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Background: The purpose of this study was to examine whether select baseline characteristics influenced the likelihood of an overweight/obese, older adult experiencing a clinically meaningful gait speed response (±0.05 m/s) to caloric restriction (CR).Methods: Individual level data from 1 188 older adults participating in 8, 5/6-month, weight loss interventions were pooled, with treatment arms collapsed into CR (n = 667) or no CR (NoCR; n = 521) categories. Exercise assignment was equally distributed across groups (CR: 65.3% vs NoCR: 65.4%) and did not interact with CR (p = .88). Poisson risk ratios (95% confidence interval [CI]) were used to examine whether CR assignment interacted with select baseline characteristic subgroups: age (≥65 years), sex (female/male), race (Black/White), body mass index (BMI; ≥35 kg/m2), comorbidity (diabetes, hypertension, cardiovascular disease) status (yes/no), gait speed (<1.0 m/s), or inflammatory burden (C-reactive protein ≥3 mg/L, interleukin-6 ≥2.5 pg/mL) to influence achievement of ±0.05 m/s fast-paced gait speed change. Main effects were also examined.Results: The study sample (69.5% female, 80.1% White) was 67.6 ± 5.3 years old with a BMI of 33.8 ± 4.4 kg/m2. Average weight loss achieved in the CR versus NoCR group was -8.3 ± 5.9% versus -1.1 ± 3.8%; p < .01. No main effect of CR was observed on the likelihood of achieving a clinically meaningful gait speed improvement (risk ratio [RR]: 1.09 [95% CI: 0.93, 1.27]) or gait speed decrement (RR: 0.77 [95% CI: 0.57, 1.04]). Interaction effects were nonsignificant across all subgroups.Conclusion: The proportion of individuals experiencing a clinically meaningful gait speed change was similar for CR and NoCR conditions. This finding is consistent across several baseline subgroupings. [ABSTRACT FROM AUTHOR]

Background: Residential environments are associated with older adults' health, but underlying physiologic causal mechanisms are not well understood. As adults age, street blocks are likely more relevant to their health than the larger neighborhood environment. This study examined the effects of adverse street block conditions on aging biomarkers among older adults.Methods: We included community-dwelling Medicare beneficiaries aged 67 and older with 2017 biomarker data from the nationally representative National Health and Aging Trends Study (n = 4357). Street block disorder in 2016 was measured using interviewer report of any trash/glass/litter, graffiti, or vacant buildings on participants' blocks. Propensity score models were used to create balanced groups with regard to multiple 2015 participant characteristics, including demographic, socioeconomic, residence, and early-life characteristics. Linear regressions modeled street block disorder as a predictor of 4 aging biomarkers, hemoglobin A1C, high-sensitivity C-reactive protein, interleukin-6, and cytomegalovirus antibodies, before and after applying propensity score weighting.Results: Adjusting for participant sociodemographic characteristics and applying propensity score weights, living on a block with any disorder was associated with 2% higher mean hemoglobin A1C levels (95% confidence interval [CI]: 0.002-0.03), 13% higher C-reactive protein (95% CI: 0.03-0.23), 10% higher interleukin-6 (95% CI: 0.02-0.19), and 19% more cytomegalovirus antibodies (95% CI: 0.09-0.29) compared to living on a block with no disorder.Conclusions: Street block disorder predicted subsequent aging biomarkers after applying a propensity score approach to account for confounding among a national sample of older adults. Targeting street-level residential contexts for intervention may reduce the risk for poor health in older adults. [ABSTRACT FROM AUTHOR]

Frailty is highly prevalent in old age and confers an important mortality risk. Although the causes of frailty are multiple, immunosenescence (IS)-predominantly driven by cytomegalovirus (CMV)-has been implicated in its pathophysiology. Thus far, research examining the association between IS and frailty states is sparse and equivocal. On the other hand, evidence is mounting in support of the view that frailty can be reversed, especially for those in the pre-frail stage. Therefore, we aimed to clarify the impact of CMV on IS and its relevance to pre-frailty. One hundred seventy-three persons aged 80 to 99 years were enrolled. Pre-frailty was defined according to Fried's criteria. Anti-CMV IgG and serum IL-6 were measured using Architect iSystem and Luminex, respectively. T-cell phenotypes were determined using flow cytometry. The prevalence of pre-frailty was 52.6%, increased with age (p = .001), and was greater in men than women (p = .044). No relationship was found between pre-frailty and positive CMV serology. Further, CMV-seropositivity was significantly associated with less naïve cells, more memory and senescence-prone phenotypes (all p < .001). After adjusting for potential confounders, only IL-6, age and sex were predictive of pre-frailty. We conclude that the presence of pre-frailty is independent from CMV infection in very old subjects. [ABSTRACT FROM AUTHOR]

Background: Interplays between inflammation and mitochondrial biology are reported. Here, we examined the cross-sectional interrelationships of mitochondrial DNA copy number (mtDNACN) and inflammation and their interaction with physical functioning.Methods: A total of 1990 community-dwelling adults aged 65 years and older who were participating in the Healthy Aging Longitudinal Study in Taiwan underwent measurements of peripheral-blood leukocytes MtDNACN, multiple inflammatory markers, grip strength, and gait speed.Results: Principal components analysis revealed two inflammatory factors: factor 1 (high-sensitivity C-reactive protein [hs-CRP], white blood cell count, fibrinogen and interleukin-6 [IL-6]); factor 2 (tumor necrosis factor receptor 1, D-dimer and soluble interleukin-6 receptor). Participants with severe physical functioning impairment (low grip strength and gait speed) had higher (p < .05) levels of factor 1 and 2, but not mtDNACN, than did those with moderately impaired (low grip strength or gait speed) and normal physical functioning. MtDNACN was negatively related to factor 1 (r = -.221, p < .001) but not factor 2 (r = -.002, p = .938). Increased factor 1 was strongly associated with higher odds of physical functioning impairment in those with a low mtDNACN (adjusted odds ratios [OR] of moderate physical function impairment 1.21, 95% CI 1.01-1.44; adjusted OR of severe physical function impairment 1.52, 95% CI 1.25-1.85) but not in those with a high mtDNACN (p for interaction = .016).Conclusions: A low mtDNACN was associated with an inflammation exhibiting elevated hs-CRP, IL-6, fibrinogen, and white blood cell count, and strengthened the association of this inflammation with physical functioning impairment. [ABSTRACT FROM AUTHOR]

Background: Habitual (non-exercise) physical activity (PA) declines with age, and aging-related increases in inflammation and fatigue may be important contributors to variability in PA.Methods: This study examined the association of objectively-measured PA (accelerometry over 7 days) with inflammation (plasma interleukin-6 and C-reactive protein) and with self-reported fatigue (SF-36 Vitality) at baseline and 18 months after a diet-induced weight loss, exercise, or diet-induced weight loss plus exercise intervention in 167 overweight/obese, middle-aged, and older adults.Results: At baseline, individuals with higher plasma interleukin-6, as well as those who reported feeling less energetic (more fatigued), took less steps per day and had lower PA energy expenditure and minutes of light and moderate-vigorous PA (p < .05 for all). At the 18-month follow-up, inflammation was lower in both weight loss groups, fatigue was reduced in all three groups with larger decreases in the combined group, and mean levels of habitual PA were not changed in any group. In longitudinal analyses with all groups combined, we found that participants reporting larger increases in vitality (eg, declines in fatigue) had greater increases in PA (p < .05 for all). Also, changes in steps/d and physical activity energy expenditure were indirectly associated with changes in interleukin-6 (β [SEM] for steps/d = -565 [253]; β [SEM] for physical activity energy expenditure = -22.4 [10.17]; p < .05).Conclusions: Levels of habitual PA are lower in middle-aged and older adults with higher levels of chronic inflammation and greater self-reported fatigue. In addition, participants who experienced greater declines in inflammation during the interventions had greater declines in fatigue and larger increases in PA. [ABSTRACT FROM AUTHOR]

Obesity and aging share an impaired immune system and oxidative and inflammatory stress. Therefore, the hypothesis of obesity as a possible model of premature immunosenescence has been proposed. In this study, we investigated whether adult obese mice, as a consequence of being fed with a fat-rich diet during their adolescence, showed premature immunosenescence and if this was aggravated with aging. Peritoneal cell suspensions were obtained when ICR/CD1 obese female mice were adults (28 weeks) and old (72 weeks), and several functions and antioxidant defenses were evaluated. The results showed that the chemotaxis of both macrophages and lymphocytes, phagocytosis of macrophages, activity of natural killer cells, proliferative response of lymphocytes, interleukin-1β, tumor necrosis factor-alpha, interleukin-6, interleukin-2, and interleukin-10 released in leukocyte cultures, as well as antioxidant and oxidant capacity were significantly impaired in adult obese mice with respect to adult nonobese mice, with values similar to those in chronologically old mice. When these obese animals grew older, although having been fed with a standard diet, they showed a higher deterioration of their immune functions in comparison with the old control group. In conclusion, these results demonstrate that a high fat intake during adolescence can produce an obesity state in adult age associated with a premature immunosenescence, which is aggravated through aging. [ABSTRACT FROM AUTHOR]

Background: Levels of the proinflammatory cytokine interleukin-18 (IL-18) are raised in old age and are associated with reduced physical functioning. Previous studies have indicated that the C allele of the rs5744256 polymorphism in the IL-18 gene is strongly associated with reduced circulating IL-18 levels. This variant has previously been associated with improved locomotor performance in old age, but the finding requires independent replication. [ABSTRACT FROM PUBLISHER]