Summary Ageing is a dynamic process, and trends in the health status of older adults aged at least 60 years vary over time because of several factors. We examined reported trends in morbidity and ...mortality in older adults during the past two decades to identify patterns of ageing across the world. We showed some evidence for compression of morbidity (ie, a reduced amount of time spent in worse health), in four types of studies: 1) of good quality based on assessment criteria scores; 2) those in which a disability-related or impairment-related measure of morbidity was used; 3) longitudinal studies; or 4) studies undertaken in the USA and other high-income countries. Many studies, however, reported contrasting evidence (ie, for an expansion of morbidity), but with different methods, these measures are not directly comparable. Expansion of morbidity was more common when trends in chronic disease prevalence were studied. Our secondary analysis of data from longitudinal ageing surveys presents similar results. However, patterns of limitations in functioning vary substantially between countries and within countries over time, with no discernible explanation. Data from low-income countries are very sparse, and efforts to obtain information about the health of older adults in less-developed regions of the world are urgently needed. We especially need studies that focus on refining measurements of health, functioning, and disability in older people, with a core set of domains of functioning, that investigate the effects of these evolving patterns on the health-care system and their economic implications.
Young adults in couple (pair-bond) relationships reported on the positive and negative aspects of their relationships and had blood drawn and assayed for oxytocin and vasopressin. Elevated plasma ...oxytocin was associated with distress in the pairbond relationship for women, but not for men. Vasopressin, which is closely related to oxytocin in molecular structure and significantly related to male pair-bond behavior in animal studies, was elevated in men experiencing distress in the pair-bond relationship, but not in women. Controlling for estradiol and testosterone did not alter these findings. We conclude that plasma oxytocin in women and plasma vasopressin in men may be biomarkers of distressed pair-bond relationships.
Background Insomnia symptoms are associated with vulnerability to age-related morbidity and mortality. Cross-sectional data suggest accelerated biological aging may be a mechanism through which sleep ...influences risk. A novel method for determining age acceleration using epigenetic methylation to DNA has demonstrated predictive utility as an epigenetic clock and prognostic of age-related morbidity and mortality. Methods We examined the association of epigenetic age and immune cell aging with sleep in the Women’s Health Initiative (WHI) study (N=2,078; Age M(SD)=64.5(7.1) with assessment of insomnia symptoms (restlessness, difficulty falling asleep, waking at night, trouble getting back to sleep, and early awakenings), sleep duration (short-sleep 5 or less; long-sleep >8hrs), epigenetic age, naïve T cell (CD8+CD45RA+CCR7+), and late differentiated T cells (CD8+CD28-CD45RA-). Results Insomnia symptoms were related to advanced epigenetic age, B(SE)=1.02(.37),P=0.005, after adjustments for covariates. Insomnia symptoms were also associated with more late differentiated T cells (B(SE)=.59(.21),P=.006), but not with naïve T cells. Self-reported short and long sleep duration were unrelated to epigenetic age. Short sleep, but not long sleep, was associated with fewer naïve T cells (P<.005) and neither were related to late differentiated T cells. Conclusions Symptoms of insomnia were associated with increased epigenetic age of blood tissue, and were associated with higher counts of late differentiated CD8+ T cells. Short sleep was unrelated to epigenetic age and late differentiated cell counts, but was related to a decline in naïve T cells. In this large population based study of women in the United States, insomnia symptoms are implicated in accelerated aging.
Early adversity and adult health outcomes Taylor, Shelley E; Way, Baldwin M; Seeman, Teresa E
Development and psychopathology,
08/2011, Letnik:
23, Številka:
3
Journal Article
Recenzirano
Adversity in childhood has effects on mental and physical health, not only in childhood but across the lifespan. A chief task of our research has been to define the pathways by which childhood ...experience has these surprising health outcomes, often decades later. The concept of allostatic load, which refers to dysregulations across major biological regulatory systems that have cumulative interacting adverse effects over time, provides a mechanism for understanding these relations and defining specific pathways. To chart these pathways, we examine early childhood socioeconomic status, family environment, and genetic predispositions as antecedents to socioemotional functioning/psychological distress; and neural responses to threat that have downstream effects on major stress regulatory systems, ultimately culminating in risks to mental and physical health outcomes. This integrative approach to investigating the impact of childhood experience on adult health outcomes illustrates the significance of multilevel integrative approaches to understanding developmental psychopathology more generally.
We investigated trends in disability among older Americans from 1988 through 2004 to test the hypothesis that more recent cohorts show increased burdens of disability.
We used data from 2 National ...Health and Nutrition Examination Surveys (1988-1994 and 1999-2004) to assess time trends in basic activities of daily living, instrumental activities, mobility, and functional limitations for adults aged 60 years and older. We assessed whether changes could be explained by sociodemographic, body weight, or behavioral factors.
With the exception of functional limitations, significant increases in each type of disability were seen over time among respondents aged 60 to 69 years, independent of sociodemographic characteristics, health status, relative weight, and health behaviors. Significantly greater increases occurred among non-Whites and persons who were obese or overweight (2 of the fastest-growing subgroups within this population). We detected no significant trends among respondents aged 70 to 79 years; in the oldest group (aged>or=80 years), time trends suggested lower prevalence of functional limitations among more recent cohorts.
Our results have significant and sobering implications: older Americans face increased disability, and society faces increased costs to meet the health care needs of these disabled Americans.
Short sleep and poor sleep quality are associated with risk of cardiovascular disease, diabetes, cancer, and mortality. This study examines the contribution of sleep duration and sleep quality on a ...multisystem biological risk index that is known to be associated with morbidity and mortality.
Analyses include a population-based sample from the Midlife Development in the United States survey recruited to the Biomarker substudy. A total of 1,023 participants aged 54.5 years (SD = 11.8), 56% female and 77.6% white, were included in the analyses. A multisystem biological risk index was derived from 22 biomarkers capturing cardiovascular, immune, lipid-metabolic, glucose-metabolic, sympathetic, parasympathetic, and hypothalamic-pituitary-adrenal systems. Self-reported average sleep duration was categorized as short (<5 hrs), below normal (5 to <6.5 hrs), normal (6.5 to <8.5 hrs), and long sleepers (8.5+ hrs). Sleep quality was determined using the Pittsburgh Sleep Quality Index categorized as normal (≤5) and poor quality (>5) sleep.
Linear mixed effect models adjusting for age, gender, race, education, income, BMI, and health status were performed. As compared to normal sleepers, multisystem biological risk in both short (B(SE) = .38(.15), p<.01) and long sleepers (B(SE) = .28(.11), p<.01) were elevated. Poor quality sleep alone was associated with elevated multisystem biological risk (B(SE) = .15(.06), p = .01), but was not significant after adjustment for health status. All short sleepers reported poor sleep quality. However in the long sleepers, only those who reported poor sleep quality exhibited elevated multisystem biological risk (B(SE) = .93(.3), p = .002).
Self-reported poor sleep quality with either short or long sleep duration is associated with dysregulation in physiological set points across regulatory systems, leading to elevated multisystem biological risk. Physicians should inquire about sleep health in the assessment of lifestyle factors related to disease risk, with evidence that healthy sleep is associated with lower multisystem biological risk.
Abstract
Study Objectives
Variable daily sleep (ie, higher intraindividual variability; IIV) is associated with negative health consequences, but potential physiological mechanisms are poorly ...understood. This study examined how the IIV of sleep timing, duration, and quality is associated with physiological dysregulation, with diurnal cortisol trajectories as a proximal outcome and allostatic load (AL) as a multisystem distal outcome.
Methods
Participants are 436 adults (M
age ± standard deviation = 54.1 ± 11.7, 60.3% women) from the Midlife in the United States study. Sleep was objectively assessed using 7-day actigraphy. Diurnal cortisol was measured via saliva samples (four/day for 4 consecutive days). AL was measured using 23 biomarkers from seven systems (inflammatory, hypothalamic–pituitary–adrenal axis, metabolic glucose and lipid, cardiovascular, parasympathetic, sympathetic) using a validated bifactor model. Linear and quadratic effects of sleep IIV were estimated using a validated Bayesian model.
Results
Controlling for covariates, more variable sleep timing (p = .04 for risetime, p = .097 for bedtime) and total sleep time (TST; p = .02), but not mean sleep variables, were associated with flatter cortisol diurnal slope. More variable sleep onset latency and wake after sleep onset, later average bedtime, and shorter TST were associated with higher AL adjusting for age and sex (p-values < .05); after controlling for all covariates, however, only later mean bedtime remained significantly associated with higher AL (p = .04).
Conclusions
In a community sample of adults, more variable sleep patterns were associated with blunted diurnal cortisol trajectories but not with higher multisystem physiological dysregulation. The associations between sleep IIV and overall health are likely complex, including multiple biopsychosocial determinants and require further investigation.
We examined the joint contributions of self-reported adverse childhood experiences (ACEs) and recent life events (RLEs) to inflammation at midlife, by testing 3 competing theoretical models: stress ...generation, stress accumulation, and early life stress sensitization. We aimed to identify potential mediators between adversity and inflammation. Participants were 1,180 middle-aged and older adults from the Midlife in the United States (MIDUS) Biomarker Project (M age = 57.3 years, SD = 11.5; 56% female). A composite measure of inflammation was derived from 5 biomarkers: serum levels of C-reactive protein, interleukin-6, fibrinogen, E-selectin, and ICAM-1. Participants provided self-report data regarding ACEs, RLEs, current lifestyle indices (cigarette smoking, alcohol consumption, physical exercise, waist circumference), current depressive symptoms, and demographic/biomedical characteristics. We also used indices of hypothalamic-pituitary-adrenocortical outflow (12-hr urinary cortisol) and sympathetic nervous system output (12-hr urinary norepinephrine and epinephrine). Analyses indicated that ACEs and RLEs were independently associated with higher levels of inflammation, controlling for each other's effects. Their interaction was not significant. The results were consistent with the hypothesis that associations between ACEs and inflammation were mediated through higher urinary norepinephrine output, greater waist circumference, smoking, and lower levels of exercise, whereas higher waist circumference and more smoking partially mediated the association between RLEs and inflammation. In support of the stress accumulation model, ACEs and RLEs had unique and additive contributions to inflammation at midlife, with no evidence of synergistic effects. Results also suggested that norepinephrine output and lifestyle indices may help explain how prior stressors foster inflammation at midlife.
This chapter focuses on evidence linking socio‐economic status (SES) to “downstream” peripheral biology. Drawing on the concept of allostatic load, we examine evidence linking lower SES with greater ...cumulative physiological toll on multiple major biological regulatory systems over the life course. We begin by reviewing evidence linking lower SES to poorer trajectories of aging in multiple, individual physiological systems, followed by evidence of the resulting cumulative, overall burdens of physiological dysregulation seen among those of lower SES. The role of cumulative physiological dysregulation in mediating SES gradients in morbidity and mortality is then examined. We conclude with discussion of the question of interactions between SES (and other such environmental factors) and genetic endowment, and their potential consequences for patterns of physiological activity—an area of research that appears poised to contribute significantly to our understanding of how social conditions “get under the skin” to affect health and aging.
Childhood abuse increases adult risk for morbidity and mortality. Less clear is how this “toxic” stress becomes embedded to influence health decades later, and whether protective factors guard ...against these effects. Early biological embedding is hypothesized to occur through programming of the neural circuitry that influences physiological response patterns to subsequent stress, causing wear and tear across multiple regulatory systems. To examine this hypothesis, we related reports of childhood abuse to a comprehensive 18-biomarker measure of multisystem risk and also examined whether presence of a loving parental figure buffers against the impact of childhood abuse on adult risk. A total of 756 subjects (45.8% white, 42.7% male) participated in this ancillary substudy of the Coronary Artery Risk Development in Young Adults Study. Childhood stress was determined by using the Risky Families Questionnaire, a well-validated retrospective self-report scale. Linear regression models adjusting for age, sex, race, parental education, and oral contraceptive use found a significant positive relationship between reports of childhood abuse and multisystem health risks B (SE) = 0.68 (0.16); P < 0.001. Inversely, higher amounts of reported parental warmth and affection during childhood was associated with lower multisystem health risks B (SE) = −0.40 (0.14); P < 0.005. A significant interaction of abuse and warmth (P < 0.05) was found, such that individuals reporting low levels of love and affection and high levels of abuse in childhood had the highest multisystem risk in adulthood.
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