Telomeres, the protective DNA-protein complexes at the ends of linear chromosomes, are important for genome stability. Leukocyte or peripheral blood mononuclear cell (PBMC) telomere length is a potential biomarker for human aging that integrates genetic, environmental, and lifestyle factors and is associated with mortality and risks for major diseases. However, only a limited number of studies have examined longitudinal changes of telomere length and few have reported data on sorted circulating immune cells. We examined the average telomere length (TL) in CD4+, CD8+CD28+, and CD8+CD28− T cells, B cells, and PBMCs, cross-sectionally and longitudinally, in a cohort of premenopausal women. We report that TL changes over 18 months were correlated among these three T cell types within the same participant. Additionally, PBMC TL change was also correlated with those of all three T cell types, and B cells. The rate of shortening for B cells was significantly greater than for the three T cell types. CD8+CD28− cells, despite having the shortest TL, showed significantly more rapid attrition when compared to CD8+CD28+ T cells. These results suggest systematically coordinated, yet cell type-specific responses to factors and pathways contribute to telomere length regulation.

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.

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.

Our analysis exhibits the potential for machine learning to move government agencies toward a more data-informed approach to evaluating risk and providing social services. Overall, such efforts will improve the efficiency of allocating resource-intensive interventions.

IntroductionPrior cross-national studies of socioeconomic inequalities in obesity have only compared summary indices of inequality but not specific, policy-relevant dimensions of inequality: (a) shape of the socioeconomic gradient in obesity, (b) magnitude of differentials in obesity across socioeconomic levels and, (c) level of obesity at any given socioeconomic level. We use unique data on two highly comparable societies – U.S. and Canada - to contrast each of these inequality dimensions.MethodsData came from the 2002/2003 Joint Canada/U.S. Survey of Health. We calculated adjusted prevalence ratios (APRs) for obesity (compared to normal weight) by income quintile and education group separately for both nations and, between Canadians and Americans in the same income or education group.ResultsIn the U.S., every socioeconomic group except the college educated had significant excess prevalence of obesity. By contrast in Canada, only those with less than high school were worse off, suggesting that the shape of the socioeconomic gradient differs in the two countries. U.S. differentials between socioeconomic levels were also larger than in Canada (e.g., PR quintile 1 compared to quintile 5 was 1.82 in the U.S. [95 % CI: 1.52-2.19] but 1.45 in Canada [95 % CI: 1.10-1.91]). At the lower end of the socioeconomic gradient, obesity was more prevalent in the U.S. than in Canada.ConclusionsOur results suggest there is variation between U.S. and Canada in different dimensions of socioeconomic inequalities in obesity. Future research should examine a broader set of nations and test whether specific policies or environmental exposures can explain these differences.

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The effect of T cell growth factor (TCGF) on the cell cycle of four T cell lines that differed in their response to TCGF was studied. Activated normal marmoset T cells (OH-1) were totally dependent on the addition of TCGF for long-term proliferation. In the absence of TCGF, the cells were incapable of traversing the cell cycle and became arrested in G1. The addition of TCGF to arrested OH-1 cells stimulated them to enter the S phase after a lag phase of 24 to 33 hr. The TCGF-stimulated cells reached a maximum of cells in the S phase by 12 hr after the initiation of DNA synthesis. TCGF was required for a minimum of 18 hr before cells would enter the S phase. In the absence of TCGF, activated owl monkey (8I) and human (RG) lymphocytes displayed a TCGF-sensitive block; addition of TCGF stimulated these cells to enter the S phase after 12 and 16 hr, respectively. In contrast, an owl monkey tumor-derived T cell line (OMT-1), not dependent on exogenous TCGF for proliferation, was able to progress slowly through the cell cycle without a TCGF-sensitive block. These cells responded to TCGF by showing an initial increase in cells that entered the S phase after a lag of 6 hr and a continuing movement of additional cells into S over the course of the next several hours.