Rethinking morbidity compression.
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ABSTRACT:
SUBMITTER: Seaman R
PROVIDER: S-EPMC7250949 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Current measures of population health lack indicators capturing the variability in age-at-morbidity onset, an important marker to assess the timing patterns of individuals' health deterioration and evaluate the compression of morbidity. We provide global, regional, and national estimates of the variability in morbidity onset from 1990 to 2019 using indicators of healthy lifespan inequality (HLI). Using data from the Global Burden of Disease Study 2019, we reconstruct age-at-death distributions to calculate lifespan inequality (LI), and age-at-morbidity onset distributions to calculate HLI. We measure LI and HLI with the standard deviation. Between 1990 and 2019, global HLI decreased from 24.74 years to 21.92, and has been decreasing in all regions except in high-income countries, where it has remained stable. Countries with high HLI are more present in sub-Saharan Africa and south Asia, whereas low HLI values are predominant in high-income countries and central and eastern Europe. HLI tends to be higher for females than for males, and HLI tends to be higher than LI. Globally, between 1990 and 2019 HLI at age 65 increased from 6.83 years to 7.44 for females, and from 6.23 to 6.96 for males. Improvements in longevity are not necessarily accompanied by further reductions in HLI among longevity vanguard countries. Morbidity is compressing, except in high-income countries, where it stagnates. The variability in the ages at morbidity onset tends to be larger than the variability in lifespans, and such divergence broadens over time. As longevity increases worldwide, the locus of health inequality is moving from death-related inequalities to disease- and disability-centered ones.
| S-EPMC10080172 | biostudies-literature
Project description:BackgroundIncreases in life expectancy are hypothesised to be associated with shorter proportional time spent with morbidity (compression of morbidity). We assessed whether this has occurred among older adults in the USA during the 1990s and 2000s.MethodsWe used data from the Health and Retirement Study to estimate a morbidity score based on eight chronic conditions and compare it (1) prospectively between two age-matched cohorts in 1992 and 2004 over a 6-year follow-up, and (2) retrospectively in the three waves prior to death among respondents who die in (1998-2004) and (2004-2010).ResultsProspective assessment shows significantly higher prevalence in 6 of eight chronic conditions in the 2000s, with 37% higher diabetes prevalence. A retrospective evaluation shows significantly higher prevalence in 7 of eight chronic conditions in the three waves prior to death for (2004-2010) versus (1998-2004), with 41% higher prevalence of arthritis. Importantly, the farther away from time of death, the higher the average number of chronic conditions in (2004-2010).ConclusionsUsing the largest longitudinal ageing study in the USA, we found no clear evidence of compression of morbidity as measured by self-reported chronic disease. Older adults in the USA may be experiencing greater disease burden in recent times.
| S-EPMC5486403 | biostudies-literature
Project description:BackgroundThe compression of morbidity model posits a breakpoint in the adult lifespan that separates an initial period of relative health from a subsequent period of ever increasing morbidity. Researchers often assume that such a breakpoint exists; however, this assumption is hitherto untested.PurposeTo test the assumption that a breakpoint exists--which we term a morbidity tipping point--separating a period of relative health from a subsequent deterioration in health status. An analogous tipping point for healthcare costs was also investigated.MethodsFour years of adults' (N = 55,550) morbidity and costs data were retrospectively analyzed. Data were collected in Pittsburgh, PA between 2006 and 2009; analyses were performed in Rochester, NY and Ann Arbor, MI in 2012 and 2013. Cohort-sequential and hockey stick regression models were used to characterize long-term trajectories and tipping points, respectively, for both morbidity and costs.ResultsMorbidity increased exponentially with age (P<.001). A morbidity tipping point was observed at age 45.5 (95% CI, 41.3-49.7). An exponential trajectory was also observed for costs (P<.001), with a costs tipping point occurring at age 39.5 (95% CI, 32.4-46.6). Following their respective tipping points, both morbidity and costs increased substantially (Ps<.001).ConclusionsFindings support the existence of a morbidity tipping point, confirming an important but untested assumption. This tipping point, however, may occur earlier in the lifespan than is widely assumed. An "avalanche of morbidity" occurred after the morbidity tipping point-an ever increasing rate of morbidity progression. For costs, an analogous tipping point and "avalanche" were observed. The time point at which costs began to increase substantially occurred approximately 6 years before health status began to deteriorate.
| S-EPMC4427176 | biostudies-literature
Project description:BACKGROUND:Super-Seniors are healthy, long-lived individuals who were recruited at age 85?years or older with no history of cancer, cardiovascular disease, diabetes, dementia, or major pulmonary disease. In a 10-year follow-up, we aimed to determine whether surviving Super-Seniors showed compression of morbidity, and to test whether the allele frequencies of longevity-associated variants in APOE and FOXO3 were more extreme in such long-term survivors. METHODS:Super-Seniors who survived and were contactable were re-interviewed 10?years after initial characterization. Health and lifestyle were characterized via questionnaire. Geriatric tests including the Timed Up and Go (TUG), Geriatric Depression Scale (GDS), Instrumental Activities of Daily Living (IADL) and the Mini-Mental State Exam (MMSE) were administered, and data were compared to results from on average 10?years earlier. As well, genotype and allele frequencies for SNPs rs7412 and rs429358 in APOE, and rs2802292 in FOXO3 were compared to the frequencies in the original collection of Super-Seniors and mid-life controls. RESULTS:Of the 480 Super-Seniors recruited from 2004 to 2007, 13 were alive, contactable, and consented to re-interview (mean age?=?100.1?±?3.3). Eight of these 13 participants (62%) still met Super-Senior health criteria. Diseases that occurred in late life were cardiovascular (5 of 13; 38%) and lung disease (1 of 13; 8%). MMSE and IADL scores declined in the decade between interviews, and GDS and TUG scores increased. The surviving group of centenarians had a higher frequency of APOE and FOXO3 longevity-associated variants even when compared to the original long-lived Super-Senior cohort. CONCLUSIONS:Although physical and mental decline occurred in the decade between interviews, the majority of Super-Seniors re-interviewed still met the original health criteria. These observations are consistent with reports of compression of morbidity at extreme ages, particularly in centenarians. The increased frequency of longevity- associated variants in this small group of survivors is consistent with studies that reported genetics as a larger contributor to longevity in older age groups.
| S-EPMC6394013 | biostudies-literature
Project description:Importance:Prior studies have demonstrated lower all-cause mortality in individuals who are overweight compared with those with normal body mass index (BMI), but whether this may come at the cost of greater burden of cardiovascular disease (CVD) is unknown. Objective:To calculate lifetime risk estimates of incident CVD and subtypes of CVD and to estimate years lived with and without CVD by weight status. Design, Setting, and Participants:In this population-based study, we used pooled individual-level data from adults (baseline age, 20-39, 40-59, and 60-79 years) across 10 large US prospective cohorts, with 3.2 million person-years of follow-up from 1964 to 2015. All participants were free of clinical CVD at baseline with available BMI index and CVD outcomes data. Data were analyzed from October 2016 to July 2017. Exposures:World Health Organization-standardized BMI categories. Main Outcomes and Measures:Total CVD and CVD subtype, including fatal and nonfatal coronary heart disease, stroke, congestive heart failure, and other CVD deaths. Heights and weights were measured directly by investigators in each study, and BMI was calculated as weight in kilograms divided by height in meters squared. We performed (1) modified Kaplan-Meier analysis to estimate lifetime risks, (2) adjusted competing Cox models to estimate joint cumulative risks for CVD or noncardiovascular death, and (3) the Irwin restricted mean to estimate years lived free of and with CVD. Results:Of the 190?672 in-person examinations included in this study, the mean (SD) age was 46.0 (15.0) years for men and 58.7 (12.9) years for women, and 140?835 patients (73.9%) were female. Compared with individuals with a normal BMI (defined as a BMI of 18.5 to 24.9), lifetime risks for incident CVD were higher in middle-aged adults in the overweight and obese groups. Compared with normal weight, among middle-aged men and women, competing hazard ratios for incident CVD were 1.21 (95% CI, 1.14-1.28) and 1.32 (95% CI, 1.24-1.40), respectively, for overweight (BMI, 25.0-29.9), 1.67 (95% CI, 1.55-1.79) and 1.85 (95% CI, 1.72-1.99) for obesity (BMI, 30.0-39.9), and 3.14 (95% CI, 2.48-3.97) and 2.53 (95% CI, 2.20-2.91) for morbid obesity (BMI, ?40.0). Higher BMI had the strongest association with incident heart failure among CVD subtypes. Average years lived with CVD were longer for middle-aged adults in the overweight and obese groups compared with adults in the normal BMI group. Similar patterns were observed in younger and older adults. Conclusions and Relevance:In this study, obesity was associated with shorter longevity and significantly increased risk of cardiovascular morbidity and mortality compared with normal BMI. Despite similar longevity compared with normal BMI, overweight was associated with significantly increased risk of developing CVD at an earlier age, resulting in a greater proportion of life lived with CVD morbidity.
| S-EPMC5875319 | biostudies-literature
Project description:BackgroundThere is debate around the composition of life years gained from smoking elimination. The aim of this study was to conduct a systematic review of the literature to synthesize existing evidence on the effect of smoking status on health expectancy and to examine whether smoking elimination leads to compression of morbidity.MethodsFive databases were systematically searched for peer-reviewed articles. Studies that presented quantitative estimates of health expectancy for smokers and non-/never-smokers were eligible for inclusion. Studies were searched, selected and reviewed by two reviewers who extracted the relevant data and assessed the risk of bias of the included articles independently.ResultsThe search identified 2491 unique records, whereof 20 articles were eligible for inclusion (including 26 cohorts). The indicators used to measure health included disability/activity limitations (n=9), health-related quality of life (EQ-5D) (n=2), weighted disabilities (n=1), self-rated health (n=9), chronic diseases (n=6), cardiovascular diseases (n=4) and cognitive impairment (n=1). Available evidence showed consistently that non-/never-smokers experience more healthy life years throughout their lives than smokers. Findings were inconsistent on the effect of smoking on the absolute number of unhealthy life years. Findings concerning the time proportionally spent unhealthy were less heterogeneous: nearly all included articles reported that non-/never-smokers experience relatively less unhealthy life years (e.g. relative compression of morbidity).ConclusionsSupport for the relative compression of morbidity due to smoking elimination was evident. Further research is needed into the absolute compression of morbidity hypothesis since current evidence is mixed, and methodology of studies needs to be harmonized.
| S-EPMC8071592 | biostudies-literature
Project description:BackgroundOne of the principles underpinning our understanding of ageing is that DNA damage induces a stress response that shifts cellular resources from growth towards maintenance. A contrasting and seemingly irreconcilable view is that prompting growth of, for example, skeletal muscle confers systemic benefit.MethodsTo investigate the robustness of these axioms, we induced muscle growth in a murine progeroid model through the use of activin receptor IIB ligand trap that dampens myostatin/activin signalling. Progeric mice were then investigated for neurological and muscle function as well as cellular profiling of the muscle, kidney, liver, and bone.ResultsWe show that muscle of Ercc1Δ/- progeroid mice undergoes severe wasting (decreases in hind limb muscle mass of 40-60% compared with normal mass), which is largely protected by attenuating myostatin/activin signalling using soluble activin receptor type IIB (sActRIIB) (increase of 30-62% compared with untreated progeric). sActRIIB-treated progeroid mice maintained muscle activity (distance travel per hour: 5.6 m in untreated mice vs. 13.7 m in treated) and increased specific force (19.3 mN/mg in untreated vs. 24.0 mN/mg in treated). sActRIIb treatment of progeroid mice also improved satellite cell function especially their ability to proliferate on their native substrate (2.5 cells per fibre in untreated progeroids vs. 5.4 in sActRIIB-treated progeroids after 72 h in culture). Besides direct protective effects on muscle, we show systemic improvements to other organs including the structure and function of the kidneys; there was a major decrease in the protein content in urine (albumin/creatinine of 4.9 sActRIIB treated vs. 15.7 in untreated), which is likely to be a result in the normalization of podocyte foot processes, which constitute the filtration apparatus (glomerular basement membrane thickness reduced from 224 to 177 nm following sActRIIB treatment). Treatment of the progeric mice with the activin ligand trap protected against the development of liver abnormalities including polyploidy (18.3% untreated vs. 8.1% treated) and osteoporosis (trabecular bone volume; 0.30 mm3 in treated progeroid mice vs. 0.14 mm3 in untreated mice, cortical bone volume; 0.30 mm3 in treated progeroid mice vs. 0.22 mm3 in untreated mice). The onset of neurological abnormalities was delayed (by ~5 weeks) and their severity reduced, overall sustaining health without affecting lifespan.ConclusionsThis study questions the notion that tissue growth and maintaining tissue function during ageing are incompatible mechanisms. It highlights the need for future investigations to assess the potential of therapies based on myostatin/activin blockade to compress morbidity and promote healthy ageing.
| S-EPMC6596402 | biostudies-literature
Project description:ObjectivesCompression of morbidity postulates that as the populations age, the age of onset of disease is postponed. The objective of this study is to test for evidence of compression of morbidity in Spain.MethodsWe calculated the age and sex-specific incidence of myocardial infarction, heart failure, cerebrovascular disease, as well as bladder, prostate, breast, lung, and colon cancer among hospital discharges covering 99.5 % of the Spanish population, approximately 40 million inhabitants for two non-overlapping periods, 1997-2000 and 2007-2010, and estimated the length of life spent with disease using the Sullivan method.ResultsWe found that expansion of morbidity due to an earlier age-specific onset of incident disease and increase in life expectancy was the norm in Spain. Notable exceptions were cardiovascular disease in women (-0.2 % time spent with disease) and lung cancer for men (-0.9 % time spent with disease) from 1997-2000 to 2007-2010.ConclusionsCompression of morbidity is often cited by policy makers when discussing adjustments to the health-care system. If morbidity is measured by age at onset of disease, the burden of morbidity has increased in Spain.
| S-EPMC7446746 | biostudies-literature
Project description:Concern for megafauna is increasing among scientists and non-scientists. Many studies have emphasized that megafauna play prominent ecological roles and provide important ecosystem services to humanity. But, what precisely are 'megafauna'? Here, we critically assess the concept of megafauna and propose a goal-oriented framework for megafaunal research. First, we review definitions of megafauna and analyse associated terminology in the scientific literature. Second, we conduct a survey among ecologists and palaeontologists to assess the species traits used to identify and define megafauna. Our review indicates that definitions are highly dependent on the study ecosystem and research question, and primarily rely on ad hoc size-related criteria. Our survey suggests that body size is crucial, but not necessarily sufficient, for addressing the different applications of the term megafauna. Thus, after discussing the pros and cons of existing definitions, we propose an additional approach by defining two function-oriented megafaunal concepts: 'keystone megafauna' and 'functional megafauna', with its variant 'apex megafauna'. Assessing megafauna from a functional perspective could challenge the perception that there may not be a unifying definition of megafauna that can be applied to all eco-evolutionary narratives. In addition, using functional definitions of megafauna could be especially conducive to cross-disciplinary understanding and cooperation, improvement of conservation policy and practice, and strengthening of public perception. As megafaunal research advances, we encourage scientists to unambiguously define how they use the term 'megafauna' and to present the logic underpinning their definition.
| S-EPMC7126068 | biostudies-literature
Project description:Classification of the human gut microbiome into distinct types, or "enterotypes," provides an attractive framework for understanding microbial variation in health and disease. However, as discussed here, several different methods of collapsing enterotype variation into a few discrete clusters suggest that enterotype distribution is continuous and can vary widely within an individual.
| S-EPMC5558460 | biostudies-literature