Cross-border ties, nativity, and inflammatory markers in a population-based prospective study of Latino adults

Even after migration, immigrants and their descendants may continue to have ties to family and friends who remain in places of origin. Recent research suggests that these cross-border social ties have implications for health, although this scholarship has been limited to self-reported outcomes. Using data from the Sacramento Area Latino Study on Aging (SALSA), we estimate associations between cross-border social ties and inflammatory biomarkers among Latino adults (n = 1786). We find that immigrants who maintained any cross-border connection to family and friends in Latin America had significantly lower levels of baseline interleukin-6 (IL-6) and C-reactive protein (CRP) compared to their US-born counterparts with no cross-border ties. These results held for values of CRP at five-year follow-up for men only. In contrast, US-born women with cross-border ties to family and friends in Latin America had both significantly higher levels of CRP and significantly lower levels of tumor necrosis factor-alpha (TNF-α) at five-year follow-up relative to their US-born counterparts with no cross-border ties. We find descriptively that men who have cross-border ties are also less likely to be socially isolated within local contexts. Considering place-of-origin social connections may contribute critical nuance to studies of immigrant health, including disparities in inflammatory markers that may serve as indicators of underlying chronic disease

Associations between chronic caregiving stress and T cell markers implicated in immunosenescence

Chronic psychological stress is associated with accelerated biological aging, immune dysfunction, and premature morbidity and mortality. Changes in the relative proportions of T cell subpopulations are thought to be a characteristic of immunological aging; however, understanding of whether these changes are associated with chronic psychological stress is incomplete. This study investigated associations between chronic caregiving stress and distributions of T cell phenotypes in a sample of high stress mothers of children with Autism Spectrum Disorder (caregivers; n = 91) and low stress mothers of neurotypical children (controls; n = 88). Immune markers assessed were naïve (CD45RA + CD62L+), central memory (CD45RA-CD62L+), and effector memory (CD45RA-CD62L-) CD4+ and CD8+ T cells. We also examined the ratio of effector to naïve (E:N) CD4+ and CD8+ T cells. In models adjusted for age, body mass index, race/ethnicity, and antidepressant use, caregivers displayed higher percentages of effector memory CD8+ and CD4+ T cells as well as lower percentages of naïve CD8+ T cells and central memory CD8+ and CD4+ T cells compared to controls. Caregivers also displayed significantly higher E:N ratios for both CD4+ and CD8+ T cells. These findings were also independent of cytomegalovirus infection status. Furthermore, higher parental stress, across both groups, was related to several immune parameters. These findings provide preliminary evidence that chronic parental caregiving stress is associated with changes in relative proportions of T cell subpopulations that are consistent with accelerated immunological aging

Major depressive disorder and accelerated cellular aging: results from a large psychiatric cohort study

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<0.01) and longer symptom duration in the past 4 years (P=0.01) were associated with shorter TL. Our results demonstrate that depressed patients show accelerated cellular aging according to a 'dose-response' gradient: those with the most severe and chronic MDD showed the shortest TL. We also confirmed the imprint of past exposure to depression, as those with remitted MDD had shorter TL than controls. © 2014 Macmillan Publishers Limited

Anxiety disorders and accelerated cellular ageing

Background: Anxiety disorders increase the risk of onset of several ageing-related somatic conditions, which might be the consequence of accelerated cellular ageing. Aims: To examine the association between anxiety status and leukocyte telomere length (LTL) as an indicator of cellular ageing. Method: Data 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). Results: Patients 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. Conclusions: Patients 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

The reward-based eating drive scale: a self-report index of reward-based eating

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 reward-based 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

Dysregulated relationship of inflammation and oxidative stress in major depression

► The relationship of inflammation to oxidation may be disturbed in untreated major depression; this may reflect or contribute to increased risk of co-morbid medical illnesses. Chronic inflammation and oxidative stress have been implicated in the pathophysiology of Major Depressive Disorder (MDD), as well as in a number of chronic medical conditions. The aim of this study was to examine the relationship between peripheral inflammatory and oxidative stress markers in un-medicated subjects with MDD compared to non-depressed healthy controls and compared to subjects with MDD after antidepressant treatment. We examined the relationships between IL-6, IL-10, and the IL-6/IL-10 inflammatory ratio vs. F2-isoprostanes (F2-IsoP), a marker of oxidative stress, in un-medicated MDD patients (n=20) before and after 8weeks of open-label sertraline treatment (n=17), compared to healthy non-depressed controls (n=20). Among the un-medicated MDD subjects, F2-IsoP concentrations were positively correlated with IL-6 concentrations (p<0.05) and were negatively correlated with IL-10 concentrations (p<0.01). Accordingly, F2-IsoP concentrations were positively correlated with the ratio of IL-6/IL-10 (p<0.01). In contrast, in the control group, there were no significant correlations between F2-IsoPs and either cytokine or their ratio. After MDD subjects were treated with sertraline for 8weeks, F2-IsoPs were no longer significantly correlated with IL-6, IL-10 or the IL-6/IL-10 ratio. These data suggest oxidative stress and inflammatory processes are positively associated in untreated MDD. Our findings are consistent with the hypothesis that the homeostatic buffering mechanisms regulating oxidation and inflammation in healthy individuals become dysregulated in untreated MDD, and may be improved with antidepressant treatment. These findings may help explain the increased risk of comorbid medical illnesses in MDD