Search

Establishing typical values of the steroid hormone cortisol at rest and after challenge is critical for understanding how environmental factors impact stress regulation and overall development, beginning at birth. Yet most extant samples are small or based upon low-risk populations, and few studies address the potential role of maternal weight during pregnancy in their study designs or sampling strategy. Here we report basal and reactivity levels of salivary cortisol within a racially and ethnically diverse sample of 132 infants approximately one month of age (Age in days: M = 37.61, SD = 7.27) born to lower income overweight or obese mothers. Reactivity was assessed in response to a multi-domain infant stressor paradigm, which included assessment via the Newborn Behavioral Observation (NBO) system and extensive anthropometric measurements. Sample means for basal, post stressors, and reactivity to the NBO were significantly lower than those reported in reviews of low-risk samples. Parity was associated with cortisol levels such that first-born infants had lower resting cortisol and higher reactivity than infants born to multiparous women. Latino infants had lower basal cortisol. No other demographic characteristics significantly predicted cortisol. The variability in cortisol levels present in this sample suggests that considerable psychophysiological diversity may exist in samples of low-SES or high-risk participants. Findings provide useful ranges for samples of racially and ethnically diverse newborns from low-income families.

Energy is required to sustain life and enable stress adaptation. At the cellular level, energy is largely derived from mitochondria – unique multifunctional organelles with their own genome. Four main elements connect mitochondria to stress: 1) Energy is required at the molecular, (epi)genetic, cellular, organ, and systemic levels to sustain components of stress responses; 2) Glucocorticoids and other steroid hormones are produced and metabolized by mitochondria; 3) Reciprocally, mitochondria functionally respond to neuroendocrine and metabolic stress mediators; and 4) Experimentally manipulating mitochondrial functions alters physiological and behavioral responses to psychological stress. Thus, mitochondria are endocrine organelles that provide both the energy and signals that enable and direct stress adaptation. Neural networks regulating social behavior – as well as psychopathological processes – are also influenced by mitochondrial energetics. An integrative view of stress as an energy-driven process opens new opportunities to study mechanisms of adaptation and regulation across the lifespan.

Major depressive disorder (MDD) has been linked to mitochondrial defects, which could manifest in mitochondrial DNA (mtDNA) polymorphisms or mutations. Additionally, copy number of mtDNA (mtDNA-cn) can be quantified in peripheral blood mononuclear cells (PBMC)s, indirectly reflecting cellular energetics, or in the circulating cell-free mtDNA (ccf-mtDNA) levels, which may reflect a fraction of the mitochondrial genome released during cellular stress. Few studies have examined ccf-mtDNA in MDD, and no studies have tested its relationship with intracellular mtDNA-cn or with antidepressant treatment response. Here, mtDNA levels were quantified in parallel from: (i) PBMCs and (ii) cell-free plasma of 50 unmedicated MDD subjects and 55 controls, in parallel with PBMC telomere length (TL) and antioxidant enzyme glutathione peroxidase (GpX) activity. MtDNA measures were repeated in 19 MDD subjects after 8 weeks of open-label SSRI treatment. In analyses adjusted for age, sex, BMI, and smoking, MDD subjects had significantly elevated levels of ccf-mtDNA (F = 20.6, p = 0.00002). PBMC mtDNA-cn did not differ between groups (p > 0.4). In preliminary analyses, we found that changes in ccf-mtDNA with SSRI treatment differed between SSRI responders and non-responders (F = 6.47, p = 0.02), with the non-responders showing an increase in ccf-mtDNA and responders not changing. Baseline ccf-mtDNA was positively correlated with GpX (r = 0.32, p = 0.001), and PBMC mtDNA correlated positively with PBMC TL (r = 0.38, p = 0.0001). These data suggest that plasma ccf-mtDNA and PBMC mtDNA-cn reflect different cellular processes and that the former may be more reflective of certain aspects of MDD pathophysiology and of the response to SSRI antidepressants.

ObjectiveWe examined effects of daily rumination and suppression in response to stressors on objective and subjective sleep among mothers.DesignParticipants were 183 mothers, including chronically stressed mothers of children with an autism spectrum disorder (M-ASD; n=92) and age-matched mothers of neurotypical children (M-NT; n=91). In an intensive longitudinal design, participants provided reports of daily rumination and suppression, nightly objective actigraphy-defined sleep and nightly subjective sleep quality for seven consecutive days at baseline, 9months and 18months.Main outcome measuresTotal sleep time, sleep fragmentation, sleep onset latency, and subjective sleep quality.ResultsAmong M-NT with above average depressive symptoms, higher daily rumination was associated with shorter total sleep time. Rumination was associated with more sleep fragmentation among M-NT at the trend level. Rumination was not associated with sleep onset latency among M-NT, or with any sleep outcomes among M-ASD. Suppression was not associated with any sleep outcomes.ConclusionWe provide novel evidence of the effect of rumination on objectively measured sleep duration among M-NT. Coping was not related to sleep among M-ASD. Given the prevalence of poor sleep among mothers, future work should examine modifiable factors perpetuating sleep disturbance.

Background: Metabolic syndrome (MetS) is thought to promote biological aging, which might lead to cardiovascular and aging-related complications. This large-scale study investigated longitudinal relationships between MetS, its components, and cellular aging markers: leukocyte mitochondrial DNA copy number (mtDNAcn) and telomere length (TL). Methods: We included 989 participants from the Coronary Artery Risk Development in Young Adults Study. MtDNAcn [study year (Y) 15, Y25] and TL (Y15, Y20, Y25) were measured via quantitative polymerase chain reaction. MetS components [waist circumference, triglycerides, high-density lipoprotein (HDL) cholesterol, systolic blood pressure, and fasting glucose] were determined (Y15, Y20, Y25). Generalized estimated equation and linear regression models, adjusting for sociodemographics and lifestyle, were used to examine associations between MetS and cellular aging at all time points, baseline MetS and 10-year changes in cellular aging, baseline cellular aging and 10-year changes in MetS, and 10-year changes in MetS and 10-year changes in cellular aging. Results: MtDNAcn and TL were negatively associated with age [mtDNAcn unstandardized β (B) = 24.76; P < 0.001; TL B = -51.53; P < 0.001] and positively correlated (r = 0.152; P < 0.001). High triglycerides were associated with low mtDNAcn and low HDL cholesterol with short TL. Greater Y15 waist circumference (B = -7.23; P = 0.05), glucose (B = 013.29; P = 0.001), number of metabolic dysregulations (B = -7.72; P = 0.02), and MetS (B = -28.86; P = 0.006) predicted greater 10-year decrease in mtDNAcn but not TL. The 10-year increase in waist circumference was associated with 10-year telomere attrition (B = -27.61; P = 0.04). Conclusions: Our longitudinal data showed that some metabolic dysregulations were associated with mtDNAcn and TL decreases, possibly contributing to accelerated cellular aging but not the converse.

Telomeres are the protective end-complexes at the termini of eukaryotic chromosomes. Telomere attrition can lead to potentially maladaptive cellular changes, block cell division, and interfere with tissue replenishment. Recent advances in the understanding of human disease processes have clarified the roles of telomere biology, especially in diseases of human aging and in some aging-related processes. Greater overall telomere attrition predicts mortality and aging-related diseases in inherited telomere syndrome patients, and also in general human cohorts. However, genetically caused variations in telomere maintenance either raise or lower risks and progression of cancers, in a highly cancer type–specific fashion. Telomere maintenance is determined by genetic factors and is also cumulatively shaped by nongenetic influences throughout human life; both can interact. These and other recent findings highlight both causal and potentiating roles for telomere attrition in human diseases.

We used a Stress and Coping model to examine the association of dispositional mindfulness, defined as the tendency to intentionally bring nonjudgmental attention and awareness to one’s experience in the present moment, with psychological and physical health in adults with HIV. Data were collected at baseline of a randomized controlled trial of Mindfulness-Based Stress Reduction (MBSR). Four facets of mindfulness (acting with attention/awareness, nonjudging of inner experience, observing, and describing) were examined as correlates of appraisal, positive and negative affect, coping, and indicators of psychological well-being and physical health. We found that mindfulness was inversely related to depression, stress appraisal, and negative affect, and positively related to positive affect. Mindfulness was also inversely related to escape/avoidance and self-blame forms of coping. Mediational analyses indicate that perceived stress and negative affect were the most consistent mediators of the association of mindfulness and psychological well-being. The findings from this paper contribute to a growing understanding of the potential adaptive role of mindfulness in people living with the stress of serious illness.

Telomeres are the protective caps at the ends of eukaryotic chromosomes. Each time a somatic cell divides, a portion of the telomeric DNA fails to replicate; thus, telomeres naturally shorten with mitosis.1,2 Telomerase, the cellular enzyme that can counteract shortening by elongating and protecting telomeres, is kept at low levels in normal human cells.3 When telomeres become too short, cells lose the ability to grow and divide.4,5 Human genetic mutations that result in short telomeres are associated with a group of conditions collectively called “telomere syndromes” that resemble premature onset of diseases of aging, 6 consistent with a role of telomere shortening in human aging in the general population.7 Recent studies have found that shorter leukocyte telomere length is associated with numerous age-related diseases, including cardiovascular disease,8–11 type 2 diabetes,12,13 dementia,14–16 and cancer,17,18 independent of chronological age. While a number of studies have also reported that shorter telomeres are associated with increased mortality,17,19–30 others have failed to find an association between telomere length and survival 31–34 (see the appendix for a summary of findings). In general, studies that have not found an association between telomere length and mortality have examined older populations. Inconsistencies in the literature may be due to differences in sample size and measurement techniques, the use of population versus clinical samples, or unknown biologic differences between those who survive to extreme old age and those with earlier mortality.35,36 Using data from the National Health and Nutrition Examination Survey (NHANES) 1999–2002, the current study examined the association between leukocyte telomere length and mortality in a large, nationally representative, socioeconomically and ethnically diverse sample of US adults. This study addressed the following research questions: (1) Is telomere length associated with all-cause mortality in adults aged 50–84? (2) Is telomere length associated with cause-specific mortality? (3) Do associations between telomere length and mortality vary according to age, sex, race/ethnicity, or socioeconomic status (SES)? Although prior research has shown that older age, male sex, white race, and low SES are associated with shorter telomere length,37,38 it is not known whether the relationship between telomere length and mortality differs according to sociodemographic characteristics. Answering this question could help determine whether telomere length is a comparable indicator of mortality risk across population subgroups.

Residents of distressed urban areas suffer early aging-related disease and excess mortality. Using a community-based participatory research approach in a collaboration between social researchers and cellular biologists, we collected a unique data set of 239 black, white, or Mexican adults from a stratified, multistage probability sample of three Detroit neighborhoods. We drew venous blood and measured telomere length (TL), an indicator of stress-mediated biological aging, linking respondents’ TL to their community survey responses. We regressed TL on socioeconomic, psychosocial, neighborhood, and behavioral stressors, hypothesizing and finding an interaction between poverty and racial-ethnic group. Poor whites had shorter TL than nonpoor whites; poor and nonpoor blacks had equivalent TL; and poor Mexicans had longer TL than nonpoor Mexicans. Findings suggest unobserved heterogeneity bias is an important threat to the validity of estimates of TL differences by race-ethnicity. They point to health impacts of social identity as contingent, the products of structurally rooted biopsychosocial processes.

Background: Food insecurity is associated with adverse mental health outcomes. Given that federal food assistance programs, such as the Supplemental Nutrition Assistance Program (SNAP), aim to alleviate food insecurity, there may be heterogeneity in the association between food insecurity and depression by SNAP participation status. Objective: With the use of data from the 2005–2010 NHANES, we examined the associations between household food security and depression and whether these differed by SNAP participation. Methods: The study population was restricted to 3518 adults with household incomes #130% of the federal poverty level. Food insecurity was assessed with the 18-item US Household Food Security Survey Module; a score of $3 was considered food insecure. Depression was assessed with the 9-item Patient Health Questionnaire and was defined as a score of $10. Multivariate logistic regression models examined the associations between food insecurity and depression, adjusting for sociodemographic and health characteristics. Results:The overall prevalence of depression was 9.3%, ranging from 6.7% among SNAP nonparticipants to 12.8% among SNAP participants. For every depressive symptom, there was a dose-response relation, such that a higher prevalence was observed with worsening food insecurity. After multivariate adjustment, food insecurity was positively associated with depression (P-trend < 0.0001), but SNAP participation modified this relation (P-interaction = 0.03). Among low-income, eligible nonparticipants, very low food security was significantly associated with higher odds of depression (OR: 5.10; 95% CI: 3.09, 8.41). Among SNAP participants, very low food security was also associated with higher odds of depression but at a lower magnitude (OR: 2.21; 95% CI: 1.54, 3.17). Conclusion: The complex relation between food insecurity and mental health may vary on the basis of SNAP participation status. Programmatic efforts to address the risk of depression among their beneficiaries may positively affect the mental health of low-income adults. J Nutr doi: 10.3945/jn.114.199414.

Telomere biology plays a fundamental role in genomic integrity, cellular regeneration, physiology, aging, disease risk, and mortality. The initial setting of telomere length (TL) in early life has important implications for telomere maintenance and related disorders throughout the life span. However, little is known about the predictors of this initial setting.Given the established role of estrogen on adult TL and the role of estriol (E3) in the context of fetal development, the goal of this study was to test the hypothesis that higher maternal E3 concentration during early pregnancy is associated with longer infant telomere length.Study participants comprised a cohort of N = 100 infants followed prospectively from intrauterine life and birth through early childhood from a population-based, representative sample of pregnant mothers recruited in early pregnancy at university-based obstetric clinics in Southern California. Maternal unconjugated E3 concentrations were assessed in plasma in early gestation (around wk 15). Infant TL was assessed in buccal cells at approximately 15 months of age.After accounting for the effects of potential confounding maternal and infant variables, there was a significant, independent effect of maternal E3 concentration on infant TL (unstandardized β = 0.297; P = .001; 95% Cl, 0.121-0.473). Specifically, a one-multiple-of-the-median (MoM) increase in maternal E3 concentration during early pregnancy was associated with a 14.42% increase in infant TL.This study supports the concept of developmental plasticity of the telomere biology system and highlights specifically the role of a potentially modifiable intrauterine factor for additional mechanistic and clinical investigation.

Many psychiatric illnesses are associated with early mortality and with an increased risk of developing physical diseases that are more typically seen in the elderly. Moreover, certain psychiatric illnesses may be associated with accelerated cellular aging, evidenced by shortened leukocyte telomere length (LTL), which could underlie this association. Shortened LTL reflects a cell's mitotic history and cumulative exposure to inflammation and oxidation as well as the availability of telomerase, a telomere-lengthening enzyme. Critically short telomeres can cause cells to undergo senescence, apoptosis or genomic instability, and shorter LTL correlates with poorer health and predicts mortality. Emerging data suggest that LTL may be reduced in certain psychiatric illnesses, perhaps in proportion to exposure to the psychiatric illnesses, although conflicting data exist. Telomerase has been less well characterized in psychiatric illnesses, but a role in depression and in antidepressant and neurotrophic effects has been suggested by preclinical and clinical studies. In this article, studies on LTL and telomerase activity in psychiatric illnesses are critically reviewed, potential mediators are discussed, and future directions are suggested. A deeper understanding of cellular aging in psychiatric illnesses could lead to re-conceptualizing them as systemic illnesses with manifestations inside and outside the brain and could identify new treatment targets.

We examined the prospective associations of objective and subjective measures of stress during pregnancy with infant stress reactivity and regulation, an early-life predictor of psychopathology. In a racially and ethnically diverse low-income sample of 151 mother–infant dyads, maternal reports of stressful life events (SLE) and perceived stress (PS) were collected serially over gestation and the early postpartum period. Infant reactivity and regulation at 6 months of age was assessed via maternal report of temperament (negativity, surgency, and regulation) and infant parasympathetic nervous system physiology (respiratory sinus arrhythmia [RSA]) during the Still Face Paradigm. Regression models predicting infant temperament showed higher maternal prenatal PS predicted lower surgency and self-regulation but not negativity. Regression models predicting infant physiology showed higher numbers of SLE during gestation predicted greater RSA reactivity and weaker recovery. Tests of interactions revealed SLE predicted RSA reactivity only at moderate to high levels of PS. Thus, findings suggest objective and subjective measures of maternal prenatal stress uniquely predict infant behavior and physiology, adjusting for key pre- and postnatal covariates, and advance the limited evidence for such prenatal programming within high-risk populations. Assessing multiple levels of maternal stress and offspring stress reactivity and regulation provides a richer picture of intergenerational transmission of adversity.

© 2017 Elsevier B.V. Background Oxidative stress is implicated in both depression and anxiety, but it is currently unclear whether this relates to syndromal diagnoses or trans-diagnostic dimensional symptoms. We examined the relationship between oxidative stress and severity of depression and anxiety symptoms in individuals with Major Depressive Disorder (MDD). Methods Plasma oxidative stress markers F2-isoprostanes and oxidized glutathione (GSSG), and the antioxidant reduced glutathione (GSH), were assessed in 69 physically healthy, medication-free MDD subjects. Symptoms of anxiety and depression were assessed using the Hamilton Anxiety (HAM-A) and Hamilton Depression (HAM-D) Rating Scales. Total HAM-A and HAM-D scores, along with “core” anxiety and depression subscales, and individual HAM-D items “psychic anxiety” and “depressed mood,” were related to oxidative stress markers. Analyses controlled for age, sex, BMI, and smoking. Results Total HAM-A ratings were positively associated with F2-isoprostanes (β=.26, p=.042) and GSSG (β=.25, p=.049), but not GSH (β=.05, p=.711). Core anxiety severity was positively associated with F2-isoprostanes (β=.34, p=.012) and GSSG, although this did not reach significance (β=.24, p=.074). None of the biological markers were significantly associated with total HAM-D or core depression ratings (all p>.13). Subjects scoring high on “psychic anxiety” had elevated F2-isoprostanes (p=.030) and GSSG (p=.020). This was not seen with “depressed mood” scores (all p>.12). Limitations We assessed peripheral oxidative markers, but their relationship to the brain is unclear. Conclusions Oxidative stress is more closely related to anxiety than depression symptoms in MDD. This highlights the importance of relating oxidative stress to specific symptoms and could provide new insights into the biological correlates of affective disorders.

The aim of this study was to examine whether baseline chronic stress and impulsive risk-taking synergistically predict changes in visceral fat among healthy mothers in an observational, longitudinal, 18-month study.A prospective cohort of 113 adult women (age, mean ± SD: 42.83 ± 4.70; BMI, mean ± SD: 24.86 ± 4.32; 74%, n = 84 white) completed assessments at baseline and 18-month follow-up. Chronically stressed mothers caring for a child with an autism spectrum disorder ("caregivers"; n = 72 participants) were compared with lower stress mothers caring for a neurotypical child ("controls"; n = 41). This study objectively assessed impulsive risk-taking by using the Behavioral Analog Risk Task at baseline and assessed visceral fat at baseline and 18-month follow-up by using bioelectrical impedance (ViScan; Tanita Corporation, Tokyo, Japan).The interaction of baseline chronic caregiving stress and impulsive risk-taking predicted an 18-month change in visceral fat, such that greater impulsive risk-taking was associated with greater 18-month increases in visceral fat among caregivers (ß = 0.423; P = 0.005) but not among controls (ß = -0.030; P = 0.802), both in unadjusted models and after accounting for covariates. Neither chronic stress nor impulsive risk-taking independently predicted 18-month changes in visceral fat.The combination of high chronic stress and high impulsive risk-taking may increase risk for visceral fat gain over time and therefore may be an important intervention target in obesity prevention.

High-quality relationships have been shown to be beneficial for physical and mental health. This study examined overall relationship satisfaction and perceived stress as well as daily reports of partner support, partner conflict, and physical intimacy obtained over the course of one week in a sample of 129 high and low stress mothers. Telomere length was examined in whole blood, as well as the two cell subpopulations: peripheral blood mononuclear cells (PBMCs) and granulocytes. Telomerase activity was measured in PBMCs. Analyses revealed no statistically significant associations of telomere length with current relationship satisfaction, daily support or conflict, or perceived stress. In contrast, women who reported any sexual intimacy during the course of the week had significantly longer telomeres measured in whole blood and PBMCs, but not in granulocytes. These relationships held covarying for age, body mass index, perceived stress, the relationship indices, and caregiver status. Sexual intimacy was not significantly related to PBMC telomerase activity. These data provide preliminary data that sexual intimacy is associated with longer telomere length. Future studies investigating these associations are warranted.

Leukocyte telomere length is shorter in response to chronic disease processes associated with inflammation such as diabetes mellitus and coronary artery disease. Data from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2002 was used to explore the relationship between leukocyte telomere length and presumed NAFLD, as indicated by elevated serum alanine aminotransferase (ALT) levels, obesity, or abdominal obesity. Logistic regression models were used to evaluate the relationship between telomere length and presumed markers of NAFLD adjusting for possible confounders. There was no relationship between elevated ALT levels, abdominal obesity, or obesity and telomere length in adjusted models in NHANES (OR 1.13, 95% CI 0.48–2.65; OR 1.17, 95% CI 0.52–2.62, resp.). Mexican-American men had shorter telomere length in relation to presumed NAFLD (OR 0.07, 95% CI 0.006–0.79) and using different indicators of NAFLD (OR 0.012, 95% CI 0.0006–0.24). Mexican origin with presumed NAFLD had shorter telomere length than men in other population groups. Longitudinal studies are necessary to evaluate the role of telomere length as a potential predictor to assess pathogenesis of NALFD in Mexicans.

© Copyright 2017, Mary Ann Liebert, Inc. 2017. Background and Objective: Sleep disturbance is a common problem among adults with obesity. Mindfulness interventions have been shown to improve sleep quality in various populations but have not been investigated in adults with obesity. The aim of this study was to compare the effects of a mindfulness-based weight-loss intervention with an active control on self-reported sleep quality among adults with obesity. Method: This study was a secondary analysis of a randomized controlled trial and included 194 adults with a body mass index in the range 30-45 kg/m2. The treatment intervention included mindfulness-based eating and stress-management practices, and the active control intervention included training in progressive muscle relaxation (PMR). Both groups received identical diet and exercise guidelines in 17 group sessions conducted over 5.5 months that were matched for time, attention, and social support. The primary outcome of this analysis was between-group change in self-reported sleep quality, which was assessed using the Pittsburgh Sleep Quality Index (PSQI) global score at baseline and at 6, 12, and 18 months. Results: Between-group differences in mean PSQI change scores in the mindfulness group (n = 100) compared to the control group (n = 94) were -0.27 (-0.68, 1.22; p = 0.58) at 6 months, -0.57 (-0.35, 1.50; p = 0.22) at 12 months, and -0.50 (-0.53, 1.53; p = 0.34) at 18 months, all in the direction of more sleep improvement in the mindfulness group but none reaching statistical significance. In the mindfulness group, average weekly minutes of meditation practice time was associated with improved sleep quality from baseline to 6 months. Conclusions: No statistically significant evidence was found that a weight-loss program that incorporates mindfulness improves self-reported sleep quality compared to a control diet/exercise intervention that included PMR. Within the mindfulness group, average weekly minutes of mindfulness practice was associated with improved sleep quality.

African American men in the USA experience poorer aging-related health outcomes compared to their White counterparts, partially due to socioeconomic disparities along racial lines. Greater exposure to socioeconomic strains among African American men may adversely impact health and aging at the cellular level, as indexed by shorter leukocyte telomere length (LTL). This study examined associations between socioeconomic factors and LTL among African American men in midlife, a life course stage when heterogeneity in both health and socioeconomic status are particularly pronounced. Using multinomial logistic regression, we examined associations between multiple measures of SES and tertiles of LTL in a sample of 92 African American men between 30 to 50 years of age. Reports of greater financial strain were associated with higher odds of short versus medium LTL (odds ratio (OR)=2.21, p = 0.03). Higher income was associated with lower odds of short versus medium telomeres (OR=0.97, p = 0.04). Exploratory analyses revealed a significant interaction between educational attainment and employment status (χ 2 = 4.07, p = 0.04), with greater education associated with lower odds of short versus long telomeres only among those not employed (OR=0.10, p = 0.040). Cellular aging associated with multiple dimensions of socioeconomic adversity may contribute to poor aging-related health outcomes among African American men. Subjective appraisal of financial difficulty may impact LTL independently of objective dimensions of SES. Self-appraised success in fulfilling traditionally masculine gender roles, including being an economic provider, may be a particularly salient aspect of identity for African American men and have implications for cellular aging in this population.

OBJECTIVE/BACKGROUND: Poor sleep quality is common in pregnancy and associated with increased psychological distress, which has adverse consequences for families. Emerging theory suggests that mindfulness-based interventions may help reduce cognitive and emotional reactivity to stressful events. The current study examines the effects of a mindfulness-based intervention on the relationship between poor sleep quality and increased depression symptom severity and perceived stress during pregnancy. Additionally, we explored the prevalence of poor sleep quality in this unique sample and the impact of intervention on sleep quality. PARTICIPANTS: Participants were 215 ethnically diverse, overweight and obese, predominantly low-income pregnant women drawn from a study examining the impact of an 8-week mindfulness-based program (Mindful Moms Training; MMT) to reduce excessive gestational weight gain, stress, and depression compared to treatment as usual (TAU). METHODS: Participants reported global sleep quality, depressive symptoms, and perceived stress at baseline and post-intervention. RESULTS: Most participants (63%) were categorized as poor sleepers at baseline. MMT participants did not experience significantly greater improvement in sleep quality compared to TAU participants. Baseline poor global sleep quality predicted increased depression symptom severity for all participants. Baseline poor global sleep quality predicted increased perceived stress for the TAU group only; this association was not evident in the MMT group. CONCLUSIONS: Poor sleep quality is prevalent in overweight and obese predominantly low-income pregnant women. Poor sleep quality was associated with worsening psychological distress, but mindfulness training significantly attenuated the influence of poor sleep on perceived stress.

Introduction.Preliminary investigations of cross-sectional samples have linked trait mindfulness with measures related to the hypothalamic–pituitary–adrenal (HPA)-mediated stress response and to the inflammatory system, suggesting that this is one potential pathway linking mindfulness based interventions and health. However, no previous studies explored the association between the trait mindfulness construct and markers of cellular ageing.Methods.In the current study we examined in a sample of healthy mothers (n = 92) of a child with Autism Spectrum Disorder (i.e. women showing high levels of chronic psychological stress) the prospective associations between a multidimensional scale of trait mindfulness, the Five Facet Mindfulness Questionnaire (FFMQ), and telomerase activity (TA), a marker of cellular ageing and telomere homeostasis. Participants’ trait mindfulness and TA were assessed at baseline as well as 9 and 18 month follow-up.Results.Analysis showed that higher levels of baseline mindfulness on FFMQ observation and describe subscales were related to increase in TA from baseline to 9 month (r = 0.27, P = 0.03 and r = 0.24, P = .04, respectively). Additionally, the FFMQ Describe subscale was related to increase in TA from baseline to 18 month (r = .30, P = .02). Results are reported following covariate adjustment of age, BMI, ethnicity, and education.Discussion.Our results showed that higher levels of baseline mindfulness are associated with higher increases in TA after 9 months and 18 months, with increased TA reportedly being associated with decreased oxidative damage, increased telomere length and overall more functional cellular physiology. These findings support a role of mindfulness-related interventions to increase general and mental health.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Cadmium and lead are ubiquitous environmental contaminants that might increase risks of cardiovascular disease and other aging-related diseases, but their relationships with leukocyte telomere length (LTL), a marker of cellular aging, are poorly understood. In experimental studies, they have been shown to induce telomere shortening, but no epidemiologic study to date has examined their associations with LTL in the general population. We examined associations of blood lead and cadmium (n = 6,796) and urine cadmium (n = 2,093) levels with LTL among a nationally representative sample of US adults from the National Health and Nutrition Examination Survey (1999-2002). The study population geometric mean concentrations were 1.67 µg/dL (95% confidence interval (CI): 1.63, 1.70) for blood lead, 0.44 µg/L (95% CI: 0.42, 0.47) for blood cadmium, and 0.28 µg/L (95% CI: 0.27, 0.30) for urine cadmium. After adjustment for potential confounders, the highest (versus lowest) quartiles of blood and urine cadmium were associated with -5.54% (95% CI: -8.70, -2.37) and -4.50% (95% CI: -8.79, -0.20) shorter LTLs, respectively, with evidence of dose-response relationship (P for trend < 0.05). There was no association between blood lead concentration and LTL. These findings provide further evidence of physiological impacts of cadmium at environmental levels and might provide insight into biological pathways underlying cadmium toxicity and chronic disease risks.

Several psychiatric disorders, including major depressive disorder (MDD), are associated with increased blood markers of oxidative stress. The relevance of this to the oxidation-sensitive hippocampus (HC) is unknown. We investigated the relationship between peripheral oxidative stress markers and HC volume in unmedicated individuals with MDD (n=16) and healthy controls (n=19). To conserve power, our primary analysis was carried out in the combined group of subjects, and secondary analyses examined each group separately. Oxidative stress markers (oxidized glutathione (GSSG)) and antioxidants (reduced glutathione (GSH), glutathione peroxidase (Gpx), and Vitamin C) were assessed, and a "total net antioxidant score" was calculated. 4-T MRI estimated total HC volume and HC subfield (CA1, CA1-CA2 transition zone, subiculum and CA3/dentate gyrus [CA3&DG]) volumes. Across groups, the antioxidant score was significantly and positively correlated with total HC volume and CA3&DG subfield volume (normalized to total intracranial volume), adjusting for age and sex. Similar relationships were observed in each individual group but missed statistical significance, likely due to type II errors, with the exception of a significant correlation between the antioxidant score and CA3&DG volume in the MDD group. These preliminary data are consistent with oxidative stress being associated with smaller total HC and CA3&DG subfield volumes.

Mammalian aging can be delayed with genetic, dietary, and pharmacologic approaches. Given that the elderly population is dramatically increasing and that aging is the greatest risk factor for a majority of chronic diseases driving both morbidity and mortality, it is critical to expand geroscience research directed at extending human healthspan.

Telomere length has been hypothesized to be a marker of cumulative exposure to stress, and stress is an established cause of depression and anxiety disorders. The goal of this study was to examine the relationship between depression, anxiety and telomere length, and to assess whether this relationship is moderated by race/ethnicity, gender, and/or antidepressant use. Data were from the National Health and Nutrition Examination Survey, 1999–2002. Telomere length was assessed using the quantitative polymerase chain reaction method of telomere length relative to standard reference DNA. Past year major depression (MD), generalized anxiety disorder (GAD) and panic disorder (PD), as well as depressed affect and anxious affect, were assessed using the Composite International Diagnostic Inventory (N=1,290). Multiple linear regression was used to assess the relationship between depression and anxiety disorders and telomere length. Among women, those with GAD or PD had shorter telomeres than those with no anxious affect (β: −0.07, p0.05). Among respondents currently taking an antidepressant, those with MD had shorter telomeres than those without (β: −.26, p.05). Neither depressive nor anxiety disorders were directly associated with telomere length in young adults. There was suggestive evidence that pharmacologically-treated MD is associated with shorter telomere length, likely reflecting the more severe nature of MD that has come to clinical attention.

To combat the obesity epidemic, interventions and treatments often recommend low-calorie dieting. Calorie restriction (CR) as a weight intervention, however, is often unsuccessful, as most people cannot sustain the behavior. Yet one small group has maintained extreme CR over years - members of the CR Society and followers of The CR Way. This study examined stable psychosocial characteristics of these individuals to identify traits that may promote success at long-term CR. In 65 participants, we measured diet, eating behaviors, and personality traits comparing calorie restrictors with two age-, gender-, ethnicity-, and education-matched comparison groups (normal weight and overweight/obese). We first tested whether the CR group restricted calories without indications of eating disorder pathology, and second, what crystallized psychosocial characteristics set them apart from their nonrestricting comparisons. Results indicated the CR group averaged 10 years of CR but scored lower than comparison groups on measures of disordered eating (p < .001) and psychopathology (p < .001). Particularly against overweight/obese participants, CR participants scored lower on neuroticism (p < .04) and hostility (p < .01), and were stronger in future time orientation (p < .05). Overall, CR profiles reflected high self-control and well being, except for having few close relationships. This study suggests a potential predisposition for successful long-term CR without disordered eating. Since modifying trait factors may be unrealistic, there may be psychosocial boundaries to the capacity for sustaining CR. Paralleling a movement toward personalized medicine, this study points toward a personalized behavioral medicine model in behavioral nutrition and treatment of overweight/obesity.

Overweight and obese individuals differ in their degree of hedonic eating. This may reflect adaptations in reward-related neural circuits, regulated in part by opioidergic activity. We examined an indirect, functional measure of central opioidergic activity by assessing cortisol and nausea responses to acute opioid blockade using the opioid antagonist naltrexone in overweight/obese women (mean BMI=31.1±4.8) prior to the start of a mindfulness-based intervention to reduce stress eating. In addition, we assessed indices of hedonic-related eating, including eating behaviors (binge eating, emotional eating, external eating, restraint) and intake of sweets/desserts and carbohydrates (Block Food Frequency); interoceptive awareness (which is associated with dysregulated eating behavior); and level of adiposity at baseline. Naltrexone-induced increases in cortisol were associated with greater emotional and restrained eating and lower interoceptive awareness. Naltrexone-induced nausea was associated with binge eating and higher adiposity. Furthermore, in a small exploratory analysis, naltrexone-induced nausea predicted treatment response to the mindfulness intervention, as participants with more severe nausea at baseline maintained weight whereas those with little or no nausea responses tended to gain weight. These preliminary data suggest that naltrexone-induced cortisol release and nausea may help identify individuals who have greater underlying food reward dependence, which leads to an excessive drive to eat. Future research is needed to confirm this finding and to test if these markers of opioidergic tone might help predict success in certain types of weight management programs.

Author(s): Rehkopf, David H; Dow, William H; Rosero-Bixby, Luis; Lin, Jue; Epel, Elissa S; Blackburn, Elizabeth H | Abstract: ObjectivesPeripheral blood leukocyte telomere length (LTL) is increasingly being used as a biomarker of aging, but its natural variation in human populations is not well understood. Several other biomarkers show seasonal variation, as do several determinants of LTL. We examined whether there was monthly variation in LTL in Costa Rica, a country with strong seasonal differences in precipitation and infection.MethodsWe examined a longitudinal population-based cohort of 581 Costa Rican adults age 60 and above, from which blood samples were drawn between October 2006 and July 2008. LTL was assayed from these samples using the quantitative PCR method. Multivariate regression models were used to examine correlations between month of blood draw and LTL.ResultsTelomere length from peripheral blood leukocytes varied by as much as 200 base pairs depending on month of blood draw, and this difference is not likely to be due to random variation. A moderate proportion of this association is statistically accounted for by month and region specific average rainfall. We found shorter telomere length associated with greater rainfall.ConclusionsThere are two possible explanations of our findings. First, there could be relatively rapid month-to-month changes in LTL. This conclusion would have implications for understanding the natural population dynamics of telomere length. Second, there could be seasonal differences in constituent cell populations. This conclusion would suggest that future studies of LTL use methods to account for the potential impact of constituent cell type.

Background Leukocyte telomere length (LTL) is an indicator of general systemic aging, with shorter LTL being associated with several chronic diseases of aging and earlier mortality. Identifying factors related to LTL among African Americans may yield insights into mechanisms underlying racial disparities in health. Purpose To test whether the combination of more frequent reports of racial discrimination and holding a greater implicit anti-black racial bias is associated with shorter LTL among African-American men. Methods Cross-sectional study of a community sample of 92 African-American men aged between 30 and 50 years. Participants were recruited from February to May 2010. Ordinary least squares regressions were used to examine LTL in kilobase pairs in relation to racial discrimination and implicit racial bias. Data analysis was completed in July 2013. Results After controlling for chronologic age and socioeconomic and health-related characteristics, the interaction between racial discrimination and implicit racial bias was significantly associated with LTL (b=−0.10, SE=0.04, p =0.02). Those demonstrating a stronger implicit anti-black bias and reporting higher levels of racial discrimination had the shortest LTL. Household income-to-poverty threshold ratio was also associated with LTL (b=0.05, SE=0.02, p Conclusions Results suggest that multiple levels of racism, including interpersonal experiences of racial discrimination and the internalization of negative racial bias, operate jointly to accelerate biological aging among African-American men. Societal efforts to address racial discrimination in concert with efforts to promote positive in-group racial attitudes may protect against premature biological aging in this population.

Sleep disturbance is a key behavioral risk factor for chronic medical conditions observed at high rates among overweight and obese individuals. Systemic inflammation, including that induced by stress, may serve as a common biological mechanism linking sleep, adiposity, and disease risk. To investigate these relationships, 48 postmenopausal women (mean age=61.8) completed a standardized laboratory stress task during which time blood was collected at baseline and 30+, 50+ and 90+ minutes after stressor onset to assess circulating levels of interleukin (IL)-6, IL-10, and IL-6/IL-10 ratio. Self-reported global sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI) while adiposity was estimated by body mass index. Sagittal diameter was obtained in clinic to estimate visceral abdominal adiposity. Multi-level growth curve models revealed that poorer self-reported sleep quality was associated with greater stress-induced increases in IL-6/IL-10 ratio. In terms of adiposity, higher sagittal diameter, but not BMI, was associated with greater IL-6 reactivity (p’s

Background: Mitochondrial DNA copy number (mtDNA-cn), which represents the number of mitochondrial genomes per cell, can be quantified in peripheral blood mononuclear cells (PBMC) and is thought to ...

Key Points Question Is naturally occurring short-term change in leukocyte telomere length related to structural plasticity of the brain, and can telomere length be influenced through mental training? Findings In this randomized clinical trial of 298 healthy adults, the mental training intervention did not affect leukocyte telomere length. Naturally occurring change in leukocyte telomere length over 3 consecutive 3-month intervals was significantly associated with cortical thickness change in the left precuneus extending to the posterior cingulate cortex. Meaning This study provides the first evidence to date for an association between short-term change in leukocyte telomere length and brain structure, suggesting that these processes may be mechanistically linked; the mental training used did not influence leukocyte telomere length of healthy, middle-aged adults., Importance Telomere length is associated with the development of age-related diseases and structural differences in multiple brain regions. It remains unclear, however, whether change in telomere length is linked to brain structure change, and to what extent telomere length can be influenced through mental training. Objectives To assess the dynamic associations between leukocyte telomere length (LTL) and cortical thickness (CT), and to determine whether LTL is affected by a longitudinal contemplative mental training intervention. Design, Setting, and Participants An open-label efficacy trial of three 3-month mental training modules with healthy, meditation-naive adults was conducted. Data on LTL and CT were collected 4 times over 9 months between April 22, 2013, and March 31, 2015, as part of the ReSource Project. Data analysis was performed between September 23, 2016, and June 21, 2019. Of 1582 eligible individuals, 943 declined to participate; 362 were randomly selected for participation and assigned to training or retest control cohorts, with demographic characteristics matched. The retest control cohorts underwent all testing but no training. Intention-to-treat analysis was performed. Interventions Training cohort participants completed 3 modules cultivating interoception and attention (Presence), compassion (Affect), or perspective taking (Perspective). Main Outcomes and Measures Change in LTL and CT. Results Of the 362 individuals randomized, 30 participants dropped out before study initiation (initial sample, 332). Data were available for analysis of the training intervention in 298 participants (n = 222 training; n = 76 retest control) (175 women [58.7%]; mean [SD] age, 40.5 [9.3] years). The training modules had no effect on LTL. In 699 observations from all 298 participants, mean estimated changes in the relative ratios of telomere repeat copy number to single-copy gene (T/S) were for no training, 0.004 (95% CI, −0.010 to 0.018); Presence, −0.007 (95% CI, −0.025 to 0.011); Affect, −0.005 (95% CI, −0.019 to 0.010); and Perspective, −0.001 (95% CI, −0.017 to 0.016). Cortical thickness change data were analyzed in 167 observations from 67 retest control participants (37 women [55.2%], mean [SD] age, 39.6 [9.0] years). In this retest control cohort subsample, naturally occurring LTL change was related to CT change in the left precuneus extending to the posterior cingulate cortex (mean t161 = 3.22; P, This randomized clinical trial examines the effect of mental attention training on leukocyte telomere length and cortical thickness among healthy adults.

Background Diet patterns have a profound influence on glycemic control for individuals with type 2 diabetes mellitus (T2DM), and craving-related eating is an important obstacle to dietary adherence. A growing body of research suggests that carbohydrate-restricted (CR) diets can improve glycemic control and reduce medication dependence in T2DM. However, limited data speak to the effects of long-term adherence to CR diets. Mindful eating training has been shown to reduce craving-related eating in overweight populations but has yet to be examined as a behavioral support for dietary adherence in T2DM. This trial examines behavioral mechanisms, particularly craving-related eating, through which mindful eating training might improve adherence to CR dietary recommendations in T2DM. This will clarify the importance of focusing on craving-related eating in the optimization of dietary adherence interventions. Objective The aim of this trial is to determine whether providing training in mindful eating increases adherence to a CR dietary recommendation in T2DM. Methods We are randomizing 60 participants to receive a CR diet with or without mindful eating training (12-week group intervention) and are following participants for 12 weeks after intervention completion. We hypothesize that participants who receive mindful eating training (relative to those who do not) will demonstrate greater adherence to the CR diet. Results Our primary outcome is change in craving-related eating, as assessed using an ecological momentary assessment mobile phone–based platform. Secondary behavioral pathway outcomes include changes in stress-related eating, impulsivity, glycemic control, weight change, dietary adherence, and resumption of dietary adherence after dietary nonadherence. Conclusions This theory-driven trial will shed light on the impact of mindfulness training on mechanisms that may impact dietary adherence in T2DM. Trial Registration ClinicalTrials.gov NCT03207711; https://clinicaltrials.gov/ct2/show/NCT03207711 (Archived by WebCite at http://www.webcitation.org/73pXscwaU) International Registered Report Identifier (IRRID) DERR1-10.2196/11002

What can a speech reveal about someone's state? We tested the idea that greater stress reactivity would relate to lower linguistic cognitive complexity while speaking. In Study 1, we tested whether heart rate and emotional stress reactivity to a stressful discussion would relate to lower linguistic complexity. In Studies 2 and 3, we tested whether a greater cortisol response to a standardized stressful task including a speech (Trier Social Stress Test) would be linked to speaking with less linguistic complexity during the task. We found evidence that measures of stress responsivity (emotional and physiological) and chronic stress are tied to variability in the cognitive complexity of speech. Taken together, these results provide evidence that our individual experiences of stress or "stress signatures"-how our body and mind react to stress both in the moment and over the longer term-are linked to how complex our speech under stress.

BackgroundSocial connections moderate the effects of high negative affect on health. Affective states (anger, fear, and anxiety) predict interleukin-6 (IL-6) reactivity to acute stress; in turn, this reactivity predicts risk of cardiovascular disease progression.PurposeHere, we examined whether perceived social support mitigates the relationship between negative affect and IL-6 stress reactivity.MethodForty-eight postmenopausal women completed a standardized mental lab stressor with four blood draws at baseline and 30, 50, and 90 min after the onset of the stressor and anger, anxiety, and fear were assessed 10 min after task completion. Participants self-rated levels of social support within a week prior to the stressor.ResultsOnly anger was related to IL-6 stress reactivity-those experiencing high anger after the stressor had significant increases in IL-6. IL-6 reactivity was marginally associated with perceived support, but more strikingly, perceived support mitigated anger associations with IL-6 stress reactivity.ConclusionSupportive ties can dampen the relationship of anger to pro-inflammatory reactivity to acute stress. Implications to cardiovascular disease are discussed.

Low socioeconomic status (SES) during childhood and adolescence has been found to predict greater susceptibility to common cold viruses in adults. Here, we test whether low childhood SES is associated with shorter leukocyte telomere length in adulthood, and whether telomere length mediates the association between childhood SES and susceptibility to acute upper respiratory disease in adulthood. At baseline, 196 healthy volunteers reported whether they currently owned their home and, for each year of their childhood, whether their parents owned the family home. Volunteers also had blood drawn for assessment of specific antibody to the challenge virus, and for CD8+CD28− T-lymphocyte telomere length (in a subset, n = 135). They were subsequently quarantined in a hotel, exposed to a virus (rhinovirus [RV] 39) that causes a common cold and followed for infection and illness (clinical cold) over five post-exposure days. Lower childhood SES as measured by fewer years of parental home ownership was associated with shorter adult CD8+CD28− telomere length and with an increased probability of developing infection and clinical illness when exposed to a common cold virus in adulthood. These associations were independent of adult SES, age, sex, race, body mass, neuroticism, and childhood family characteristics. Associations with infections and colds were also independent of pre-challenge viral-specific antibody and season. Further analyses do not support mediating roles for smoking, alcohol consumption or physical activity but suggest that CD8+CD28− cell telomere length may act as a partial mediator of the associations between childhood SES and infection and childhood SES and colds.

Summary Background Telomere shortness in human beings is a prognostic marker of ageing, disease, and premature morbidity. We previously found an association between 3 months of comprehensive lifestyle changes and increased telomerase activity in human immune-system cells. We followed up participants to investigate long-term effects. Methods This follow-up study compared ten men and 25 external controls who had biopsy-proven low-risk prostate cancer and had chosen to undergo active surveillance. Eligible participants were enrolled between 2003 and 2007 from previous studies and selected according to the same criteria. Men in the intervention group followed a programme of comprehensive lifestyle changes (diet, activity, stress management, and social support), and the men in the control group underwent active surveillance alone. We took blood samples at 5 years and compared relative telomere length and telomerase enzymatic activity per viable cell with those at baseline, and assessed their relation to the degree of lifestyle changes. Findings Relative telomere length increased from baseline by a median of 0·06 telomere to single-copy gene ratio (T/S)units (IQR–0·05 to 0·11) in the lifestyle intervention group, but decreased in the control group (−0·03 T/S units, −0·05 to 0·03, difference p=0·03). When data from the two groups were combined, adherence to lifestyle changes was significantly associated with relative telomere length after adjustment for age and the length of follow-up (for each percentage point increase in lifestyle adherence score, T/S units increased by 0·07, 95% CI 0·02–0·12, p=0·005). At 5 years, telomerase activity had decreased from baseline by 0·25 (–2·25 to 2·23) units in the lifestyle intervention group, and by 1·08 (–3·25 to 1·86) units in the control group (p=0·64), and was not associated with adherence to lifestyle changes (relative risk 0·93, 95% CI 0·72–1·20, p=0·57). Interpretation Our comprehensive lifestyle intervention was associated with increases in relative telomere length after 5 years of follow-up, compared with controls, in this small pilot study. Larger randomised controlled trials are warranted to confirm this finding. Funding US Department of Defense, NIH/NCI, Furlotti Family Foundation, Bahna Foundation, DeJoria Foundation, Walton Family Foundation, Resnick Foundation, Greenbaum Foundation, Natwin Foundation, Safeway Foundation, Prostate Cancer Foundation.

Chronic psychological stress appears to accelerate biological aging, and oxidative damage is an important potential mediator of this process. However, the mechanisms by which psychological stress promotes oxidative damage are poorly understood. This study investigates the theory that cortisol increases in response to an acutely stressful event have the potential to either enhance or undermine psychobiological resilience to oxidative damage, depending on the body's prior exposure to chronic psychological stress. In order to achieve a range of chronic stress exposure, forty-eight post-menopausal women were recruited in a case-control design that matched women caring for spouses with dementia (a chronic stress model) with similarly aged control women whose spouses were healthy. Participants completed a questionnaire assessing perceived stress over the previous month and provided fasting blood. Three markers of oxidative damage were assessed: 8-iso-prostaglandin F(2α) (IsoP), lipid peroxidation, 8-hydroxyguanosine (8-oxoG) and 8-hydroxy-2'-deoxyguanosine (8-OHdG), reflecting oxidative damage to RNA/DNA respectively. Within approximately one week, participants completed a standardized acute laboratory stress task while salivary cortisol responses were measured. The increase from 0 to 30 min was defined as "peak" cortisol reactivity, while the increase from 0 to 15 min was defined as "anticipatory" cortisol reactivity, representing a cortisol response that began while preparing for the stress task. Women under chronic stress had higher 8-oxoG, oxidative damage to RNA (p

The present study investigated the relationship between posttraumatic stress disorder (PTSD) and emotional eating in a sample of medically healthy and medication-free adults. Participants with PTSD (n = 44) and control participants free of lifetime psychiatric history (n = 49) completed a measure of emotional eating. Emotional eating is the tendency to eat or overeat in response to negative emotions. PTSD participants exhibited greater emotional eating than control participants (η(2) = .20) and emotional eating increased with higher PTSD symptom severity (R(2) = .11). Results supported the stress-eating-obesity model whereby emotional eating is a maladaptive response to stressors. Over time, this could lead to weight gain, particularly abdominal stores, and contribute to higher risk for comorbid medical disorders. Findings suggest the importance of future longitudinal research to understand whether emotional eating contributes to the high rates of obesity, diabetes, and heart disease in PTSD.