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PubMed1999

Longevity of British breeds of dog and its relationships with sex, size, cardiovascular variables and disease.

The results of a questionnaire provided data about owners' perceptions of the cause of death of over 3000 British dogs. The mean age at death (all breeds, all causes) was 11 years one month, but in dogs dying of natural causes it was 12 years eight months. Only 8 per cent of dogs lived beyond 15, and 64 per cent of dogs died of disease or were euthanased as a result of disease. Nearly 16 per cent of deaths were attributed to cancer, twice as many as to heart disease. Neutered females lived longer than males or intact females, but among dogs dying of natural causes entire females lived slightly longer. In neutered males the importance of cancer as a cause of death was similar to heart disease. Mongrels lived longer than average but several breeds lived longer than mongrels, for example, Jack Russells, miniature poodles and whippets. There was no correlation between longevity and cardiovascular parameters (heart rate, systolic, diastolic, pulse and mean arterial pressure, or the combination of heart rate and pulse pressure) but smaller dogs had longer lifespans. The results also include breed differences in lifespan, susceptibility to cancer, road accidents and behavioural problems as a cause of euthanasia.

Accidents, Traffic↗

PubMed1982

Effect of sodium chloride on longevity in mice.

The effects of dietary sodium chloride on the longevity, body weight, and food consumption in a normotensive strain (A/J) of mice was studied. Four groups of 50 mice each were fed diets containing 0.5 (control group), 1.5, 2.5, and 4.5% sodium chloride. The mean life span was 115.2 wk in the control group, and 115.5, 110,5, and 116.1 wk for groups 2, 3, and 4, with no significant differences from the control group. No differences were present in food consumption, but a graded weight loss was present after the 20th wk, which persisted throughout the experiment. No significant effect of salt loading was demonstrable on the extravascular fluid movement in either acute experiments or in the long-term dietary sodium chloride groups.

Animals↗

PubMed1985

Effect of voluntary exercise on longevity of rats.

The purpose of this study was to obtain information regarding the effects of exercise on longevity in rats. The exercise used was voluntary activity wheel running. The runners gradually decreased their running from approximately 4 to approximately 1 mile/day as they aged from 9 to 30 mo. The runners lived slightly but significantly longer than sedentary freely eating controls and sedentary pair-fed controls (1,012 +/- 138 vs. 923 +/- 160 and 928 +/- 186 days) but significantly less long than food-restricted paired-weight sedentary controls (1,113 +/- 150 days). Although the exercise improved survival, it did not result in an extension of life-span. In contrast, the food-restricted paired-weight sedentary rats showed a true increase in life-span. The paired-weight rats also had a significantly reduced incidence of malignancies compared with the other three groups. However, there was no significant difference between the runners and the freely eating or pair-fed sedentary controls in the cause of death. These results provide evidence that exercise improves survival but does not result in an extension of life-span in rats.

Animals↗

PubMed1991

Interaction between exercise and food restriction: effects on longevity of male rats.

Male rats that exercise in running wheels have a longer average survival than freely eating sedentary controls but, in contrast to food-restricted sedentary controls of the same weight, show no extension of maximal life span (J. Appl. Physiol. 59: 826-831, 1985). To test the possibility that exercise may counteract a life-extending effect of decreased availability of energy for certain biological processes such as cell proliferation, we examined the combined effects of exercise and food restriction on longevity of male rats. As before, wheel running improved average length of life, 978 +/- 172 vs. 875 +/- 175 (SD) days, for the sedentary controls (P less than 0.01) without increasing maximal life span. Paired-weight controls, food restricted (approximately 30% below ad libitum) to weight the same as the runners, showed increases in both average (1,056 +/- 144 days) and maximal life span. Food-restricted runners, with intake restricted to the same extent (approximately 30%), had an increased mortality rate over the first approximately 50% of their survival curve up to approximately 900 days of age; their average life span (995 +/- 226) was similar to that of the control group of runners and shorter than that of their paired-weight food-restricted sedentary controls (1,088 +/- 159 days, P less than 0.05). However, after approximately 900 days of age the food-restricted runners' survival became similar to that of the food-restricted sedentary groups, with a comparable increase in maximal life span. Thus the exercise did not counteract the increase in maximal life span induced by food restriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1998

Apolipoprotein E polymorphism is not associated with longevity or disability in a sample of Italian octo- and nonagenarians.

BACKGROUND: Apolipoprotein E (apo E) is a protein associated with plasma lipoproteins. Apo E polymorphism has been related to significant modifications of lipoprotein profile, as well as to the incidence of different pathologies including cardiovascular disease, Alzheimer's disease, and vascular dementia. Furthermore, it was proposed that apo E polymorphism might be involved in the aging selection process. OBJECTIVE: The purposes of the present study were the following: (1) to evaluate apo E polymorphism in 'successful' and 'unsuccessful' aging, defined as the absence or presence of disability and severe chronic diseases (mainly cardiovascular disease and dementia), respectively; (2) to evaluate the impact of apo E polymorphism on plasma lipids in very old individuals free of or affected by disability. METHODS: 253 Italian subjects including 100 free-living healthy octo- and nonagenarians, 62 disabled octo- and nonagenarians, and 91 healthy adult controls, all matched for origin were studied. Apo E phenotypes were determined by PhastSystem (Pharmacia). Lipoprotein parameters (total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, lipoprotein (a), and apoprotein A-I and B) were measured by standardized methods. ADL were evaluated by the Katz index. RESULTS: The frequency of sigma2, sigma3, and sigma4 alleles was 0.062, 0.887, and 0.051 respectively in the entire sample; no differences in alleles distribution were found between the three groups. When the subjects were divided according to the E type (E2 type: E2/E2 and E2/E3; E3 type: E3/E3; E4 type: E3/E4 and E4/E4), no differences in lipoprotein parameters emerged, but a trend toward higher total and LDL-cholesterol from the E2 to the E4 type was observed. The sigma4 allele had a raising effect, while sigma2 had a lowering effect on total cholesterol levels, but these effects were much less profound in the disabled octo- and nonagenarians. CONCLUSIONS: We conclude that (1) the frequency of the sigma4 allele is very low in this sample of subjects from central Italy; (2) no differences emerged in sigma4 distribution between healthy and disabled octo- and nonagenarians, and adult controls; the very low frequency of sigma4 allele might contribute to this finding; (3) our data do not support the hypothesis of a possible association between apo E polymorphism and longevity or disability in this population.

Aged↗

PubMedDate not supplied

Ageing and longevity are related to growth hormone/insulin-like growth factor-1 secretion.

BACKGROUND: It is known that the growth process is related to an individual's life-span, but the role of growth hormone (GH) secretion in human ageing remains unknown. OBJECTIVE: This study has focussed on the influence of GH on ageing parameters and on its relationship with human longevity. METHODS: To deal with the first issue, we compared ageing parameters of young (up to 39) and old (over 70) individuals having similar insulin-like growth factor-1 (IGF-1) blood levels. For the second one, the decline in IGF-1 levels was studied comparing its behaviour in the first half with that in the second half of adult life. The latter represents the period of life in which mortality progressively increases. Two hundred and five healthy individuals were chosen as subjects, well distributed by gender and age (between 19 and 93 years). RESULTS: Old males with IGF-1 levels similar to young ones do not show the age-dependent decrease in serum testosterone and lean body mass, nor the increase in fat body mass. Other hormone-metabolic and nutritional parameters do not reveal any change compared with the results of all individuals. In females, the results do not allow to assume any IGF-1 influence. The behaviour of the linear regression in the second half of adult life of males, which becomes flat because old men having low IGF-1 blood levels die earlier, is consistent with these results. This effect, which is supported by predictive analysis, is not observed in females, i.e. the IGF-1 level declines in the second half of the women's adult life are only a little flatter than in the first half. Finally, extrapolating the regressions obtained in the first half of adulthood, the age at which the curve crosses the x-axis is 110 years for males and 132 for females. CONCLUSIONS: The presented study of IGF-1 levels suggests that the GH secretion in adulthood plays a determinant role not only for some regressive manifestations, but also for life potential.

Adult↗

PubMed1989

Evidence for a relationship between longevity of mammalian species and a lens growth parameter.

The lens growth was studied in a number of curves representing 16 mammalian species. Emphasis was placed on determining the length of the lens development stage. All the lens curves studied went through a growth crisis: It is a period of apparent growth slowing down, lasting linear during the resting lifespan (adult stage). The growth crisis occurred at a length that was characteristic for the species and was shown to be directly correlated with the species maximum lifespan potential. These results may indicate the prevalence of a common functional basis regulating the lens growth and thus operating in the longevity of mammalian species.

Animals↗

PubMed1994

Age determination and longevity in amphibians.

Methods of age determination of amphibians by counting annual layers in the bone tissue and data on longevity of amphibians (both anurans and urodeles) in nature are presented. Age compositions of amphibian populations are discussed and their variations analysed.

Age Determination by Skeleton↗

PubMed1995

Effect of maternal diabetes on longevity in offspring of spontaneously hypertensive rats.

We studied the effect of maternal diabetes induced by neonatal streptozotocin treatment on the longevity of the male offspring in spontaneously hypertensive rats (SHR). Maternal diabetes significantly decreased the survival in the offspring as compared with the control (p < 0.01). Mean age at death was 14.9 +/- 0.6 months in the offspring from the diabetic dams and 17.9 +/- 1.1 months in that from the control. The life span was significantly correlated with the birth weight (rs = 0.55, p = 0.009). These findings suggest that a diabetic pregnancy may accelerate an age-related degenerative process of the offspring in SHR.

Animals↗

PubMed1976

Sports and longevity.

The mortality of 396 Finnish champion skiers born from 1845 to 1910 was followed up to the end of 1967. Their median life expectancy was 73.0 years, ie.e 4.3 years longer than that for the Finnish male population during the same period. Former skiers have low blood pressure, seldom smoke and are physically active. Increased longevity has been reported also for American college oarsmen and baseball players.

Adolescent↗

PubMed1997

Genetic cholesteryl ester transfer protein deficiency is extremely frequent in the Omagari area of Japan. Marked hyperalphalipoproteinemia caused by CETP gene mutation is not associated with longevity.

Low levels of HDL cholesterol have been clearly demonstrated to be associated with an increased incidence of coronary heart disease, strongly suggesting that HDL particles have an antiatherogenic function. However, little information has been available concerning the atherogenicity of a marked hyperalphalipoproteinemia (HALP). There is no agreement about whether plasma cholesteryl ester transfer protein (CETP) deficiency is associated with an antiatherogenic state or not, although this disorder was reported to be one of the major causes of marked HALP. In the current study, we have found a unique area (Omagari City, Akita Prefecture, Japan) where CETP deficiency caused by a G-to-A mutation at the 5' splice donor site of intron 14 in the CETP gene is extremely frequent. In Omagari City, the mutation was detected more than 20 times more frequently and the prevalence of a marked HALP with plasma HDL cholesterol > or = 2.58 mmol/L (100 mg/dL) was 5 to 10 times higher than in other areas of Japan. This discovery has made it possible to perform a large population-based study concerning the atherogenicity of a marked elevation of HDL cholesterol in a genetically more homogeneous population. There was a statistically significant U-shaped relationship between HDL cholesterol levels and the incidence of ischemic changes in electrocardiograms. In cases of HDL cholesterol < 1.81 mmol/L (70 mg/dL), the incidence increased in proportion to the levels of HDL cholesterol. The frequency of the CETP gene mutation was higher in patients with coronary heart disease than in healthy control subjects. In subjects aged > 80 years, the prevalence of both marked HALP and the intron 14 splicing defect was significantly lower than in the younger generation. The current study indicated for the first time that a marked HALP caused by CETP gene mutation may not represent a longevity syndrome, suggesting the importance of reevaluation of the clinical significance and pathophysiology of a marked HALP.

Aged↗

PubMed2001

Hypothesis: pulse pressure and human longevity.

In exploration of the association between pulse pressure and longevity in humans, 3 hypotheses are briefly discussed: the fetal origin hypothesis, antagonistic pleiotropy, and the telomere hypothesis of cellular aging. The implications of these hypotheses serve to draw a critical distinction between biologic age (aging) and chronological age and, thereby, offer an answer to a question that presently matters most in the field of hypertension: Why has it been so difficult to disentangle the genetic components of essential hypertension and to identify the variant genes responsible for elevated blood pressure in a large segment of the human population?

Aging↗

PubMed2004

Silent information regulator 2alpha, a longevity factor and class III histone deacetylase, is an essential endogenous apoptosis inhibitor in cardiac myocytes.

Yeast silent information regulator 2 (Sir2), a nicotinamide adenine dinucleotide-dependent histone deacetylase (HDAC) and founding member of the HDAC class III family, functions in a wide array of cellular processes, including gene silencing, longevity, and DNA damage repair. We examined whether or not the mammalian ortholog Sir2 affects growth and death of cardiac myocytes. Cardiac myocytes express Sir2alpha predominantly in the nucleus. Neonatal rat cardiac myocytes were treated with 20 mmol/L nicotinamide (NAM), a Sir2 inhibitor, or 50 nmol/L Trichostatin A (TSA), a class I and II HDAC inhibitor. NAM induced a significant increase in nuclear fragmentation (2.2-fold) and cleaved caspase-3, as did sirtinol, a specific Sir2 inhibitor, and expression of dominant-negative Sir2alpha. TSA also modestly increased cell death (1.5-fold) but without accompanying caspase-3 activation. Although TSA induced a 1.5-fold increase in cardiac myocyte size and protein content, NAM reduced both. In addition, NAM caused acetylation and increases in the transcriptional activity of p53, whereas TSA did not. NAM-induced cardiac myocyte apoptosis was inhibited in the presence of dominant-negative p53, suggesting that Sir2alpha inhibition causes apoptosis through p53. Overexpression of Sir2alpha protected cardiac myocytes from apoptosis in response to serum starvation and significantly increased the size of cardiac myocytes. Furthermore, Sir2 expression was increased significantly in hearts from dogs with heart failure induced by rapid pacing superimposed on stable, severe hypertrophy. These results suggest that endogenous Sir2alpha plays an essential role in mediating cell survival, whereas Sir2alpha overexpression protects myocytes from apoptosis and causes modest hypertrophy. In contrast, inhibition of endogenous class I and II HDACs primarily causes cardiac myocyte hypertrophy and also induces modest cell death. An increase in Sir2 expression during heart failure suggests that Sir2 may play a cardioprotective role in pathologic hearts in vivo.

Acetylation↗

PubMed1992

Nutritional improvement, cardiovascular diseases and longevity in Japan.

1. Nutritional conditions have improved remarkably for the past 40 years in Japan; major improvements are increases in protein intake (69.7 in 1955 to 79.2g/day per capita in '88), and fat intake (20.3 in '55 to 58.3 g/day per capita in '88), both of which are significantly related statistically to the gradual reduction of stroke mortality (r = -0.74, not significant; r = -0.78, p < 0.05) and to a remarkable extension of average life span (r = 0.91, p < 0.01; r = 0.98, p < 0.001) in the Japanese. 2. Average heights of 12-year old male and female children, correlating significantly with these nutritional improvements, are significantly positively correlated with average life spans (men and women respectively; r = 0.97, p < 0.001). 3. Thus, general nutritional improvements among the Japanese are regarded as the major contributory factor to the recent achievement of top-ranked position for longevity in the world.

Body Height↗

PubMed2002

Enhanced longevity in tau mutant Syrian hamsters, Mesocricetus auratus.

The single-gene mutation tau in the Syrian hamster shortens the circadian period by about 20% in the homozygous mutant and simultaneously increases the mass-specific metabolic rate by about 20%. Both effects might be expected to lead to a change in longevity. To test such expectations, the life span of male and female hamsters from three genotypes (wild-type, heterozygous, and homozygous tau mutants, all derived from heterozygote crosses to randomize the genetic background) was recorded in constant darkness. Male hamsters lived significantly longer than females: the overall average life span was 96.9 weeks (SE = 2.5, n = 118) for males and 82.0 weeks (SE = 2.1, n = 99) for females. To our surprise, male and female homozygous mutant hamsters lived significantly longer rather than shorter compared to wild-types. For males, the difference between the two genotypes was on average 14%; for females, the difference was 16%. The mortality rate of wild-type males was significantly different from that of homozygous tau males but not different from that of heterozygotes. Overall, survival of wild-type females was statistically distinguishable from both heterozygous and homozygous mutant females. Male and female wild-type hamsters were heavier than homozygote mutants throughout the entire life span, and heterozygous mutants had intermediate weights. There was no correlation between body mass and life span, and the causes of the extended life span in tau mutant hamsters remain unresolved.

Animals↗

PubMed1993

Nutritional and non-nutritional factors for 'healthy' longevity.

The far-reaching effects of the ageing of populations is being increasingly appreciated. Lengthening longevity, associated with decreasing family size, evokes rising charges, socioeconomically, and on health services. Information on these and other parameters is presented for developed and developing populations. Examples are given, with lessons to be learned, of long-living segments of populations, past and present. The roles of diet, physical activity, and smoking and alcohol consumption also of attitudes, are discussed. It is concluded that if the middle-aged and elderly could be persuaded to follow long-term practices associated with good public health, then morbidity could be compressed, and disability-free years extended. However, this goal could only be achieved with a high level of motivation.

Family Characteristics↗

PubMed2006

Search for genetic variants in the p66Shc longevity gene by PCR-single strand conformational polymorphism in patients with early-onset cardiovascular disease.

BACKGROUND: Among the possible candidate genes for atherosclerosis experimental data point towards the longevity gene p66Shc. The p66Shc gene determines an increase of intracellular reactive oxygen species (ROS), affecting the rate of oxidative damage to nucleic acids. Knock-out p66Shc-/- mice show reduction of systemic oxidative stress, as well as of plasma LDL oxidation, and reduced atherogenic lesions. Thus, p66Shc may play a pivotal role in controlling oxidative stress and vascular dysfunction in vivo. METHODS: We searched for sequence variations in the p66Shc specific region of the Shc gene and its upstream promoter by PCR-SSCP in a selected group of early onset coronary artery disease (CAD) subjects (n. 78, mean age 48.5 +/- 6 years) and in 93 long-living control subjects (mean age 89 +/- 6 years). RESULTS: The analysis revealed two variant bands. Sequencing of these variants showed two SNPs: -354T>C in the regulatory region of p66Shc locus and 92C>T in the p66 specific region (CH2). Both these variants have never been described before. The first substitution partially modifies the binding consensus sequence of the Sp1 transcription factor, and was detected only in two heterozygous carriers (1 CAD subjects and 1 control subject). The 92C>T substitution in the CH2 region consists in an amino acid substitution at codon 31 (proline to leucine, P31L), and was detected in heterozygous status only in one CAD subject. No subjects homozygous for the two newly described SNPs were found. CONCLUSION: Only two sequence variations in the p66Shc gene were observed in a total of 171 subjects, and only in heterozygotes. Our observations, in accordance to other studies, suggest that important variations in the p66Shc gene may be extremely rare and probably this gene is not involved in the genetic susceptibility to CAD.

Adaptor Proteins, Signal Transducing↗

PubMed1995

Mental status examination of an exceptional case of longevity J. C. aged 118 years.

BACKGROUND: The mental status examination of an extreme case of longevity, J. C., aged 118 years and 9 months, is documented in order to further knowledge regarding profiles of morbidity in the extremely elderly. J. C. is presently considered to have the longest authenticated life-span in the history of the human species. METHOD: Neuropsychological tests were improvised taking into account the subject's severe perceptual deficits. The examination was carried out over a six-month period. A CT scan was also conducted. RESULTS: The subject's performance on tests of verbal memory and language fluency is comparable to that of persons with the same level of education in their eighties and nineties. Frontal lobe functions are relatively spared and there is no evidence of depressive symptomatology or other functional illness. Cognitive functioning was found to slightly improve over a six-month period. CONCLUSIONS: The subject shows no evidence of progressive neurological disease. A high initial level of intellectual ability may have constituted a protective factor.

Aged↗