scholarly journals Aging as a consequence of selection to reduce the environmental risk of dying

2021 ◽  
Vol 118 (22) ◽  
pp. e2102088118
Author(s):  
Stig W. Omholt ◽  
Thomas B. L. Kirkwood

Each animal in the Darwinian theater is exposed to a number of abiotic and biotic risk factors causing mortality. Several of these risk factors are intimately associated with the act of energy acquisition as such and with the amount of reserve the organism has available from this acquisition for overcoming temporary distress. Because a considerable fraction of an individual’s lifetime energy acquisition is spent on somatic maintenance, there is a close link between energy expenditure on somatic maintenance and mortality risk. Here, we show, by simple life-history theory reasoning backed up by empirical cohort survivorship data, how reduction of mortality risk might be achieved by restraining allocation to somatic maintenance, which enhances lifetime fitness but results in aging. Our results predict the ubiquitous presence of senescent individuals in a highly diverse group of natural animal populations, which may display constant, increasing, or decreasing mortality with age. This suggests that allocation to somatic maintenance is primarily tuned to expected life span by stabilizing selection and is not necessarily traded against reproductive effort or other traits. Due to this ubiquitous strategy of modulating the somatic maintenance budget so as to increase fitness under natural conditions, it follows that individuals kept in protected environments with very low environmental mortality risk will have their expected life span primarily defined by somatic damage accumulation mechanisms laid down by natural selection in the wild.

2019 ◽  
Vol 38 (6) ◽  
pp. 589-594 ◽  
Author(s):  
Angela Gentile ◽  
María Florencia Lucion ◽  
María del Valle Juarez ◽  
María Soledad Areso ◽  
Julia Bakir ◽  
...  

Renal Failure ◽  
2007 ◽  
Vol 29 (7) ◽  
pp. 823-828 ◽  
Author(s):  
Beril Akman ◽  
Ayse Bilgic ◽  
Gulsah Sasak ◽  
Siren Sezer ◽  
Atilla Sezgin ◽  
...  

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A273-A273
Author(s):  
Xi Zheng ◽  
Ma Cherrysse Ulsa ◽  
Peng Li ◽  
Lei Gao ◽  
Kun Hu

Abstract Introduction While there is emerging evidence for acute sleep disruption in the aftermath of coronavirus disease 2019 (COVID-19), it is unknown whether sleep traits contribute to mortality risk. In this study, we tested whether earlier-life sleep duration, chronotype, insomnia, napping or sleep apnea were associated with increased 30-day COVID-19 mortality. Methods We included 34,711 participants from the UK Biobank, who presented for COVID-19 testing between March and October 2020 (mean age at diagnosis: 69.4±8.3; range 50.2–84.6). Self-reported sleep duration (less than 6h/6-9h/more than 9h), chronotype (“morning”/”intermediate”/”evening”), daytime dozing (often/rarely), insomnia (often/rarely), napping (often/rarely) and presence of sleep apnea (ICD-10 or self-report) were obtained between 2006 and 2010. Multivariate logistic regression models were used to adjust for age, sex, education, socioeconomic status, and relevant risk factors (BMI, hypertension, diabetes, respiratory diseases, smoking, and alcohol). Results The mean time between sleep measures and COVID-19 testing was 11.6±0.9 years. Overall, 5,066 (14.6%) were positive. In those who were positive, 355 (7.0%) died within 30 days (median = 8) after diagnosis. Long sleepers (>9h vs. 6-9h) [20/103 (19.4%) vs. 300/4,573 (6.6%); OR 2.09, 95% 1.19–3.64, p=0.009), often daytime dozers (OR 1.68, 95% 1.04–2.72, p=0.03), and nappers (OR 1.52, 95% 1.04–2.23, p=0.03) were at greater odds of mortality. Prior diagnosis of sleep apnea also saw a two-fold increased odds (OR 2.07, 95% CI: 1.25–3.44 p=0.005). No associations were seen for short sleepers, chronotype or insomnia with COVID-19 mortality. Conclusion Data across all current waves of infection show that prior sleep traits/disturbances, in particular long sleep duration, daytime dozing, napping and sleep apnea, are associated with increased 30-day mortality after COVID-19, independent of health-related risk factors. While sleep health traits may reflect unmeasured poor health, further work is warranted to examine the exact underlying mechanisms, and to test whether sleep health optimization offers resilience to severe illness from COVID-19. Support (if any) NIH [T32GM007592 and R03AG067985 to L.G. RF1AG059867, RF1AG064312, to K.H.], the BrightFocus Foundation A2020886S to P.L. and the Foundation of Anesthesia Education and Research MRTG-02-15-2020 to L.G.


Gerontology ◽  
2021 ◽  
pp. 1-9
Author(s):  
Timothy A. Donlon ◽  
Randi Chen ◽  
Kamal H. Masaki ◽  
Bradley J. Willcox ◽  
Brian J. Morris

<b><i>Introduction:</i></b> Genetic variation in the phosphatidylinositol 3-kinase reregulatory subunit 1 gene (<i>PIK3R1</i>) is associated with longevity. <b><i>Objective:</i></b> The aim of the study was to determine whether cardiovascular disease (CVD) affects this association. <b><i>Methods:</i></b> We performed a longitudinal study of longevity-associated <i>PIK3R1</i> single-nucleotide polymorphism <i>rs7709243</i> genotype by CVD status in 3,584 elderly American men of Japanese ancestry. <b><i>Results:</i></b> At baseline (1991–1993), 2,254 subjects had CVD and 1,314 did not. The follow-up until Dec 31, 2019 found that overall, men with a CVD had higher mortality than men without a CVD (<i>p</i> = 1.7 × 10<sup>−5</sup>). However, survival curves of CVD subjects differed according to <i>PIK3R1</i> genotype. Those with longevity-associated <i>PIK3R1 TT</i>/<i>CC</i> had survival curves similar to those of subjects without a CVD (<i>p</i> = 0.11 for <i>TT</i>/<i>CC</i>, and <i>p</i> = 0.054 for <i>TC</i>), whereas survival curves for CVD subjects with the <i>CT</i> genotype were significantly attenuated compared with survival curves of subjects without a CVD (<i>p</i> = 0.0000012 compared with <i>TT</i>/<i>CC</i>, and <i>p</i> = 0.0000028 compared with <i>TC</i>). Men without CVD showed no association of longevity-associated genotype with life span (<i>p</i> = 0.58). Compared to subjects without any CVD, hazard ratios for mortality risk were 1.26 (95% CI, 1.14–1.39; <i>p</i> = 0.0000043) for <i>CT</i> subject with CVD and 1.07 (95% CI 0.99–1.17; <i>p</i> = 0.097) for <i>CC</i>/<i>TT</i> subjects with CVD. There was no genotypic effect on life span for 1,007 subjects with diabetes and 486 with cancer. <b><i>Conclusion:</i></b> Our study provides novel insights into the basis for <i>PIK3R1</i> as a longevity gene. We suggest that the <i>PIK3R1</i> longevity genotype attenuates mortality risk in at-risk individuals by protection against cellular stress caused by CVD.


2006 ◽  
Vol 18 (6) ◽  
pp. 274-274
Author(s):  
J Walker ◽  
H Christensen ◽  
T Windsor ◽  
A George

1985 ◽  
Vol 110 (4_Suppl) ◽  
pp. S21-S26 ◽  
Author(s):  
R. J. Jarrett ◽  
M. J. Shipley

Summary. In 168 male diabetics aged 40-64 years participating in the Whitehall Study, ten-year age adjusted mortality rates were significantly higher than in non-diabetics for all causes, coronary heart disease, all cardiovascular disease and, in addition, causes other than cardiovascular. Mortality rates were not significantly related to known duration of the diabetes. The predictive effects of several major mortality risk factors were similar in diabetics and non-diabetics. Excess mortality rates in the diabetics could not be attributed to differences in levels of blood pressure or any other of the major risk factors measured. Key words: diabetics; mortality rates; risk factors; coronary heart disease. There are many studies documenting higher mortality rates - particularly from cardiovascular disease -in diabetics compared with age and sex matched diabetics from the same population (see Jarrett et al. (1982) for review). However, there is sparse information relating potential risk factors to subsequent mortality within a diabetic population, information which might help to explain the increased mortality risk and also suggest preventive therapeutic approaches. In the Whitehall Study, a number of established diabetics participated in the screening programme and data on mortality rates up to ten years after screening are available. We present here a comparison of diabetics and non-diabetics in terms of relative mortality rates and the influence of conventional risk factors as well as an analysis of the relationship between duration of diabetes and mortality risk.


Author(s):  
M. Hidalgo de la Cruz ◽  
J.A. Miranda Acuña ◽  
E. Luque Buzo ◽  
B. Chavarria Cano ◽  
E. Esteban de Antonio ◽  
...  

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