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Reports from the front line in the fight against aging. The science of healthy life extension. Activism and advocacy for longer, healthier lives.
Reason
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- August 30, 2010
- 11:07 PM
- 38 views
Thyroid Function and Inherited Human Longevity
by Reason in Fight Aging!
There is good reason to believe that levels of thyroid hormones, and the changes in thyroid function they represent, influence human longevity. These are amongst a number of hormones in the human body that touch on almost everything you would expect to influence life span over time: metabolic rate, cell growth, use and processing of food, and so forth. You might recall studies on the thyroid hormone triiodothyronine, or T3, for example: The hypothalamo-pituitary-thyroid axis has been widely implicated in modulating the aging process. Life extension effects associated with low thyroid hormone levels have been reported in multiple animal models. In human populations, an association was observed between low thyroid function and longevity at old age ... These findings suggest that the favorable role of low thyroid hormone metabolism on health and longevity in model organism is applicable to humans as well. Here is another, more recent study of a human population that pulls in more confirming data: The objective of the study was to test whether low thyroid activity associated with extreme longevity constitutes a heritable phenotype, which could contribute to the familial longevity observed in the Leiden Longevity Study. ... Eight hundred fifty-nine nonagenarian siblings (median age 92.9...... Read more »
Rozing MP, Houwing-Duistermaat JJ, Slagboom PE, Beekman M, Frölich M, de Craen AJ, Westendorp RG, & van Heemst D. (2010) Familial Longevity Is Associated with Decreased Thyroid Function. The Journal of clinical endocrinology and metabolism. PMID: 20739380
- August 19, 2010
- 10:17 PM
- 59 views
Anoxia Tolerance and Species Longevity
by Reason in Fight Aging!
I noticed a paper on longevity in turtles today that speculates on a link between species life span and tolerance of low-oxygen environments. It seems to be as interesting a line of research as any opened up by the comparison of differences in biochemistry and longevity between species. Why are long-lived species long-lived, and can we expect the answers to translate, as for calorie restriction research, into potential benefits for human health? Forever young: mechanisms of natural anoxia tolerance and potential links to longevity While mammals cannot survive oxygen deprivation for more than a few minutes without sustaining severe organ damage, some animals have mastered anaerobic life. Freshwater turtles belonging to the Trachemys and Chrysemys genera are the champion facultative anaerobes of the vertebrate world, often surviving without oxygen for many weeks at a time. The physiological and biochemical mechanisms that underlie anoxia tolerance in turtles include profound metabolic rate depression, post-translational modification of proteins, strong antioxidant defenses, activation of specific stress-responsive transcription factors, and enhanced expression of cytoprotective proteins. Turtles are also known for their incredible longevity and display characteristics of "negligible senescence". We propose that the robust stress-tolerance mechanisms that permit long term anaerobiosis by turtles may also...... Read more »
Krivoruchko A, & Storey KB. (2010) Forever young: mechanisms of natural anoxia tolerance and potential links to longevity. Oxidative medicine and cellular longevity, 3(3), 186-98. PMID: 20716943
- August 11, 2010
- 12:32 AM
- 69 views
Impairment of Blood Vessels in the Brain Isn't a Good Thing
by Reason in Fight Aging!
Exercise correlates with a reduced risk of suffering dementia in later life, just as excess visceral fat is correlated with an increased risk of later developing dementia. The underlying mechanisms are somewhat different, but they both boil down to the quality of the blood vessels in your brain. Impaired blood vessels mean a lower blood flow or the breakages and lesions of vascular dementia - neither of which is good for you in the long term. Another issue to consider in this context is the ongoing impact of atherosclerosis, the build-up of fatty material on blood vessel walls. This can result in sudden death due to blockage and rupture of larger deposits, but the condition harms your brain across the years leading up to that point: Atherosclerosis, dementia, and Alzheimer disease in the Baltimore Longitudinal Study of aging cohort We examined the relationship between systemic atherosclerosis, Alzheimer type pathology, and dementia in autopsies from 200 participants in the Baltimore Longitudinal Study of Aging, a prospective study of the effect of aging on cognition, 175 of whom had complete body autopsies. ... we found that the presence of intracranial but not coronary or aortic atherosclerosis significantly increased the odds of dementia....... Read more »
Dolan H, Crain B, Troncoso J, Resnick SM, Zonderman AB, & Obrien RJ. (2010) Atherosclerosis, dementia, and Alzheimer disease in the Baltimore Longitudinal Study of aging cohort. Annals of neurology, 68(2), 231-40. PMID: 20695015
- August 10, 2010
- 12:27 AM
- 81 views
An Addendum on Solar Radiation, Reliability Theory, and Longevity
by Reason in Fight Aging!
A few years ago, I pointed out some speculative work on environmental radiation during embryonic development and its possible effects on later longevity: Speculation on Solar Radiation and Longevity More on Solar Radiation and Life Expectancy The amount of [solar] radiation varies according to where you are in the world, what time of year it is and cyclic changes in the sun’s behaviour. The Equator generally gets the most radiation, and in the northern hemisphere, the usual radiation peaks will be in June and July, but there will be variations from year to year according to "solar cycles." Every 11 years the Sun goes through a cycle when the magnetic field changes and the number of sunspots grows and dwindles. This affects the amounts of radiation produced. The Maine researchers suggest that high radiation levels either stress the immune system of embryos and foetuses or cause small mutations in their DNA, which can either predispose or protect from disease, mould brain characteristics and influence length of life. The reliability theory of aging and longevity models complex organisms such as humans as an array of systems composed of many redundant component parts. It suggests that we are all born with a...... Read more »
Shamir L. (2010) Does cosmic weather affect infant mortality rate?. Journal of environmental health, 73(1), 20-3. PMID: 20687328
- July 13, 2010
- 09:40 PM
- 112 views
Analysis of Gene Expression and Longevity is Forging Ahead
by Reason in Fight Aging!
The process of gene expression, in which a gene is used as a blueprint to construct a protein, is anything but static. Levels of gene expression for individual genes rise and fall with environmental circumstances, health, injury, and over the course of aging. It's a tremendously complex system, with a lot of feedback loops and switches, but fortunately the cost of analyzing gene expression profiles over a whole genome is falling rapidly. It is now feasible to run hundreds of such profiles over the course of a study. At the same time the tools of analysis are starting to catch up with the amount of data being generated: researchers are able to more rapidly and effectively draw conclusions from the mountainous databases they construct. So, for example, see this study on flies, which compares groups of flies selected for their longevity versus a control group of average length lives. It demonstrates that systematically sweeping the whole genome for changes in gene expression with age is a viable way to evaluate the importance of other lines of research and find new avenues for future study: We evaluated the gene expression profile in young, middle-aged, and old male flies, finding that 530...... Read more »
Sarup P, Sørensen P, & Loeschcke V. (2010) Flies selected for longevity retain a young gene expression profile. Age (Dordrecht, Netherlands). PMID: 20607427
- July 8, 2010
- 11:24 PM
- 121 views
Immunosenescence and What Can Be Done About It
by Reason in Fight Aging!
Immunosenescence is the steady degeneration of the immune system that occurs with age. For the adaptive immune system at least, researchers have a good picture as to why and how this happens - which means that they also have starting points to develop ways to reverse immunosenescence. Here is an open access review paper on the topic: The elderly frequently suffer from severe infections. Vaccination could protect them against several infectious diseases, but it can be effective only if cells that are capable of responding are still present in the repertoire. Recent vaccination strategies in the elderly might achieve low effectiveness due to age-related immune impairment. ... Ageing dampens the ability of B cells to produce antibodies against novel antigens. Exhausted memory B lymphocyte subsets replace naive cells. Decline of cell-mediated immunity is the consequence of multiple changes, including thymic atrophy, reduced output of new T lymphocytes, accumulation of anergic memory cells, and deficiencies in cytokines production. Persistent viral and parasitic infections contribute to the loss of immunosurveillance and premature exhaustion of T cells. In essence, the immune system fails because the thymus, source of immune cells, ceases production and withers away. At the same time, the population of immune...... Read more »
Ongrádi, J., & Kövesdi, V. (2010) Factors that may impact on immunosenescence: an appraisal. Immunity , 7(1), 7. DOI: 10.1186/1742-4933-7-7
- July 1, 2010
- 12:42 AM
- 112 views
An Update on Progeria Research
by Reason in Fight Aging!
Hutchinson-Gilford Progeria Syndrome (HGPS, or just "progeria") is perhaps the best known of the accelerated aging conditions. Considerable progress has been made over the past decade in uncovering the biochemical mechanisms of this disease, and in the process it has come to seem plausible that a viable therapy for progeria may have some modest use in tackling normal aging as well. The same follows for other accelerated aging conditions, meaning that it's worth keeping an eye on this field of medical research. With this in mind, here is an open access paper that outlines some of the latest advances in progeria research. Matters look a lot closer to a viable therapy than they did a few years back, and studies continue to show that the changing biology of normal aging shares - to a lesser degree - some of the unwanted biochemical signatures of progeria: Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare premature aging disorder caused by a [mutation within the] LMNA gene encoding A-type nuclear lamins. [Nuclear lamins are fibrous proteins providing structural function and transcriptional regulation in the cell nucleus.] ... We analyzed global gene expression changes in fibroblasts from human subjects with HGPS and found that a...... Read more »
Marji J, O'Donoghue SI, McClintock D, Satagopam VP, Schneider R, Ratner D, J Worman H, Gordon LB, & Djabali K. (2010) Defective lamin A-Rb signaling in Hutchinson-Gilford Progeria Syndrome and reversal by farnesyltransferase inhibition. PloS one, 5(6). PMID: 20559568
- June 28, 2010
- 11:37 PM
- 151 views
Regeneration of Tooth Enamel: Cavities Healed in Mice
by Reason in Fight Aging!
Dental researchers are forging ahead with their branch of tissue engineering and regenerative medicine. It hasn't been long since engineered growth in situ of replacement teeth was demonstrated in rats, and now a research group has shown they can regenerate tooth enamel in mice, thereby healing cavities: A new peptide, embedded in a soft gel or a thin, flexible film and placed next to a cavity, encourages cells inside teeth to regenerate in about a month ... The gel or thin film contains a peptide known as MSH, or melanocyte-stimulating hormone. Previous experiments [showed] that MSH encourages bone regeneration. Bone and teeth are fairly similar, so the French scientists reasoned that if the MSH were applied to teeth, it should help healing as well. To test their theory, the French scientists applied either a film or gel, both of which contained MSH, to cavity-filled mice teeth. After about one month, the cavities had disappeared. You can also take a look at the research paper if interested, though it's fairly dense. It is an excellent example of what can be achieved where materials science meets biotechnology and the life sciences, and overall a very encouraging proof of concept. It is reasonable...... Read more »
Fioretti, F., Mendoza-Palomares, C., Helms, M., Al Alam, D., Richert, L., Arntz, Y., Rinckenbach, S., Garnier, F., Haïkel, Y., Gangloff, S.... (2010) Nanostructured Assemblies for Dental Application. ACS Nano, 4(6), 3277-3287. DOI: 10.1021/nn100713m
- June 25, 2010
- 10:24 PM
- 197 views
Another Illustration as to Why There Will Be Many, Many Genetic Contributions to Longevity
by Reason in Fight Aging!
As I mentioned not so long ago, there will most likely prove to be a great many subtle and overlapping genetic variants of human longevity. However, very few of them will be important in the sense that they will lead to ways to significantly increase human life span through new medicine. The effective way to greatly increase human longevity is to learn to repair the biochemical damage of aging, not to tinker with metabolism to slow down the rate at which damage occurs. In any case, here is an excellent illustration as to why there will be thousands of genetic variations that contribute to human longevity: the effects on life expectancy of known single gene variants may be enhanced or diminished by other variations that do not themselves directly contribute to longevity. Combinations of genetic variants are probably just as important as single gene differences, in other words: The search for longevity-determining genes in human has largely neglected the operation of genetic interactions. We have identified a novel combination of common variants of three genes that has a marked association with human lifespan and healthy aging. ... Haplotype analysis was performed in three candidate genes, and the haplotype combinations were...... Read more »
Michal Jazwinski S, Kim S, Dai J, Li L, Bi X, Jiang JC, Arnold J, Batzer MA, Walker JA, Welsh DA.... (2010) HRAS1 and LASS1 with APOE are associated with human longevity and healthy aging. Aging cell. PMID: 20569235
- June 18, 2010
- 10:44 PM
- 175 views
Naked Mole Rats Do Not Suffer From Cancer
by Reason in Fight Aging!
When it comes to wandering Methuselah's zoo in search of comparisons between species that might lead to greater understanding of human longevity - and how to increase it - the naked mole rat stands out as a prominent point of interest. It lives for something like nine times longer than some similar rodent species, and appears to have unusually resilient biochemistry for a mammal. Naked Mole-Rats and Negligible Senescence Built Differently, Down in the Membranes You might recall that different fatty acid or lipid composition in cell membranes was floated as a reason for the ninefold longevity of naked mole-rats over related rodent species. Plenty of oxidative stress in the older mole-rats, but little sign of biochemical damage resulting from it - in comparison to those other rodents long since aged to death, that is. Better, more damage-resistant building blocks down at the molecular level might be the cause. The concept of "better membranes" has a theory of aging to go along with it: the membrane pacemaker hypothesis. Follow that link if you care to find out more. Naked mole rats are not just very long-lived, however. They also appear to be immune to cancer. No naked mole rat has...... Read more »
Liang S, Mele J, Wu Y, Buffenstein R, & Hornsby PJ. (2010) Resistance to experimental tumorigenesis in cells of a long-lived mammal, the naked mole-rat (Heterocephalus glaber). Aging cell. PMID: 20550519
- June 17, 2010
- 12:38 AM
- 139 views
Ash-2, Another Longevity Gene in Worms
by Reason in Fight Aging!
Researchers have been turning up quite the trove of longevity-influencing genes and processes in nematode worms of late. Here is the latest: Study identifies proteins that modulate life span in worms The gene with the most pronounced effect, Ash-2, makes a protein that functions as a methyltransferase - meaning it works together with other proteins to add a chemical tag called a methyl group to a component of a cell's DNA packaging machinery, which is known as a histone. The presence or absence of this tag affects whether the DNA remains wound up tightly like thread on a spool, or unfurls to allow its genes to be expressed. Inhibiting Ash-2 activity reduces the number of methyl tags on the histone, which keeps the DNA inaccessible and somehow extends the animal's life by as much as 30 percent. ... The researchers found that Ash-2 is highly expressed in the germline, or reproductive cells, as well as in newly formed eggs. These cells also had high levels of the methyl tag. When Greer blocked the expression of Ash-2 in worms that lacked normal reproductive cells, he found that this no longer extended worm life span, suggesting that an intact germline is necessary...... Read more »
Greer, E., Maures, T., Hauswirth, A., Green, E., Leeman, D., Maro, G., Han, S., Banko, M., Gozani, O., & Brunet, A. (2010) Members of the H3K4 trimethylation complex regulate lifespan in a germline-dependent manner in C. elegans. Nature. DOI: 10.1038/nature09195
- June 12, 2010
- 12:26 AM
- 167 views
Structural Causes of Increasing Life Expectancy
by Reason in Fight Aging!
As I'm sure you're all aware by now, human life expectancy for both young and old in the most developed regions of the world is slowly increasing, and this has been the case for some time. As medical technology advances and our wealth grows, we benefit in ways that lead to less biochemical damage to the complex machinery of our body accumulated over the course of a lifetime - and thus a greater likelihood of living longer. That the medical and research establishments have achieved this ongoing benefit even in advance of any structured, deliberate, large-scale efforts to slow or (more preferably) repair the consequences of aging bodes well for the future. The scientific community should be able to achieve far more impressive results when they are actually trying to directly tackle aging. I noticed an open access paper today (PDF version included) that applies some mathematical wizardry so as to break out the most important structural contributions to increasing longevity. I think you'll find it interesting: The ongoing increase in life expectancy in developed countries is associated with changes in the shape of the survival curve. These changes can be characterized by two main, distinct components: (i) the decline...... Read more »
Rousson, V., & Paccaud, F. (2010) A set of indicators for decomposing the secular increase of life expectancy. Population Health Metrics, 8(1), 18. DOI: 10.1186/1478-7954-8-18
- June 10, 2010
- 10:17 PM
- 148 views
Building the Foundation of Tomorrow's Immune System
by Reason in Fight Aging!
The human immune system of tomorrow will look, conceptually, a lot like today's software defenses: Scientists are making real inroads into replicating and controlling the cells and mechanisms of our immune system. Producing immune cells, directing their actions, deciphering the biochemistry of pathogens - all these pieces are waiting to be put together as a bioartificial immune system, many times more selective, efficient and resistant to damage than the basic version we're all equipped with. ... One might imagine the future providers of immune system technology looking a lot like today's providers of anti-virus software for your computers, harvesting information on potential infections and streaming update information to bioartificial antibody manufactories in your bloodstream. Wireless anti-virus nanotechnology in the blood may seem like a far future vision, but the first building blocks of that technology are already emerging from present day research. For example, it won't be long before clinics can assemble massive doses of artificial antibodies to order and then infuse them into your body. Antibodies are the immune system's weapons, molecules tailored to a specific threat that either directly kill attackers or flag them for ingestion and destruction by white blood cells. An infusion of antibodies produced in...... Read more »
Hoshino, Y., Koide, H., Urakami, T., Kanazawa, H., Kodama, T., Oku, N., & Shea, K. (2010) Recognition, Neutralization, and Clearance of Target Peptides in the Bloodstream of Living Mice by Molecularly Imprinted Polymer Nanoparticles: A Plastic Antibody. Journal of the American Chemical Society, 132(19), 6644-6645. DOI: 10.1021/ja102148f
- June 10, 2010
- 09:13 AM
- 145 views
There Will Be Ten Thousand Subtle Gene Variants of Human Longevity
by Reason in Fight Aging!
There will be ten thousand subtle gene variants of human longevity. Or rather, these differences between individuals most likely exist now and will be steadily uncovered in the years ahead as the cost of DNA sequencing continues to fall. Most of these longevity-associated genetic variants will look much like this one: an association discovered by comparing long-lived people to average members of the population, and neither terribly exciting nor particularly exploitable: Cytokines are crucial for the regulation of inflammation development in humans. Many studies have shown that variations in cytokine genes might play a role in determining human longevity. This study examined the changes in the gene pool relevant to the -308 G/A polymorphism in the promoter region of the proinflammatory cytokine tumour necrosis factor (TNF)-alpha gene and the -1082 G/A polymorphism in the promoter region of anti-inflammatory cytokine interleukin (IL)-10 gene with aging and survival selection occurs in the Jordanian population. .. the IL-10 genotype and allele frequencies were significantly associated with longevity in men but not in women. We should expect to see subtle associations with human longevity in genes associated with processes known to be important in long-term health - such as the inflammatory response, or indeed...... Read more »
Khabour OF, & Barnawi JM. (2010) Association of longevity with IL-10 -1082 G/A and TNF-alpha-308 G/A polymorphisms. International journal of immunogenetics. PMID: 20518833
- May 27, 2010
- 12:22 AM
- 166 views
EGF Pathway Found to Influence Nematode Longevity
by Reason in Fight Aging!
Researchers have uncovered what might be a new set of genes and protein mechanisms that influence healthy longevity: the epidermal growth factor or EGF pathway. The work was carried out in nematode worms, but the track record of such metabolic influences upon longevity carrying through into higher animals is pretty good so far. The epidermal growth factor (EGF) peptide induces cellular proliferation through the EGF receptor ... Inhibitors of the EGF receptor are being pursued as potential cancer therapies and EGF may stimulate wound healing. Mutation of the EGF receptor has been associated with cancer in humans. The best known of the metabolic mechanisms influencing longevity are those involved in insulin metabolism and calorie restriction - there may be some overlap between the two when all is said and done. The researchers here were in fact surprised to find that the results of their work did not point to insulin metabolism. Here's a reference to the paper: Improving health of the rapidly growing aging population is a critical medical, social, and economic goal. Identification of genes that modulate healthspan, the period of mid-life vigor that precedes significant functional decline, will be an essential part of the effort to design anti-aging...... Read more »
Iwasa H, Yu S, Xue J, & Driscoll M. (2010) Novel EGF Pathway Regulators Modulate C. elegans Healthspan and Lifespan via EGF Receptor, PLC-gamma and IP3R Activation. Aging cell. PMID: 20497132
- May 20, 2010
- 12:48 AM
- 165 views
Trehalose and Nematode Worm Longevity
by Reason in Fight Aging!
Researchers interested in metabolic manipulation as a path to extended healthy longevity continue to identify potential compounds to feed into the long drug development process. Many such compounds begin with worm or fly life span studies, as the major known genes associated with metabolism and life span are conserved between species - all the way from worms up to we humans. If a compound can make a fly live longer and can be shown to act on genes and mechanisms already associated with calorie restriction or insulin metabolism, then you'll probably see interest in pushing forward to testing in mammals. Here is an example of this sort of research: Trehalose is a disaccharide of glucose found in diverse organisms and is suggested to act as a stress protectant against heat, cold, desiccation, anoxia, and oxidation. Here, we demonstrate that treatment of [nematode worms of the species] Caenorhabditis elegans with trehalose starting from the young-adult stage extended the mean life span by over 30% without any side effects. Surprisingly, trehalose treatment starting even from the old-adult stage shortly thereafter retarded the age-associated decline in survivorship and extended the remaining life span by 60%. Demographic analyses of age-specific mortality rates revealed that...... Read more »
Honda Y, Tanaka M, & Honda S. (2010) Trehalose extends longevity in the nematode Caenorhabditis elegans. Aging cell. PMID: 20477758
- May 18, 2010
- 11:43 PM
- 184 views
Applying Reliability Theory to Aging
by Reason in Fight Aging!
Reliability theory is, put very simply, a way of modeling and predicting the failure modes and mean time to failure of complex systems with many redundant parts subject to wear and tear. Reliability theory has seen a great deal of use in the electronics industry, amongst many others, but the human body is also a complex system that can be considered in these terms. Looking at our life spans and age-related illnesses in the context of reliability theory and the accumulating failure of redundant systems can add a great deal to our understanding of aging and our expectations for longevity science. In recent years there has been more interest in this topic amongst aging researchers. I'm sure that Leonid Gavrilov and Natalia Gavrilova, who produced some of the important papers in this space, will be pleased to see that more researchers are now rigorously applying reliability theory to aging and longevity: Aging in mouse brain is a cell/tissue-level phenomenon exacerbated by proteasome loss Biological aging is often described by its phenotypic effect on individuals. Still, its causes are more likely found on the molecular level. Biological organisms can be considered as reliability-engineered, robust systems and applying reliability theory to their...... Read more »
Mao L, Roemer I, Nebrich G, Klein O, Koppelstaetter A, Hin SC, Hartl D, & Zabel C. (2010) Aging in mouse brain is a cell/tissue-level phenomenon exacerbated by proteasome loss. Journal of proteome research. PMID: 20469937
- May 13, 2010
- 11:24 PM
- 170 views
Mitochodrial DNA in the Nucleus and Species Life Span Differences
by Reason in Fight Aging!
A large merged double edition of the journal Rejuvenation Research is now online, bringing with it a lot of papers to look through. I thought I'd direct your attention to one of those many papers, as it presents an interesting evolutionary background to the SENS approach to the mitochondrial DNA damage that accumulates with age. Our mitochondria are biological power plants within our cells, the evolved descendants of symbiotic bacterial species. They convert food into ATP, the chemical used as fuel by cells. Mitochondria have their own DNA, a relic left over from when they were some form of free-living species. Over time, portions of that mitochondrial DNA have become incorporated into our own nuclear DNA at the heart of the cell. By evolutionary considerations, these changes must have prospered and spread because they provided some form of advantage. One thing to consider in this respect is that nuclear DNA is far better protected from damage than mitochondrial DNA. Indeed, one root cause of aging is that our mitochondrial DNA is battered over the years by side-effects of the chemical reactions that produce ATP. This is not a problem suffered by nuclear DNA to anywhere near the same degree. So...... Read more »
Muradian, K., Lehmann, G., & Fraifeld, V. (2010) NUMT (“New Mighty”) Hypothesis of Longevity. Rejuvenation Research, 13(2-3), 152-155. DOI: 10.1089/rej.2009.0974
- May 5, 2010
- 08:47 PM
- 210 views
Grow Fat and Suffer the Consequences
by Reason in Fight Aging!
Excess visceral fat tissue and other side-effects of the sort of high-calorie, low-exercise lifestyle required to pack on the fat will do you great harm in the long term. Getting fat is a choice is for the vast majority of people, a choice made again and again day after day by deciding to eat more calories and skip exercise in favor of other activities. For 99.9% of the audience here: you're not special, and there's nothing in your genes that's making it noticeably easier to gain weight or harder to lose it. But if you let yourself become fat, just as so many other people are doing in this age of comparative wealth and low-cost calories, then it will come back to bite you. See this paper, for example: In the second half of the 20th century it became obvious that a relentless increase in diabetes type 2 (DM) affecting the economically affluent countries, is gradually afflicting also the developing world. This review juxtaposes the threat that the DM epidemic represents to mankind, with the astonishing recent discoveries on the role of obesity and of the body fat in this metabolic disorder. Presently, the highest prevalence of DM is in...... Read more »
Ginter E, & Simko V. (2010) Diabetes type 2 pandemic in 21st century. Bratislavske lekarske listy, 111(3), 134-7. PMID: 20437822
- April 29, 2010
- 09:28 PM
- 237 views
The Immune System Wears Out Faster With Stress
by Reason in Fight Aging!
If the immune system is chronically stressed, such as by organ transplants or HIV infection, then it ages noticeably faster - in effect the immune system wears down with overuse like a burdened machine. You might look on this sort of outcome as a much faster burn through the normal process of immune system use and degeneration with age, and it has consequences in terms of health and life expectancy. For example: Study links liver transplantation to accelerated cellular aging The University of Cambridge research team investigated whether the chronic immune stress of liver disease and organ transplantation accelerates aging of the immune system, which in turn contributes to excess morbidity and mortality in established liver graft recipients. Study leader Dr. Graeme Alexander explains, "There is a marked increase in the prevalence of cardiac disease, malignancy, cerebrovascular disease and infections in patients with established liver grafts, affecting a majority of cases eventually and which in the past have been attributed to agents used to suppress immune responses. However, an alternative (and not exclusive) hypothesis is that liver transplant recipients develop premature immune senescence which is also associated with these same pathologies, perhaps consequent to chronic [immune system activation]." Early immune...... Read more »
Desai S, & Landay A. (2010) Early immune senescence in HIV disease. Current HIV/AIDS reports, 7(1), 4-10. PMID: 20425052
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