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PubMed2004

Association of the mitochondrial DNA haplogroup J with longevity is population specific.

Evidences are accumulating on the effects of the variability of mitochondrial DNA (mtDNA) on many complex traits. In particular, mtDNA haplogroup J has been reported to increase the individual chance to attain longevity in northern Italians, Northern Irish and Finns. However, since the genetic contribution to longevity may be population specific, we wanted to verify if haplogroup J does affect longevity also in a southern European population having a different genetic and environmental history. We analysed a population sample (883 subjects, 371 males and 521 females; age range 18-108 years) from southern Italy for the presence of haplogroup J. No frequency increase of this mtDNA haplogroup was found in the older cohorts, suggesting that, in this population, haplogroup J does not play a significant role in longevity. This finding shows that, as for other genetic factors, the association of mtDNA inherited variability with longevity is population specific.

Adolescent↗
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↗
PubMed1990

Somatotype and longevity of former university athletes and nonathletes.

A longitudinal study was conducted on 398 athletes and 369 nonathletes who were born before 1920 and attended Michigan State University. The subjects were compared to determine if intercollegiate athletic competition accounts for significant variation in longevity when considered with somatotype. Because some of the subjects were still alive at the time of the study, the BMDP Statistical Software was used to do a survival analysis with covariates. Preliminary comparisons considered the differences in somatotype between athletes and nonathletes. Two sample t-tests indicated that athletes were more mesomorphic and less ectomorphic (p less than .05) than nonathletes. When comparing the relationship between somatotype and longevity, the pooled data of athletes and nonathletes indicated that endomorphs were shorter lived than the other three comparison groups. When only the athletes were considered, similar results were found. However, the nonathlete group exhibited differences only between the mesomorphic and endomorphic groups. The endomorphs were shorter lived. Longevity was examined by using the Cox proportional hazards regression method with somatotype and athlete/nonathlete status as covariates. Somatotype, by itself, was found to be significantly related to longevity, (p less than .001). Athletic status was not significantly related to longevity, either by itself or when entered into the model with somatotype.

Age Factors↗
PubMed2006

Genes, ageing and longevity in humans: problems, advantages and perspectives.

Many epidemiological data indicate the presence of a strong familial component of longevity that is largely determined by genetics, and a number of possible associations between longevity and allelic variants of genes have been described. A breakthrough strategy to get insight into the genetics of longevity is the study of centenarians, the best example of successful ageing. We review the main results regarding nuclear genes as well as the mitochondrial genome, focusing on the investigations performed on Italian centenarians, compared to those from other countries. These studies produced interesting results on many putative "longevity genes". Nevertheless, many discrepancies are reported, likely due to the population-specific interactions between gene pools and environment. New approaches, including large-scale studies using high-throughput techniques, are urgently needed to overcome the limits of traditional association studies performed on a limited number of polymorphisms in order to make substantial progress to disentangle the genetics of a trait as complex as human longevity.

Aged, 80 and over↗
PubMed2006

Uncoupling the relationship between fatty acids and longevity.

Research into different species has verified the negative correlation between longevity and the level of reactive oxygen species (ROS) production. ROS creates oxidative damage and, consequently, fuels the aging process. As such, the astonishing longevity of avian species correlates well with their lower levels of ROS production, in comparison to mammals of similar size. Apart from this inter-species difference, caloric restriction (CR) is a widely-documented means of increasing intra-species longevity, and it works by decreasing ROS production. However, little is known about the mechanisms responsible, either for the retardation of aging in CR or for the longevity of long-living species. Recent findings have shown an increase in uncoupling protein (UCP) activity with lower ROS levels, after CR stress. These UCPs are stimulated by fatty acids. Moreover, in numerous studies, fatty acids have been demonstrated to generate a reduction in ROS generation. Thus, the decreased ROS production seen in both CR and longer lifespan may occur via up-regulation of free fatty acid stimulation of UCP activity. Consequently, free fatty acids may play an important regulatory role in longevity, by reducing ROS, via actions on UCPs.

Aging↗
PubMed2006

Artificial selection on male longevity influences age-dependent reproductive effort in the black field cricket Teleogryllus commodus.

Although the trade-off between reproductive effort and longevity is central to both sexual selection and evolutionary theories of aging, there has been little synthesis between these fields. Here, we selected directly on adult longevity of male field crickets Teleogryllus commodus and measured the correlated responses of age-dependent male reproductive effort, female lifetime fecundity, and several other life-history traits. Male longevity responded significantly to five generations of divergent selection. Males from downward-selected lines commenced calling sooner and reached their peak calling effort at a younger age. They called more per night and, despite living less than half as long, called more overall than males selected for increased longevity. Females from the downward-selected lines lived significantly shorter lives than females from the upward-selected lines but still produced the same number of offspring. Nymph survival, development time, and body size and weight at eclosion did not show significant correlated response to selection on male longevity, despite evidence for substantial genetic variation in each of these traits. Collectively, our findings directly support the antagonistic pleiotropy model of aging and suggest an important role for sexual selection in the aging process.

Aging↗
PubMed2000

Genetic, behavioral and environmental determinants of male longevity in Caenorhabditis elegans.

Males of the nematode Caenorhabditis elegans are shorter lived than hermaphrodites when maintained in single-sex groups. We observed that groups of young males form clumps and that solitary males live longer, indicating that male-male interactions reduce life span. By contrast, grouped or isolated hermaphrodites exhibited the same longevity. In one wild isolate of C. elegans, AB2, there was evidence of copulation between males. Nine uncoordinated (unc) mutations were used to block clumping behavior. These mutations had little effect on hermaphrodite life span in most cases, yet many increased male longevity even beyond that of solitary wild-type males. In one case, the neuronal function mutant unc-64(e246), hermaphrodite life span was also increased by up to 60%. The longevity of unc-4(e120), unc-13(e51), and unc-32(e189) males exceeded that of hermaphrodites by 70-120%. This difference appears to reflect a difference in sex-specific life span potential revealed in the absence of male behavior that is detrimental to survival. The greater longevity of males appears not to be affected by daf-2, but is influenced by daf-16. In the absence of male-male interactions, median (but not maximum) male life span was variable. This variability was reduced when dead bacteria were used as food. Maintenance on dead bacteria extended both male and hermaphrodite longevity.

Animals↗
PubMed2000

Why do life spans differ? Partitioning mean longevity differences in terms of age-specific mortality parameters.

Populations typically differ in mean life spans because of genetic, environmental, or experimental factors. In this paper methods are presented that clarify the relationship between differences in the longevity of two populations and differences in their underlying age-specific patterns of mortality. Data are examined from rodent and fruit fly (Drosophila melanogaster) experiments that investigated the longevity effects of a variety of environmental and genetic manipulations, including temperature, dietary restriction, laboratory selection for increased longevity, and severe inbreeding. Analyses suggest that longevity differences mediated by temperature and dietary restriction result predominantly from differences in the rate of increase in mortality with age. Increases in longevity through laboratory selection result primarily from a reduction in baseline mortality and not a slowing of the rate of aging. Although the methods are applied primarily in the context of simple mathematical models of mortality (e.g., the Gompertz model), they are quite general and can be applied to mortality models of arbitrary complexity. Mathematica protocols ("notebooks") and computer software have been developed to perform all the analyses discussed and are available from the first author.

Age Factors↗
PubMed2001

Searching for human longevity genes: the future history of gerontology in the post-genomic era.

Over the last 30 years, a number of genetic and environmental factors that lead to decreased length of life have been identified. Unfortunately, much less progress has been achieved in identifying genes associated with longevity that protect from common diseases or slow the aging process. Recent compelling evidence supports a role for important genetic and environmental interactions on longevity in lower organisms. Although less is known in humans, commonality in molecular and biological processes, evolutionary arguments, and epidemiological data would strongly suggest that similar mechanisms also apply. The completion of the Human Genome Project and the rapid innovations in technology will make possible the identification of human longevity-assurance genes. This article reviews such evidence, its implications for the identification of human longevity-assurance genes, and the significance of finding longevity genes to human health and disease.

Aged↗
PubMed2003

More favorable midlife cardiovascular risk factor levels in male twins and mortality after 25 years of follow-up is related to longevity of their parents.

BACKGROUND: Genetic studies of life span in humans have used broad survival measures, most commonly longevity, which is moderately correlated between parents and offspring. We examined whether genetic cardiovascular disease risk factors in male twin offspring are related to longevity of their parents in the National Heart, Lung, and Blood Institute twin study. METHODS: Cholesterol levels, body mass index, blood pressures, and pulmonary function measured over the first three examinations (average subject age 48, 58, and 63 years, respectively) were compared with the twins' paternal, maternal, and parental mean longevity divided into upper versus lower quintiles. The presence of an apolipoprotein E epsilon 4 allele typed from DNA collected at Exam 3 and mortality in the twin cohort through 1997 were also examined in relation to parental longevity quintiles. RESULTS: Twins, particularly whose fathers died at younger ages, had significantly higher total cholesterol (p <.05), ratio of total cholesterol to high-density lipoprotein (p <.01), and blood pressures (p <.01) in middle age. This relationship decreased at the subsequent two examinations, but consistently, twins with longer-lived parents tended to have better risk factor profiles. A twin death (mean age 65) was significantly more common in families with mothers (p <.001) and, to a lesser extent, fathers who died early. An apolipoprotein epsilon 4 allele was more common in families with parents' age at death in the lowest quintile (p <.05). CONCLUSIONS: Systolic blood pressures, cholesterol levels, and the presence of the apolipoprotein E epsilon 4 allele likely contribute to the observed familial correlations in longevity that have been reported in the literature.

Apolipoproteins E↗
PubMed2006

Chromosome 4q25, microsomal transfer protein gene, and human longevity: novel data and a meta-analysis of association studies.

Recently, chromosome 4q25 was linked to exceptional human longevity, and a haplotype of the positional candidate microsomal transfer protein (MTP) gene was associated to the phenotype in U.S. Caucasians. We investigated whether linkage to 4q25 could be detected in 164 nonagenarian sibships of the Leiden Longevity Study. Additionally, we compared the MTP -493G/T and Q95H allele and haplotype frequencies in the Leiden Longevity Study (379 nonagenarians, 525 of their offspring, and 251 partners of their offspring) and in the Leiden 85-Plus Study (655 octogenarians and 244 young controls). The latter study population was followed for at least 7 years, providing the opportunity to perform also prospective analyses using the longitudinal data. We found neither evidence for linkage at 4q25 nor association of the MTP locus with longevity in nonagenarian individuals. Meta-analyses of all previous studies implied that the association in U.S. Caucasians may have its source in admixture of the U.S. control population rather than in the genetic effect of the locus on exceptional longevity.

Adult↗
PubMed2000

Longevity and the costs of reproduction in a historical human population.

It has been argued that the priority that natural selection places on reproduction negatively affects other processes such as longevity and the problem posed by this trade-off underlies the disposable soma theory for the evolution of human ageing. Here we examine the relationship between reproduction and longevity in a historical human population (the Krummhörn, north-west Germany 1720-1870). In our initial analyses, we found no support for the hypothesized negative effects of reproduction on longevity: married women who remained childless lived no longer than women who reproduced and women who had few children lived no longer than women who had many children. However, more detailed analyses in relation to socio-economic class revealed that the extent to which reproduction has an effect on longevity is a function of the level of economic deprivation. We found that, when possible sources of confound were controlled for (e.g. duration of marriage and amount of time spent in fecund marriage), there is an increasingly strong relationship between longevity and reproduction with increasing poverty.

Aged↗
PubMed2006

Longevity and ageing: appraising the evolutionary consequences of growing old.

Senescence or ageing is an increase in mortality and/or decline in fertility with increasing age. Evolutionary theories predict that ageing or longevity evolves in response to patterns of extrinsic mortality or intrinsic damage. If ageing is viewed as the outcome of the processes of behaviour, growth and reproduction then it should be possible to predict mortality rate. Recent developments have shown that it is now possible to integrate these ecological and physiological processes and predict the shape of mortality trajectories. By drawing on the key exciting developments in the cellular, physiological and ecological process of longevity the evolutionary consequences of ageing are reviewed. In presenting these ideas an evolutionary demographic framework is used to argue how trade-offs in life-history strategies are important in the maintenance of variation in longevity within and between species. Evolutionary processes associated with longevity have an important role in explaining levels of biological diversity and speciation. In particular, the effects of life-history trait trade-offs in maintaining and promoting species diversity are explored. Such trade-offs can alleviate the effects of intense competition between species and promote species coexistence and diversification. These results have important implications for understanding a number of core ecological processes such as how species are divided among niches, how closely related species co-occur and the rules by which species assemble into food-webs. Theoretical work reveals that the proximate physiological processes are as important as the ecological factors in explaining the variation in the evolution of longevity. Possible future research challenges integrating work on the evolution and mechanisms of growing old are briefly discussed.

Aging↗
PubMed2004

Clinical phenotype of families with longevity.

OBJECTIVES: To determine whether offspring of centenarians acquired protection from age-related diseases. DESIGN: Case-control study. SETTING: The study was part of the Longevity Genes Project at Albert Einstein College of Medicine. PARTICIPANTS: Centenarians (n=145), offspring of centenarians (n=180), and spouses of the offspring of centenarians (n=75) as a control group. Two additional groups served as controls: age-matched Ashkenazi Jews, and an age-matched control group from the Third National Health and Nutrition Examination Survey. MEASUREMENTS: Self-reported family history of longevity; prevalence of hypertension, diabetes mellitus, heart attacks, and strokes; and objective measurements of body mass index and fat mass. RESULTS: Parents of centenarians (born in approximately 1870) had a markedly greater ( approximately sevenfold) "risk" for longevity (reaching ages 90-99), supporting the notion that genetics contributed to longevity in these families. The offspring of long-lived parents had significantly lower prevalence of hypertension (by 23%), diabetes mellitus (by 50%), heart attacks (by 60%), and strokes (no events reported) than several age-matched control groups. CONCLUSION: Offspring of centenarians may inherit significantly better health. The authors suggest that a cohort of these subjects and their spouses is ideal to study the phenotype and genotype of longevity and its interaction with the environment.

Aged↗
PubMed2002

Metabolic alterations and shifts in energy allocations are corequisites for the expression of extended longevity genes in Drosophila.

Evolutionary theories suggest that the expression of extended longevity depends on the organism's ability to shift energy from reproduction to somatic maintenance. New data led us to reexamine our older data and integrate the two into a larger picture of the genetic and metabolic alterations required if the animal is to live long. Our Ra normal-lived control strain can express any one of three different extended longevity phenotypes, only one of which involves significant and proportional increases in both mean and maximum longevity and thus a delayed onset of senescence. This phenotype is dependent on the up-regulation of the antioxidant defense system (ADS) genes and enzymes. Animals that express this phenotype typically have a pattern of altered specific activities in metabolically important enzymes, suggesting they are necessary to support the NAD+/NADP+ reducing system required for the continued high ADS enzyme activities. Fecundity data suggests that the energy required for this higher level of somatic maintenance initially came from a reduced egg production. This was only transient, however, for the females significantly increased their fecundity in later generations while still maintaining their longevity. The energy required for this enhanced fecundity was probably obtained from an increased metabolic efficiency, for the mitochondria of the La long-lived strain are metabolically more efficient and have a lower leakage of reactive oxygen species (ROS) to the cytosol. Selection pressures that do not lead to these shifts in energy allocations result in extended longevity phenotypes characterized by increased early survival or increased late survival but not by a delayed onset of senescence.

Animals↗
PubMed2005

Genetics of longevity and aging.

Longevity, i.e., the property of being long-lived, has its natural limitation in the aging process. Longevity has a strong genetic component, as has become apparent from studies with a variety of organisms, from yeast to humans. Genetic screening efforts with invertebrates have unraveled multiple genetic pathways that suggest longevity is promoted through the manipulation of metabolism and the resistance to oxidative stress. To some extent, these same mechanisms appear to act in mammals also, despite considerable divergence during evolution. Thus far, evidence from population-based studies with humans suggests the importance of genes involved in cardiovascular disease as important determinants of longevity. The challenge is to test if the candidate longevity genes that have emerged from studies with model organisms exhibit genetic variation for life span in human populations. Future investigations are likely to involve large-scale case-control studies, in which large numbers of genes, corresponding to entire gene functional modules, will be assessed for all possible sequence variation and associated with detailed phenotypic information on each individual over extended periods of time. This should eventually unravel the genetic factors that contribute to each particular aging phenotype.

Aging↗
PubMed1993

Relationship of baseline major risk factors to coronary and all-cause mortality, and to longevity: findings from long-term follow-up of Chicago cohorts.

The focus here is on relationships between major risk factors and long-term mortality from coronary heart disease (CHD) and all causes, and on longevity, in Chicago cohorts: 25-year follow-up for Peoples Gas (PG) men aged 25-39 (n = 1,119), 30-year follow-up for PG men aged 40-59 (n = 1,235), 24-year follow-up for Western Electric (WE) men aged 40-55 (n = 1,882); also 15-year follow-up for five cohorts of the Chicago Heart Association (CHA) Study: men aged 25-39 (n = 7,873), 40-59 (n = 8,515), 60-74 (n = 1,490), and women aged 40-59 (n = 7,082) and 60-74 (n = 1,243); also 12-year findings for very low risk men (n = 11,098) and other men (n = 350,564) screened for the Multiple Risk Factor Intervention Trial (MRFIT). With a high degree of consistency, multivariate analyses showed independent positive relationships of baseline serum cholesterol, blood pressure and cigarette use to risk of death from CHD and all causes. For the WE cohort, with baseline nutrient data, dietary cholesterol was also independently related to these mortality risks. Combined risk factor impact was strong for both men and women of all baseline ages. Thus, for WE men, favorable compared to observed levels of serum cholesterol, blood pressure, cigarette use and dietary cholesterol were estimated to result in 24-year risk of CHD death 69% lower, all-cause death 42% lower and longevity 9 years greater. For CHA middle-aged and older women, favorable baseline levels of serum cholesterol, blood pressure and cigarette use were estimated to yield 15-year-CHD risk lower by about 60% and longevity greater by about 5 years. For MRFIT, very low risk men (serum cholesterol < 182 mg/dl, systolic/diastolic blood pressure < 120/<80), nonsmokers, nondiabetic, no previous heart attack), compared to all others, observed 12-year death rates were lower by 89% for CHD, 79% for stroke, 86% for all cardiovascular diseases, 30% for cancers, 21% for other causes, 53% for all causes, and longevity was estimated to be more than 9 years longer. These findings indicate great potentials for prevention of the CHD epidemic and for increased longevity with health for men and women, through improved life-styles and consequent lower risk factor levels.

Adult↗
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↗