39 replies to this topic

[ImmInst]

Related Articles Constituents isolated from Cordyceps militaris suppress enhanced inflammatory mediator's production and human cancer cell proliferation.

J Ethnopharmacol. 2010 Jul 12;

Authors: Rao YK, Fang SH, Tzeng YM

ETHNOPHARMACOLOGICAL RELEVANCE: Cordyceps militaris has long been used as a traditional Chinese medicine to promote longevity, for treatment of inflammation and cancer complications. AIM OF THE STUDY: The purpose of this study is to isolate the pure compounds from the extracts of Cordyceps militaris obtained through solid state cultivation process, and evaluate their anti-inflammatory and anticancer properties. MATERIALS AND METHODS: Silica gel column chromatographic purification of Cordyceps militaris extracts resulted in the isolation of ten pure compounds (1-10). The compounds 1-10 were examined for their growth inhibitory properties against nitric oxide (NO), tumor necrosis factor (TNF)-alpha and interleukin (IL)-12 enhanced production from LPS/IFN-gamma-stimulated macrophages. Additionally, the anti-proliferation effects of 1-10 on human cancer cell lines, colon (colon 205), prostate (PC-3), and hepatoma (HepG2) cells were also analyzed. RESULTS: Compound 8 displayed potent growth inhibition on NO, TNF-alpha and IL-12 production with an IC(50) value of 7.5, 6.3, and 7.6mug/ml, respectively. A similar inhibitory trend on these inflammatory mediators was observed for 3, 7, 9 and 10 with an IC(50) values ranging 10.8mug/ml to 17.2mug/ml. On the other hand, compounds 3 and 8 were potent anti-proliferative agents with an IC(50) value of 35.6mug/ml and 32.6mug/ml toward PC-3 and colon 205 cell lines, respectively. The compounds 1 and 2 showed potent anti-proliferation in PC-3 and colon 205 cells, while only 3 displayed such effect in HepG2 cells. CONCLUSION: The present study provides scientific supporting information for the ethnopharmacological use of Cordyceps militaris as an anti-inflammatory and anticancer agent.

PMID: 20633630 [PubMed - as supplied by publisher]



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A high-fat diet impairs neurogenesis: Involvement of lipid peroxidation and brain-derived neurotrophic factor.

Neurosci Lett. 2010 Jul 26;

Authors: Park HR, Park M, Choi J, Park KY, Chung HY, Lee J

Obesity is a growing global health problem that contributes to diabetes, hypertension, cardiovascular diseases, dementia, and cancer. The increased consumption of saturated fats in a high fat diet (HFD) contributes to obesity, neurodegenerative diseases, long-term memory loss, and cognitive impairment. We tested whether HFD influences adult hippocampal neurogenesis. Male C57BL/6 mice were divided into 2 groups and maintained on either a normal diet (ND) or HFD. Seven weeks of HFD significantly decreased the numbers of newly generated cells in the dentate gyrus of the hippocampus without neuronal loss. HFD also increased the level of malondialdehyde (MDA) and decreased the level of brain-derived neurotrophic factor (BDNF) in the hippocampus. The toxic effects of MDA were evaluated on neural progenitor cells (NPCs). MDA reduced the growth of NPCs, but BDNF treatment restored NPCs proliferation. The present data indicate that a HFD impairs hippocampal neurogenesis and NPCs proliferation through increased lipid peroxidation and decreased BDNF.

PMID: 20670674 [PubMed - as supplied by publisher]



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[James Cain]

HFD increases plasma free fatty acids and causes oxidative stress followed by
the accumulation of peroxidized lipids

It's the greater FFA release associated with over-nutrition and hypertrophic obesity that results in the inflammation and impaired neurogenesis (along with many other obesity pathologies), and not the high fat diet per se. These results would have been the same with a normal diet, except they used a diet-induced model of obesity. A high fat diet isn't a problem as much as overeating on any diet.

What really gets me is this...

The increased consumption of saturated fats in a high fat diet (HFD) contributes to obesity, neurodegenerative diseases, long-term memory loss, and cognitive impairment

Yet they base the findings of their paper on lipid peroxidation. Saturated fat, in the right context, wouldn't be as bad as (poly)unsaturated fats in this regard. They refer to supplemental materials for the diet breakdown, which isn't available either in the available full-text, but should be available in the issue of Neuroscience when it gets printed. I'd be willing to bet it has plenty of vegetable oils. Regardless, the over-nutrition is the real culprit. You can see the full effect of this here (table of animal characteristics).

[ImmInst]

DAF-16/FOXO: Many Paths To a Single Fork(head) in The Road.

Antioxid Redox Signal. 2010 Aug 1;

Authors: Tissenbaum HA

The C. elegans FOXO transcription factor homolog DAF-16 functions as a central mediator of multiple biological processes such as longevity, development, fat storage, stress resistance, development and reproduction. In C. elegans, similar to other systems, DAF-16 functions as the downstream target of a conserved, well-characterized insulin/IGF-1 signaling (IIS) pathway. This cascade is comprised of an insulin/IGF-1 receptor, which signals through a conserved PI 3-kinase/AKT pathway that ultimately down-regulates DAF-16/FOXO activity. Importantly, studies have shown that multiple pathways intersect with the IIS pathway and impinge on DAF-16 for their regulation. Therefore in C. elegans, the single FOXO family member, DAF-16, integrates signals from several pathways and then regulates its many downstream target genes.

PMID: 20673162 [PubMed - as supplied by publisher]



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[ImmInst]

[Study on the longevity related mitochondrial genome variation in Bama elderly population in Guangxi province.]

Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2010 Aug;27(4):423-7

Authors: Lv Z, Zheng C, Kong F, Feng J, Jiang W, Hu C, Li H, Lv Y, Zhang G, Yang Z

OBJECTIVE: To investigate the human mitochondrial DNA (mtDNA) variations associated with longevity in Bama elderly population from Guangxi. METHODS: Mitochondrial genome of 20 individuals over 96 years of age was sequenced, and seven target single nucleotide polymorphism(SNPs) were observed by comparing with the standard rCRS sequence, and two were tested by polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) method in a larger population including 208 individuals of 90-113 years old, and 586 unrelated control individuals from Guangxi. RESULTS: The 4824G frequency of the mtDNA4824A/G locus increased with age both in the long-lived elderly and in controls. And it was significantly higher in controls than that in long-lived population (P<0.05). CONCLUSION: The mtDNA4824 A/G is not only an age-related locus, its mutation is also negatively correlated with longevity.

PMID: 20677150 [PubMed - in process]



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[ImmInst]

Related Articles Longevity health sciences and mental health as future medicine.

Ann N Y Acad Sci. 2010 Jun;1197:184-7

Authors: Riga S, Riga D, Mihailescu A, Motoc D, Mos L, Schneider F

Longevity health sciences and mental health are fields of public health and of preventive and integrative medicine. The antagonism between health construction and human pathology is substantiated by two opposite fundamental pathways: the health-longevity tetrad versus the aging-disease cascade. It is necessary that the current paradigm of contemporary medicine be replaced by the advanced paradigm of future medicine. A societal cost-benefit rate is decisive for health-longevity promotion. This is why the WHO public health strategy keeps forwarding the societal medical target into the global health-longevity field.

PMID: 20536848 [PubMed - indexed for MEDLINE]



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[ImmInst]

Related Articles Metabolic networks of longevity.

Cell. 2010 Jul 9;142(1):9-14

Authors: Houtkooper RH, Williams RW, Auwerx J

Molecular and cellular networks implicated in aging depend on a multitude of proteins that collectively mount adaptive and contingent metabolic responses to environmental challenges. Here, we discuss the intimate links between metabolic regulation and longevity and outline new approaches for analyzing and manipulating such links to promote human health span.

PMID: 20603007 [PubMed - indexed for MEDLINE]



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Related Articles How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis).

Exp Gerontol. 2010 Jun;45(6):410-8

Authors: Ristow M, Zarse K

Recent evidence suggests that calorie restriction and specifically reduced glucose metabolism induces mitochondrial metabolism to extend life span in various model organisms, including Saccharomyces cerevisiae, Drosophila melanogaster, Caenorhabditis elegans and possibly mice. In conflict with Harman's free radical theory of aging (FRTA), these effects may be due to increased formation of reactive oxygen species (ROS) within the mitochondria causing an adaptive response that culminates in subsequently increased stress resistance assumed to ultimately cause a long-term reduction of oxidative stress. This type of retrograde response has been named mitochondrial hormesis or mitohormesis, and may in addition be applicable to the health-promoting effects of physical exercise in humans and, hypothetically, impaired insulin/IGF-1-signaling in model organisms. Consistently, abrogation of this mitochondrial ROS signal by antioxidants impairs the lifespan-extending and health-promoting capabilities of glucose restriction and physical exercise, respectively. In summary, the findings discussed in this review indicate that ROS are essential signaling molecules which are required to promote health and longevity. Hence, the concept of mitohormesis provides a common mechanistic denominator for the physiological effects of physical exercise, reduced calorie uptake, glucose restriction, and possibly beyond.

PMID: 20350594 [PubMed - indexed for MEDLINE]



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[ImmInst]

Related Articles 10 tips for living to 100.

US News World Rep. 2009 Oct;146(9):82-3

Authors: Kotz D



PMID: 19806874 [PubMed - indexed for MEDLINE]



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Related Articles Longevity depends on a balance between proinflammatory and anti-inflammatory factors: use of TCMS and natural products.

Curr Drug Discov Technol. 2010 Mar 1;7(1):13-21

Authors: Lien EJ, Lien LL, Wang J

During the course of our investigation of longevity promoting natural products and Chinese herbs in the last 15 years, we come to the conclusion that in order to have healthy, productive and graceful maturing, it is necessary to maintain a dynamic balance between proinflammatory and anti-inflammatory loads. This may also help to prevent cancer as well as premature degeneration of various organ systems. Modern life style and food intake tend to overload proinflammatory factors. To overcome this it is desirable to regularly consume fresh fruits, vegetables and multiple grains, various beans including soybeans and/or minimally processed, unbleached products. When this is not sufficient or possible, taking proper dietary supplements under the guidance of knowledgeable health professional can be helpful.

PMID: 20156138 [PubMed - indexed for MEDLINE]



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Related Articles Systems biology and longevity: an emerging approach to identify innovative anti-aging targets and strategies.

Curr Pharm Des. 2010;16(7):802-13

Authors: Cevenini E, Bellavista E, Tieri P, Castellani G, Lescai F, Francesconi M, Mishto M, Santoro A, Valensin S, Salvioli S, Capri M, Zaikin A, Monti D, de Magalhães JP, Franceschi C

Human aging and longevity are complex and multi-factorial traits that result from a combination of environmental, genetic, epigenetic and stochastic factors, each contributing to the overall phenotype. The multi-factorial process of aging acts at different levels of complexity, from molecule to cell, from organ to organ systems and finally to organism, giving rise to the dynamic "aging mosaic". At present, an increasing amount of experimental data on genetics, genomics, proteomics and other -omics are available thanks to new high-throughput technologies but a comprehensive model for the study of human aging and longevity is still lacking. Systems biology represents a strategy to integrate and quantify the existing knowledge from different sources into predictive models, to be later tested and then implemented with new experimental data for validation and refinement in a recursive process. The ultimate goal is to compact the new acquired knowledge into a single picture, ideally able to characterize the phenotype at systemic/organism level. In this review we will briefly discuss the aging phenotype in a systems biology perspective, showing four specific examples at different levels of complexity, from a systemic process (inflammation) to a cascade-process pathways (coagulation) and from cellular organelle (proteasome) to single gene-network (PON-1), which could also represent targets for anti-aging strategies.

PMID: 20388091 [PubMed - indexed for MEDLINE]



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[ImmInst]

Related Articles Scoring more than ten plus century - Antiquity in gerontology?

Indian J Med Res. 2010 Apr;131:586-7

Authors: Sinha JK, Ghosh S



PMID: 20424313 [PubMed - indexed for MEDLINE]



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[aLurker]

The actual list

[ImmInst]

Related Articles SH2B regulation of growth, metabolism, and longevity in both insects and mammals.

Cell Metab. 2010 May 5;11(5):427-37

Authors: Song W, Ren D, Li W, Jiang L, Cho KW, Huang P, Fan C, Song Y, Liu Y, Rui L

SH2B1 is a key regulator of body weight in mammals. Here, we identified dSH2B as the Drosophila homolog of SH2B1. dSH2B bound to Chico and directly promoted insulin-like signaling. Disruption of dSH2B decreased insulin-like signaling and somatic growth in flies. dSH2B deficiency also increased hemolymph carbohydrate levels, whole-body lipid levels, life span, and resistance to starvation and oxidative stress. Systemic overexpression of dSH2B resulted in opposite phenotypes. dSH2B overexpression in fat body decreased lipid and glucose levels, whereas neuron-specific overexpression of dSH2B decreased oxidative resistance and life span. Genetic deletion of SH2B1 also resulted in growth retardation, obesity, and type 2 diabetes in mice; surprisingly, life span and oxidative resistance were reduced in SH2B1 null mice. These data suggest that dSH2B regulation of insulin-like signaling, growth, and metabolism is conserved in SH2B1, whereas dSH2B regulation of oxidative stress and longevity may be conserved in other SH2B family members.

PMID: 20417156 [PubMed - indexed for MEDLINE]



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[ImmInst]

Related Articles [Effect of Ligusticum chuanxiong extract on lifespan of Caenorhabditis elegans and its underlying molecular mechanisms]

Zhongguo Zhong Yao Za Zhi. 2010 Apr;35(8):1042-5

Authors: Wang X, Wang X, Wang D, Li L, Niu X

OBJECTIVE: To explore the effect of Ligusticam chuanxiong extract (CXE) on lifespan of Caenorhabditis elegans and investigate its underlyirig molecular mechanisms. METHOD: The lifespan assay was carried out on animals grouped into blank control group and CXE groups with concentration from low to high: 12.5, 25, 50, 100 mg x L(-1) by examining the effect of CXE on mean lifespan and maximum lifespan of C. elegans. According to the result of lifespan assay, we cultured the animals with the optimal concentration of CXE for 10 days, and tested the expression change of aging-related genes between the control and CXE group by realtime RT-PCR (qRT-PCR). RESULT: Compared with the control, 25, 50, 100 mg x L(-1) CXE all significantly extended the mean lifespan (15.7%, 9.1%, 6.2% respectively) and the maximum lifespan (15.0%, 6.8%, 6.6% respectively) of C. elegans. After treatment with 25 mg x L(-1) CXE the expression of hsp-70, skn-1 were obviously up-regulated while the expression of akt-2, tub-1 were significantly down-regulated. CONCLUSION: CXE significantly extend the lifespan of C. elegans, and the underlying molecular mechanism is related with genes of Insulin/IGF-1 signaling pathway and dietary restriction system.

PMID: 20617690 [PubMed - indexed for MEDLINE]



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[ImmInst]

Related Articles Antioxidant enzyme activities are not broadly correlated with longevity in 14 vertebrate endotherm species.

Age (Dordr). 2010 Jun;32(2):255-70

Authors: Page MM, Richardson J, Wiens BE, Tiedtke E, Peters CW, Faure PA, Burness G, Stuart JA

The free radical theory of ageing posits that accrual of oxidative damage underlies the increased cellular, tissue and organ dysfunction and failure associated with advanced age. In support of this theory, cellular resistance to oxidative stress is highly correlated with life span, suggesting that prevention or repair of oxidative damage might indeed be essential for longevity. To test the hypothesis that the prevention of oxidative damage underlies longevity, we measured the activities of the five major intracellular antioxidant enzymes in brain, heart and liver tissue of 14 mammalian and avian species with maximum life spans (MLSPs) ranging from 3 years to over 100 years. Our data set included Snell dwarf mice in which life span is increased by approximately 50% compared to their normal littermates. We found that CuZn superoxide dismutase, the major cytosolic superoxide dismutase, showed no correlation with MLSP in any of the three organs. Similarly, neither glutathione peroxidase nor glutathione reductase activities correlated with MLSP. MnSOD, the sole mitochondrial superoxide dismutase in mammals and birds, was positively correlated with MLSP only for brain tissue. This same trend was observed for catalase. For all correlational data, effects of body mass and phylogenetic relatedness were removed using residual analysis and Felsenstein's phylogenetically independent contrasts. Our results are not consistent with a causal role for intracellular antioxidant enzymes in longevity, similar to recent reports from studies utilising genetic modifications of mice (Pérez et al., Biochim Biophys Acta 1790:1005-1014, 2009). However, our results indicate a specific augmentation of reactive oxygen species neutralising activities in brain associated with longevity.

PMID: 20431992 [PubMed - indexed for MEDLINE]



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Related Articles Personality and health, subjective well-being, and longevity.

J Pers. 2010 Feb;78(1):179-216

Authors: Friedman HS, Kern ML, Reynolds CA

Personality traits can be employed to guide understanding of trajectories to health and longevity, but long-term longitudinal study and multifaceted assessment of healthy aging are crucial. Following up on the life span study initiated by Lewis Terman, we assessed 4 validated factors of personality in young adulthood in 1940, constructed a multifactor measure of participants' healthy aging in 1986, and collected death certificates through 2007 (to determine longevity) on a sample of 1,312 Terman participants (732 men). Neuroticism predicted worse physical health and subjective well-being in old age and, for women, higher mortality risk, but for men, neuroticism predicted decreased mortality risk. For both sexes, extraversion predicted old-age social competence, whereas conscientiousness predicted men's old-age productivity. Differential patterns of association between personality traits and healthy aging components are informative about individual personality characteristics and long-term health outcomes.

PMID: 20433617 [PubMed - indexed for MEDLINE]



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Related Articles Search for mechanisms of exceptional human longevity.

Rejuvenation Res. 2010 Apr-Jun;13(2-3):262-4

Authors: Gavrilova NS, Gavrilov LA

This study presents initial findings of a new ongoing research project aimed to identify important predictors and mechanisms of exceptional human longevity. For this purpose the detailed data on long-lived people surviving to 100 years in the Unites States are collected, validated, and analyzed. The study found that being born to a young mother is an important predictor of person's longevity. The study also found that the "stout" body build at age 30 years (being in the heaviest 15% of population) significantly decreases chances of survival to 100 years. These findings demonstrate that early-life and mid-life personal characteristics play an important role in human longevity.

PMID: 20370503 [PubMed - indexed for MEDLINE]



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Related Articles Decreased energy metabolism extends life span in Caenorhabditis elegans without reducing oxidative damage.

Genetics. 2010 Jun;185(2):559-71

Authors: Van Raamsdonk JM, Meng Y, Camp D, Yang W, Jia X, Bénard C, Hekimi S

On the basis of the free radical and rate of living theories of aging, it has been proposed that decreased metabolism leads to increased longevity through a decreased production of reactive oxygen species (ROS). In this article, we examine the relationship between mitochondrial energy metabolism and life span by using the Clk mutants in Caenorhabditis elegans. Clk mutants are characterized by slow physiologic rates, delayed development, and increased life span. This phenotype suggests that increased life span may be achieved by decreasing energy expenditure. To test this hypothesis, we identified six novel Clk mutants in a screen for worms that have slow defecation and slow development and that can be maternally rescued. Interestingly, all 11 Clk mutants have increased life span despite the fact that slow physiologic rates were used as the only screening criterion. Although mitochondrial function is decreased in the Clk mutants, ATP levels are normal or increased, suggesting decreased energy utilization. To determine whether the longevity of the Clk mutants results from decreased production of ROS, we examined sensitivity to oxidative stress and oxidative damage. We found no evidence for systematically increased resistance to oxidative stress or decreased oxidative damage in the Clk mutants despite normal or elevated levels of superoxide dismutases. Overall, our findings suggest that decreased energy metabolism can lead to increased life span without decreased production of ROS.

PMID: 20382831 [PubMed - indexed for MEDLINE]



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Related Articles Orion: a glimpse of hope in life span extension?

Rejuvenation Res. 2010 Apr-Jun;13(2-3):359-61

Authors: Muradian K, Bondar V, Bezrukov V, Zhukovsky O, Polyakov V, Utko N

Orion is a multicomponent drug based on derivatives of taurocholic acid and several other compounds. Application of Orion into the feeding medium of Drosophila melanogaster resulted in increased life span and survival at stressful conditions. Two paradoxical features of the drug should be stressed: The "age-threshold" (life span extension was observed only when the drug was applied starting from the second half of life) and induction of "centenarian" flies (older 100 days). Orion enhanced survival at heat shock (38 degrees C) and acidic (pH = 1.6) or alkaline (pH = 11.8) feeding mediums, but not at oxidative stresses modeled by 100% oxygen or application of hydrogen peroxide (H(2)O(2)).

PMID: 20426615 [PubMed - indexed for MEDLINE]



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Related Articles Caenorhabditis elegans life span studies: the challenge of maintaining synchronous cohorts.

Rejuvenation Res. 2010 Apr-Jun;13(2-3):347-9

Authors: Gruber J, Poovathingal SK, Schaffer S, Ng LF, Gunawan R, Halliwell B

Due to its many advantages, the nematode worm Caenorhabditis elegans (C. elegans) is commonly employed as a convenient model for aging studies as well as for testing life span effects of chemical compounds. However, some challenges exist in the context of such life span studies, particularly in relation to generation and maintenance of synchronized cohorts, and these challenges are not always fully appreciated. Here we discuss the impact of incomplete control of nematode proliferation on life span studies and suggest some solutions to minimize these artefacts.

PMID: 20426619 [PubMed - indexed for MEDLINE]



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Related Articles HLA and KIR frequencies in Sicilian Centenarians.

Rejuvenation Res. 2010 Apr-Jun;13(2-3):314-8

Authors: Listì F, Caruso C, Colonna-Romano G, Lio D, Nuzzo D, Candore G

Several studies suggest that human longevity appears to be linked inextricably with optimal functioning of the immune system, suggesting that specific genetic determinants may reside in loci that regulate the immune response, as human leukocyte antigen (HLA) and killer cell immunoglobulin-like receptor (KIR) genes. It has been suggested that longevity is associated with positive selection of alleles (i.e., HLA-DR11) or haplotypes (i.e., HLA-B8,DR3) that confer resistance to infectious disease(s). On the other hand, the cytolytic activity of natural killer (NK) cells is controlled by activating and inhibitory cell-surface receptors, including KIR. The genetic diversity of the KIR loci with respect to successful aging has been analyzed only in one study performed in the Irish population. Although two KIR genes (2DS3, 2DL5) displayed an initial increased frequency in the aged group, the significance of this association was lost when repeated in a second cohort. We have evaluated by polymerase chain reaction-sequence-specific primers (PCR-SSP) HLA-DRB1 and KIR receptors/HLA ligands frequencies in centenarians and controls from Sicily. Our results demonstrate an increase of the HLA DRB1*18 allele in male centenarians (p = 0.0266, after Bonferroni correction). Concerning KIR, no significant difference was observed after Bonferroni correction. However, our findings suggest that HLA/KIR/longevity associations are population specific, being heavily affected by the population-specific genetic and environmental history. This kind of study is important to better understand aging and longevity, hence enhancing the planning of antiaging strategies.

PMID: 20426625 [PubMed - indexed for MEDLINE]



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Related Articles NUMT ("new mighty") hypothesis of longevity.

Rejuvenation Res. 2010 Apr-Jun;13(2-3):152-5

Authors: Muradian KK, Lehmann G, Fraifeld VE

Maximum life span (MLS) and abundance of mitochondrial DNA (mtDNA) insertions in the nuclear DNA (NUMTs) were analyzed in 17 animal species with completely sequenced mitochondrial and nuclear genomes. Highly significant positive correlations were found between MLS and NUMT number, total size, or density (both in mammals and all animal species). In mammals, NUMT abundance correlated positively with the mtDNA guanine content and negatively with adenine and thymine contents, but did not correlate with such longevity-associated variables as the body mass and resting metabolic rate.

PMID: 20462381 [PubMed - indexed for MEDLINE]



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Related Articles Applied Healthspan engineering.

Rejuvenation Res. 2010 Apr-Jun;13(2-3):265-80

Authors: Larrick JW, Mendelsohn A

According to the Homeric Hymn to Aphrodite, when Eos asked Zeus for Tithonus to be granted immortality, she forgot to ask for eternal youth. Applied Healthspan Engineering (AHE) seeks to address this problem. All organisms have a minimal level of functional reserve required to sustain life that eventually declines to a point incompatible with survival at death. AHE seeks to maintain or restore optimal functional reserve of critical tissues and organs. Tissue reserve correlates with well being. Diet, physical exercise, and currently available small-molecule-based therapeutics may attenuate the rate of decline of specific organs or organ systems, but are unlikely to restore lost reserve. Inherent evolutionary-derived limitations in tissue homeostasis and cell maintenance necessitate the development of therapies to enhance regenerative processes and possibly replace whole organs or tissues. AHE supports the study of cell, tissue, and organ homeostatic mechanisms to derive new regenerative and tissue replacement therapies to extend the period of human health.

PMID: 20462384 [PubMed - indexed for MEDLINE]



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Related Articles How do masculinity, paternity leave, and mortality associate? -A study of fathers in the Swedish parental & child cohort of 1988/89.

Soc Sci Med. 2010 Aug;71(3):576-83

Authors: Månsdotter A, Lundin A

One of the proposed causes for the gender gap in longevity is the attitudes and practices culturally prescribed for men, often conceptualised as 'masculinity'. It has also been suggested that paternity leave, indicating a change from breadwinning to caring, could benefit men's lifetime health. In this study, the objective was to examine associations between 'masculinity' (assessed at the age of 18-19 years), paternity leave (1988-1990), and mortality patterns (1991-2008) based on a population of Swedish men who had a child in 1988/89 (N=72,569). 'Masculinity' was measured during the compulsory military conscription process by a psychologist based on leisure and occupational interests, and paternity leave was measured in fulltime days by registry data. The main finding was that low 'masculinity' ranking increased the risk of all-cause mortality, and mortality from alcohol and violent causes, while taking paternity leave between 30 and 135 days decreased the risk of all-cause mortality. However, the weak association found between 'masculinity' and paternity leave indicates that entering a caring role as a father is not predicted by 'masculinity' assessed in late adolescence, and that the studied phenomena influence male mortality independently of each other.

PMID: 20538394 [PubMed - indexed for MEDLINE]



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Related Articles Three measures of longevity: time trends and record values.

Demography. 2010 May;47(2):299-312

Authors: Canudas-Romo V

This article examines the trend over time in the measures of "typical" longevity experienced by members of a population: life expectancy at birth, and the median and modal ages at death. The article also analyzes trends in record values observed for all three measures. The record life expectancy at birth increased from a level of 44 years in Sweden in 1840 to 82 years in Japan in 2005. The record median age at death shows increasing patterns similar to those observed in life expectancy at birth. However, the record modal age at death changes very little until the second half of the twentieth century: it moved from a plateau level, around age 80, to having a similar pace of increase as that observed for the mean and the median in most recent years. These findings explain the previously observed uninterrupted increase in the record life expectancy. The cause of this increase has changed over time from a dominance of child mortality reductions to a dominance of adult mortality reductions, which became evident by studying trends in the record modal age at death.

PMID: 20608098 [PubMed - indexed for MEDLINE]



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Related Articles Holter heart rate variability: are we measuring physical activity?

Am J Cardiol. 2010 Aug 1;106(3):448-9

Authors: Fortrat JO, de Germain V, Custaud MA



PMID: 20643263 [PubMed - indexed for MEDLINE]



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Related Articles Female fertility and longevity.

Age (Dordr). 2010 Mar;32(1):79-84

Authors: Mitteldorf J

Does bearing children shorten a woman's life expectancy? Pleiotropic theories of aging predict that it should, and in particular, the Disposable Soma theory predicts unequivocally that this effect should be inescapable. But many demographic studies, historic and current, have found no such effect. In this context,the Caerphilly cohort study stands apart as the sole test that corroborates the theory. Why has this study found an effect that others fail to see? Their analysis is based on Poisson regression, a statistical technique that is accurate only if the underlying data are Poisson distributed.But the distribution of the number of children born to women in the Caerphilly data based departs strongly from Poisson at the high end. This makes the result overly sensitive to a handful of women with 15 children or more who lived before 1700. When these five women are removed from a database of more than 2,900, the Poisson regression no longer shows a significant result. Bilinear regression relating life span to fertility and date of birth results in a small positive coefficient for fertility, in agreement with the main trend of reported results.

PMID: 19731082 [PubMed - indexed for MEDLINE]



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[Blud]

This doesn't seem like a very meaningful study to me. The fair comparison would be between women with
children and (voluntary and not due to some disease) childless women. Ideally it would be a study of twins, where one is childless. They were searching for some "dose response" effect for mothers, and it is not clear whether they have taken into account that healthy women with robust bodies will get pregnant more often and have more children than the less robust ones and still live as long as the second group, all due to their good genes.

[John Schloendorn]

Can we get rid of this spam? This once useful forum is completely clogged.