration and better subjective quality predicted greater positive emotions and lower negative emotions upon waking, and lower levels of peak perceived stressfulness, but not peak positivity ratings. Daily experiences did not predict sleep duration. Conversely, negative affect in the evening and greater peak perceived stressfulness during the day predicted worse sleep quality that night, whereas positive affect and positive events were not related to sleep. Although correlational, these findings suggest that good sleep can improve waking affect and help mitigate the impact of stressful experiences but does not amplify responses to the positive events of the day. In turn, daily perceived stress reactivity impairs sleep quality. These novel findings show stronger bidirectional relationships between sleep with daily stress, than sleep with daily positivity.
Supplementary information:
The online version contains supplementary material available at 10.1007/s42761-022-00112-x.
... p=0.008). The result is consistent and corroborates with the studies conducted by Prather et al. [26], [27], and Wentz et al. [28]. The three studies This occurs because chronic deficiency of sleep duration (short sleep duration or sleep disturbances) increases the systemic inflammatory response, which can cause inflammation. ...
During the coronavirus desease 2019 (COVID-19) pandemic, athletes must be able to adapt to new habits, such as: social restriction, change of competition schedule, and sending back home. This situation has led to an 18.2% increase in sleep disturbances. This study aimed to look at the sleep duration of adolescent athletes during the COVID-19 pandemic and its impact on athlete’s health conditions. A total of 126 adolescent athletes from 15 sports were recruited in this cross-sectional study. Adequate sleep duration was assessed according to the American Academy of Sleep Medicine criteria. Data on health conditions, medical history, injury history, were taken using a questionnaire. Behavioral assessment was assessed through the strengths and difficulties questionnaire. About 80.2% of adolescent athletes had insufficient sleep, and there was a significant relationship between sleep duration and disease incidence with a relative risk (RR) of 3.31 (1.32-8.28) 95% convidence interval (CI). There was no significant relationship between adequate sleep duration and health conditions (p>0.05). Things that may be the cause of sleep disturbances; use of electronic devices (37.6%), environmental conditions (53.4%), and worry (9%). In the end, this indicates adolescent athletes face difficulties in achieving adequate sleep duration during this pandemic and a continuous surveillance system is needed to monitor athletes outside the dormitory.
... [12] Low socioeconomic status [13] and parental separation during childhood [14] were other risk factors for URTIs. Shorter sleep duration was a risk factor for URTIs, [15] but other research found that this was only observed in low socioeconomic groups [16] Poor self-rated general health was also identified as a risk factor for URTIs. [17] An underlying assumption of most of the above studies was that the psychological factors influenced the immune system, which increased the risk of infection. ...
... However, various factors such as the increase in life pressure or irregular nightlife habits have led to more and more people suffering from sleep disorders all over the world. Poor sleep and/or lack of sleep have been linked to all kinds of illnesses, starting from poor cognitive efficiency and neurological dysfunction to an elevated threat for type 2 diabetes, coronary heart illness, most cancers and Alzheimer's disease (AD) [26]. Some evidence suggests that the characteristics of the gastrointestinal microbiome and metabolism of the host are associated with its sleep and circadian rhythm [27]. ...
Gut microbiota homeostasis in the organism and insomnia have been reported to influence each other. In the study, a method of 16S rRNA gene sequencing combined with ultra-high performance liquid chromatography-mass/mass spectrometry was adopted to evaluate the effects of Lilium brownie (LB) on intestinal flora and metabolic profiles of serum, hypothalamus and hippocampus in insomnia rat induced by p‑chlorophenylalanine (PCPA). It was observed that the imbalance in the diversity and abundance of gut microbiota induced by PCPA was restored after LB intervention. Among these, the Porphyromonadaceae, Lactobacillus and Escherichia were significantly adjusted at the genus level by PCPA and LB, respectively. It was also found that the most of metabolic phenotypes in serum, hypothalamus and hippocampus perturbed by PCPA were regulated towards normal after LB intervention, especially 5-hydroxy-l-tryptophan of the hypothalamus involving in 5-HT metabolism. Moreover, the arachidonic acid metabolism in serum, hypothalamus and hippocampus, and the serotonergic synapse in hypothalamus and hippocampus were the most fundamentally and significantly affected pathways after LB intervention. The results of correlation analysis showed that several floras including Pseudoruegeria have an outstanding contribution to the change of differential metabolites. In brief, the results confirm that gut microbiota is significantly returned to normal and may interact with the corresponding metabolites to relieve insomnia under LB intervention.
... Whereas, only 0¢89% and 0¢14% of URIs related deaths and DALYs, respectively, were attributable to all the risk factors assessed in GBD 2019, and risk factors for the high incidence rates were not estimated. Previous studies had put forward several possible risk factors for the morbidity of URIs, such as inadequate sleep duration and psychological stress [38][39][40][41]. In the future, more extensive and comprehensive evaluations of risk factors are necessary to evaluate the URIs-related burden. ...
Background
Upper respiratory infections (URIs) are among the most common diseases. However, the related burden has not been comprehensively evaluated. Thus, we designed the present study to describe the global and regional burden of URIs from 1990 to 2019.
Methods
A secondary analysis was performed on the incidence, mortality, and disability-adjusted life years (DALYs) of URIs in different sex and age groups, from 21 geographic regions, 204 countries and territories, between 1990 and 2019, using the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019. Countries and territories were categorized according to Socio-demographic Index (SDI) quintiles.
Findings
Globally, the incident cases of URIs reached 17·2 (95% uncertainty interval: 15·4 to 19·3) billion in 2019, which accounted for 42·83% (40·01% to 45·77%) cases from all causes in the GBD 2019 study. The age-standardized incidence rate remained stable from 1990 to 2019, while significant decreases were found in the mortality and DALY rate. The highest age-standardized incidence rates from 1990 to 2019 and the highest age-standardized DALY rates after 2011 were observed in high SDI regions. Among all the age groups, children under five years old suffered from the highest incidence and DALY rates, both of which were decreased with increasing age. Fatal consequences of URIs occurred mostly in the elderly and children under five years old.
Interpretation
The present study provided comprehensive estimates of URIs burden for the first time. Our findings, highlighting the substantial incidence and considerable DALYs due to URIs, are expected to attract more attention to URIs and provide future explorations in the prevention and treatment with epidemiological evidence.
... Prather AA, Janicki-Deverts D, Adler NE, Hall M, Cohen S. [31]. ...
... There are multiple pathways through which sleep might influence weight. For example, short sleep duration is associated with preferences for fatty food and skipping breakfast (Nishiura, Noguchi, & Hashimoto, 2010) and with consumption of sugar-sweetened beverages (Prather, Janicki-Deverts, Adler, Hall, & Cohen, 2017). However, several studies have found an association between sleep and obesity even after controlling for energy intake and physical activity (Patel & Hu, 2008), suggesting that additional mechanisms may be at play. ...
Men appear to gain weight during the transition to parenthood, and fathers are heavier than non-fathers. Paternal perinatal weight gain may set weight trajectories in midlife and have long-term health implications. Since men do not undergo the physical demands of pregnancy and breastfeeding, the specific mechanisms underlying weight gain in new fathers warrant investigation. This review aims to stimulate research on paternal perinatal weight gain by suggesting testable potential mechanisms that 1) show change across the transition to parenthood; and 2) play a role in weight and body composition. We identify seven mechanisms, within three categories: behavioral mechanisms (sleep, physical activity, and diet), hormonal mechanisms (testosterone and cortisol), and psychological mechanisms (depression and stress). We also discuss direct effects of partner pregnancy influences (e.g., “couvade syndrome”) on men’s body weight. In presenting each mechanism, we discuss how it may be affected by the transition to parenthood, and then review its role in body composition and weight. Next, we describe bidirectional and interactive effects, discuss timing, and present three broad research questions to propel theoretical development.
... Conceivably, sleep disturbance increases vulnerability to a range of infectious agents many of which elicit the formation of effector memory CD8 + cells. For instance, short ( 6 h) sleepers were found to be at increased risk for developing a cold after a rhinovirus challenge (Prather et al., 2017(Prather et al., , 2015. ...
A subset of individuals with major depressive disorder (MDD) have impaired adaptive immunity characterized by a greater vulnerability to viral infection and a deficient response to vaccination along with a decrease in the number and/or activity of T cells and natural killer cells (NKC). Nevertheless, it remains unclear which specific subsets of lymphocytes are altered in MDD, a shortcoming we address here by utilizing an advanced fluorescence-activated cell sorting (FACS) method that allows for the differentiation of important functionally-distinct lymphocyte sub-populations. Furthermore, despite evidence that sleep disturbance, which is a core symptom of MDD, is itself associated with alterations in lymphocyte distributions, there is a paucity of studies examining the contribution of sleep disturbance on lymphocyte populations in MDD populations. Here, we measured differences in the percentages of 13 different lymphocytes and 6 different leukocytes in 54 unmedicated MDD patients (partially remitted to moderate) and 56 age and sex-matched healthy controls (HC). The relationship between self-reported sleep disturbance and cell counts was evaluated in the MDD group using the Pittsburgh Sleep Quality Index (PSQI). The MDD group showed a significantly increased percentage of CD127low/CCR4⁺ Treg cells, and memory Treg cells, as well as a reduction in CD56⁺CD16⁻ (putative immunoregulatory) NKC counts, the latter, prior to correction for body mass index. There also was a trend for higher effector memory CD8⁺ cell counts in the MDD group versus the HC group. Further, within the MDD group, self-reported sleep disturbance was associated with an increased percentage of effector memory CD8⁺ cells but with a lower percentage of CD56⁺CD16⁻ NKC. These results provide important new insights into the immune pathways involved in MDD, and provide novel evidence that MDD and associated sleep disturbance increase effector memory CD8⁺ and Treg pathways. Targeting sleep disturbance may have implications as a therapeutic strategy to normalize NKC and memory CD8⁺ cells in MDD.
Background
Acute diarrhea is the most frequent diagnosis among ill travelers. Sleep loss may weaken the body's defense against pathogens and increase susceptibility to infection. The relationship between sleep and infectious diarrhea has not been studied and was assessed utilizing data from a controlled human infection model (CHIM) for enterotoxigenic Escherichia coli (ETEC).
Methods
During a CHIM assessing the efficacy of an immunoprophylactic targeting ETEC against moderate-to-severe diarrhea (MSD) following challenge, we measured sleep via actigraphy over an 8-day inpatient period. We hypothesized better sleep pre-challenge would predict illness symptomatology following challenge.
Results
Among 57 participants (aged 34.4 ± 8.1 years, 64% male), there was no relationship between sleep metrics and incidence of MSD. However, longer total sleep time the night preceding ETEC challenge was associated with lower maximum 24 hour diarrhea volume (B = −1.80, p = 0.01) and total diarrhea volume (B = −2.45, p = 0.01).
Conclusions
This novel study showed that shorter sleep duration predicted diarrhea severity over the course of an ETEC infection. Future work should experimentally manipulate sleep to further clarify its impact on diarrhea-related outcomes for ETEC and other important enteric pathogens.
Economic aspects of health care have never been more important than they are today. In the modern healthcare climate of increasing costs on the one hand and limited resources on the other hand, patients, payers, policymakers, and multiple stakeholders are increasingly attuned to healthcare costs and value derived from healthcare services. The purpose of this chapter is to introduce and briefly review the scientific domain of sleep health economics. First, we present a very brief overview of health economics science. Second, we review several key studies regarding economic aspects of sleep disorders and their treatments. Finally, we suggest future directions for health economic research in sleep medicine.KeywordsSleepEconomicsCostsUtilizationQuality of lifeTreatment
Objective
There is a need for a brief affect scale that also encompasses different components of affect relevant for researchers interested in physiological and health outcomes. The Subcomponents of Affect Scale (SAS) meets this need. This 18-item scale has nine positive and nine negative affect items encompassing six subscales (calm, well-being, vigour, depression, anxiety, anger). Previous research using the SAS has demonstrated its predictive validity, but no work has tested its subscale structure or longitudinal validity.
Design
Data from the Common Cold Project in which individuals (N = 610) completed the SAS over the course of seven days were used.
Results
Confirmatory factor analysis demonstrated the reliability of the subscale structure of the SAS across seven days (positive affect subscale structure: CFIs ≥ 0.98; negative affect subscale structure: CFIs ≥ 0.94 with day 6 CFI = 0.91) and tests of factorial invariance showed the scale is valid to use over time.
Conclusions
These results confirm the psychometric validity of the subscale structure of the SAS and imply that the subscales can be used longitudinally, allowing for its use in health research as well as non-health research that can benefit from its subscale structure and longitudinal capabilities.
Objective:
Insufficient sleep and circadian disruption have been linked to immune system dysregulation. The aim of this study was to examine the associations between self-reported sleep duration and work schedule with reports of head and chest colds among adults 18 years and older in the United States.
Methods:
Associations between self-reported habitual sleep duration and work schedule (regular daytime, regular evening, regular nighttime, rotating, other) with reports head and chest colds in the past 2 weeks were examined using data from the 2010 and 2015 National Health Interview Survey. Adults who slept 7-8 hours or reported a regular daytime work schedule were considered the reference group. Multivariate logistic regressions, incorporating sampling weights, were computed adjusting for sociodemographic and health characteristics.
Results:
Analyses revealed in fully adjusted models that compared to 7- 8 hours sleepers, those sleeping 5 or fewer hours were 44% more likely to report a cold (odds ratio [OR] = 1.44, 95% confidence interval [CI] 1.29-1.61) while those sleeping 9 or more hours were 20% more likely (OR = 1.20, 95% CI 1.06-1.36). Participants who reported a rotating work schedule were 20% more likely to report a cold (OR = 1.20, 95% CI 1.07-1.36) than those reporting a regular daytime work schedule.
Conclusions:
Short and long sleep duration, as well as a rotating shift work schedule, were associated with increased reports of head and chest colds in a nationally representative sample of US adults. Sleep and circadian function may serve as relevant targets to reduce susceptibility to infectious illness.
The aim of the present article is to describe bi-directional interactions between fatigue and infection with common cold producing viruses. Over one hundred years ago, researchers started to investigate the association between been fatigue and infection. Studies of psychological risk factors for upper respiratory tract illnesses (URTIs) have been carried out for over fifty years. Early research did not control for exposure and also often relied on self-report rather than clinical and virological assessment. Research on experimentally-induced URTIs has demonstrated that susceptibility to infection is increased by stress. Other research has shown that job insecurity, few social contacts, emotional disposition, early childhood experiences, sleep problems and self-rated health are key risk factors for infection. This article provides an interpretation of these results in terms of chronic fatigue increasing susceptibility to infection. Infection and illness also lead to changes in behaviour. These effects include greater fatigue, impaired attention and slower motor speed. Such effects occur not only when the person has symptoms but in the incubation period, with sub-clinical infections, and after the symptoms have gone. Those with URTIs are also more sensitive to other negative factors such as prolonged work, and this has implications for safety-critical jobs. Ingestion of caffeine, which is an established countermeasure for fatigue, can reduce the behavioural malaise induced by URTIs. Further support for the use of a fatigue framework comes from a secondary analysis of data on real-life colds. Previous research has demonstrated that chronic fatigue leads to greater effects of acute fatigue. The new analysis showed that those with high levels of fatigue prior to developing a cold had larger behavioural impairments when they became ill.
The aim of the present article is to describe bi-directional interactions between fatigue and infection with common cold producing viruses. Over one hundred years ago, researchers started to investigate the association between been fatigue and infection. Studies of psychological risk factors for upper respiratory tract illnesses (URTIs) have been carried out for over fifty years. Early research did not control for exposure and also often relied on self-report rather than clinical and virological assessment. Research on experimentally-induced URTIs has demonstrated that susceptibility to infection is increased by stress. Other research has shown that job insecurity, few social contacts, emotional disposition, early childhood experiences, sleep problems and self-rated health are key risk factors for infection. This article provides an interpretation of these results in terms of chronic fatigue increasing susceptibility to infection. Infection and illness also lead to changes in behaviour. These effects include greater fatigue, impaired attention and slower motor speed. Such effects occur not only when the person has symptoms but in the incubation period, with sub-clinical infections, and after the symptoms have gone. Those with URTIs are also more sensitive to other negative factors such as prolonged work, and this has implications for safety-critical jobs. Ingestion of caffeine, which is an established countermeasure for fatigue, can reduce the behavioural malaise induced by URTIs. Further support for the use of a fatigue framework comes from a secondary analysis of data on real-life colds. Previous research has demonstrated that chronic fatigue leads to greater effects of acute fatigue. The new analysis showed that those with high levels of fatigue prior to developing a cold had larger behavioural impairments when they became ill.
Background
Growing evidence suggests that sleep plays an important role in immunological memory, including antibody responses to vaccination. However, much of the prior research has been carried out in the laboratory limiting the generalizability of the findings. Furthermore, no study has sought to identify sensitive periods prior to or after vaccination where sleep may have a stronger influence on antibody responses.Methods
Eighty-three healthy young adults completed 13 days of sleep diaries and received the trivalent influenza vaccine on day 3 of the study. Measures of self-reported sleep duration, sleep efficiency, and subjective sleep quality were assessed on each day. Antibody levels to the influenza viral strains were quantified at baseline and 1 and 4 months following influenza vaccination.ResultsShorter sleep duration, averaged over the collection period, was associated with fewer antibodies to the A/New Caledonia viral strain 1 and 4 months later, independent of baseline antibodies, age, sex, and cohort year. Analyses focused on nightly sleep on the days preceding and after the vaccination revealed that shorter sleep duration on the two nights before the vaccination predicted fewer antibodies 1 and 4 months later. Measures of self-reported sleep efficiency and subjective quality were unrelated to antibody responses to the influenza vaccination.Conclusion
These findings provide further support for an association between sleep duration and antibody responses to the influenza vaccine and suggest that perhaps sleep on nights prior to vaccination are critical. If replicated, these findings may support sleep as a target for enhancing vaccination efficacy.
Background
Disparities in adult morbidity and mortality may be rooted in patterns of biological dysfunction in early life. We sought to examine the association between pathogen burden and a cumulative deficits index (CDI), conceptualized as a pre-clinical marker of an unhealthy biomarker profile, specifically focusing on patterns across levels of social disadvantage.
Methods
Using the data from the National Health and Nutrition Examination Survey 2003–2004 wave (aged 20–49 years), we examined the association of pathogen burden, composed of seven pathogens, with the CDI. The CDI comprised 28 biomarkers corresponding to available clinical laboratory measures. Models were stratified by race/ethnicity and education level.
Results
The CDI ranged from 0.04 to 0.78. Nearly half of Blacks were classified in the high burden pathogen class compared with 8% of Whites. Among both Mexican Americans and other Hispanic groups, the largest proportion of individuals were classified in the common pathogens class. Among educational classes, 19% of those with less than a high school education were classified in the high burden class compared with 7% of those with at least a college education. Blacks in the high burden pathogen class had a CDI 0.05 greater than those in the low burden class (P < 0.05). Whites in the high burden class had a CDI only 0.03 greater than those in the low burden class (P < 0.01).
Discussion
Our findings suggest there are significant social disparities in the distribution of pathogen burden across race/ethnic groups, and the effects of pathogen burden may be more significant for socially disadvantaged individuals.
In this article, the authors evaluate the possible roles of negative emotions and cognitions in the association between socioeconomic status (SES) and physical health, focusing on the outcomes of cardiovascular diseases and all-cause mortality. After reviewing the limited direct evidence, the authors examine indirect evidence showing that (a) SES relates to the targeted health outcomes, (b) SES relates to negative emotions and cognitions, and (c) negative emotions and cognitions relate to the targeted health outcomes. The authors present a general framework for understanding the roles of cognitiveemotional factors, suggesting that low-SES environments are stressful and reduce individuals' reserve capacity to manage stress, thereby increasing vulnerability to negative emotions and cognitions. The article concludes with suggestions for future research to better evaluate the proposed model.
Short sleep duration and poor sleep continuity have been implicated in the susceptibility to infectious illness. However, prior research has relied on subjective measures of sleep, which are subject to recall bias. The aim of this study was to determine whether sleep, measured behaviorally using wrist actigraphy, predicted cold incidence following experimental viral exposure.
A total of 164 healthy men and women (age range, 18 to 55 y) volunteered for this study. Wrist actigraphy and sleep diaries assessed sleep duration and sleep continuity over 7 consecutive days. Participants were then quarantined and administered nasal drops containing the rhinovirus, and monitored over 5 days for the development of a clinical cold (defined by infection in the presence of objective signs of illness). Logistic regression analysis revealed that actigraphy- assessed shorter sleep duration was associated with an increased likelihood of development of a clinical cold. Specifically, those sleeping <5 h (odds ratio [OR]= 4.50, 95% confidence interval [CI], 1.08-18.69) or sleeping between 5 to 6 h (OR = 4.24, 95% CI, 1.08-16.71) were at greater risk of developing the cold compared to those sleeping >7 h per night; those sleeping 6.01 to 7 h were at no greater risk (OR = 1.66; 95% CI 0.40-6.95). This association was independent of prechallenge antibody levels, demographics, season of the year, body mass index, psychological variables, and health practices. Sleep fragmentation was unrelated to cold susceptibility. Other sleep variables obtained using diary and actigraphy were not strong predictors of cold susceptibility.
Shorter sleep duration, measured behaviorally using actigraphy prior to viral exposure, was associated with increased susceptibility to the common cold.
Copyright © 2015 Associated Professional Sleep Societies, LLC. All rights reserved.
Peritoneal exudates from rats which have survived an infection with L. monocytogenes can protect cyclophosphamide-treated recipients against a Listeria challenge. They are more effective in this respect than cells obtained from the spleen or thoracic duct lymph. Since exudate cells from normal rats and inocula prepared from the resident peritoneal cell populations of infected donors are unable to inhibit the challenge infection, the protective cells must belong to a class of lymphocytes that emerges from the blood in response to inflammation. It is significant therefore that thoracic duct lymphocytes formed during an acute Listeria infection can move into exudates induced by a variety of inflammatory stimuli. The affinity of newly formed lymphocytes for inflamed tissue points to a mechanism whereby the host marshalls its cellular defenses at sites of bacterial invasion. The tendency of short-lived lymphocytes to leave inflamed vessels might also explain their short-circulating life-span.
Sleep disturbance is associated with inflammatory disease risk and all-cause mortality. Here, we assess global evidence linking sleep disturbance, sleep duration, and inflammation in adult humans.
A systematic search of English language publications was performed, with inclusion of primary research articles that characterized sleep disturbance and/or sleep duration or performed experimental sleep deprivation and assessed inflammation by levels of circulating markers. Effect sizes (ES) and 95% confidence intervals (CI) were extracted and pooled using a random effect model.
A total of 72 studies (n > 50,000) were analyzed with assessment of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor α (TNFα). Sleep disturbance was associated with higher levels of CRP (ES .12; 95% CI = .05-.19) and IL-6 (ES .20; 95% CI = .08-.31). Shorter sleep duration, but not the extreme of short sleep, was associated with higher levels of CRP (ES .09; 95% CI = .01-.17) but not IL-6 (ES .03; 95% CI: -.09 to .14). The extreme of long sleep duration was associated with higher levels of CRP (ES .17; 95% CI = .01-.34) and IL-6 (ES .11; 95% CI = .02-20). Neither sleep disturbances nor sleep duration was associated with TNFα. Neither experimental sleep deprivation nor sleep restriction was associated with CRP, IL-6, or TNFα. Some heterogeneity among studies was found, but there was no evidence of publication bias.
Sleep disturbance and long sleep duration, but not short sleep duration, are associated with increases in markers of systemic inflammation.
Copyright © 2015 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
Sleep disturbances are most prevalent among older adults and often go untreated. Treatment options for sleep disturbances remain limited, and there is a need for community-accessible programs that can improve sleep.
To determine the efficacy of a mind-body medicine intervention, called mindfulness meditation, to promote sleep quality in older adults with moderate sleep disturbances.
Randomized clinical trial with 2 parallel groups conducted from January 1 to December 31, 2012, at a medical research center among an older adult sample (mean [SD] age, 66.3 [7.4] years) with moderate sleep disturbances (Pittsburgh Sleep Quality Index [PSQI] >5).
A standardized mindful awareness practices (MAPs) intervention (n = 24) or a sleep hygiene education (SHE) intervention (n = 25) was randomized to participants, who received a 6-week intervention (2 hours per week) with assigned homework.
The study was powered to detect between-group differences in moderate sleep disturbance measured via the PSQI at postintervention. Secondary outcomes pertained to sleep-related daytime impairment and included validated measures of insomnia symptoms, depression, anxiety, stress, and fatigue, as well as inflammatory signaling via nuclear factor (NF)-κB.
Using an intent-to-treat analysis, participants in the MAPs group showed significant improvement relative to those in the SHE group on the PSQI. With the MAPs intervention, the mean (SD) PSQIs were 10.2 (1.7) at baseline and 7.4 (1.9) at postintervention. With the SHE intervention, the mean (SD) PSQIs were 10.2 (1.8) at baseline and 9.1 (2.0) at postintervention. The between-group mean difference was 1.8 (95% CI, 0.6-2.9), with an effect size of 0.89. The MAPs group showed significant improvement relative to the SHE group on secondary health outcomes of insomnia symptoms, depression symptoms, fatigue interference, and fatigue severity (P < .05 for all). Between-group differences were not observed for anxiety, stress, or NF-κB, although NF-κB concentrations significantly declined over time in both groups (P < .05).
The use of a community-accessible MAPs intervention resulted in improvements in sleep quality at immediate postintervention, which was superior to a highly structured SHE intervention. Formalized mindfulness-based interventions have clinical importance by possibly serving to remediate sleep problems among older adults in the short term, and this effect appears to carry over into reducing sleep-related daytime impairment that has implications for quality of life.
clinicaltrials.gov Identifier: NCT01534338.
Study objectives:
To investigate the comparative efficacy of cognitive behavioral therapy (CBT), Tai Chi Chih (TCC), and sleep seminar education control (SS) on the primary outcome of insomnia diagnosis, and secondary outcomes of sleep quality, fatigue, depressive symptoms, and inflammation in older adults with insomnia.
Design:
Randomized controlled, comparative efficacy trial.
Setting:
Los Angeles community.
Patients:
123 older adults with chronic and primary insomnia.
Interventions:
Random assignment to CBT, TCC, or SS for 2-hour group sessions weekly over 4 months with follow-up at 7 and 16 months.
Measurements:
Insomnia diagnosis, patient-reported outcomes, polysomnography (PSG), and high-sensitivity C-reactive protein (CRP) levels.
Results:
CBT performed better than TCC and SS in remission of clinical insomnia as ascertained by a clinician (P < 0.01), and also showed greater and more sustained improvement in sleep quality, sleep parameters, fatigue, and depressive symptoms than TCC and SS (all P values < 0.01). As compared to SS, CBT was associated with a reduced risk of high CRP levels (> 3.0 mg/L) at 16 months (odds ratio [OR], 0.26 [95% CI, 0.07-0.97] P < 0.05). Remission of insomnia was associated with lower levels of CRP (P < 0.05) at 16 months. TCC was associated with improvements in sleep quality, fatigue, and depressive symptoms as compared to SS (all P's < 0.05), but not insomnia remission. PSG measures did not change.
Conclusions:
Treatment of late-life insomnia is better achieved and sustained by cognitive behavioral therapies. Insomnia treatment and remission reduces a marker of inflammatory risk, which has implications for cardiovascular morbidity and diabetes observed with sleep disturbance in epidemiologic surveys.
Sleep has a critical role in promoting health. Research over the past decade has documented that sleep disturbance has a powerful influence on the risk of infectious disease, the occurrence and progression of several major medical illnesses including cardiovascular disease and cancer, and the incidence of depression. Increasingly, the field has focused on identifying the biological mechanisms underlying these effects. This review highlights the impact of sleep on adaptive and innate immunity, with consideration of the dynamics of sleep disturbance, sleep restriction, and insomnia on (a) antiviral immune responses with consequences for vaccine responses and infectious disease risk and (b) proinflammatory immune responses with implications for cardiovascular disease, cancer, and depression. This review also discusses the neuroendocrine and autonomic neural underpinnings linking sleep disturbance and immunity and the reciprocal links between sleep and inflammatory biology. Finally, interventions are discussed as effective strategies to improve sleep, and potential opportunities are identified to promote sleep health for therapeutic control of chronic infectious, inflammatory, and neuropsychiatric diseases. Expected final online publication date for the Annual Review of Psychology Volume 66 is November 30, 2014. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.
Childhood adversity, defined in terms of material hardship or physical or emotional maltreatment has been associated with risk for infection with cytomegalovirus (CMV) among children and adolescents, and with CMV reactivation in children and adults. The present study examined whether different dimensions of childhood experience—those pertaining to socioeconomic status (SES), physical environment, or family relationships—relate differentially to CMV serostatus and reactivation during adulthood. Participants were 140 healthy adults, aged 18–55 years (41% female; 64% white). Childhood environments were assessed retrospectively and included family SES (parental housing tenure); childhood neighborhood environment (urban residence; physical conditions; safety; and social atmosphere); residential exposures (parental smoking and physical condition of home); family relationships (parental divorce; warmth; harmony; dysfunction; parental bonding); and overall perceived stress during childhood. Approximately 39% (n = 53) of participants were CMV+. In individual analyses controlling for age, sex, race, body mass, current adult SES and smoking status, fewer years of parental home ownership, having a parent who smoked, and living in a poorly maintained or unsafe neighborhood each were associated with greater odds of infection with CMV. By comparison, in individual analyses limited to CMV+ participants, less family warmth, less harmony, greater dysfunction, and suboptimal parental bonding each were related to higher antibody levels, independent of the aforementioned covariates. Findings were not attributable to current adult perceptions of psychological stress or relative levels of emotional stability. These results suggest that different types of childhood adversity may be associated with differential effects on CMV infection and latency.
We ask whether subjective socioeconomic status (SES) predicts who develops a common cold when exposed to a cold virus.
193 healthy men and women ages 21-55 years were assessed for subjective (perceived rank) and objective SES, cognitive, affective and social dispositions, and health practices. Subsequently, they were exposed by nasal drops to a rhinovirus or influenza virus and monitored in quarantine for objective signs of illness and self-reported symptoms.
Infection, signs and symptoms of the common cold, and clinical illness (infection and significant objective signs of illness).
Increased subjective SES was associated with decreased risk for developing a cold for both viruses. This association was independent of objective SES and of cognitive, affective and social disposition that might provide alternative spurious (third factor) explanations for the association. Poorer sleep among those with lesser subjective SES may partly mediate the association between subjective SES and colds.
Increased Subjective SES is associated with less susceptibility to upper respiratory infection, and this association is independent of objective SES, suggesting the importance of perceived relative rank to health.
Socioeconomic status (SES) is consistently associated with health outcomes, yet little is known about the psychosocial and behavioral mechanisms that might explain this association. Researchers usually control for SES rather than examine it. When it is studied, only effects of lower, poverty-level SES are generally examined. However, there is evidence of a graded association with health at all levels of SES, an observation that requires new thought about domains through which SES may exert its health effects. Variables are highlighted that show a graded relationship with both SES and health to provide examples of possible pathways between SES and health end points. Examples are also given of new analytic approaches that can better illuminate the complexities of the SES-health gradient.
To satisfy the need in personality research for factorially univocal measures of each of the 5 domains that subsume most English-language terms for personality traits, new sets of Big-Five factor markers were investigated. In studies of adjective-anchored bipolar rating scales, a transparent format was found to produce factor markers that were more univocal than the same scales administered in the traditional format. Nonetheless, even the transparent bipolar scales proved less robust as factor markers than did parallel sets of adjectives administered in unipolar format. A set of 100 unipolar terms proved to be highly robust across quite diverse samples of self and peer descriptions. These new markers were compared with previously developed ones based on far larger sets of trait adjectives, as well as with the scales from the NEO and Hogan personality inventories. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Chronic sleep deficiency, defined as a state of inadequate or mistimed sleep, is a growing and underappreciated determinant of health status. Sleep deprivation contributes to a number of molecular, immune, and neural changes that play a role in disease development, independent of primary sleep disorders. These changes in biological processes in response to chronic sleep deficiency may serve as etiological factors for the development and exacerbation of cardiovascular and metabolic diseases and, ultimately, a shortened lifespan. Sleep deprivation also results in significant impairments in cognitive and motor performance which increase the risk of motor vehicle crashes and work-related injuries and fatal accidents. The American Academy of Sleep Medicine and the Sleep Research Society have developed this statement to communicate to national health stakeholders the current knowledge which ties sufficient sleep and circadian alignment in adults to health.
Seven experts on personality measurement here discuss the viability of public-domain personality measures, focusing on the International Personality Item Pool (IPIP) as a prototype. Since its inception in 1996, the use of items and scales from the IPIP has increased dramatically. Items from the IPIP have been translated from English into more than 25 other languages. Currently over 80 publications using IPIP scales are listed at the IPIP Web site (http://ipip.ori.org), and the rate of IPIP-related publications has been increasing rapidly. The growing popularity of the IPIP can be attributed to five factors: (1) It is cost free; (2) its items can be obtained instantaneously via the Internet; (3) it includes over 2000 items, all easily available for inspection; (4) scoring keys for IPIP scales are provided; and (5) its items can be presented in any order, interspersed with other items, reworded, translated into other languages, and administered on the World Wide Web without asking permission of anyone. The unrestricted availability of the IPIP raises concerns about possible misuse by unqualified persons, and the freedom of researchers to use the IPIP in idiosyncratic ways raises the possibility of fragmentation rather than scientific unification in personality research.
Stress often co-occurs with inadequate sleep duration, and both are believed to impact mood and emotion. It is not yet known whether inadequate sleep simply increases the intensity of subsequent stress responses or interacts with stressors in more complicated ways. To address this issue, we investigated the effects of one night of total sleep deprivation on subjective stress and mood in response to low-stress and high-stress cognitive testing conditions in healthy adult volunteers in two separate experiments (total N = 53). Sleep was manipulated in a controlled, laboratory setting and stressor intensity was manipulated by changing difficulty of cognitive tasks, time pressure, and feedback about performance. Sleep-deprived participants reported greater subjective stress, anxiety, and anger than rested controls following exposure to the low-stressor condition, but not in response to the high-stressor condition, which elevated negative mood and stress about equally for both sleep conditions. These results suggest that sleep deprivation lowers the psychological threshold for the perception of stress from cognitive demands but does not selectively increase the magnitude of negative affect in response to high-stress performance demands. (PsycINFO Database Record (c) 2012 APA, all rights reserved).
Sleep and the circadian system exert a strong regulatory influence on immune functions. Investigations of the normal sleep-wake cycle showed that immune parameters like numbers of undifferentiated naïve T cells and the production of pro-inflammatory cytokines exhibit peaks during early nocturnal sleep whereas circulating numbers of immune cells with immediate effector functions, like cytotoxic natural killer cells, as well as anti-inflammatory cytokine activity peak during daytime wakefulness. Although it is difficult to entirely dissect the influence of sleep from that of the circadian rhythm, comparisons of the effects of nocturnal sleep with those of 24-h periods of wakefulness suggest that sleep facilitates the extravasation of T cells and their possible redistribution to lymph nodes. Moreover, such studies revealed a selectively enhancing influence of sleep on cytokines promoting the interaction between antigen presenting cells and T helper cells, like interleukin-12. Sleep on the night after experimental vaccinations against hepatitis A produced a strong and persistent increase in the number of antigen-specific Th cells and antibody titres. Together these findings indicate a specific role of sleep in the formation of immunological memory. This role appears to be associated in particular with the stage of slow wave sleep and the accompanying pro-inflammatory endocrine milieu that is hallmarked by high growth hormone and prolactin levels and low cortisol and catecholamine concentrations.
Both higher socioeconomic status (SES) and supportive personal relationships confer health benefits, including better immune function. This study assessed the joint impact of SES and social support on the expression of a latent herpesvirus, Epstein-Barr virus (EBV), in a group of highly stressed women.
Two-hundred and twenty four women either awaiting further evaluation following an abnormal mammogram or newly diagnosed with breast cancer completed questionnaires and provided blood samples to assess EBV viral capsid antigen (VCA) IgG antibody titers.
More highly educated women with more support from friends had lower EBV VCA antibody titers, reflecting a stronger cellular immune response to the latent virus; however, among less educated women, friend support was not associated with EBV antibody titers. As revealed in an ancillary analysis, more highly educated women with more friend support had lower systolic blood pressure (SBP); however, friend support was not associated with SBP among less educated women. Neither depression nor perceived stress mediated these associations. Neither cancer status nor cancer stage among those diagnosed with cancer was significantly related to these outcomes.
Lower SES women may not reap the same immunological benefits from friend support when experiencing a stressful life event as their higher SES counterparts.
Psychological stress and sleep disturbances are highly prevalent and are both implicated in the etiology of cardiovascular diseases. Given the common co-occurrence of psychological distress and sleep disturbances including short sleep duration, this study examined the combined effects of these two factors on blood pressure reactivity to immediate mental challenge tasks after well-rested and sleep-deprived experimental conditions.
Participants (n = 20) were healthy young adults free from current or past sleep, psychiatric, or major medical disorders. Using a within-subjects crossover design, we examined acute stress reactivity under two experimental conditions: after a night of normal sleep in the laboratory and after a night of total sleep deprivation. Two standardized psychological stress tasks were administered, a Stroop color-word naming interference task and a speech task, which were preceded by a prestress baseline period and followed by a poststress recovery period. Each period was 10 minutes in duration, and blood pressure recordings were collected every 2.5 minutes throughout each period. Mean blood pressure responses during stress and recovery periods were examined with a mixed-effects analysis of covariance, controlling for baseline blood pressure.
There was a significant interaction between sleep deprivation and stress on systolic blood pressure (F(2,82.7) = 4.05, p = .02). Systolic blood pressure was higher in the sleep deprivation condition compared with the normal sleep condition during the speech task and during the two baseline periods.
Sleep deprivation amplified systolic blood pressure increases to psychological stress. Sleep loss may increase cardiovascular risk by dysregulating stress physiology.
AimsTo assess the relationship between duration of sleep and morbidity and mortality from coronary heart disease (CHD), stroke, and total cardiovascular disease (CVD).Methods and resultsWe performed a systematic search of publications using MEDLINE (19662009), EMBASE (from 1980), the Cochrane Library, and manual searches without language restrictions. Studies were included if they were prospective, follow-up >3 years, had duration of sleep at baseline, and incident cases of CHD, stroke, or CVD. Relative risks (RR) and 95 confidence interval (CI) were pooled using a random-effect model. Overall, 15 studies (24 cohort samples) included 474 684 male and female participants (follow-up 6.925 years), and 16 067 events (4169 for CHD, 3478 for stroke, and 8420 for total CVD). Sleep duration was assessed by questionnaire and incident cases through certification and event registers. Short duration of sleep was associated with a greater risk of developing or dying of CHD (RR 1.48, 95 CI 1.221.80, P < 0.0001), stroke (1.15, 1.001.31, P 0.047), but not total CVD (1.03, 0.931.15, P 0.52) with no evidence of publication bias (P 0.95, P 0.30, and P 0.46, respectively). Long duration of sleep was also associated with a greater risk of CHD (1.38, 1.151.66, P 0.0005), stroke (1.65, 1.451.87, P < 0.0001), and total CVD (1.41, 1.191.68, P < 0.0001) with no evidence of publication bias (P 0.92, P 0.96, and P 0.79, respectively).Conclusion
Both short and long duration of sleep are predictors, or markers, of cardiovascular outcomes.
BACKGROUND. Congenital cytomegalovirus (CMV) infection causes permanent disabilities in more than 5500 children each year in the United States. The likelihood of congenital infection and disability is highest for infants whose mothers were CMV seronegative before conception and who acquire infection during pregnancy. METHODS. To provide a current, nationally representative estimate of the seroprevalence of CMV in the United States and to investigate trends in CMV infection, serum samples from the National Health and Nutrition Examination Survey (NHANES) 1999-2004 were tested for CMV-specific immunoglobulin G antibody, and results were compared with those from NHANES III (1988-1994). Individuals aged 6-49 years (21,639 for NHANES III and 15,310 for NHANES 1999-2004) were included. RESULTS. For NHANES 1999-2004, the overall age-adjusted CMV seroprevalence was 50.4%. CMV seroprevalence was higher among non-Hispanic black and Mexican American children compared with non-Hispanic white children and increased more quickly in subsequent age groups. CMV seropositivity was independently associated with older age, female sex, foreign birthplace, low household income, high household crowding, and low household education. Compared with NHANES 1988-1994, the overall age-adjusted CMV seroprevalence for NHANES 1999-2004 was not significantly different. CONCLUSIONS. Many women of reproductive age in the United States are still at risk of primary CMV infection during pregnancy. There is an urgent need for vaccine development and other interventions to prevent and treat congenital CMV. The substantial disparities in CMV risk among seronegative women suggest that prevention strategies should include an emphasis on reaching racial or ethnic minorities and women of low socioeconomic status.
Lower social class is associated with diminished resources and perceived subordinate rank. On the basis of this analysis, the authors predicted that social class would be closely associated with a reduced sense of personal control and that this association would explain why lower class individuals favor contextual over dispositional explanations of social events. Across 4 studies, lower social class individuals, as measured by subjective socioeconomic status (SES), endorsed contextual explanations of economic trends, broad social outcomes, and emotion. Across studies, the sense of control mediated the relation between subjective SES and contextual explanations, and this association was independent of objective SES, ethnicity, political ideology, and self-serving biases. Finally, experimentally inducing a higher sense of control attenuated the tendency for lower subjective SES individuals to make more contextual explanations (Study 4). Implications for future research on social class as well as theoretical distinctions between objective SES and subjective SES are discussed.
To assess the relationship between habitual sleep disturbances and the incidence of type 2 diabetes and to obtain an estimate of the risk.
We conducted a systematic search of publications using MEDLINE (1955-April 2009), EMBASE, and the Cochrane Library and manual searches without language restrictions. We included studies if they were prospective with follow-up >3 years and had an assessment of sleep disturbances at baseline and incidence of type 2 diabetes. We recorded several characteristics for each study. We extracted quantity and quality of sleep, how they were assessed, and incident cases defined with different validated methods. We extracted relative risks (RRs) and 95% CI and pooled them using random-effects models. We performed sensitivity analysis and assessed heterogeneity and publication bias.
We included 10 studies (13 independent cohort samples; 107,756 male and female participants, follow-up range 4.2-32 years, and 3,586 incident cases of type 2 diabetes). In pooled analyses, quantity and quality of sleep predicted the risk of development of type 2 diabetes. For short duration of sleep (< or =5-6 h/night), the RR was 1.28 (95% CI 1.03-1.60, P = 0.024, heterogeneity P = 0.015); for long duration of sleep (>8-9 h/night), the RR was 1.48 (1.13-1.96, P = 0.005); for difficulty in initiating sleep, the RR was 1.57 (1.25-1.97, P < 0.0001); and for difficulty in maintaining sleep, the RR was 1.84 (1.39-2.43, P < 0.0001).
Quantity and quality of sleep consistently and significantly predict the risk of the development of type 2 diabetes. The mechanisms underlying this relation may differ between short and long sleepers.
Extremes of sleep duration have been associated with adverse health outcomes. The mechanism is unclear but may be related to increased inflammation. We sought to assess the association between sleep duration and inflammatory biomarkers.
A total of 614 individuals from the Cleveland Family Study completed questionnaires about sleep habits and underwent polysomnography. A morning fasting blood sample was assayed for 5 inflammatory cytokines.
In this cohort, mean (SD) habitual sleep duration based on self-report was 7.6 (1.6) h and mean sleep duration by polysomnography (PSG) on the night prior to blood sampling was 6.2 (1.3) h. After adjusting for obesity and apnea severity, each additional hour of habitual sleep duration was associated with an 8% increase in C-reactive protein (CRP) levels (P=0.004) and 7% increase in interleukin-6 (IL-6) levels (P=0.0003). These associations were independent of self-reported sleepiness. In contrast, PSG sleep duration was inversely associated with tumor necrosis factor alpha (TNFa) levels. For each hour reduction in sleep, TNFalpha levels increased by 8% on average (P=0.02). Sleep duration was not associated with IL-1 or IL-10.
Increases in habitual sleep durations are associated with elevations in CRP and IL-6 while reduced PSG sleep duration is associated with elevated TNFa levels. Activation of pro-inflammatory pathways may represent a mechanism by which extreme sleep habits affect health.
Sleep quality is thought to be an important predictor of immunity and, in turn, susceptibility to the common cold. This article examines whether sleep duration and efficiency in the weeks preceding viral exposure are associated with cold susceptibility.
A total of 153 healthy men and women (age range, 21-55 years) volunteered to participate in the study. For 14 consecutive days, they reported their sleep duration and sleep efficiency (percentage of time in bed actually asleep) for the previous night and whether they felt rested. Average scores for each sleep variable were calculated over the 14-day baseline. Subsequently, participants were quarantined, administered nasal drops containing a rhinovirus, and monitored for the development of a clinical cold (infection in the presence of objective signs of illness) on the day before and for 5 days after exposure.
There was a graded association with average sleep duration: participants with less than 7 hours of sleep were 2.94 times (95% confidence interval [CI], 1.18-7.30) more likely to develop a cold than those with 8 hours or more of sleep. The association with sleep efficiency was also graded: participants with less than 92% efficiency were 5.50 times (95% CI, 2.08-14.48) more likely to develop a cold than those with 98% or more efficiency. These relationships could not be explained by differences in prechallenge virus-specific antibody titers, demographics, season of the year, body mass, socioeconomic status, psychological variables, or health practices. The percentage of days feeling rested was not associated with colds.
Poorer sleep efficiency and shorter sleep duration in the weeks preceding exposure to a rhinovirus were associated with lower resistance to illness.
A number of immunological functions are dependent on circadian rhythms and regular sleep. This has impact on the type and magnitude of immune responses following antigenic challenge, for example in vaccination. Little is known about the underlying mechanisms. One possibility may be the circadian and sleep-dependent modulation of CD4(+)CD25(-) T cell responses by CD4(+)CD25(+) natural regulatory T cells (nT(reg)). In a variety of studies, nT(reg) have been shown to regulate T cell responses negatively. Thus, we investigated the influence of sleep and circadian rhythm on the number and function of nT(reg) as well as on the function of CD4(+)CD25(-) T cells. Seven healthy young men were examined under defined conditions on two occasions, i.e. during sleep and sleep deprivation. Venous blood was drawn periodically; numbers of nT(reg), suppressive activity of nT(reg), interleukin-2 production and proliferation of CD4(+)CD25(-) T cells were explored in vitro. nT(reg) counts revealed a significant circadian rhythm with highest levels during the night (mean 95 nT(reg)/microl) and lowest levels during the day (mean 55 nT(reg)/microl). During normal sleep, the suppressive activity of nT(reg) was highest at 02.00 h and somewhat lower at 15.00 h. Surprisingly, almost no suppressive activity was present at 07.00 h. Deprivation of sleep abrogated this rhythm. CD4(+)CD25(-) T cell proliferation was dampened significantly by sleep deprivation. This is the first study in human cells to show that nT(reg) number and function follow a rhythm across the 24-h period. Furthermore, sleep deprivation severely disturbs the functional rhythm of nT(reg) and CD4(+)CD25(-) T cells.
Prolonged and severe sleep deprivation is associated with alterations of natural and cellular immune function. To determine whether alterations of immune function also occur after even a modest loss of sleep, the effects of early-night partial sleep deprivation on circulating numbers of white blood cells, natural killer (NK) cell number and cytotoxicity, lymphokine-activated killer (LAK) cell number and activity, and stimulated interleukin-2 (IL-2) production were studied in 42 medically and psychiatrically healthy male volunteers. After a night of sleep deprivation between 10 P.M. and 3 A.M., a reduction of natural immune responses as measured by NK cell activity, NK activity per number of NK cells, LAK activity, and LAK activity per number of LAK precursors (CD16,56, CD25) was found. In addition, concanavalin A-stimulated IL-2 production was suppressed after sleep deprivation due to changes in both adherent and nonadherent cell populations. After a night of recovery sleep, NK activity returned to baseline levels and IL-2 production remained suppressed. These data implicate sleep in the modulation of immunity and demonstrate that even a modest disturbance of sleep produces a reduction of natural immune responses and T cell cytokine production.
This preliminary study compared the associations between objective and subjective socioeconomic status (SES) with psychological and physical variables among 157 healthy White women, 59 of whom subsequently participated in a laboratory stress study. Compared with objective indicators, subjective social status was more consistently and strongly related to psychological functioning and health-related factors (self-rated health, heart rate, sleep latency, body fat distribution, and cortisol habituation to repeated stress). Most associations remained significant even after controlling for objective social status and negative affectivity. Results suggest that, in this sample with a moderately restricted range on SES and health, psychological perceptions of social status may be contributing to the SES–health gradient.
Perceived control is a personality characteristic that contributes to well-being, but few studies have attempted to integrate the functions of perceived control with those of other determinants of health. This research tested two hypotheses about the functions of perceived control: (a) individual differences in perceived control would account for socioeconomic differences in self-rated health status; (b) performance of health-related behaviors would account for the health benefits of perceived control. Using data from adult, nonproxy respondents in the National Population Health Survey of Canada (1995; n = 11, 110), confirmatory factor analysis supported a measurement model of self-rated health status composed of two correlated factors: physical health (i.e., chronic conditions. restricted activities, self-rated general health, physical functional capacity) and mental health (i.e., distress, depression). Structural equation modeling supported the first hypothesis, but not the second, regarding perceived control as a determinant of self-rated physical and mental health. Health-related behaviors partially mediated age differences in self-rated health, but different behaviors functioned in this way for men than for women. The findings suggest that psychological process, that of perceiving control over life events, underlies social inequality in health. Health-related behaviors appear not to serve as the primary mechanism through which perceived control influences health.
In this article, the authors evaluate the possible roles of negative emotions and cognitions in the association between socioeconomic status (SES) and physical health, focusing on the outcomes of cardiovascular diseases and all-cause mortality. After reviewing the limited direct evidence, the authors examine indirect evidence showing that (a) SES relates to the targeted health outcomes, (b) SES relates to negative emotions and cognitions, and (c) negative emotions and cognitions relate to the targeted health outcomes. The authors present a general framework for understanding the roles of cognitive-emotional factors, suggesting that low-SES environments are stressful and reduce individuals' reserve capacity to manage stress, thereby increasing vulnerability to negative emotions and cognitions. The article concludes with suggestions for future research to better evaluate the proposed model.
The present report meta-analyzes more than 300 empirical articles describing a relationship between psychological stress and parameters of the immune system in human participants. Acute stressors (lasting minutes) were associated with potentially adaptive upregulation of some parameters of natural immunity and downregulation of some functions of specific immunity. Brief naturalistic stressors (such as exams) tended to suppress cellular immunity while preserving humoral immunity. Chronic stressors were associated with suppression of both cellular and humoral measures. Effects of event sequences varied according to the kind of event (trauma vs. loss). Subjective reports of stress generally did not associate with immune change. In some cases, physical vulnerability as a function of age or disease also increased vulnerability to immune change during stressors.
Objective:
The purpose of this study is to assess the role of psychological stress in the expression of illness among infected subjects and to test the plausibility of local proinflammatory cytokine production as a pathway linking stress to illness.
Methods:
After completing a measure of psychological stress, 55 subjects were experimentally infected with an influenza A virus. Subjects were monitored in quarantine daily for upper respiratory symptoms, mucus production, and nasal lavage levels of interleukin (IL)-6.
Results:
Higher psychological stress assessed before the viral challenge was associated with greater symptom scores, greater mucus weights, and higher IL-6 lavage concentrations in response to infection. The IL-6 response was temporally related to the two markers of illness severity, and mediation analyses indicated that these data were consistent with IL-6 acting as a major pathway through which stress was associated with increased symptoms of illness. However, this pattern of data is also consistent with increases in IL-6 occurring in response to tissue damage associated with illness symptoms.
Conclusions:
Psychological stress predicts a greater expression of illness and an increased production of IL-6 in response to an upper respiratory infection.
Childhood adversity, defined in terms of material hardship or physical or emotional maltreatment has been associated with risk for infection with cytomegalovirus (CMV) among children and adolescents, and with CMV reactivation in children and adults. The present study examined whether different dimensions of childhood experience—those pertaining to socioeconomic status (SES), physical environment, or family relationships, relate differentially to CMV serostatus and reactivation during adulthood. Participants were 140 healthy adults, aged 18-55 years (41% female; 64% white). Childhood environments were assessed retrospectively and included family SES (parental housing tenure); childhood neighborhood environment (urban residence; physical conditions; safety; and social atmosphere); residential exposures (parental smoking and physical condition of home); family relationships (parental divorce; warmth; harmony; dysfunction; parental bonding); and overall perceived stress during childhood. Approximately 39% (n = 53) of participants were CMV+. In individual analyses controlling for age, sex, race, body mass, current adult SES and smoking status, fewer years of parental home ownership, having a parent who smoked, and living in a poorly maintained or unsafe neighborhood each were associated with greater odds of infection with CMV. By comparison, in individual analyses limited to CMV+ participants, less family warmth, less harmony, greater dysfunction, and suboptimal parental bonding each were related to higher antibody levels, independent of the aforementioned covariates. Findings were not attributable to current adult perceptions of psychological stress or relative levels of emotional stability. These results suggest that different types of childhood adversity may be associated with differential effects on CMV infection and latency.
Inflammatory processes are implicated in a number of diseases for which there are known socioeconomic status (SES) disparities, including heart disease and diabetes. Growing evidence also suggests SES gradients in levels of peripheral blood markers of inflammation. However, we know little about potential gender and racial/ethnic differences in associations between SES and inflammation, despite the fact that the burden of inflammation-related diseases varies by gender and race. The present study examines SES (education and income) gradients in levels of two inflammatory biomarkers, C-reactive protein (CRP) and interleukin-6 (IL-6), in a biethnic (White and Black) sample of men and women (n = 3,549, aged 37–55 years) in the USA from the CARDIA Study. Health status, behavioral and psychosocial variables that may underlie SES differences in inflammatory biomarker levels were also examined. Age-adjusted CRP and IL-6 levels were inversely associated with education level in each race/gender group except Black males. Income gradients were also observed in each race/gender group for IL-6 and in White females and males for CRP. In general, differences in CRP and IL-6 levels between low and high SES groups were reduced in magnitude and significance with the addition of health status, behavioral, and psychosocial variables, although the impact of the addition of model covariates varied across race/gender groups and different SES-inflammation models. Overall, findings indicate SES gradients in levels of inflammation burden in middle-aged White and Black males and females.
Good sleep is essential to good health. Yet for most of its history, sleep medicine has focused on the definition, identification, and treatment of sleep problems. Sleep health is a term that is infrequently used and even less frequently defined. It is time for us to change this. Indeed, pressures in the research, clinical, and regulatory environments require that we do so. The health of populations is increasingly defined by positive attributes such as wellness, performance, and adaptation, and not merely by the absence of disease. Sleep health can be defined in such terms. Empirical data demonstrate several dimensions of sleep that are related to health outcomes, and that can be measured with self-report and objective methods. One suggested definition of sleep health and a description of self-report items for measuring it are provided as examples. The concept of sleep health synergizes with other health care agendas, such as empowering individuals and communities, improving population health, and reducing health care costs. Promoting sleep health also offers the field of sleep medicine new research and clinical opportunities. In this sense, defining sleep health is vital not only to the health of populations and individuals, but also to the health of sleep medicine itself.
Buysse DJ. Sleep health: can we define it? Does it matter? SLEEP 2014;37(1):9-17.
The gradient between socioeconomic status (SES) and health is well established: Many measures of health show that health increases as SES increases. However, the mechanisms underlying this association are not well understood. Behavioral, cognitive, and affective tendencies that develop in response to the greater psychosocial stress encountered in low-SES environments may partially mediate the impact of SES on health. Although these tendencies might be helpful for coping in the short term, over time they may contribute to the development of allostatic load, which increases vulnerability to disease. Debate remains regarding the direction of causation between SES and health, the impact of income inequality, the interaction of SES with race-ethnicity and gender, and the effects of SES over the life course.
Objective:
To examine the hypothesis that diverse ties to friends, family, work, and community are associated with increased host resistance to infection.
Design:
After reporting the extent of participation in 12 types of social ties (eg, spouse, parent, friend, workmate, member of social group), subjects were given nasal drops containing 1 of 2 rhinoviruses and monitored for the development of a common cold.
Setting:
Quarantine.
Participants:
A total of 276 healthy volunteers, aged 18 to 55 years, neither seropositive for human immunodeficiency virus nor pregnant.
Outcome measures:
Colds (illness in the presence of a verified infection), mucus production, mucociliary clearance function, and amount of viral replication.
Results:
In response to both viruses, those with more types of social ties were less susceptible to common colds, produced less mucus, were more effective in ciliary clearance of their nasal passages, and shed less virus. These relationships were unaltered by statistical controls for prechallenge virus-specific antibody, virus type, age, sex, season, body mass index, education, and race. Susceptibility to colds decreased in a dose-response manner with increased diversity of the social network. There was an adjusted relative risk of 4.2 comparing persons with fewest (1 to 3) to those with most (6 or more) types of social ties. Although smoking, poor sleep quality, alcohol abstinence, low dietary intake of vitamin C, elevated catecholamine levels, and being introverted were all associated with greater susceptibility to colds, they could only partially account for the relation between social network diversity and incidence of colds.
Conclusions:
More diverse social networks were associated with greater resistance to upper respiratory illness.
Health disparities (differences in health by socioeconomic groups) are a pressing issue in our society. This article provides an overview of a multilevel approach that seeks to understand the mechanisms underlying health disparities by considering factors at the individual, family, and neighborhood levels. In addition, we describe an approach to connecting these factors to various levels of biological processes (systemic inflammation, cellular processes, and genomic pathways) that drive disease pathophysiology. In the second half of the article, we address the question of why some low-socioeconomic-status (low-SES) individuals manage to maintain good physical health. We identify naturally occurring psychosocial factors that help buffer these individuals from adverse physiological responses and pathogenic processes leading to chronic disease. What is protective for low-SES individuals is not the same as what is protective for high-SES individuals, and this needs to be taken into account in interventions aimed at reducing health disparities. Expected final online publication date for the Annual Review of Clinical Psychology Volume 9 is March 26, 2013. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.
This chapter focuses on evidence linking socio-economic status (SES) to "downstream" peripheral biology. Drawing on the concept of allostatic load, we examine evidence linking lower SES with greater cumulative physiological toll on multiple major biological regulatory systems over the life course. We begin by reviewing evidence linking lower SES to poorer trajectories of aging in multiple, individual physiological systems, followed by evidence of the resulting cumulative, overall burdens of physiological dysregulation seen among those of lower SES. The role of cumulative physiological dysregulation in mediating SES gradients in morbidity and mortality is then examined. We conclude with discussion of the question of interactions between SES (and other such environmental factors) and genetic endowment, and their potential consequences for patterns of physiological activity--an area of research that appears poised to contribute significantly to our understanding of how social conditions "get under the skin" to affect health and aging.
The brain is the key organ of stress reactivity, coping, and recovery processes. Within the brain, a distributed neural circuitry determines what is threatening and thus stressful to the individual. Instrumental brain systems of this circuitry include the hippocampus, amygdala, and areas of the prefrontal cortex. Together, these systems regulate physiological and behavioral stress processes, which can be adaptive in the short-term and maladaptive in the long-term. Importantly, such stress processes arise from bidirectional patterns of communication between the brain and the autonomic, cardiovascular, and immune systems via neural and endocrine mechanisms underpinning cognition, experience, and behavior. In one respect, these bidirectional stress mechanisms are protective in that they promote short-term adaptation (allostasis). In another respect, however, these stress mechanisms can lead to a long-term dysregulation of allostasis in that they promote maladaptive wear-and-tear on the body and brain under chronically stressful conditions (allostatic load), compromising stress resiliency and health. This review focuses specifically on the links between stress-related processes embedded within the social environment and embodied within the brain, which is viewed as the central mediator and target of allostasis and allostatic load.
To examine the associations between income and education and three markers of inflammation: interleukin-6 (IL-6), C-reactive protein (CRP), and fibrinogen. Socioeconomic status is inversely linked with health outcomes, but the biological processes by which social position "gets under the skin" to affect health are poorly understood.
Cross-sectional analyses involved participants (n = 704) from the second wave of the national population-based Survey of Midlife Development in the United States (MIDUS). Data on pretax household-adjusted income and educational attainment were collected by questionnaire and telephone interview, respectively. Detailed medical history interviews, inventories of medication, and fasting blood samples for assessment of inflammatory proteins were obtained during an overnight clinic stay.
All three inflammatory proteins were inversely associated with both income and education in bivariate analyses. However, multivariate regression models, adjusting for potential confounds, showed that only low income predicted higher levels of inflammatory proteins. Moreover, inclusion of IL-6 in the regression models for CRP and fibrinogen eliminated the associations with income.
These results suggest that income explains the association between education and peripheral inflammation. In short, the reason that higher education is linked to reduced peripheral inflammation is because it reduces the risk for low income status, which is what is directly associated with reduced peripheral inflammation. The findings also suggest that the links between income and both CRP and fibrinogen are mediated by IL-6. These observations help to sharpen our understanding of the relationship between social position and biological markers of illness in the United States.
Research over the past several decades has documented psychosocial influences on the development and progression of several major medical illnesses. The field is now increasingly focused on identifying the biological and behavioral mechanisms underlying these effects. This review takes stock of the knowledge accumulated in the biological arena to date and highlights conceptual and methodological approaches that have proven especially productive. It emphasizes the value of a disease-centered approach that "reverse engineers" adverse health outcomes into their specific biological determinants and then identifies psychologically modulated neuroendocrine and immunologic dynamics that modulate those pathological processes at the cellular and molecular levels.
Despite the prevalence of sleep complaints among psychiatric patients, few questionnaires have been specifically designed to measure sleep quality in clinical populations. The Pittsburgh Sleep Quality Index (PSQI) is a self-rated questionnaire which assesses sleep quality and disturbances over a 1-month time interval. Nineteen individual items generate seven "component" scores: subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, use of sleeping medication, and daytime dysfunction. The sum of scores for these seven components yields one global score. Clinical and clinimetric properties of the PSQI were assessed over an 18-month period with "good" sleepers (healthy subjects, n = 52) and "poor" sleepers (depressed patients, n = 54; sleep-disorder patients, n = 62). Acceptable measures of internal homogeneity, consistency (test-retest reliability), and validity were obtained. A global PSQI score greater than 5 yielded a diagnostic sensitivity of 89.6% and specificity of 86.5% (kappa = 0.75, p less than 0.001) in distinguishing good and poor sleepers. The clinimetric and clinical properties of the PSQI suggest its utility both in psychiatric clinical practice and research activities.
This paper presents the results of a randomized, double-blind, placebo-controlled study of the efficacy of chlorpheniramine in relieving the symptoms and attenuating the pathophysiologic correlates of a rhinovirus "common cold." Forty healthy, adult, nonatopic subjects were randomly assigned to one of two treatment groups: active drug and placebo. On study Day 0, all subjects were challenged intranasally with rhinovirus type 39 (dose = 100 TCID50). Subjects were cloistered from Day 2 to Day 7, at which time they were treated with either chlorpheniramine or placebo. From 3 days before challenge to study Day 19, subjects had nasal patency assessed by rhinomanometry, eustachian tube function assessed by the 9-step test and sonotubometry, middle ear pressure assessed by tympanometry and nasal clearance assessed by the dyed-saccharin technique. Symptom diaries were maintained throughout the period of follow-up. During cloister, symptoms also were scored by interview, nasal secretions were quantified and nasal washings were performed for viral culture. Results showed that 19 (95%) subjects in the active-treatment group and 18 (90%) subjects in the placebo-treatment group shed virus. Symptomatic colds were observed in 63% of the active-treated and 83% of the placebo-treated subjects. Symptoms increased on Day 1 and peaked at Days 4 to 5. Detrimental changes in other measured functions consistent with those previously reported were observed. During the period of treatment, significant differences in the average symptom scores favoring the active-treatment group were observed for sneezing. Also, weight of expelled secretions was greater and mucociliary clearance rate less on some cloister days for the placebo-treated group. No significant differences between treatment groups in the objective measures of nasal congestion or the response of the middle ear and eustachian tube were documented.
This paper presents evidence from three samples, two of college students and one of participants in a community smoking-cessation program, for the reliability and validity of a 14-item instrument, the Perceived Stress Scale (PSS), designed to measure the degree to which situations in one's life are appraised as stressful. The PSS showed adequate reliability and, as predicted, was correlated with life-event scores, depressive and physical symptomatology, utilization of health services, social anxiety, and smoking-reduction maintenance. In all comparisons, the PSS was a better predictor of the outcome in question than were life-event scores. When compared to a depressive symptomatology scale, the PSS was found to measure a different and independently predictive construct. Additional data indicate adequate reliability and validity of a four-item version of the PSS for telephone interviews. The PSS is suggested for examining the role of nonspecific appraised stress in the etiology of disease and behavioral disorders and as an outcome measure of experienced levels of stress.
Socioeconomic status (SES) is an important predictor of a range of health and illness outcomes. Research seeking to identify the extent to which this often-reported effect is due to protective benefits of higher SES or to toxic elements of lower social status has not yielded consistent or conclusive findings. A relatively novel hypothesis is that these effects are due to chronic stress that is associated with SES; lower SES is reliably associated with a number of important social and environmental conditions that contribute to chronic stress burden, including crowding, crime, noise pollution, discrimination, and other hazards or stressors. In other words, chronic stress may capture much of the variance in health and social outcomes associated with harmful aspects of lower social status. Low SES is generally associated with distress, prevalence of mental health problems, and with health-impairing behaviors that are also related to stress. Research targeting this hypothesis is needed to determine the extent to which stress is a pathway linking SES and health.
The influence of low socioeconomic status on cardiovascular disease may be mediated in part by sustained activation of stress-related autonomic and neuroendocrine processes. We hypothesized that low socioeconomic status would be associated with heightened ambulatory blood pressure and cortisol output over the working day.
One hundred eight men and 94 women from the Whitehall II epidemiological cohort participated. Blood pressure and heart rate were monitored every 20 minutes over a working day and evening, and salivary cortisol was sampled on waking up and at 2-hour intervals. Measures were also taken under resting laboratory conditions. Socioeconomic status was indexed by grade of employment.
Resting blood pressure, heart rate, and cortisol did not differ by grade. Ambulatory systolic pressure was greater in the morning in the lower (128.9 +/- 15.7 mm Hg) than the intermediate (122.6 +/- 12.5 mm Hg) and higher grades (123.3 +/- 12.7 mm Hg) after adjustment for age, sex, smoking, and alcohol intake (p =.019). Heart rate was also raised in the morning in the lower grade participants. Differences in morning systolic pressure and heart rate were independent of concurrent physical activity. Cortisol concentration was greater in lower than higher grade men (9.54 +/- 4.1 vs. 7.38 +/- 2.8 nmol/liter, p =.008) but was more elevated in higher than lower grade women (7.84 +/- 2.5 vs. 6.35 +/- 1.9 nmol/liter, p =.014). Differences remained significant after adjustment for age, time of awakening, smoking, and alcohol intake.
Socioeconomic differences in blood pressure and cortisol may reflect stress-related activation of biological pathways that contribute to variations in disease risk.
Recent human studies suggested a supportive influence of regular nocturnal sleep on immune responses to experimental infection (vaccination). We hypothesized here that sleep could ease such responses by shifting the balance between T helper 1 (Th1) and T helper 2 (Th2) cytokine activity towards Th1 dominance thereby favoring cellular over humoral responses to infection. We compared the Th1/Th2 cytokine balance in 14 healthy men during regular nocturnal sleep (between 23:00 and 07:00 h) and while remaining awake during the same nocturnal interval, in a within-subject cross-over design. Blood was collected every 2 h. Production of T cell derived cytokines--interferon-gamma (IFN-gamma), interleukin-2 (IL-2), interleukin-4 (IL-4), and tumor necrosis factor-alpha (TNF-alpha)--was measured at the single cell level using multiparametric flow cytometry. Also, several immunoactive hormones--prolactin, growth hormone (GH), thyroid stimulating hormone (TSH), cortisol, and melatonin--were measured, the release of which is known to be regulated by sleep. Compared with wakefulness, early nocturnal sleep induced a shift in the Th1/Th2 cytokine balance towards increased Th1 activity, as indicated by an increased (p <.05) ratio of IFN-gamma/IL-4 producing T helper cells. However, the Th1 shift was only of moderate size and replaced by Th2 dominance during late sleep (p <.05). It could be mediated via release of prolactin and GH which both were distinctly increased during sleep (p <.001). Though unexpected, the most pronounced effect of sleep on T cell cytokine production was a robust decrease in TNF-alpha producing CD8+ cells probably reflecting increased extravasation of cytotoxic effector and memory T cells.
Psychosocial factors moderate the expression of illness during upper respiratory virus infections but past attempts to define mediational pathways were not successful. Here, we used a model of experimental rhinovirus infection in humans to evaluate three proinflammatory cytokines for their potential role in mediating the previously documented association between positive emotional style and illness. After assessing emotional style in 327 healthy adults, each was exposed to one of two strains of rhinovirus and followed for 5 days in quarantine. Symptoms/signs, nasal lavage IL-1beta, IL-6, and IL-8 protein, and viral shedding were assessed at baseline and on each of the 5 days after exposure. Virus-specific antibody was assessed at baseline and 28 days after challenge. An analysis of the data for 234 subjects with documented infection showed that nasal IL-1beta, IL-6, and IL-8 protein levels were all associated with greater illness expression but IL-6 was by far the best predictor of nasal signs and symptoms. Lower positive emotional style was associated with greater objective and subjective markers of illness and these associations were decreased substantially by controlling for IL-6 but not for IL-1beta or IL-8. These results are consistent with the hypothesis that IL-6 acts as a biological mediator in linking positive emotional style to illness expression during rhinovirus infection.
Sleep deprivation is known to impair a range of functions, including immune regulation and metabolic control, as well as neurocognitive processes, such as learning and memory [1]. But evidence for the role of sleep in regulating our emotional brain-state is surprisingly scarce, and while the dysregulation of affective stability following sleep loss has received subjective documentation 2 and 3, any neural examination remains absent. Clinical evidence suggests that sleep and emotion interact; nearly all psychiatric and neurological disorders expressing sleep disruption display corresponding symptoms of affective imbalance [4]. Independent of sleep, knowledge of the basic neural and cognitive mechanisms regulating emotion is remarkably advanced. The amygdala has a well-documented role in the processing of emotionally salient information, particularly aversive stimuli 5 and 6. The extent of amygdala engagement can also be influenced by a variety of connected systems, particularly the medial-prefrontal cortex (MPFC); the MPFC is proposed to exert an inhibitory, top-down control of amygdala function, resulting in contextually appropriate emotional responses 5 and 6. We have focused on this network and using functional magnetic resonance image (fMRI) have obtained evidence, reported here, that a lack of sleep inappropriately modulates the human emotional brain response to negative aversive stimuli (see Supplemental data available on-line with this issue).
Low socioeconomic position is known to be associated with cardiovascular events and atherosclerosis. Reasons for these associations remain a topic of research. Inflammation could be an important mediating mechanism linking socioeconomic position to cardiovascular risk.
This cross-sectional study used data from the baseline examination of the Multi-Ethnic Study of Atherosclerosis (MESA), a study of 6814 men and women 45 to 84 years of age. Race- and ethnicity-stratified regression analyses were used to estimate associations of household income and education with C-reactive protein and interleukin-6 before and after adjustment for infection and medication use, psychosocial factors, behaviors, adiposity, and diabetes mellitus. Low income was associated with higher concentrations of interleukin-6 in all race/ethnic groups. Percent differences associated with 1-SD-lower income were 9% (95% confidence interval [CI], 7 to 11), 6% (95% CI, 1 to 10), 8% (95% CI, 4 to 11), and 8% (95% CI, 3 to 13) for whites, Chinese, blacks, and Hispanics. Low levels of education were associated with higher levels of interleukin-6 only among whites and blacks (percent difference in interleukin-6 associated with 1-SD-lower education: 9% [95% CI, 6 to 12] among Whites, and 7% [95% CI, 3 to 10] among blacks). Similar patterns were observed for C-reactive protein. Adiposity was the single most important factor explaining socioeconomic position associations, especially among blacks and whites. A smaller effect was seen for psychosocial factors and behaviors in all race groups.
Both household income and education are associated with inflammation, but associations vary across race/ethnic groups. Associations likely result from socioeconomic position patterning of adiposity and other factors.