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At least 19 recordsLinked to original sources

PubMed2026

Parental longevity and polygenic longevity scores in relation to ageing-related factors in a population of 70-year-olds followed over six years: The Gothenburg H70 Birth Cohort Study.

As societies age, a deeper understanding of ageing-related factors that contribute to longevity is needed. We therefore investigated possible longevity factors (social, medical, and biological) in relation to parental longevity (PL) and polygenic longevity scores (PGLSs). We examined 1126 70-year-olds from the Swedish population-based Gothenburg H70 Birth Cohort study in 2014-2016 (response rate 72%), with follow-up in 2019-2022 (response rate 77.6%). Comprehensive examinations included self-reported information on parents' ages, socioeconomic factors, mental, cardiovascular, and neurological health, anthropometry, laboratory data, and genotyping to construct two continuous PGLSs variables (with and without the APOE locus). PL groups were categorised as high if both parents survived to age 85 (17.2%); medium if one parent had survived (43.3%), and low if neither parent had survived to age 85 (39.4%). Higher PL and higher PGLSs were related to less hypertension, higher educational level, better childhood, and current socioeconomic status. In addition, higher PL was associated with higher MMSE score, total cholesterol, HDL-cholesterol (HDL-c) and LDL-cholesterol (LDL-c), lower BMI, homocysteine and inflammatory markers (IL-6, CRP) levels, and less smoking, whereas higher PGLSs was related to less myocardial infarction. At follow-up, high-PL was associated with less increase in plasma pTau217. PGLSs were mainly related to socioeconomic and cardiovascular factors, while individuals with long-lived parents, in addition, had several other characteristics of longevity, such as less inflammation, homocysteine, and markers of dementia. PL may be a proxy for biological ageing and used as a screening for ageing-related disorders in the context of prevention.

APOE↗

PubMed1978

A look at the basic correlates of longevity: is longevity a superficial trait?

Nature appears to have distributed life spans, whether long or short, entirely upon the possession or non-possession of a few physiologically superficial characteristics, namely, immunity of mature, full-sized specimens from the effects of: (1) predation, (2) competition, (3) fire, (4) disease, and (5) the existence of a definite usefulness for long life spans in bridging lengthy periods unfavorable to the reproduction and/or maturation of offspring. Extremely strong correlations are presented in proof of the above relationships. Since longevity mechanisms can closely correlate to superficial traits, it is unlikely that they comprise an integral part of basic structural or biochemical processes. In the case of trees, all five of the above traits are apparently required for the achievement of potential life spans in excess of 1000 years. By contrast, the longest live animal species appear to fully possess only (1) and (3) of the five prerequisite traits above. This observation may fully account for the fact that maximum life spans of trees are 30-40 times greater than those of the longest lived animals.

Animals↗

PubMed1979

An attempt to select for increased longevity in Drosophila melanogaster.

Eight generations of selection towards a higher longevity were made in a wild strain of Drosophila melanogaster. Two control lines were also observed. Absolutely no response to selection was obtained whilst a major increase in longevity occurred between F2 and F4 in the three lines under observation. It is shown that the major increase in longevity is due neither to genetic drift, nor to changes in classical environmental conditions. The absence of response to selection is demonstrated to be due neither to a too low selection differential, nor to the absence of genetic variability in the strain, nor to inaccuracy in the measurements, nor to recurrent reproduction at an old age. The impossibility to select towards a higher longevity and the total absence of relation between parental and offspring longevities demonstrate that the very large phenotypic variability displayed by longevity in wild strains of D. melanogaster does not depend on a precise set of specific genes or polygenes with additive action. The results are briefly discussed in relation with inbreeding depression and heterosis for longevity and with similar results obtained in experiments of selection for duration of development.

Animals↗

PubMed2026

Elevated mitochondrial superoxide promotes longevity through a mitochondria-to-nucleus kinase signaling pathway.

The reactive oxygen species superoxide is generated by mitochondria during the process of producing energy. While superoxide can cause oxidative damage to the cell, we and others have shown that a mild increase in mitochondrial superoxide extends longevity in multiple model organisms. To elucidate the molecular mechanisms involved, we identified transcriptional changes in mitochondrial superoxide dismutase deletion mutants (sod-2 worms) using RNA sequencing. sod-2 mutants exhibit a number of changes in nuclear gene expression resulting from elevated mitochondrial superoxide suggesting that mitochondria-to-nucleus signaling is contributing to their longevity. Gene ontology enrichment analysis demonstrated that genes involved in innate immunity and cuticle formation are significantly upregulated in sod-2 worms. To identify kinases involved in this lifespan-extending pathway, we completed a targeted RNA interference screen to examine the contribution of selected kinases to sod-2 longevity. From this screen, we found 25 kinases which are required for the long lifespan of sod-2 mutants including mak-2, which has a role in a kinase signaling pathway involved in axon regeneration. Disruption of mak-2 specifically reduces sod-2 lifespan but not wild-type longevity and also decreases resistance to multiple exogenous stressors. In examining other genes that act with mak-2 in established signaling pathways, we identified a SEK-3/PMK-3/MAK-2/CEBP-1 signaling pathway that is specifically required for sod-2 longevity but not wild-type lifespan. Combined these results suggest a novel role for kinases with established roles in axon regeneration in promoting longevity through a mitochondria-to-nucleus signaling pathway.

Aging↗

PubMed1992

Sublethal effects of insecticides on adult longevity and fecundity of German cockroaches (Dictyoptera: Blattellidae).

The effects of sublethal concentrations of chlorpyrifos, cyfluthrin, and hydramethylnon on adult longevity and fecundity of German cockroaches, Blattella germanica (L.), were investigated. Longevity of males declined linearly with increasing doses of insecticide. An LD50 of cyfluthrin decreased male longevity by 52%, whereas an LD50 of hydramethylnon reduced male longevity by 81%. Longevity of females increased linearly with increasing sublethal doses of chlorpyrifos, whereas all doses of both cyfluthrin and hydramethylnon decreased longevity of females. Fecundity increased linearly with increasing sublethal doses of chlorpyrifos. Number of oothecae formed, oothecae hatched, and number of offspring produced in each ootheca increased with increasing sublethal concentrations of chlorpyrifos. In contrast, fecundity declined with increasing sublethal concentrations of cyfluthrin and hydramethylnon. Formation of the first ootheca occurred approximately 8 d after mating for untreated females but generally longer with sublethal concentrations of all insecticides. The period between oothecae hatch and the formation of subsequent oothecae increased with successive oothecae in all treatments.

Animals↗

PubMed1977

Extension of longevity in Drosophila mojavensis by environmental ethanol: differences between subraces.

Drosophila mojavensis adults, which breed and feed on necrotic cacti, show an increase in longevity when exposed to atmospheric ethanol. The increase in longevity is accompanied by retention of mature ovarioles and is independent of diet. Differences in longevity among strains from different localities were detected for females. Strains from Arizona and Sonora, Mexico, showed the greatest increase in longevity, while strains from Baja California, Mexico, showed the least increase. These differences may be controlled by the alcohol dehydrogenase locus, the octanol dehydrogenase locus, and modifier genes, because the aduld response is correlated with the frequency of alcohol dehydrogenase alleles, as well as second chromosomal inversions containing the octanol dehydrogenase locus. The longevity response is also consistent with the more uneven distribution and availability of the host plant in Arizona and Sonora, Mexico. Strains from Arizona and Sonora, Mexico, have a high frequency of Adh-S, the allele whose product is heat and pH tolerant. The host plant, organpipe cactus, exhibits extremes in temperature and pH in the same geographic region. Strains from Baja California, Mexico, possess a high frequency of Adh-F, whose product is heat and pH sensitive. The substrate in this region, agria cactus, has moderate temperature and pH extremes and contains relatively high concentrations of isopropanol. Isopropanol is presumable a selective agen favorable to Adh-F. The environmental heterogeneity that is proposed for maintaining the alleles at the alcohol dehydrogenase locus is the interaction of substrate alcohol content with temperature and pH. Substrates that do not contain appreciable amounts of isopropanol and are exposed to high temperatures and exhibit variable pH favor Adh-S, while substrates containing isopropanol and having moderate temperatures and pH favor Adh-F.

Alcohol Oxidoreductases↗

PubMed1975

Longevity, growth rate and related traits among strains of Tribolium castaneum.

Longevity of eight laboratory strains of the flour beetle Tribolium castaneum, with various geographic backgrounds, was studied under constant laboratory conditions of 33 degrees C and 70% relative humidity in standard medium (95% whole wheat flour and 5% dried yeast) during a period of 227 days starting from the egg stage. The eggs were collected from the same parents, first a few days after emergence and afterwards at intervals of 13, 9, 10 and 11 days. Mean survival time (MST) was found to be strain-specified. It ranges from 128.6 days for KJ (Kyoto, Japan) to 174.2 days for ES (Edinburgh, Scotland). MST was highly correlated with the percentage of adults alive after 227 days, which did not change the ranking order of strain longevity. Parental age had no effect on longevity. The mean adult longevity of the strains was correlated with the available data on adult weight, growth rate, viability and productivity. There was no relationship between adult weight and longevity. LIfe span was found to depend on growth rate (measured as 13-day larval weight), percent viability (from 13-day larvae to adulthood) and productivity. Developmental time was also found to influence adult life span within certain limits (two extreme strains deviated). The data suggest that ageing and death in T. castaneum is under genetic control and support the idea that ageing, allied to development, is genetically controlled.

Age Factors↗

PubMed1977

Body weight change over the life span and longevity for C57BL/6J mice and mutations which differ in maximal body weight.

Body weights were obtained monthly for mutant groups with the C57BL/6J genetic background which differ in body weight (bg, c,J Ay, ob), and for a control group (C57BL/6J) (n = 16, N = 80). The mean longevity was significantly lower for all mutant groups compared with the mean longevity of the control group. Although obese mice (ob) had a shorter life span than other mutant groups, mice which also attained a very high body weight (yellow, Ay) did not differ significantly in longevity from thin mutant mice. Moreover, peak body weight was positively correlated with longevity for all mouse groups. All mouse groups showed a terminal decline in body weight except the albino group which gained weight throughout life. In general, long-lived mice obtained a greater terminal weight loss than short-lived mice within groups. The major finding of this study was that within each group there was a negative relationship obtained between growth rate and longevity.

Aging↗

PubMed1979

[Theories of longevity (author's transl)].

Any modern theory of longevity has to take into account the multifactorial combined effect of biological-medical, social and psychological factors and of factors pertaining to molecular biology, each with their different weighting. For this reason research into greater-than-average life expectancy and longevity is only possible on an interdisciplinary basis. Many theories of longevity despite convincing arguments also have their weak points. Critical analysis of the theories available to date reveals that longevity rests on an optimal combination of two major factors: 1. on a genetic predisposition in people with longevity in the family--this is the case in most instances. 2. on additional exogenous factors of a social, psychological, ecological and medical kind.

Aged↗

PubMed1992

Selection on stress resistance increases longevity in Drosophila melanogaster.

Tests for the causal involvement of specific physiological mechanisms in the control of aging require evidence that these mechanisms can be used to increase longevity or reproductive lifespan. Selection for later reproduction in Drosophila has been shown to lead to increased longevity, as well as increased resistance to starvation and desiccation stresses. Selection for increased resistance to starvation and desiccation in Drosophila melanogaster is here shown to lead to increased longevity, indicating that alleles that increase stress resistance also may increase longevity. The responses of desiccation and starvation resistance to selection are partly independent of each other, indicating a multiplicity of physiological mechanisms involved in selectively postponed aging, and thus aging in general.

Animals↗

PubMed1992

Intrapair differences of physical aging and longevity in identical twins.

The genetic and environmental contributions to physical aging (hair graying, balding, presbyopia) and longevity (age at death) were examined by within-pair comparison in monozygotic (MZ) and dizygotic (DZ) twins in later adulthood. Physical aging was investigated on 135 pairs of adult twins aged over 50. Hair graying and hair loss (baldness) showed significantly higher rates of concordance in the MZ twins than in the DZ twins. The intrapair difference of the degree of hair graying was negligible in 79%, slight in 15% and striking in 5% among the MZ pairs; while negligible in 40%, slight in 50% and striking in 10% among the DZ pairs. The intrapair difference of the degree of hair loss was negligible in 92%, slight in 8% (and striking in none) among the MZ pairs; while negligible in 69%, slight in 25% and striking in 6% among the DZ pairs. The age at onset of presbyopia showed a slightly higher rate of concordance in the MZ than in the DZ pairs. Longevity (age at death) was surveyed on 184 pairs of twins who died at over 40 years of age. The intrapair difference of longevity was 6.65 +/- 5.6 years (maximum 18.0; minimum 0.04) in the MZ pairs, and 8.66 +/- 7.2 years (maximum 18.6; minimum 2.9) in the DZ pairs. The MZ pairs showed a slightly smaller within-pair difference of longevity than the DZ pairs.

Aged↗

PubMed2026

Genetic trade-offs in fertility and longevity explain the maintenance of disease-associated alleles in humans.

Genetic variants that increase the risk for complex diseases persist in human populations, despite adverse effects on health and longevity. Life-history theory predicts that such alleles can be maintained by trade-offs arising from pleiotropy, yet direct genomic evidence has been limited. We asked whether disease-associated variants persist because they enhance reproduction, despite costs to health and lifespan. By analysing genome-wide data across 62 diseases, longevity and fertility, we show that disease-risk alleles are, on average, associated with reduced longevity and increased fertility. Moreover, the subset of alleles that increase both fertility and disease risk appear to have been favoured by natural selection over the past 50,000 years. Using Mendelian randomization, we detect a causal effect of genetic liability to disease on longevity, but no robust evidence for a causal effect on fertility; importantly, these estimates remain stable after adjusting for socioeconomic factors. At the individual level, we compared offspring numbers between affected and unaffected individuals with high polygenic disease risk. For most diseases, affected individuals had more children than unaffected ones. But for early-onset diseases, the pattern reverses, indicating reproductive costs of early morbidity. Together, these results support antagonistic pleiotropy and help explain the persistence of disease-risk alleles in human populations.

Humans↗

PubMed1976

Effect of family size and mother's longevity.

A prospective study of the mother's longevity and of her completed family size has been conducted on the basis of historical demographic records. We show that 1 to 5 pregnancies is associated with the greatest longevity in weakly inbred women and 11 pregnancies is associated with greatest longevity in more inbred women. Taking into account maternal inbreeding, completely sterile women and those who had a large number of pregnancies have an equal mean longevity. It is suggested that repeated pregnancies produce a cumulative hormonal effect, the distribution of which, following family size, should be bell-shaped.

Consanguinity↗

PubMed1975

Life-span and the inheritance of longevity of inbred mice.

Measures of life-span were obtained for male and female A/J, BALB/cJ, C57BL/6J, and DBA/2J inbred mouse strains and the six possible hybrid combinations (N equals 500, 10 groups, 25 male and 25 female per group). C57BL/6J mice were long lived, while A/J, BALB/cJ and DBA/2J mice were short lived, with the exception of female BALB/cJ mice, which lived as long as C57BL/6J mice. Female BALB/cJ and two female hybrid mouse groups with a BALB/cJ parent lived longer than males, but significant sex differences were not obtained for other groups. In general, the mode of inheritance of longevity was overdominant. For a second study (N equals 400) of the longevity of A/J and C57BL/6J strains and F1 and F2 hybrids it was estimated that one genetic factor was associated with longevity and the coefficient of genetic determination for longevity was estimated as between .48 and .79.

Analysis of Variance↗

PubMed1992

Nutritional factors for longevity in Okinawa--present and future.

Several factors, such as environment and heredity, are presumed to be related to longevity. Of these nutrition is believed to function as a regulatory factor. Okinawa prefecture is well known as the leading area for longevity in the world. We therefore examined present and past nutrition records together with the background of all the 88 centenarians (18 male, 70 female) who are living in Okinawa in 1991. Their leading occupation was agriculture, and they were in work until the 8th decade. They took rice or potato as carbohydrate with abundant vegetables and vegetable protein or fish protein. Although they did not take a rich diet it was well balanced, and was assumed to be related to longevity because of the decreased incidence of atherosclerosis; together with a good genetic background, suggested by the accumulation of longevity in their siblings.

Aged↗

PubMed1992

Sublethal effects of larval methoprene exposure on adult mosquito longevity.

Larvae of Aedes aegypti were exposed to sublethal concentrations of the insect growth regulator, methoprene, and the glycogen content of pupae and surviving adults was compared and effects on adult longevity determined. The glycogen reserves in both male and female Ae. aegypti pupae were significantly reduced as a result of methoprene exposure. The longevity of adult females was also significantly reduced, but exposure affected neither the longevity nor the glycogen content of adult males. Adult sugar feeding increased the amount of glycogen in both treated and control females. The reduced longevity of adult females from larval methoprene treatment appeared not to be directly related to reduced glycogen, but rather reflected neuroendocrine abnormalities induced by this juvenile hormone analogue.

Aedes↗

PubMed1979

Evolution of human longevity: a critical overview.

Evolution of longevity of the ungulates, carnivores and primates is reviewed. Special emphasis is focused on recent evolutionary history of longevity along the hominid ancestral-descendant sequence leading to modern man. Maximum life span potential (MLP) or the change in MLP is predicted in extinct species by (1) a phylogenetic analysis of the MLP of present living species and (2) an empirical equation using brain and body weight estimates from fossils. Both of these methods indicate MLP generally increased during mammalian evolution and at an extremely fast rate during the appearance of the hominid species. These results suggest that relatively few genetic alterations were necessary during the recent evolutionary history of man to significantly extend his innate ability to maintain mental and physical health. Much evidence indicates these genetic alterations principally involve regulatory genes, which control a conserved set of structural genes. Evolution of longevity in man could therefore be a result of simple changes in temporal and quantitative expression. Whether these genetic alterations result from mutational changes and/or chromosomal rearrangement cannot yet be evaluated.

Aging↗

PubMed1979

Polygamy and the evolution of human longevity.

An alternative to previous explanations of the rapid increase in man's longevity and intelligence during the several million years of his recent evolution from pre-hominid, clearly shorter-lived and less intelligent, primate ancestors is presented. The general thesis is that a very greatly accelerated rate of incorporation of favorable genes or gene combinations can be achieved in surprisingly few generations among social animals provided that dominant males become the patriarchs of many descendents by virtue of their partial or complete monopoly on available females. The conclusion is that man probably differs from his ancesters of 0.5 to 5 million years ago by many thousands of genes (both structural and regulatory) rather than the dozens or few hundreds that have been postulated on the basis of more classical treatments of selection pressures, gene frequency changes and mutation rates. The concepts developed here formally apply only to two alternative alleles, rather than to groups of genes which segregate independently, or to characters determined by multiple alleles. The appropriate mathematical treatment of the latter real situation is not readily visualized; nor is account taken of the likelihood that different tribes of pre-humans developed different specializations via the above mechanisms which were then (later) combined into an emerging human stock through matings between members of different tribes. The very great variability both in longevity and in intelligence between different races of animals such as dogs, which have been the objects of deliberate genetic selection by humans for particular heritable traits, may parallel our own recent history, even though the selection mechanism (deliberate human selection vs. polygamous dominance) is quite different in the two cases. The onset of civilizations consisting of amalgums between smaller, previously competing tribes, together with the humanitarian responsibilities to each other we share as a species, ironically has probably arrested further evolution of human longevity (and perhaps of intelligence) in the modern world. Possibly even retrogressive changes are occurring, except in those rare sub-populations in which special social and cultural practices tend to favor selective perpetuation of characteristics which are usually viewed as beneficial.

Alleles↗