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PubMed2001

Familial excess longevity in Utah genealogies.

We evaluated the influence of family history on longevity by examining longevity in a cohort of 78,994 individuals drawn from the Utah Population Database (UPDB) who were born between 1870 and 1907, and lived to at least age 65. We examined Mendelian genetic and social modes of transmission of excess longevity (the difference between observed and expected longevity) by varying weighted kinship contributions over different classes of relatives. The genetic component of the variation in excess longevity measured as heritability, h2, was approximately 0.15 (95% confidence interval [CI] 0.12-0.18). Among siblings of probands who reached the 97th percentile of excess longevity (+ 14.8 years, currently age 95 for men and 97 for women), the relative risk of recurrence (lambdas) was 2.30 (95% CI 2.08-2.56). In sibships whose relatives were in the top 15% of the distribution for familial excess longevity, the value of lambdas increased substantially, indicating that considering the longevity of distant relatives may be helpful in the selection of families in which to identify genes influencing aging and longevity.

Aged↗
PubMed2002

Temperature-induced shifts in associations of longevity with body size in Drosophila melanogaster.

One of the hypotheses of growing interest in studies of responses to thermal environments suggests that trade-offs and other trait associations may be altered by temperature. Here, the commonly observed positive association between body size and longevity was examined at two adult test temperatures, 14 degrees C and 25 degrees C, in cold-stress-selected lines (S) and their controls (C) in 25 degrees C-reared Drosophila melanogaster. Thorax length (TL) and developmental time (DT) were also scored in 25 degrees C-reared individuals before and after one generation of truncation selection on longevity. The topography of the selection surface that relates longevity to thorax and wing size was temperature dependent and differed both between lines and between sexes. Longevity increased monotonically with body size (TL) in C and S females at 25 degrees C but, surprisingly, longevity decreased with body size in S individuals at 14 degees C. Body size did not diverge between S and C lines and showed no response to longevity selection. However, DT increased by 25 degrees C-longevity selection in C individuals and decreased by 14 degrees C-longevity selection in S individuals. These results suggest that trait associations (including the commonly observed trade-off between body size and DT) can greatly depend on temperature, as a shift in the sign of the correlation is possible at low temperature. Genotype x temperature interaction is an important source of variation in the relationship between soma size and longevity.

Acclimatization↗
PubMed2004

Evaluating longevity of composite beef females using survival analysis techniques.

Objectives were to 1) identify risk factors affecting the longevity of beef females, 2) evaluate the utility of measures collected early in life in predicting longevity, and 3) estimate the heritability of longevity when females were culled primarily for not being pregnant following a 45-d breeding season. Data were from 1,379 Composite Gene Combination (CGC; 1/2 Red Angus, 1/4 Charolais, 1/4 Tarentaise) cows born from 1982 through 1999 at the USDA-ARS, Fort Keogh Livestock and Range Research Laboratory, Miles City, MT, and first calving at approximately 2 yr of age. The length of productive life was modeled using Cox regression to identify factors affecting the longevity of beef females. Age at first calving and calf birth weight did not influence longevity. Cows that experienced dystocia were at greater risk of being culled than those that calved without assistance (P < 0.01). On average, as breeding value for cow weight increased, the risk of being culled decreased (P < 0.01), whereas the risk of being culled increased with increasing maternal breeding values for preweaning gain (P < 0.05). Traits measured before 1 yr of age were not useful in predicting the subsequent longevity of cows. The heritability of functional longevity was estimated to be 0.14. Relatively low heritability and the lack of indicators of longevity expressed early in life suggest that genetic improvement of longevity will be difficult. Matching the genetic potential of cows for size and milk production to the production environment such that rebreeding performance is not compromised by concurrent lactation seems to be a consideration in retaining beef females when open cows are culled.

Animals↗
PubMed2003

[Longevity in gerontology and in Judaism--quantity years or quality years?].

In this day and age, we have been granted longevity--both a blessing and a curse. Longevity has resulted in new diseases, illnesses and long-term disabilities due to the shift from death caused by acute infectious diseases and by chronic diseases such as cancer, cardiac and vascular diseases, to morbidity caused by chronic cases of arthritis, Alzheimer's and sensory disabilities--auditory and visual. Chronic diseases are characterized by long-term illness and result in escalating reduction in functioning, with an increase in the elderly person's dependence on his family or society. What do we mean when we say 'longevity'? Do we add days to our lives or perhaps life to our days? What can we expect? How do we achieve longevity? I have looked into the Torah, into the words of the Sages and into the findings of geriatric research. I have found that, both in gerontology, and in the words of the Sages, longevity is accompanied by quality of life. In gerontology, 'quality of life' is measured as being active and independent, including the ability to carry out routine daily activities (ADL). Katz and his colleagues have used the terms 'active life expectancy' and 'dependent life expectancy'. The ability to predict active life expectancy is no less important than predicting mortality, and particularly how to achieve active life expectancy. The Sages praise longevity, accompanied by wisdom: "In the elderly, wisdom, and in wisdom, long life' (Job). In addition, they say: 'For longevity and years of life and peace shall be granted to you' (Proverbs), to teach the blessing of longevity accompanied by wisdom. To achieve longevity, one should maintain regular habits that reduce the risk of illness such as physical exercise, a balanced diet, no smoking, and have a relaxed attitude to self-importance and to financial matters, while emphasizing the routine and stable elements of one's daily life.

Geriatrics↗
PubMed2003

Effect of modern pacing algorithms on generator longevity: a predictive analysis.

Pulse generator (PG) longevity is of major importance to the quality of care of pacemaker patients. A series of automatic algorithms affect PG longevity. This study investigated the individual and combined effects of three algorithms incorporated in the Medtronic Kappa 700 pacemaker series: Capture Management periodically measures the stimulation threshold and adjusts the PG output, Sinus Preference allows the sinus rate to prevail in a specified range below the sensor rate, and Search AV allows an extension of the AV interval if spontaneous conduction is observed. The effects of Capture Management, Sinus Preference, and Search AV on device longevity were studied in 21 consecutive patients treated in the VDD and DDDR modes. Patients were followed for 1 year. The data were analyzed using an equation provided by the manufacturer. Capture Management was activated in 20 patients. For 11 PGs at the basic settings, longevity was extended by 5.2%, whereas reprogrammed PGs had no gain. Sinus Preference was active in four DDDR patients, who gained 12.0 +/- 5.3%atrial sensing from it, with a resultant longevity gain of1.4 +/- 0.45 months(NS). Search AV was active in 19 patients and 8 responders gained 7.8 +/- 4.4 months PG longevity. The overall longevity in this study was 106.3 +/- 8.4 months with all features as programmed, whereas the longevity without Capture Management and Search AV algorithms would be 98.2 +/- 4.9 months, saving 8.1 +/- 5.8 months(range 0-18) of battery life. Thus, two algorithms: Capture Management and Search AV, have clinical relevance in the extension of PG longevity.

Algorithms↗
PubMed2005

Why dietary restriction substantially increases longevity in animal models but won't in humans.

Caloric restriction (CR) extends maximum longevity and slows aging in mice, rats, and numerous non-mammalian taxa. The apparent generality of the longevity-increasing effects of CR has prompted speculation that similar results could be obtained in humans. Longevity, however, is not a trait that exists in a vacuum; it evolves as part of a life history and the physiological mechanisms that determine longevity are undoubtedly complex. Longevity is intertwined with reproduction and there is a cost to reproduction. The impact of this cost on longevity can be age-independent or age-dependent. Given the complexity of the physiology underlying reproductive costs and other mechanisms affecting life history, it is difficult to construct a simple model for the relationship between the particulars of the physiology involved and patterns of mortality. Consequently, we develop a hypothesis-neutral model describing the relationship between diet and longevity. Applying this general model to the special case of human longevity and diet indicates that the benefits of caloric restriction in humans would be quantitatively small.

Age Factors↗
PubMed2006

Coevolution of exceptional longevity, exceptionally high metabolic rates, and mitochondrial DNA-coded proteins in mammals.

Mammals' longevity is inversely related to mass-specific basal metabolic rate because the generation of reactive oxygen species constrains lifespan. Longevity increases with body mass because the latter is inversely related to mass-specific basal metabolic rates. In placental mammals the longevity residuals from the power laws that describe longevity as a function of mass-specific basal metabolic rates, or body mass, are positively correlated with the relative rates of evolution of cytochrome b, a generator of reactive oxygen species. Therefore, longevity is more accurately described as a function of both mass-specific basal metabolic rate and the relative rate of cytochrome b evolution. The longevity residuals from the power law that describe longevity as a function of body mass are positively correlated with the relative rate of evolution of most other mtDNA-coded proteins. In taxa with very high rate of cytochrome b evolution exceptional longevity is associated with an increase, rather than the predicted decrease, of basal metabolic rates. These finding are compatible with the hypothesis that, in placental mammals, the accelerated evolution of mtDNA-coded proteins, allowed the extension of lifespan by selecting mutations that reduce the generation of reactive oxygen species, mostly by increasing internal proton leak, that accelerates mitochondrial electron transport.

Adaptation, Physiological↗
PubMed1998

HLA-DR alleles display sex-dependent effects on survival and discriminate between individual and familial longevity.

In an effort to reassess the contribution of HLA-DRB1 polymorphisms to inter-individual variations of human longevity, we have compared their genotypic distributions between longevous and adult control groups in the French population. The longevous groups included two independent cohorts totalling 533 centenarians, and 163 nonagenarian siblings. Allelic distributions were significantly different between controls and longevous groups. Three individual alleles were mostly responsible for these differences: DR7, DR11 and DR13. Multivariate logistic analyses were performed in order to sort out interactions between gender- and age-specific genetic effects. DR7 frequency was elevated in longevous men, in centenarians as well as nonagenarian siblings [OR = 1.72 (1.2-2.5)]. DR11's influence on longevity displayed a significant interaction with sex, with an increase in women from longevous sibships [OR = 2.03 (1.4-3.0)]. DR13's frequency was increased in centenarians of both genders [OR = 1.46 (1.2-1.75)]. These results are discussed in the context of other pathophysiological effects of the implicated alleles. Our data support the direct involvement of three HLA-DR alleles in survival at very old ages. Two allele-specific effects on longevity appear to depend on gender and one on familial status for aggregation of this trait. The latter is an original finding for humans.

Adult↗
PubMed1997

Genetic correlations between longevity and conformation traits in an upgrading dairy cattle population.

Genetic correlations between longevity and conformation traits were estimated using data on Dutch Black and White cows born in 1978 (11,558 records), 1982 (39,252 records), and 1989 plus 1990 (58,864 records). Longevity traits considered were number of lactations, herd life, and stayabilities until 36 and 48 mo of age and their functional equivalents (i.e., the longevity traits corrected for production). For the 1989 plus 1990 data file, only stayabilities until 36 and 48 mo of age were considered. Conformation traits were rear legs set, front teat placement, udder depth, suspensory ligament, and subjective scores for udder, feet and legs, and type. Also investigated was a possible nonlinear relationship between conformation and longevity traits. Genetic correlations between conformation and longevity traits differed between years of birth, mainly because farmers practiced large-scale upgrading with Holstein-Friesian bulls during the period considered, which caused a change in desired type. Therefore, the predictive value of conformation traits for longevity based on data from an upgrading population, might be limited. Estimates of genetic parameters should be based on the most recent data possible, and these parameters should be reestimated over time. From the 1989 plus 1990 data file, subjective scores for udder and feet and legs had the highest predictive values for functional longevity. Quadratic relationships between conformation and longevity traits did exist, but generally the linear relationships prevailed.

Animals↗
PubMed1999

Height, body size and longevity.

Life expectancy, mortality and longevity data related to height and body size for various US and world population samples are reviewed. Research on energy restriction, smaller body size and longevity is also examined. Information sources include various medical and scientific journals, books and personal communications with researchers. Additional information is presented based on research involving eight populations of the world noted for their health, vigor and longevity. This information includes the findings of one of the authors who led research teams to study these populations. While conflicting findings exist on the cardiovascular death rates for shorter people, many examples of short populations with very little heart disease are described. Most cancer studies indicate that shorter people have significantly lower mortality risk. Considerable data suggest that shorter people generally have greater longevity than taller people, and extensive animal research supports human longevity findings. Tall populations with low mortality rates are also described. Shorter stature and smaller body weight appear to promote better health and longevity in the absence of malnutrition and infectious diseases. Several theoretical reasons for this greater longevity potential are covered. Also discussed, is the role of socioeconomic status, diet, relative weight, environment and other factors in increasing or decreasing the longevity of individuals, regardless of their heights and weights.

Body Constitution↗
PubMed1999

Genetic and environmental conditions that increase longevity in Caenorhabditis elegans decrease metabolic rate.

Mutations that increase the longevity of the soil nematode Caenorhabditis elegans could define genes involved in a process specific for aging. Alternatively, these mutations could reduce animal metabolic rate and increase longevity as a consequence. In ectotherms, longevity is often negatively correlated with metabolic rate. Consistent with these observations, environmental conditions that reduce the metabolic rate of C. elegans also extend longevity. We found that the metabolic rate of long-lived C. elegans mutants is reduced compared with that of wild-type worms and that a genetic suppressor that restored normal longevity to long-lived mutants restored normal metabolic rate. Thus, the increased longevity of some long-lived C. elegans mutants may be a consequence of a reduction in their metabolic rate, rather than an alteration of a genetic pathway that leads to enhanced longevity while maintaining normal physiology. The actual mechanism responsible for the inverse correlation between metabolic rate and longevity remains unknown.

Animals↗
PubMed1996

The impact of pulse generator longevity on the long-term costs of cardiac pacing.

The long-term costs of cardiac pacing include the device costs, the procedural costs, the follow-up costs, and the replacement costs. At present, there is significant variability in the efficiencies of the integrated circuits and the total battery capacity among different pulse generators that will influence replacement rates over time. Accordingly, we compared the influence of pulse generator longevity on the long-term costs of pacing. The longevity of pulse generators was calculated based on the electrical characteristics of the device and the percentage of time the patient is paced. Replacement rates of pulse generators were estimated for our patient population over a 20-year period, based on patient survival and pulse generator longevity. The costs of pacing over this 20-year follow-up period were then calculated. The longevity of DDDR devices presently implanted in the United States ranges from 8-14 years, assuming that patients are paced 50% of the time. Replacement rates in this population over a 20-year follow-up period were calculated to range from 0.34-0.66, and the total costs of pacing would range from $11,898-14,900 per patient. The longevity of SSIR devices ranges from 7-20 years, assuming that patients are paced 50% of the time. Replacement rates were calculated over the 20-year follow-up period to range from 0.20-0.84, and the total costs of VVIR pacing would range from $8,331-13,286. Based on the proportion of pulse generator models implanted in patients in the United States, the maximum cost differential to the health care system is approximately $424 million/year comparing the devices with the shortest and greatest longevities. Thus, pulse generator longevity may significantly influence the long-term costs of pacing. Patient survival and pulse generator system longevity should be considered when selecting the appropriate pacing system for the individual patient.

Actuarial Analysis↗
PubMed2006

Pacemaker longevity: are we getting what we are promised?

BACKGROUND: Although pacemaker manufacturers provide projections on longevity, these projections cannot be relied upon due to the assumptions of output parameters being far in excess of those programmed in clinical practice. OBJECTIVE: The purpose of this review was to compare the actual longevity to the calculated longevity of pacemakers based on battery cell characteristics taking into account individual programmed parameters, mode, degree of usage, and percent pacing. This was also compared to the manufacturers' own projected longevities. METHODS: Patients who had a pacemaker replaced between 1998 and 2003 were included (n = 124). Cell characteristics were obtained from manufacturers and programmed parameters were obtained at each visit. Stepwise calculations were done for each visit to find current drain during each interval, and then were used in a weighted average to find the total average lifetime current drain. This was subsequently used to find a calculated longevity for each pacemaker to be compared to the actual longevity observed. RESULTS: The pacemakers lasted 491+/-92 days (mean+/-SEM) less than calculated. There was also a difference between dual- and single-chamber devices (though not statistically significant). Moreover, it was found that there were significant differences between manufacturers. CONCLUSIONS: There appears to be a significant discrepancy between calculated and actual longevities, confirming that battery depletion occurs earlier than expected. This suggests that current drain expended for ancillary functions may be considerable. Another factor may be pre-implantation drain. Vigilance with programming of outputs, modes, sensors, heart rates, and ancillary functions could potentially extend longevity and postpone/obviate the need for costly repeat surgery with its attended risk of complications. Furthermore, the differences between manufacturers seem to parallel the clinical impressions.

Aged↗
PubMed2006

Longevity and the evolution of the mitochondrial DNA-coded proteins in mammals.

The amino acids sequences of the mitochondrial DNA-coded peptides of placental mammals evolved at different rates in different branches of the mammalian phylogenetic tree. Adaptive selection was suggested to account for the faster evolution of some mitochondrial DNA-coded proteins in several branches of the mammalian tree, but the driving force(s) for the accelerated evolution has not been elucidated. Mitochondria generate reactive oxygen species (ROS) that appear to constrain the life span of many species. Therefore, I tested the hypothesis that the evolution of mammalian longevity drives the accelerated evolution of mitochondrial DNA-coded peptides. Using rodents as an outgroup for a clad that included most placental mammals (excluding rodents and hedgehogs) the computed rates of amino acid substitution per site were positively correlated with genus longevity (maximal observed averaged life span) for most of the mitochondrial DNA-coded peptides. The substitution per site of ATP6, the proton conducting subunit of ATPsynthase, CYTB, the core subunit of ubiquinone oxidoreductase that participate in both electron and proton transport, and ND3, a subunit of NADH dehydrogenase, showed the strongest correlations with longevity. Additional confirmation for the hypothesis was obtained by the observation that the genetic distances between placental mammals species that belong to different orders are positively correlated with the sum of longevities of the species pairs. The substitutions per site for the entire amino acid sequence coded by the heavy strand mtDNA were also positively correlated with the average longevities of the placental mammals orders. These results support the hypothesis that the evolution of longevity in mammals drove the accelerated evolution of mtDNA-coded peptide. It is suggested that, in mammals, adaptive selection of mutations that decrease the rate of production of reactive oxygen species, directly or indirectly (e.g. by increasing proton leak), increases longevity.

Animals↗
PubMed2002

Dauer juvenile longevity and stress tolerance in natural populations of entomopathogenic nematodes: is there a relationship?

Qualitative and quantitative genetic analysis of life span in experimental adult animals predicts that resistance to stress and longevity are positively correlated, but such studies on field populations of animals are rare. We tested this hypothesis using dauer juveniles of 15 natural populations of the entomopathogenic nematode, Heterorhabditis bacteriophora, collected from diverse localities. Dauer juvenile longevity at 25 degrees C in autoclaved tap water and tolerance to major environmental stresses including heat (survival at 40 degrees C for 2 h), ultraviolet (UV) radiation (original virulence remaining after exposure to 302 nm UV for 5 min), hypoxia (survival at approximately 0% dissolved O2 at 25 degrees C for 96 h), and desiccation (survival in 25% glycerol at 25 degrees C for 72 h) differed significantly among populations. Intrinsic dauer juvenile longevity, defined as the number of weeks to 90% mortality (LT90) estimated using probit analysis of nematode survival data at 25 degrees C varied between 6 and 16 weeks among populations. Longevity was most strongly correlated with heat followed by UV and hypoxia tolerance, respectively, but showed no correlation with desiccation tolerance. The strong positive correlation of longevity with heat tolerance was further confirmed through principal components analysis which showed almost identical variance for heat and longevity. Among the stress factors, only UV tolerance was positively correlated with heat and hypoxia tolerance. Differences in longevity and stress tolerance in nematode populations isolated from a single 200 m2 grassland locality further support another hypothesis that population structure of heterorhabditid nematodes is highly fragmented, thus suggesting the existence of metapopulation dynamics.

Animals↗
PubMed2002

Longevity determination genes in Drosophila melanogaster.

Identification of longevity mutants is crucial for genetic approach to dissect the molecular mechanism of aging and longevity determination. In Drosophila melanogaster, several mutations have been shown to extend the longevity: methuselah encoding a putative G-protein coupled receptor, Indy encoding a sodium dicarboxylate cotransporter, chico encoding insulin receptor substrate, and InR encoding the insulin-like receptor. Extended longevity phenotypes were also observed in transgenic flies overexpressing antioxidant enzymes, Cu/Zn superoxide dismutase and Catalase, Cu/Zn SOD only, or a molecular chaperone, hsp70. Pleiotropism of mutations is a limitation associated with conventional mutagenesis for efficient detection of longevity determination genes. Using a conditional misexpression system, we identified Drosophila POSH (DPOSH), a scaffold protein containing RING finger and four SH3 domains, whose ubiquitous overexpression in adult stage extends the longevity. Neural-specific overexpression of DPOSH is sufficient to extend the longevity, whereas overexpression in non-neural tissues during development induces apoptosis through activation of JNK/SAPK pathway.

Animals↗
PubMed1998

Behavior pattern, arterial partial pressure of oxygen, superoxide dismutase, micro-blood-flow state and longevity or aging.

It is believed that the mechanisms of aging or longevity are multifactorial. We selected four major postnatal factors to verify the mechanisms of longevity and aging. Type B behavior is strongly associated with longevity. The frequency of Type B behavior pattern (55.5 vs. 26.6%) was significantly higher while Type A behavior pattern (2.4 vs. 5.9%) was much lower in the longevity group compared with those in the elderly group (P < 0.01). The decline of arterial partial pressure of oxygen (PaO2) might relate to the aging process which was supported by two facts: (1) low PaO2 might lead to high frequency of chromosomal aberrations, the frequency of chromosomal aberrations was 1.22+/-0.53%, 0.57+/-0.23% and 0.23+/-0.22% in PaO2 < 75, 75-84 or > or = 85 mmHg groups respectively (P < 0.025); (2) the lower the PaO2, the more serious the retina arteriosclerosis. Five mean contents of superoxide dismutase (SOD) in erythrocytes were 626+/-39, 583+/-56, 556+/-43, 547+/-49 and 557+/-40 microg/gHb in different age groups. No significant differences were found in the longevity group as compared with those in 40-89 years old age groups (P > 0.05), but a significantly lower level was found in the middle rather than the young age group (P < 0.05). The studies of thixotropy show that micro-blood-flow state also sustains a better condition in the longevity group. We consider Type B behavior pattern, a higher PaO2, a better micro-blood-flow and a higher level of SOD of erythrocytes may be beneficial for longevity.

Adolescent↗
PubMed2000

HLA, aging, and longevity: a critical reappraisal.

Despite a large number of studies, available data do not allow at present to reach definitive and clear conclusions on role of HLA on longevity, owing to major methodological problems, such as serological and molecular typing of different loci, insufficient sample sizes, different inclusion criteria and age cut-off, inappropriate mixing of data referred to people from 58 to over 100 years of age, inappropriate control matching, and neglected consideration of sex-related effects and the different genetic make-up of studied populations. However, within this confused scenario, some data emerge. First, two studies that do not fit the biases above discussed show that some HLA alleles are associated with longevity. However, some of these alleles may confer an increased risk to undergo a variety of diseases. Second, longevity may be associated with an increased homozygosity at HLA loci. Third, an intriguing association between longevity and the 8.1 ancestral haplotype (AH), which has been proven to be associated with a variety of immune dysfunctions and autoimmune diseases, apparently emerges. This association appears to be a sex-specific (males) longevity contributor, and it is particularly interesting, taking into account that a type 2 (early infancy) --> type 1 (adulthood) --> type 2 (aging) shift of cytokine profile occurs lifelong, and that individuals bearing this haplotype show a type 2 immune responsiveness (note that type 1 cytokines mainly enhance cellular responses, whereas type 2 cytokines predominantly enhance humoral responses). On the whole, the (sex specific) association of longevity with alleles or haplotypes of several genes related to risk factors for a variety of diseases (cardiovascular diseases, cancer), including HLA alleles and haplotypes, is not unexpected on the basis of previous studies on the genetics of longevity in centenarians. This association can be interpreted under the perspective of a well known evolutionary theory of aging (antagonistic pleiotropy). This theory predicts that the same gene (or allele or haplotype) can have different roles (positive or negative) in different periods of the life span. Thus, the 8.1 AH should exert a positive effect during the infancy and aging but not in adulthood, when, indeed it is associated to susceptibility to a variety of diseases.

Aged↗