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PubMed2002

Mitochondrial DNA polymorphisms associated with longevity in a Finnish population.

Sequence variation in mitochondrial DNA (mtDNA) may cause slight differences both in the functioning of the respiratory chain and in free radical production, and an association between certain mtDNA haplogroups and longevity has been suggested. In order to determine further the role of mtDNA in longevity, we studied the frequencies of mtDNA haplogroups and haplogroup clusters among elderly subjects and controls in a Finnish population. Samples were obtained from 225 persons aged 90-91 years (Vitality 90+) and from 400 middle-aged controls and 257 infants. MtDNA haplogroups were determined by restriction fragment length polymorphism. The haplogroup frequencies of the Vitality 90+ group differed from both those of the middle-aged controls ( P=0.01) and the infants ( P=0.00005), haplogroup H being less frequent than among the middle-aged subjects ( P=0.001) and infants ( P=0.00001), whereas haplogroups U and J were more frequent. Haplogroup clusters also differed between Vitality 90+ and both the middle-aged subjects ( P=0.002) and infants ( P=0.00001), the frequency of haplogroup cluster HV being lower in the former and that of UK and WIX being higher. These data suggest an association between certain mtDNA haplogroups or haplogroup clusters and longevity. Furthermore, our data appear to favour the presence of advantageous polymorphisms and support a role for mitochondria and mtDNA in the degenerative processes involved in ageing.

Adolescent↗
PubMed2006

Association between the MLH1 gene and longevity.

Perturbations in genomic stability result in cancer, a reduced life span, and premature aging. MLH1 is a mismatch repair enzyme that acts to maintain genomic stability, and a loss of MLH1 increases cancer incidence and apoptosis resistance, which suggests a link between MLH1 and longevity. We found here that MLH1 is associated with longevity by comparing a centenarian group with a control group. Our data indicate a critical role for MLH1 in longevity.

Adaptor Proteins, Signal Transducing↗
PubMed1996

Untangling genetic influences on smoking, body mass index and longevity: a multivariate study of 2464 Danish twins followed for 28 years.

A multivariate twin study was conducted in order to evaluate to what extent smoking, BMI and longevity are influenced by common genetic factors. The study was based on a 28-year follow-up of a sample of 2464 Danish twins who were born in the period 1890-1920 and who answered a questionnaire, including requests for information on smoking status, height and weight, in 1966. By 1994, approximately 2/3 of the sample had died. To compensate for the right-censoring, age at death was imputed for twins who were still alive by using survival analysis; all living subjects were more than 73 years old (mean 80 years, SD 5) in 1994. Proportions of covariance resulting from genetic and environmental factors in common and unique to the three traits were estimated from covariance matrices using the structural equation model approach. The study found no evidence for a substantial impact of common genetic factors on smoking, BMI and longevity. This suggests that only a small fraction of the genetic influences on longevity is mediated via a genetic influence on smoking and BMI and, furthermore, that it is unlikely that the associations between smoking and mortality and between BMI and mortality are confounded by common genetic factors.

Aged↗
PubMed2005

First copulation increases longevity and fecundity of Histiostoma feroniarum (Acari: Astigmata: Acaridida) females.

I investigated the influence of insemination at different life stages on female fitness in the mite Histiostoma feroniarum. In this species, males guard immature females at the tritonymph stage to inseminate them immediately after the last moulting. Four groups of females were studied (1) females inseminated 'naturally', i.e. mating occurred immediately after guarding, and then the male was removed (IF/0M), (2) 'naturally' inseminated females, where after insemination the male was replaced by two additional males (IF/2M), (3) virgin females reared without males (VF/0M) and (4) mature, virgin females to which two virgin males were added 3 days after last moulting (VF/2DM). The results show that females inseminated 'naturally' (IF/0M) have higher longevity and fecundity than either virgin (VF/0M) or late-inseminated females (VF/2DM). Furthermore, longevity and fecundity of the former (IF/0M) was also greater than that of females 'naturally' inseminated and subsequently exposed to males (IF/2M). One may suggest that seminal fluids have a positive effect on female fitness. When delayed insemination occurs, such positive effect may not be observed due to a change in features of the sperm access system. Harassment may explain decreased longevity and fecundity of females inseminated 'naturally' compared to females that received additional males.

Acaridae↗
PubMed2005

Chaperones and longevity.

That evolution of longevity may depend on alterations in the expression of relatively few regulatory genes has been inferred from the rapid increase in lifespan during evolution of the hominid species (Cutler RG (1979) Mech Ageing Dev 9: 337-354). Also the inherent immortality of the embryonic stem cells implies that replicative senescence (Hayflick L (1997) Biochem Mosc 62: 1180-1190) as possibly aging of species are epigenetic phenomena. Evidence is presented to suggest that the epigenetic changes of the longevity determinants to a significant extend concerns the molecular chaperones. Specific involvement of RNA chaperones in cell immortalization and defective RecQ-DNA chaperones in syndromes of premature aging suggest that DNA/RNA - chaperones probably rank high among the determinants of cellular and species longevity.

Animals↗
PubMed2006

Why calorie restriction would work for human longevity.

Experimentally imposed calorie restriction (CR) is shown to result in the most reproducible endpoint of lifespan extension in all animals models tested. In this presentation, the question of CR's effect on human longevity is reviewed by discussing data pertinent to the putative efficacy of CR on humans. Arguments are presented in support of this possibility based on CR's unique abilities to retard biological functional declines and to deter pathological processes, both of which are major targets of deleterious oxidative stress. To delineate the cellular and molecular mechanisms of CR's efficacy on human longevity, this review elaborates on the modulation of CR on the inflammatory process, a common risk factor for many chronic diseases. Discussions also include evidence from human data on the effect of CR in the loss of body weight, known to suppress inflammatory cytokines, subsequently leading to the reduction of chronic diseases known to compromise the functional longevity of humans.

Aging↗
PubMed2006

The potential for dietary restriction to increase longevity in humans: extrapolation from monkey studies.

Based on results emerging from long-term studies of dietary restriction in rhesus monkeys, we offer our views regarding whether dietary restriction can increase longevity in humans. Because lifespan data in monkeys remain inconclusive currently, we respond that "we do not for sure". Based on the vast literature regarding the effects of healthy, low calorie diets on health and longevity in a wide range of species, including humans, and based on data emerging from monkey studies suggesting that dietary restriction improves markers of disease risk and health, we respond that "we think so." Because it is unlikely that an experimental study will ever be designed to address this question in humans, we respond that "we think we will never know for sure." We suggest that debate of this question is clearly an academic exercise; thus, we would suggest that the more compelling discussion should focus on whether basic mechanisms of DR can be discovered and if such discoveries can lead to the development of effective DR mimetics. Even if proof that DR or DR mimetics can increase longevity in humans will likely never emerge, we would suggest that endpoints regarding disease risk and disease incidence as well as maintenance of function can be examined in human clinical trials, and that these will be highly relevant for evaluating the effectiveness of such treatments.

Aging↗
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↗
PubMedDate not supplied

A method for the isolation of longevity mutants in the nematode Caenorhabditis elegans and initial results.

The free-living nematode Caenorhabditis elegans is used as a genetically manipulable experimental system for the study of aging. Utilizing a temperature-sensitive sterile strain with a normal life span, a method is described for the isolation of mutant strains with significantly increased life spans. Eight mutant strains were isolated each having increased life spans. Two mutant strains were spontaneous dauer formers, accounting for their increased longevity. Another was chemotaxis-defective, causing reduced food intake which could account for its increased life span. Five mutants suffered from varying degrees of paralysis affecting their rate of pharyngeal pumping and food ingestion. The high correlation of the decreased rate of food ingestion of these mutants with their increased longevity is interpreted as indicating that the increased longevity is most likely due to reduced caloric intake. These results appear to indicate that specific life span genes are extremely rare or, alternatively, life span is controlled in a polygenic fashion.

Aging↗
PubMed1993

Hypergravity, aging and longevity in Drosophila melanogaster.

1. Drosophila melanogaster flies have been used in studies of the effect of hypergravity (HG) on aging and longevity. 2. There is no clear longevity decrease with the gravity level up to 4 g and, even at 7 g, flies still live for roughly 40 days. 3. The HG-related changes in fecundity suggest that flies counteract an increased metabolic demand. 4. Viability is barely affected in HG. 5. These results show that flies remain able to lay viable eggs and to live for a fairly long life, even at high HG levels. 6. The study of three behavioral traits affected by aging (climbing activity, pattern of movement, spontaneous locomotor activity) suggests that flies age faster in HG, while no HG effect is clearly detected at young age. 7. These results are observed at HG levels where longevity is not yet affected. 8. Results are discussed in relation with Pearl's rate of living theory (1928).

Aging↗
PubMed1994

A decrease of free radical production near critical targets as a cause of maximum longevity in animals.

A comprehensive study was performed on the brains of various vertebrate species showing different life energy potentials in order to find out if free radicals are important determinants of species-specific maximum life span. Brain superoxide dismutase, catalase, Se-dependent and independent GSH-peroxidases, GSH-reductase, and ascorbic acid showed significant inverse correlations with maximum longevity, whereas GSH, uric acid, GSSG/GSH, in vitro peroxidation (thiobarbituric acid test), and malondialdehyde (measured by HPLC), did not correlate with maximum life span. Superoxide dismutase, catalase, GSH-peroxidase, GSH and ascorbate results agree with those previously reported in various independent works using different animal species. GSSG/GSH, and true malondialdehyde (HPLC) results are reported for the first time in relation to maximum longevity. The results suggest that longevous species simultaneously show low antioxidant concentrations and low levels of in vivo free radical production (a low free radical turnover) in their tissues. The "free radical production hypothesis of aging" is proposed: a decrease in oxygen radical production per unit of O2 consumption near critical DNA targets (mitochondria or nucleus) increases the maximum life span of extraordinarily long-lived species like birds, primates, and man. Free radical production near these DNA sites would be a main factor responsible for aging in all the species, in those following Pearl's (Rubner's) metabolic rule as well as in those not following it.

Aging↗
PubMed1985

The comparative biology of longevity and lifetime energetics.

The relationships between longevity and cumulative energy metabolism in homeothermic vertebrates are explored interspecifically as allometric functions, and intraspecifically in terms of metabolic extension, through restriction of energy intake, hibernation, and torpor. A new equation for marsupial longevity is presented. The first evidence of age-dependent mortality in a population of hummingbirds is shown. Hummingbirds are seen to be model subjects for the study of longevity in nature.

Animals↗
PubMedDate not supplied

Reproductive life of French-Canadians in the 17-18th centuries: a search for a trade-off between early fecundity and longevity.

One of the predictions derived from Williams' (1957) evolutionary theory of senescence is the existence of a trade-off between early fecundity and longevity. The population register of the French immigrants to Québec in the 17th century and of the first Canadians in the 17th and 18th centuries was used to detect such a trade-off in a noncontraceptive human population living at a time when longevity had not been prolonged by medical care and was not artificially shortened by wars, epidemics, or other external causes. No evidence for such a trade-off could be detected in these populations which had not yet reached the demographic transition phase (i.e., the historical period when longevity began to be extended and the progeny began to be reduced). Results are discussed in connection with the various studies aiming to test the Williams' theory.

Canada↗
PubMedDate not supplied

The expression of the EF1 alpha genes of Drosophila is not associated with the extended longevity phenotype in a selected long-lived strain.

A quantitative dot blot analysis was performed to determine whether the expression of the EF-1 alpha genes of Drosophila melanogaster are associated with the extended longevity phenotype characteristic of our genetically selected long-lived strain. These data were compared to that obtained from two normal-lived strains and from two iso-chromosomal strains with an intermediate life span. The relative mRNA levels of both EF-1 alpha genes (EF-1 alpha F1 and EF-1 alpha F2) for all five strains were measured through the larval, pupal, and early adult stages, and statistically analyzed. Our findings from these studies indicate that the F2 mRNA tracks with the extended longevity; however, the F1 mRNA is the major component and, thus, the relative total expression of these genes at the mRNA level is approximately equivalent for all five strains. These conclusions suggest that the expression of the EF-1 alpha genes is not associated with the extended longevity phenotype.

Animals↗
PubMed2004

The genetics of human longevity.

Many of the genes that affect aging and longevity in model organisms, such as mice, fruit flies, and worms, have human homologs. This article reviews several genetic pathways that may extend lifespan through effects on aging, rather than through effects on diseases such as atherosclerosis or cancer. These include some of the genes involved in the regulation of DNA repair and nuclear structure, which cause the progeroid syndromes when mutated, as well as those that may affect telomere length, since shorter telomeres have been associated with shorter survival. Other potential longevity genes, such as sirtuins, are involved in regulating the response to cellular stress, including caloric restriction. The best-studied pathway involves insulin and insulin-like growth factor 1 signaling; mutations in homologs of these genes have extended lifespan up to sixfold in model organisms. Other potential candidates include mitochondrial DNA and the genes that regulate the inflammatory response. Despite the challenges in study design and analysis that face investigators in this area, the identification of genetic pathways that regulate longevity may suggest potential targets for therapy.

Aging↗
PubMed2004

Smoking and longevity: an incompatible binomial?

In Western countries data from clinical and epidemiological studies have induced the public health offices to promote a great deal of advertising and informative campaigning for smoking reduction. Cigarette smoking has been clearly linked to the most common causes of death in the elderly and contributes to the higher death rate and disability rate associated with many chronic illnesses that are common in this age group. The combination of smoking along with other risk factors like hypertension and diabetes increase high frequency diseases, disability as well as adding to an increase in mortality rate. In order to verify if a healthy lifestyle really favors longevity and how much smoking is incompatible with extreme longevity we investigated the prevalence of smokers and the total smoking exposure of a sample of centenarians in relation with residual survival and health conditions. Our sample consists of 157 centenarians living in Rome, 39 males and 118 females (ratio m/f =1:3),mean age being 101.59 +/- 1.8 years (+/-SD), 83.8% of the centenarians have never smoked,13.5 % are former smokers, and 2.7% are active smokers. The average starting age of smoking is 21.2 years, while the average age of quitting is 65.7 years with an average of 44.7 +/- 17.1 smoking years. The average number of smoked cigarettes per day is quite low,less than 10 cigarettes, so that the total average number of smoked cigarettes is 158,045,well under 280,000 which is considered the cut-off point in many studies of when tumors are noticed. There seemed to be a significant difference (p < 0.001) in gender results in smokers: among male centenarians smokers reached 46%, while female smoker centenarians reached only 8.1%. Statistically significant chronic illnesses were noted among centenarian smokers over the age of 65 (p < 0.02). Moreover, Cox's regression has shown in centenarians a lower survival rate (p < 0.05) in smokers (20.7 +/- 11.2 months) than in non-smokers (27.0 +/- 19.0 months). In conclusion, our study evidences that smoking is for all but some exceptional subjects, incompatible with successful aging and compromises life expectancy even in extreme longevity.

Aged↗
PubMed2006

Analysis of common polymorphisms in angiotensin-converting enzyme and apolipoprotein e genes and human longevity in Colombia.

BACKGROUND: Genetic analysis of human longevity may be useful for the understanding of molecular mechanisms implicated in age-related diseases. The molecular genetics of human longevity is largely unexplored in Latin American populations and other developing countries. METHODS: To explore the possibility of an association of common polymorphisms in two candidate genes and longevity in Colombia, we analyzed two polymorphisms in apolipoprotein E (APOE) and angiotensin-converting enzyme (ACE) genes in a sample of 538 Colombian subjects (18-106 years), using previously validated PCR-based methodologies. RESULTS: We found a significant decrease in ACE DD genotype (24 vs. 16%) between young and old subject groups (mean age: 45 vs. 77 years) (p = 0.03). The ACE DD genotype and D allele decrease was significant only in women. There were no differences for APOE polymorphism between young and old subjects. CONCLUSIONS: Our results are compatible with the expected age-related decrease of ACE DD genotype. Future studies examining functional single nucleotide polymorphisms (SNPs) in the ACE gene and its correlation with serum ACE activity in the older subjects and their younger relatives in this sample are warranted.

Adolescent↗