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Telomeres are the DNA–protein complexes that protect the ends of eukaryotic chromosomes. The cellular enzyme telomerase counteracts telomere shortening by adding telomeric DNA. A growing body of literature links shorter telomere length and lower telomerase activity with various age-related diseases and earlier mortality. Thus, leukocyte telomere length (LTL) and telomerase activity are emerging both as biomarkers and contributing factors for age-related diseases. However, no clinical study has directly examined telomerase activity and telomere length in different lymphocyte subtypes isolated from the same donors, which could offer insight into the summary measure of leukocyte telomere maintenance. We report the first quantitative data in humans examining both levels of telomerase activity and telomere length in four lymphocyte subpopulations from the same donors—CD4+, CD8+CD28+ and CD8+CD28− T cells and B cells, as well as total PBMCs—in a cohort of healthy women. We found that B cells had the highest telomerase activity and longest telomere length; CD4+ T cells had slightly higher telomerase activity than CD8+CD28+ T cells, and similar telomere length. Consistent with earlier reports that CD8+CD28−T cells are replicatively senescent cells, they had the lowest telomerase activity and shortest telomere length. In addition, a higher percentage of CD8+CD28− T cells correlated with shorter total PBMC TL (r = −0.26, p = 0.05). Interestingly, telomerase activities of CD4+ and CD8+CD28+ T cells from the same individual were strongly correlated (r = 0.55, r < 0.001), indicating possible common mechanisms for telomerase activity regulation in these two cell subtypes. These data will facilitate the understanding of leukocyte aging and its relationship to human health.

After experiencing a stressful or traumatic event, many individuals report positive changes in their lives, or benefit finding. Preliminary evidence suggests that benefit finding may lead to improvements in physical health. However, the mechanisms linking benefit finding to physical health outcomes have not been determined. This article describes an integrative model that identifies specific psychological and physiological pathways through which benefit finding may affect physical health. The underlying premise of the model is that benefit finding leads to more adaptive, efficient responses to future stressors, limiting exposure to stress hormones that may have damaging effects on long-term health.

Elevated circulating levels of glucocorticoids are associated with psychiatric symptoms across several different conditions. It remains unknown if this hormonal abnormality is a cause or an effect of the psychiatric conditions. For example, the hypercortisolemia observed in a subset of patients with depression may have a direct impact on the symptoms of depression, but it is also possible that the hypercortisolemia merely reflects the stress associated with depression. Further, rather than causing depression, hypercortisolemia could represent a homeostatic attempt to overcome glucocorticoid resistance. Each of these possibilities will be considered, and correlational and causal evidence will be reviewed. This article will focus on the relationships between glucocorticoids and psychiatric symptoms in Cushing's syndrome, major depression, and steroid psychosis/steroid dementia, as well as the effects of exogenously administered glucocorticoids in normal volunteers. Similarities and differences in the relationship of glucocorticoid hormones to psychiatric symptoms in these conditions will be reviewed. Possible mediators of glucocorticoid effects on the brain and behavior, as well as possible "pro-aging" effects of glucocorticoids in certain cells of the body, will be reviewed. The article concludes with a conceptual model of glucocorticoid actions in the brain that may lead to novel therapeutic opportunities.

Understanding the malleable determinants of cellular aging is critical to understanding human longevity. Telomeres may provide a pathway for exploring this question. Telomeres are the protective caps at the ends of chromosomes. The length of telomeres offers insight into mitotic cell and possibly organismal longevity. Telomere length has now been linked to chronic stress exposure and depression. This raises the question of mechanism: How might cellular aging be modulated by psychological functioning? We consider two psychological processes or states that are in opposition to one another-threat cognition and mindfulness-and their effects on cellular aging. Psychological stress cognitions, particularly appraisals of threat and ruminative thoughts, can lead to prolonged states of reactivity. In contrast, mindfulness meditation techniques appear to shift cognitive appraisals from threat to challenge, decrease ruminative thought, and reduce stress arousal. Mindfulness may also directly increase positive arousal states. We review data linking telomere length to cognitive stress and stress arousal and present new data linking cognitive appraisal to telomere length. Given the pattern of associations revealed so far, we propose that some forms of meditation may have salutary effects on telomere length by reducing cognitive stress and stress arousal and increasing positive states of mind and hormonal factors that may promote telomere maintenance. Aspects of this model are currently being tested in ongoing trials of mindfulness meditation.

In order to more fully understand associations between psychological stress and health, it is helpful for researchers to identify “psychobiomarkers,” or biological measures that are regulated in part by psychological function and that predict longevity. Telomere length appears to be such a measure. Telomeres, the protective caps at the tips of chromosomes, shorten with age, and this shortening predicts disease and longevity. Leukocyte telomere length may be best viewed through a life-span approach, as it reflects in part the cumulative number of cell divisions that have occurred and the long-term biochemical environment. Recently, a critical mass of studies demonstrated that telomeres appear to shorten with chronic stress, although the mechanisms are unknown. This paper reviews what appear to be malleable determinants of rate of telomere attrition, focusing on early life chronic stressors and metabolic adversity (poor nutrition during development, and obesity). The next generation of research will benefit from experimental and longitudinal models integrating genetic variation, social environments, life experience, and health behaviors.

DHEA and DHEAS are steroids synthesized in human adrenals, but their function is unclear. In addition to adrenal synthesis, evidence also indicates that DHEA and DHEAS are synthesized in the brain, further suggesting a role of these hormones in brain function and development. Despite intensifying research into the biology of DHEA and DHEAS, many questions concerning their mechanisms of action and their potential involvement in neuropsychiatric illnesses remain unanswered. We review and distill the preclinical and clinical data on DHEA and DHEAS, focusing on (i) biological actions and putative mechanisms of action, (ii) differences in endogenous circulating concentrations in normal subjects and patients with neuropsychiatric diseases, and (iii) the therapeutic potential of DHEA in treating these conditions. Biological actions of DHEA and DHEAS include neuroprotection, neurite growth, and antagonistic effects on oxidants and glucocorticoids. Accumulating data suggest abnormal DHEA and/or DHEAS concentrations in several neuropsychiatric conditions. The evidence that DHEA and DHEAS may be fruitful targets for pharmacotherapy in some conditions is reviewed.

Telomere length (TL) has been proposed as a marker of mitotic cell age and as a general index of human organismic aging. Short absolute leukocyte telomere length has been linked to cardiovascular-related morbidity and mortality. Our aim was to test whether the rate of change in leukocyte TL is related to mortality in a healthy elderly cohort. We examined a subsample of 236 randomly selected Caucasian participants from the MacArthur Health Aging Study (aged 70 to 79 years). DNA samples from baseline and 2.5 years later were assayed for mean TL of leukocytes. Percent change in TL was calculated as a measure of TL change (TLC). Associations between TL and TLC with 12-year overall and cardiovascular mortality were assessed. Over the 2.5 year period, 46% of the study participants showed maintenance of mean bulk TL, whereas 30% showed telomere shortening, and, unexpectedly, 24% showed telomere lengthening. For women, short baseline TL was related to greater mortality from cardiovascular disease (OR = 2.3; 95% CI: 1.0 - 5.3). For men, TLC (specifically shortening), but not baseline TL, was related to greater cardiovascular mortality, OR = 3.0 (95% CI: 1.1 - 8.2). This is the first demonstration that rate of telomere length change (TLC) predicts mortality and thus may be a useful prognostic factor for longevity.

Summary Background Telomeres are protective DNA–protein complexes at the end of linear chromosomes that promote chromosomal stability. Telomere shortness in human beings is emerging as a prognostic marker of disease risk, progression, and premature mortality in many types of cancer, including breast, prostate, colorectal, bladder, head and neck, lung, and renal cell. Telomere shortening is counteracted by the cellular enzyme telomerase. Lifestyle factors known to promote cancer and cardiovascular disease might also adversely affect telomerase function. However, previous studies have not addressed whether improvements in nutrition and lifestyle are associated with increases in telomerase activity. We aimed to assess whether 3 months of intensive lifestyle changes increased telomerase activity in peripheral blood mononuclear cells (PBMC). Methods 30 men with biopsy-diagnosed low-risk prostate cancer were asked to make comprehensive lifestyle changes. The primary endpoint was telomerase enzymatic activity per viable cell, measured at baseline and after 3 months. 24 patients had sufficient PBMCs needed for longitudinal analysis. This study is registered on the ClinicalTrials.gov website, number NCT00739791. Findings PBMC telomerase activity expressed as natural logarithms increased from 2·00 (SD 0·44) to 2·22 (SD 0·49; p=0·031). Raw values of telomerase increased from 8·05 (SD 3·50) standard arbitrary units to 10·38 (SD 6·01) standard arbitrary units. The increases in telomerase activity were significantly associated with decreases in low-density lipoprotein (LDL) cholesterol ( r =−0·36, p=0·041) and decreases in psychological distress ( r =−0·35, p=0·047). Interpretation Comprehensive lifestyle changes significantly increase telomerase activity and consequently telomere maintenance capacity in human immune-system cells. Given this finding and the pilot nature of this study, we report these increases in telomerase activity as a significant association rather than inferring causation. Larger randomised controlled trials are warranted to confirm the findings of this study. Funding US Department of Defense (US Army Medical Research Acquisition Activity W81XWH-05-1-0375, Fort Detrick, Frederick, MD, USA); Henry M Jackson Foundation for the Advancement of Military Medicine (contract 56422; Rockville MD, USA) from the National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (grant number K01AT004199; Bethesda, MD, USA); Bahna Foundation (Stamford, CT, USA); DeJoria Foundation (Los Angeles, CA, USA); Kerzner Foundation (New York, NY, USA); Bernard Osher Foundation (San Francisco, CA, USA); Walton Family Foundation (Bentonville, AK, USA); Jeff Walker Family Foundation (Wilton, CT, USA); Safeway Foundation (Pleasanton, CA, USA).

Leukocyte telomere shortening can serve as a biomarker of aging, as telomere length (TL) can decline with age and shortening is positively associated with morbidity and mortality. It is therefore important to identify psychological and behavioral factors linked to accelerated telomere shortening. Stress and poorer metabolic health (greater adiposity, insulin resistance, and cortisol) correlate with shorter telomeres. Self-reported dietary restraint (DR), defined as chronic preoccupation with weight and attempts at restricting food intake, is linked to greater perceived stress, cortisol, and weight gain, when assessed in community studies (versus in weight loss programs).To test for an association between DR and TL in healthy women across a range of ages.We examined whether DR is linked to TL in two samples, one of premenopausal women (aged 20-50 years;N = 36) and one of postmenopausal women (aged 53-69 years; N = 20).In both samples, higher levels of DR were associated with shorter leukocyte TL, independent of body mass index, smoking, and age.Chronic DR, as assessed by self-report (i.e. not caloric restriction), may be a risk factor for premature telomere shortening. Potential mechanisms are discussed.

Objective To determine whether positive affect predicts mortality among people with diabetes and among a comparison group of people with no chronic health conditions. Design Longitudinal cohort study. Main outcome measure Mortality. Results Positive affect was significantly associated with lower risk of all-cause mortality in people with diabetes (N = 715). Enjoyed life was associated with lower risk of mortality over and above the effects of negative affect or other significant predictors of mortality. In a comparison sample without chronic illness (N = 2,673), positive affect was not associated with mortality. However, when the analysis was restricted to those over the age of 65, specific positive affects, in particular hopeful and enjoyed life were significantly associated with lower risk of mortality, again independent of negative affect. Enjoyed life remained significantly predictive of lower risk of mortality in the older sample when other predictors of mortality were statistically controlled. Positive affect was particularly protective among those over the age of 65 who reported higher levels of stress. Conclusion These findings are discussed in light of possible stress-buffering functions of positive affect.

Many individuals who undergo stressful life events report that they have derived some positive benefit from the experience. Although the majority of research on benefit finding has focused on its psychological correlates, there is intriguing evidence that benefit finding may also have effects on physical health. In this paper, we review the emerging literature on benefit finding and physical health and present an integrative model in which we identify specific psychological and physiological pathways through which benefit finding may influence physical health outcomes. In particular, we consider the hypothesis that benefit finding may involve changes in a number of psychological domains – namely, changes in appraisal and coping processes, relationships, goals and priorities, and positive affect – that lead to a state of enhanced allostasis, buffering against negative effects of catabolic stress responses and promoting activity in restorative physiological systems. Empirical evidence for this model is reviewed, focusing on studies that have examined positive psychological constructs relevant to benefit finding and their effects on stress reactivity, recovery, and habituation, as well as restorative processes.

Purpose Obese individuals vary in their experience of food cravings and tendency to engage in reward-driven eating, both of which can be modulated by the neural reward system rather than physiological hunger. We examined two predictions in a sample of obese women: (1) whether opioidergic blockade reduced food-craving intensity, and (2) whether opioidergic blockade reduced an association between food-craving intensity and reward-driven eating, which is a trait-like index of three factors (lack of control over eating, lack of satiation, preoccupation with food). Methods Forty-four obese, pre-menopausal women completed the Reward-Based Eating Drive (RED) scale at study start and daily food-craving intensity on 5 days on which they ingested either a pill-placebo (2 days), a 25 mg naltrexone dose (1 day), or a standard 50 mg naltrexone dose (2 days). Results Craving intensity was similar under naltrexone and placebo doses. The association between food-craving intensity and reward-driven eating significantly differed between placebo and 50 mg naltrexone doses. Reward-driven eating and craving intensity were significantly positively associated under both placebo doses. As predicted, opioidergic blockade (for both doses 25 mg and 50 mg naltrexone) reduced the positive association between reward-driven eating and craving intensity to non-significance. Conclusions Opioidergic blockade did not reduce craving intensity; however, blockade reduced an association between trait-like reward-driven eating and daily food-craving intensity, and may help identify an important endophenotype within obesity.

Background Although there is substantial evidence of differential hypothalamic-pituitary-adrenal (HPA) axis activity in both generalized and abdominal obesity, consistent trends in obesity-related HPA axis perturbations have yet to be identified. Objectives To systematically review the existing literature on HPA activity in obesity, identify possible explanations for inconsistencies in the literature, and suggest methodological improvements for future study. Data sources Included papers used Pubmed, Google Scholar, and the University of California Library search engines with search terms body mass index (BMI), waist-to-hip ratio (WHR), waist circumference, sagittal diameter, abdominal versus peripheral body fat distribution, body fat percentage, DEXA, abdominal obesity, and cortisol with terms awakening response, slope, total daily output, reactivity, feedback sensitivity, long-term output, and 11β-HSD expression. Study eligibility criteria Empirical research papers were eligible provided that they included at least one type of obesity (general or abdominal), measured at least one relevant cortisol parameter, and a priori tested for a relationship between obesity and cortisol. Results A general pattern of findings emerged where greater abdominal fat is associated with greater responsivity of the HPA axis, reflected in morning awakening and acute stress reactivity, but some studies did show underresponsiveness. When examined in adipocytes, there is a clear upregulation of cortisol output (due to greater expression of 11β-HSD1), but in hepatic tissue this cortisol is downregulated. Overall obesity (BMI) appears to also be related to a hyperresponsive HPA axis in many but not all studies, such as when acute reactivity is examined. Limitations The reviewed literature contains numerous inconsistencies and contradictions in research methodologies, sample characteristics, and results, which partially precluded the development of clear and reliable patterns of dysregulation in each investigated cortisol parameter. Conclusions and implications The literature to date is inconclusive, which may well arise from differential effects of generalized obesity vs. abdominal obesity or from modulators such as sex, sex hormones, and chronic stress. While the relationship between obesity and adipocyte cortisol seems to be clear, further research is warranted to understand how adipocyte cortisol metabolism influences circulating cortisol levels and to establish consistent patterns of perturbations in adrenal cortisol activity in both generalized and abdominal obesity.

Several studies have reported that adults with major depressive disorder have shorter telomere length and reduced hippocampal volumes. Moreover, studies of adult populations without major depressive disorder suggest a relationship between peripheral telomere length and hippocampal volume. However, the relationship of these findings in adolescents with major depressive disorder has yet to be explored. We examined whether adolescent major depressive disorder is associated with altered peripheral telomere length and hippocampal volume, and whether these measures relate to one another. In 54 unmedicated adolescents (13–18 years) with major depressive disorder and 63 well-matched healthy controls, telomere length was assessed from saliva using quantitative polymerase chain reaction methods, and bilateral hippocampal volumes were measured with magnetic resonance imaging. After adjusting for age and sex (and total brain volume in the hippocampal analysis), adolescents with major depressive disorder exhibited significantly shorter telomere length and significantly smaller right, but not left hippocampal volume. When corrected for age, sex, diagnostic group and total brain volume, telomere length was not significantly associated with left or right hippocampal volume, suggesting that these cellular and neural processes may be mechanistically distinct during adolescence. Our findings suggest that shortening of telomere length and reduction of hippocampal volume are already present in early-onset major depressive disorder and thus unlikely to be only a result of accumulated years of exposure to major depressive disorder.

ObjectiveThe objective of the study was to investigate whether group prenatal care (Centering Pregnancy Plus [CP+]) has an impact on pregnancy weight gain and postpartum weight loss trajectories and to determine whether prenatal depression and distress might moderate these trajectories.Study designThis was a secondary analysis of a cluster-randomized trial of CP+ in 14 Community Health Centers and hospitals in New York City. Participants were pregnant women aged 14-21 years (n = 984). Medical record review and 4 structured interviews were conducted: in the second and third trimesters and 6 and 12 months postpartum. Longitudinal mixed modeling was utilized to evaluate the weight change trajectories in the control and intervention groups. Prenatal distress and depression were also assessed to examine their impact on weight change.ResultsThere were no significant differences between the intervention and control groups in baseline demographics. Thirty-five percent of the participants were overweight or obese, and more than 50% had excessive weight gain by Institute of Medicine standards. CP+ was associated with improved weight trajectories compared with controls (P < .0001): women at clinical sites randomized to group prenatal care gained less weight during pregnancy and lost more weight postpartum. This effect was sustained among women who were categorized as obese based on prepregnancy body mass index (P < .01). Prenatal depression and distress were significantly associated with higher antepartum weight gain and postpartum weight retention. Women with the highest levels of depression and prenatal distress exhibited the greatest positive impact of group prenatal care on weight trajectories during pregnancy and through 12 months postpartum.ConclusionGroup prenatal care has a significant impact on weight gain trajectories in pregnancy and postpartum. The intervention also appeared to mitigate the effects of depression and prenatal distress on antepartum weight gain and postpartum weight retention. Targeted efforts are needed during and after pregnancy to improve weight gain trajectories and overall health.

Objective Given the critical role of behavior in preventing and treating chronic diseases, it is important to accelerate the development of behavioral treatments that can improve chronic disease prevention and outcomes. Findings from basic behavioral and social sciences research hold great promise for addressing behaviorally based clinical health problems, yet there is currently no established pathway for translating fundamental behavioral science discoveries into health-related treatments ready for Phase III efficacy testing. This article provides a systematic framework for developing behavioral treatments for preventing and treating chronic diseases. Method The Obesity-Related Behavioral Intervention Trials (ORBIT) model for behavioral treatment development features a flexible and progressive process, prespecified clinically significant milestones for forward movement, and return to earlier stages for refinement and optimization. Results This article presents the background and rationale for the ORBIT model, a summary of key questions for each phase, a selection of study designs and methodologies well-suited to answering these questions, and prespecified milestones for forward or backward movement across phases. Conclusions The ORBIT model provides a progressive, clinically relevant approach to increasing the number of evidence-based behavioral treatments available to prevent and treat chronic diseases. (PsycINFO Database Record

Context: Sugar overconsumption and chronic stress are growing health concerns because they both may increase the risk for obesity and its related diseases. Rodent studies suggest that sugar consumption may activate a glucocorticoid-metabolic-brain-negative feedback pathway, which may turn off the stress response and thereby reinforce habitual sugar overconsumption. Objective: The objective of the study was to test our hypothesized glucocorticoid-metabolic-brain model in women consuming beverages sweetened with either aspartame of sucrose. Design: This was a parallel-arm, double-masked diet intervention study. Setting: The study was conducted at the University of California, Davis, Clinical and Translational Science Center's Clinical Research Center and the University of California, Davis, Medical Center Imaging Research Center. Participants: Nineteen women (age range 18–40 y) with a body mass index (range 20–34 kg/m2) who were a subgroup from a National Institutes of Health-funded investigation of 188 participants assigned to eight experimental groups. Intervention: The intervention consisted of sucrose- or aspartame-sweetened beverage consumption three times per day for 2 weeks. Main Outcome Measures: Salivary cortisol and regional brain responses to the Montreal Imaging Stress Task were measured. Results: Compared with aspartame, sucrose consumption was associated with significantly higher activity in the left hippocampus (P = .001). Sucrose, but not aspartame, consumption associated with reduced (P = .024) stress-induced cortisol. The sucrose group also had a lower reactivity to naltrexone, significantly (P = .041) lower nausea, and a trend (P = .080) toward lower cortisol. Conclusion: These experimental findings support a metabolic-brain-negative feedback pathway that is affected by sugar and may make some people under stress more hooked on sugar and possibly more vulnerable to obesity and its related conditions.

Background: Telomere length (TL) is a marker of cellular aging, with the majority of lifetime attrition occurring during the first 4 y. Little is known about risk factors for telomere shortening in childhood. Objective: We evaluated the relation between early life feeding variables and preschool TL. Design: We assessed the relation between dietary, feeding, and weight-associated risk factors measured from birth and TL from blood samples taken at 4 y of age (n = 108) and 5 y of age (n = 92) in a cohort of urban, Latino children (n = 121 individual children). Feeding variables were evaluated in children with repeat measurements (n = 77). Results: Mean TL (in bp) was associated with exclusive breastfeeding at 4–6 wk of age (adjusted coefficient: 353.85; 95% CI: 72.81, 634.89; P = 0.01), maternal TL (adjusted coefficient: 0.32; 95% CI: 0.11, 0.54; P < 0.01), and older paternal age (adjusted coefficient: 33.27; 95% CI: 4.10, 62.44; P = 0.03). The introduction of other foods or drinks in addition to breast-milk or replacement-milk substitutes before 4–6 wk of age was associated with mean TL at 4 and 5 y of age (adjusted coefficient: −457.01; 95% CI: −720.50, −193.51; P < 0.01). Infant obesity at 6 mo of age and soda consumption at 4 y of age mediated the relation in part between exclusive breastfeeding at 4–6 wk of age and mean TL at 4 and 5 y of age. High soda consumption at 3 y of age was associated with an accelerated attrition from 4 to 5 y of age (adjusted coefficient: −515.14; 95% CI: −986.06, −41.22; P = 0.03). Conclusion: Exclusive breastfeeding at 4–6 wk of age may have long-term effects on child health as evidenced by longer TL at 4 and 5 y of age.

© 2015 Elsevier Inc. Introduction: Mitochondrial abnormalities may be involved in PTSD, although few studies have examined this. Mitochondrial DNA copy number (mtDNAcn) in blood cells is an emerging systemic index of mitochondrial biogenesis and function. The present study assessed mtDNAcn in male combat-exposed veterans with PTSD compared to those without PTSD as well as its correlation with clinical scales. Methods: mtDNAcn was assessed with a TaqMan multiplex assay in granulocytes of 43 male combat veterans with (n. =43) or without (n. =44) PTSD. Twenty of the PTSD subjects had co-morbid major depressive disorder (MDD). The Clinician Administered PTSD Scale (CAPS), the Positive and Negative Affect Schedule (PANAS), the Early Trauma Inventory (ETI) and the Beck Depression Inventory II (BDI-II) were used for the clinical assessments. All analyses were corrected for age and BMI. Results: mtDNAcn was significantly lower in subjects with PTSD (p.

There are currently no commonly used or easily accessible ‘biomarkers’ of hedonic eating. Physiologic responses to acute opioidergic blockade, indexed by cortisol changes and nausea, may represent indirect functional measures of opioid-mediated hedonic eating drive and predict weight loss following a mindfulness-based intervention for stress eating. In the current study, we tested whether cortisol and nausea responses induced by oral ingestion of an opioidergic antagonist (naltrexone) correlated with weight and self-report measures of hedonic eating and predicted changes in these measures following a mindfulness-based weight loss intervention. Obese women (N = 88; age = 46.7 ± 13.2 years; BMI = 35.8 ± 3.8) elected to complete an optional sub-study prior to a 5.5-month weight loss intervention with or without mindfulness training. On two separate days, participants ingested naltrexone and placebo pills, collected saliva samples, and reported nausea levels. Supporting previous findings, naltrexone-induced cortisol increases were associated with greater hedonic eating (greater food addiction symptoms and reward-driven eating) and less mindful eating. Among participants with larger cortisol increases (+1 SD above mean), mindfulness participants (relative to control participants) reported greater reductions in food addiction symptoms, b = −0.95, SE(b) = 0.40, 95% CI [−1.74, −0.15], p = .021. Naltrexone-induced nausea was marginally associated with reward-based eating. Among participants who endorsed naltrexone-induced nausea (n = 38), mindfulness participants (relative to control participants) reported greater reductions in food addiction symptoms, b = −1.00, 95% CI [−1.85, −0.77], p = .024, and trended toward reduced reward-based eating, binge eating, and weight, post-intervention. Single assessments of naltrexone-induced cortisol increases and nausea responses may be useful time- and cost-effective biological markers to identify obese individuals with greater opioid-mediated hedonic eating drive who may benefit from weight loss interventions with adjuvant mindfulness training that targets hedonic eating.

Background/Aims: Telomere biology plays a fundamental role in genomic integrity and cell physiology. The newborn setting of telomere length (TL) likely has important implications for telomere dynamics over the lifespan; however, its determinants are poorly understood. Folate is essential for DNA integrity. The maternal compartment is the only source of folate for the developing fetus. We, therefore, tested the hypothesis that variation in maternal folate during pregnancy is associated with newborn TL. Methods: A prospective, longitudinal study was conducted in 119 mother-newborn dyads. Eligible mothers were enrolled at 9.5 (SD ±2.1) weeks gestation and followed through birth. Concentrations of maternal serum folate were measured in the first trimester of pregnancy. Newborn telomere length was measured in cord blood mononuclear cells (CBMC). Results: After accounting for the effects of other established determinants of newborn TL, each 10 ng/ml increase in maternal total folate was associated with a 5.8% increase in median TL (p = 0.03). The median TL in newborns of mother in the lowest quartile of total folate levels was approximately 10% shorter than that of newborns of mothers in the highest folate quartile. Conclusions: Our findings suggest that fetal TL exhibits developmental plasticity, and provide evidence that maternal nutrition may exert a ‘programming' effect on this system.

BackgroundAnxiety disorders increase the risk of onset of several ageing-related somatic conditions, which might be the consequence of accelerated cellular ageing.AimsTo examine the association between anxiety status and leukocyte telomere length (LTL) as an indicator of cellular ageing.MethodData are from individuals with current (n = 1283) and remitted (n = 459) anxiety disorder, and controls (n = 582) with no psychiatric disorder from the Netherlands Study of Depression and Anxiety. We determined DSM-IV anxiety diagnoses and clinical characteristics by structured psychiatric interviews and self-report questionnaires; LTL was assessed using quantitative polymerase chain reaction and converted into base pairs (bp).ResultsPatients in the current anxiety group (bp = 5431) had significantly shorter LTL compared with the control group (bp = 5506, P = 0.01) and the remitted anxiety group (bp = 5499, P = 0.03) in analyses adjusted for sociodemographics, health and lifestyle. The remitted anxiety group did not differ from the control group (P = 0.84), however, time since remission was positively related with LTL. Furthermore, anxiety severity scores were associated with LTL in the whole sample, in line with a dose–response association.ConclusionsPatients with current – but not remitted – anxiety disorder had shorter telomere length, suggesting a process of accelerated cellular ageing, which in part may be reversible after remission.

© 2015 Elsevier Ireland Ltd. Accelerated cell aging, indexed in peripheral leukocytes by telomere shortness and in peripheral blood mononuclear cells (PBMCs) by telomerase activity, has been reported in several studies of major depressive disorder (MDD). However, the relevance of these peripheral measures for brain indices that are presumably more directly related to MDD pathophysiology is unknown. In this study, we explored the relationship between PBMC telomerase activity and leukocyte telomere length and magnetic resonance imaging-estimated hippocampal volume in un-medicated depressed individuals and healthy controls. We predicted that, to the extent peripheral and central telomerase activity are directly related, PBMC telomerase activity would be positively correlated with hippocampal volume, perhaps due to hippocampal telomerase-associated neurogenesis, neuroprotection or neurotrophic facilitation, and that this effect would be clearer in individuals with increased PBMC telomerase activity, as previously reported in un-medicated MDD. We did not have specific hypotheses regarding the relationship between leukocyte telomere length and hippocampal volume, due to conflicting reports in the published literature. We found, in 25 un-medicated MDD subjects, that PBMC telomerase activity was significantly positively correlated with hippocampal volume; this relationship was not observed in 18 healthy controls. Leukocyte telomere length was not significantly related to hippocampal volume in either group (19 unmedicated MDD subjects and 17 healthy controls). Although the nature of the relationship between peripheral telomerase activity and telomere length and the hippocampus is unclear, these preliminary data are consistent with the possibility that PBMC telomerase activity indexes, and may provide a novel window into, hippocampal neuroprotection and/or neurogenesis in MDD.

The purpose of the present study was to explore the associations among benefit finding, daily positive and negative emotion, and daily cortisol slope in 71 maternal caregivers. Benefit finding was measured using the Posttraumatic Growth Inventory (PTGI; Tedeschi, R. G., & Calhoun, L. G. (1996). The Posttraumatic Growth Inventory: Measuring the positive legacy of trauma. Journal of Traumatic Stress, 9, 455–472.). Cortisol slope was not significantly correlated with any of the PTGI subscales, positive emotion, or negative emotion. However, the interactions of daily positive emotion with the PTGI subscales of Personal Strength, Appreciation of Life, and Spiritual Change were statistically significant such that higher scores on these subscales predicted a steeper (more adaptive) daily cortisol slope only for those women who also had higher levels of daily positive emotion.

Objectives: The objectives of this study were to assess whether socioeconomic status (SES) is associated with dysregulation of the cortisol diurnal rhythm and whether this association is independent of race and occurs equally in whites and blacks; and to determine if an association between SES and cortisol can be explained (is mediated) by behavioral, social, and emotional differences across the SES gradient. Methods: Seven hundred eighty-one subjects from a multisite sample representing both whites and blacks provided six saliva cortisol samples over the course of the day: at awakening, 45 minutes, 2.5 hours, 8 hours, and 12 hours after awakening, and at bedtime. Results: Both lower SES (education and income) and being black were associated with higher evening levels of cortisol. These relationships were independent of one another and SES associations with cortisol were similar across racial categories. The evidence was consistent with poorer health practices (primarily smoking), higher levels of depressive symptoms, poorer social networks and supports, and feelings of helplessness (low mastery) mediating the link between SES and cortisol. However, we found no evidence for psychosocial or behavioral mediation of the association between race and cortisol response. Conclusions: Lower SES was associated in a graded fashion with flatter diurnal rhythms as a result of less of a decline during the evening. This association occurred independent of race and the data were consistent with mediation by health practices, emotional and social factors. Blacks also showed a flatter rhythm at the end of the day. This association was independent of SES and could not be explained by behavioral, social, or emotional mediators. Key words: socioeconomic status, blacks, cortisol, health behavior, social support, social networks. CARDIA Coronary Artery Risk Development in Young Adults Study; SES socioeconomic status; HPA hypothalamic–pituitary adrenocortical; BMI body mass index; AUC area under the curve; CES-D Center for Epidemiologic Studies Depression scale; MIDUS Midlife in the U.S. Survey; PAH Physical Activities History questionnaire.

Numerous studies demonstrate links between chronic stress and indices of poor health, including risk factors for cardiovascular disease and poorer immune function. Nevertheless, the exact mechanisms of how stress gets “under the skin” remain elusive. We investigated the hypothesis that stress impacts health by modulating the rate of cellular aging. Here we provide evidence that psychological stress— both perceived stress and chronicity of stress—is significantly associated with higher oxidative stress, lower telomerase activity, and shorter telomere length, which are known determinants of cell senescence and longevity, in peripheral blood mononuclear cells from healthy premenopausal women. Women with the highest levels of perceived stress have telomeres shorter on average by the equivalent of at least one decade of additional aging compared to low stress women. These findings have implications for understanding how, at the cellular level, stress may promote earlier onset of age-related diseases.

Few studies have examined whether certain coping behaviors are associated with physical outcomes following surgery. This prospective, longitudinal study investigated the effect of active and avoidant coping behaviors on two physical outcomes over time, pain and knee function, in a group of patients experiencing knee arthroscopic surgery (n = 81). Structured interviews and physician clinical assessments were conducted preoperatively and at 3 and 24 weeks postoperatively. Coping behavior was assessed during the preoperative interview, and patients were divided into high and low avoidant and active coping groups. Using repeated measures MANCOVA/ANCOVA, avoidant coping was significantly associated with knee pain and active coping was associated with knee function. Serum cortisol levels were available for a patient subset (n = 16); higher cortisol was related to both avoidant coping and poorer functioning during early recovery. Results suggest that these divergent coping behaviors are differentially associated...

We examined the relationship between perceived emotional intelligence (PEI), measured by the Trait Meta-Mood Scale (TMMS), and psychophysiological measures of adaptive coping. The TMMS assesses perceived ability to (a) attend to moods (Attention), (b) discriminate clearly among moods (Clarity), and (c) regulate moods (Repair). Study 1 showed significant positive associations between PEI and psychological and interpersonal functioning. In Study 2, skill at mood Repair was associated with less passive coping and perceptions of repeated laboratory stressors as less threatening; Clarity was related to greater increases in negative mood, but lower cortisol release during repeated stress. In Study 3, Repair was associated with active coping and lower levels of rumination; Attention was associated with lowered cortisol and blood pressure responses to acute laboratory challenges. These findings suggest that psychophysiological responses to stress may be one potential mechanism underlying the relationship between ...

Specific types of cognitions and mental processes may lead to greater stress arousal and may subsequently impact cell longevity. The study of telomeres and telomere-related molecular systems may provide a pathway for exploring the link between psychological domains and cell physiology. Based on findings emerging from clinical and preclinical data, we hypothesize that the telomere-telomerase system contributes to explain certain biological underpinnings of psychological interventions.In this symposium we’ll present the preliminary evidence on the complex translational relationships between specific psychological domains (i.e. childhood adversities, stressful life events, mindfulness-based interventions and perceived distress), the telomere-telomerase system and clinical outcomes. Further, we’ll discuss preliminary data on the effect of mindfulness- and meditation-based interventions on cellular ageing and disease-associated molecular phenotypes.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Background: Increasing evidence suggests that childhood trauma confers risk for psychosis, perhaps through later dysregulated stress responsivity. However, few studies have examined this model in “clinical-high-risk” (CHR) individuals, prior to psychosis onset.

Glucocorticoids contribute to obesity and metabolic syndrome; however, the mechanisms are unclear, and prognostic measures are unavailable. A systems level understanding of the hypothalamic–pituitary–adrenal (HPA)–leptin axis may reveal novel insights. Eighteen obese premenopausal women provided blood samples every 10 min over 24 h, which were assayed for cortisol, adrenocorticotropin releasing hormone (ACTH) and leptin. A published personalized HPA systems model was extended to incorporate leptin, yielding three parameters: (i) cortisol inhibitory feedback signalling, (ii) ACTH–adrenal signalling, and (iii) leptin–cortisol antagonism. We investigated associations between these parameters and metabolic risk profiles: fat and lean body mass (LBM; using dual-energy X-ray absorptiometry), and insulin resistance. Decreased cortisol inhibitory feedback signalling was significantly associated with greater fat (kg; p = 0.01) and insulin resistance ( p = 0.03) but not LBM. Leptin significantly antagonized cortisol dynamics in eight women, who exhibited significantly lower 24 h mean leptin levels, LBM and higher ACTH–adrenal signalling nocturnally (all p < 0.05), compared with women without antagonism. Traditional neuroendocrine measures did not predict metabolic health, whereas a dynamic systems approach revealed that lower central inhibitory cortisol feedback signalling was significantly associated with greater metabolic risk. While exploratory, leptin–cortisol antagonism may reflect a ‘neuroendocrine starvation’ response.

Diabetes is a unique disorder in how much it requires a high degree of individual self management strategies. Anxiety and stress can affect glycemic control, and thus management of emotions may be key to good glycemic control. This study is the first to examine how anxiety and coping style, and their interaction, can affect long-term glycemic control. We measured anxiety, coping, and HbA1C, a measure for mean blood glucose levels in the previous 6-8 weeks, in 115 patients with Type 1 diabetes at baseline and roughly 5 years later. We found that coping predicted outcomes, especially for those high in trait anxiety. Trait anxiety predicted limited increases in HbA1C (mean increase = 0.02%). Lower levels of emotion-oriented coping predicted clinically significant increases in HbA1C, but only for those high on baseline trait anxiety (mean increase = 0.92%). Task-oriented coping predicted decreases in state anxiety. Use of task- and emotion-oriented coping appears especially important for highly anxious patients, both for emotional regulation and glycemic control. So, coping styles, basal anxiety and their interactions should be considered in designing follow-up and interventions with diabetic patients.

Objective: Weight discrimination is associated with increased risk of obesity. The mechanism of this relationship is unknown, but being overweight is a highly stigmatized condition and may be a source of chronic stress that contributes to the development and pathophysiology of obesity. The objective of this study was to test whether weight stigma is associated with physiological risk factors linked to stress and obesity, including hypercortisolism and oxidative stress, independent of adiposity. Method: We examined the frequency of experiencing situations involving weight stigma and consciousness of weight stigma in relation to hypothalamic-pituitary-adrenal axis activity and oxidative stress (F2-isoprostanes) in 45 healthy overweight to obese women. Results: Independent of abdominal fat, weight stigma was significantly related to measures of cortisol (including salivary measures of cortisol awakening response and serum morning levels) as well as higher levels of oxidative stress. Perceived stress mediated the relationship between weight stigma consciousness and the cortisol awakening response. Conclusion: These preliminary findings show that weight stigma is associated with greater biochemical stress, independent of level of adiposity. It is possible that weight stigma may contribute to poor health underlying some forms of obesity. © 2014 American Psychological Association.

Summary Purpose Chronic stimulation and dysregulation of the neuroendocrine system by stress may cause metabolic abnormalities. We estimated how much cortisol and psychosocial outcomes improved with a restorative yoga (relaxation) versus a low impact stretching intervention for individuals with the metabolic syndrome. Methods We conducted a 1-year multi-center randomized controlled trial (6-month intervention and 6-month maintenance phase) of restorative yoga vs. stretching. Participants completed surveys to assess depression, social support, positive affect, and stress at baseline, 6 months and 12 months. For each assessment, we collected saliva at four points daily for three days and collected response to dexamethasone on the fourth day for analysis of diurnal cortisol dynamics. We analyzed our data using multivariate regression models, controlling for study site, medications (antidepressants, hormone therapy), body mass index, and baseline cortisol values. Results Psychosocial outcome measures were available for 171 study participants at baseline, 140 at 6 months, and 132 at 1 year. Complete cortisol data were available for 136 of 171 study participants (72 in restorative yoga and 64 in stretching) and were only available at baseline and 6 months. At 6 months, the stretching group had decreased cortisol at waking and bedtime compared to the restorative yoga group. The pattern of changes in stress mirrored this improvement, with the stretching group showing reductions in chronic stress severity and perseverative thoughts about their stress. Perceived stress decreased by 1.5 points (−0.4; 3.3, p = 0.11) at 6 months, and by 2.0 points (0.1; 3.9, p = 0.04) at 1 year in the stretching compared to restorative yoga groups. Post hoc analyses suggest that in the stretching group only, perceived increases in social support (particularly feelings of belonging), but not changes in stress were related to improved cortisol dynamics. Conclusions We found significant decreases in salivary cortisol, chronic stress severity, and stress perception in the stretching group compared to the restorative yoga group. Group support during the interactive stretch classes may have contributed to these changes.

BackgroundAdverse childhood experiences (ACEs) are associated with poor physical and mental health outcomes in adulthood. Adverse childhood experiences are also associated with shortened leukocyte telomere length (LTL) in adults, suggesting accelerated cell aging. No studies have yet assessed the relationship of ACEs to LTL in individuals with major depressive disorder (MDD), despite the high incidence of antecedent ACEs in individuals with MDD. Further, no studies in any population have assessed the relationship of ACEs to the activity of telomerase, the major enzyme responsible for maintaining LTL, or the relationship between telomerase and LTL in individuals with ACEs.MethodsTwenty healthy, unmedicated adults with MDD and 20 healthy age-, sex- and ethnicity-matched controls had ACEs assessed and had blood drawn for LTL and peripheral blood mononuclear cell (PBMC) resting telomerase activity.ResultsIn healthy controls, greater ACE exposure was associated with shorter LTL (p

The rate of biological aging is modulated in part by genes interacting with stressor exposures. Basic research has shown that exposure to short-term stress can strengthen cellular responses to stress ("hormetic stress"). Hormetic stress promotes longevity in part through enhanced activity of molecular chaperones and other defense mechanisms. In contrast, prolonged exposure to stress can overwhelm compensatory responses ("toxic stress") and shorten lifespan. One key question is whether the stressors that are well understood in basic models of aging can help us understand psychological stressors and human health. The psychological stress response promotes regulatory changes important in aging (e.g., increases in stress hormones, inflammation, oxidative stress, insulin). The negative effects of severe stress are well documented in humans. Potential positive effects of acute stress (stress resistance) are less studied, especially at the cellular level. Can stress resistance slow the rate of aging in humans, as it does in model organisms? If so, how can we promote stress resistance in humans? We urge a new research agenda embracing the continuum from cellular stress to psychological stress, using basic and human research in tandem. This will require interdisciplinary novel approaches that hold much promise for understanding and intervening in human chronic disease.

Background Prepregnancy body mass index and excessive gestational weight gain (GWG) are associated with adverse maternal and infant outcomes. Because stress contributes to obesity and eating behaviors, stress reduction interventions during pregnancy may be a novel way to influence GWG, positively affect maternal and infant outcomes, and address the obesity epidemic intergenerationally. Methods Our research team is developing a mindfulness-based stress reduction and nutrition intervention for low-income, overweight and obese pregnant women, with healthy GWG as the primary outcome measure. To inform development of the intervention, we conducted focus groups with our target population. Focus group transcripts were analyzed for themes related to sources and importance of stress, relationship between stress and eating, and motivation for a stress reduction pregnancy intervention. Findings Fifty-nine low-income pregnant women from the San Francisco Bay Area participated in focus groups and completed a questionnaire. The vast majority of women (80%) reported experiencing significant stress from a variety of sources and most recognized a relationship between stress and eating in their lives. Conclusions This at-risk population seems to be extremely interested in a stress reduction intervention to support healthy GWG during pregnancy. The women in our groups described high levels of stress and a desire for programs beyond basic dietary recommendations. These findings inform practitioners and policymakers interested in pregnancy as a “window of opportunity” for behavior change that can affect the metabolic and weight trajectory both for women and their offspring.

Growing epidemiologic and laboratory evidence links short sleep duration with increased incidence of obesity; however, the behavioral mechanisms have not been fully elucidated. Sugar-sweetened beverage (SSBs) consumption has been identified as a significant contributor to weight gain. The aim of this study was to examine whether self-reported sleep duration and consumption of SSB were associated among a sample of 8,130 adults, aged 16-70 years, who participated in the 2005-2008 National Health and Nutrition Examination Survery (NHANES). Analyses revealed elevated average rates of daily SSB consumption in participants who reported sleeping ≤5 hours (Relative Difference (RD)=1.21, 95% CI 1.12, 1.31) and 6 hours per night (RD=1.15, 95% CI 1.08, 1.23) compared to those sleeping 7 to 8 hours per night (reference group). These associations were independent of age, gender, race/ethnicity, highest level of education, poverty income ratio, smoking status, marital status, BMI, self-reported health status, depressive symptoms, history of trouble sleeping, history of sleep disorders, total energy, coffee intake, and tea intake. Sub-analyses of specific types of SSBs revealed that the strongest associations emerged for regular soda consumption (caffeinated: ≤5 hours RD=1.46, 95% CI 1.27, 1.67 and 6 hours per night RD=1.18, 95% CI 1.04, 1.35; decaffeinated: ≤5 hours RD=1.15, 95% CI 1.07, 1.25 and 6 hours per night RD=1.08, 95% CI 1.02, 1.13) and non-carbonated SSBs (≤5 hours RD=1.10, 95% CI 1.03, 1.18). These associations varied by gender, race, and age group. Overall, the inverse associations between sleep duration and SSB consumption were significantly stronger among women, Caucasians, and participants in midlife. These findings provide initial observational evidence for associations between short sleep duration and increased intake of SSBs, providing a plausible behavioral pathway through which sleep may promote excess weight gain and obesity.

Consumption of sugar-sweetened beverages (SSBs) is linked to increased risks of metabolic disease, but the biological mechanisms underlying this association are still under investigation. Leukocyte telomere length maintenance underlies healthy cellular aging, and may provide a link between SSB consumption and risk of disease. Given the known effects of SSBs on oxidative stress and insulin resistance, we examined the associations between sugar-sweetened beverage, diet soda, and fruit juice consumption, and leukocyte telomere length in 5,309 healthy adults with no prior history of diabetes or cardiovascular disease, using data from the 1999-2002 National Health and Nutrition Surveys (NHANES). We hypothesized that beverages with high sugar content would be most detrimental to cellular aging. Leukocyte telomere length was assayed from DNA specimens collected from adult NHANES participants. Diet was assessed using 24-hour dietary recalls. Because 24-hour dietary recalls may not accurately reflect long-term intake, the National Cancer Institute statistical method was used to estimate usual dietary intake. After adjustment for sociodemographic characteristics, smoking behavior, physical activity, dietary quality, and body mass index (BMI), each 8-ounce daily serving of sugar-sweetened sodas was associated with shorter telomeres (β=-0.010, 95% CI -0.019, -0.001), roughly equivalent to 1.8 additional years of aging. Twenty-one percent of study participants consumed ≥20 ounces of sugar-sweetened soda a day, translating into approximately 4.4 additional years of aging for heavy soda drinkers. No significant associations were observed between consumption of diet sodas, non-carbonated SSBs, or 100% fruit juice and telomere length. In conclusion, regular consumption of sugar-sweetened sodas was associated with shorter telomeres in a nationally representative sample of healthy, nonelderly adults independent of BMI and other individual characteristics. These results suggest that SSBs may influence metabolic disease development through accelerated cell aging. Although more research is needed to confirm these associations, these findings strengthen the rationale for limiting the consumption of SSBs.

Telomere length, a reliable predictor of disease pathogenesis, can be affected by genetics, chronic stress and health behaviors. Cross-sectionally, highly stressed postmenopausal women have shorter telomeres, but only if they are inactive. However, no studies have prospectively examined telomere length change over a short period, and if rate of attrition is affected by naturalistic factors such as stress and engagement in healthy behaviors, including diet, exercise, and sleep. Here we followed healthy women over 1 year to test if major stressors that occurred over the year predicted telomere shortening, and whether engaging in healthy behaviors during this period mitigates this effect. In 239 postmenopausal, non-smoking, disease-free women, accumulation of major life stressors across a 1-year period predicted telomere attrition over the same period-for every major life stressor that occurred during the year, there was a significantly greater decline in telomere length over the year of 35 bp (P

Why are some individuals more vulnerable to persistent weight gain and obesity than are others? Some obese individuals report factors that drive overeating, including lack of control, lack of satiation, and preoccupation with food, which may stem from reward-related neural circuitry. These are normative and common symptoms and not the sole focus of any existing measures. Many eating scales capture these common behaviors, but are confounded with aspects of dysregulated eating such as binge eating or emotional overeating. Across five studies, we developed items that capture this rewardbased eating drive (RED). Study 1 developed the items in lean to obese individuals (n = 327) and examined changes in weight over eight years. In Study 2, the scale was further developed and expert raters evaluated the set of items. Study 3 tested psychometric properties of the final 9 items in 400 participants. Study 4 examined psychometric properties and race invariance (n = 80 women). Study 5 examined psychometric properties and age/gender invariance (n = 381). Results showed that RED scores correlated with BMI and predicted earlier onset of obesity, greater weight fluctuations, and greater overall weight gain over eight years. Expert ratings of RED scale items indicated that the items reflected characteristics of reward-based eating. The RED scale evidenced high internal consistency and invariance across demographic factors. The RED scale, designed to tap vulnerability to reward-based eating behavior, appears to be a useful brief tool for identifying those at higher risk of weight gain over time. Given the heterogeneity of obesity, unique brief profiling of the reward-based aspect of obesity using a self-report instrument such as the RED scale may be critical for customizing effective treatments in the general population. © 2014 Epel et al.

Patients with major depressive disorder (MDD) have an increased onset risk of aging-related somatic diseases such as heart disease, diabetes, obesity and cancer. This suggests mechanisms of accelerated biological aging among the depressed, which can be indicated by a shorter length of telomeres. We examine whether MDD is associated with accelerated biological aging, and whether depression characteristics such as severity, duration, and psychoactive medication do further impact on biological aging. Data are from the Netherlands Study of Depression and Anxiety, including 1095 current MDD patients, 802 remitted MDD patients and 510 control subjects. Telomere length (TL) was assessed as the telomere sequence copy number (T) compared to a single-copy gene copy number (S) using quantitative polymerase chain reaction. This resulted in a T/S ratio and was converted to base pairs (bp). MDD diagnosis and MDD characteristics were determined by self-report questionnaires and structured psychiatric interviews. Compared with control subjects (mean bp=5541), sociodemographic-adjusted TL was shorter among remitted MDD patients (mean bp=5459; P=0.014) and current MDD patients (mean bp=5461; P=0.012). Adjustment for health and lifestyle variables did not reduce the associations. Within the current MDD patients, separate analyses showed that both higher depression severity (P

To date, there are few known predictors of stress-induced eating. The purpose of this study was to identify whether physiological and psychological variables are related to eating after stress. Specifically, we hypothesized that high cortisol reactivity in response to stress may lead to eating after stress, given the relations between cortisol with both psychological stress and mechanisms affecting hunger. To test this, we exposed fifty-nine healthy pre-menopausal women to both a stress session and a control session on different days. High cortisol reactors consumed more calories on the stress day compared to low reactors, but ate similar amounts on the control day. In terms of taste preferences, high reactors ate significantly more sweet food across days. Increases in negative mood in response to the stressors were also significantly related to greater food consumption. These results suggest that psychophysiological response to stress may influence subsequent eating behavior. Over time, these alterations could impact both weight and health.

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.

Objective Excessive central fat puts one at greater risk of disease. In animal studies, stress-induced cortisol secretion has been shown to increase central fat. The objective of this study was to assess whether women with central fat distribution (as indicated by a high waist-to-hip ratio [WHR]), across a range of body mass indexes, display consistently heightened cortisol reactivity to repeated laboratory stressors. Methods Fifty-nine healthy premenopausal women, 30 with a high WHR and 29 with a low WHR, were exposed to consecutive laboratory sessions over 4 days (three stress sessions and one rest session). During these sessions, cortisol and psychological responses were assessed. Results Women with a high WHR evaluated the laboratory challenges as more threatening, performed more poorly on them, and reported more chronic stress. These women secreted significantly more cortisol during the first stress session than women with a low WHR. Furthermore, lean women with a high WHR lacked habituation to stress in that they continued to secrete significantly more cortisol in response to now familiar challenges (days 2 and 3) than lean women with a low WHR. Conclusions Central fat distribution is related to greater psychological vulnerability to stress and cortisol reactivity. This may be especially true among lean women, who did not habituate to repeated stress. The current cross-sectional findings support the hypothesis that stress-induced cortisol secretion may contribute to central fat and demonstrate a link between psychological stress and risk for disease.

This study explored whether self-efficacy and time perspective of homeless adults (N = 82) living in a shelter affected their coping strategies related to obtaining housing and employment. Participants with high self-efficacy searched more for housing and employment and stayed at the shelter for a shorter duration, whereas participants with low selfefficacy were more likely to request an extension of their stay at the shelter. Those high on future orientation had shorter durations of homelessness and were more likely to enroll in school and to report gaining positive benefits from their predicament. whereas those with a high present orientation had more avoidant coping strategies. Despite the predictive power of self-efficacy and future orientation of proactive search behaviors, there were no predictors of obtaining stable housing, which is a scarce resource in the area. However, a high present orientation predicted obtaining temporary housing. A present temporal perspective may be adaptive in finding short-term solutions to an unstable situation, such as homelessness. The role of time perspective in crisis situations is discussed, as well as the severe environmental constraints on the exercise of personal control over reality dictated by social, economic, and political forces.