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Fight Aging!
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- May 13, 2009
- 10:11 PM
- 876 views
Exercise, Reactive Oxygen Species, and Antioxidants
by Reason in Fight Aging!
I was slowly planning to write something about a recent study that shows antioxidant supplements blocking (one part of) the mechanism by which exercise produces (some of its) health benefits. Here I am instead reaping the benefits of procrastination. If you leave a blog post percolating for long enough, someone else will do part of your job for you: So, what actually causes [the beneficial effects of exercise on metabolism]? There has to be a signal (or set of signals) down at the molecular level that tells your cells what’s happening, and initiates changes in their metabolism. One good candidate is the formation of reactive oxygen species (ROS) in the mitochondria. Exercise most certainly increases a person’s use of oxygen, and increases the work load on the mitochondria (since that’s where all the biochemical energy is coming from, anyway). Increased mitochondrial formation of ROS has been well documented, and they have a lot of physiological effects. ... as it turns out, antioxidant supplements appear to cancel out many of the beneficial effects of exercise. Soaking up those transient bursts of reactive oxygen species keeps them from signaling. Looked at the other way, oxidative stress could be a key to preventing...... Read more »
Ristow, M., Zarse, K., Oberbach, A., Kloting, N., Birringer, M., Kiehntopf, M., Stumvoll, M., Kahn, C., & Bluher, M. (2009) Antioxidants prevent health-promoting effects of physical exercise in humans. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.0903485106
- May 19, 2009
- 09:39 PM
- 822 views
Exercise Versus Mitochondrial DNA Damage
by Reason in Fight Aging!
As you probably know by now, the well-supported mitochondrial free radical theory of aging tells us that damage to the DNA in mitochondria, the power plants of our cells, is an important root cause of aging. You can look back in the archives for an explanation as to exactly why that is the case. There's every reason to expect that methods to repair or otherwise negate mitochondrial DNA (mtDNA) damage will produce great benefits, and a reversal of one contribution to the aging process. A number of different approaches are presently in various stages in the laboratory, including the SENS Foundation's MitoSENS strategy: rather than fixing mitochondrial mutations, we can make them harmless to us. By putting "backup copies" of these few remaining genes into the nucleus, we can prevent the harm caused by any mutations that may occur of the original versions. Even without the mitochondrial DNA, the proteins that it encodes will still be produced and incorporated into the mitochondrial machinery, allowing the cellular power plants to continue humming along normally. For today, however, I'll point your attention to an open access paper on how exercise interacts with damaged mitochondrial DNA. It puts forward a mechanism (and offers...... Read more »
Tarnopolsky, M. (2009) Mitochondrial DNA shifting in older adults following resistance exercise training. Applied Physiology, Nutrition, and Metabolism, 34(3), 348-354. DOI: 10.1139/H09-022
- May 21, 2009
- 08:45 PM
- 802 views
Autophagy and Cellular Senescence
by Reason in Fight Aging!
Autophagy is the process by which cells break down unwanted biochemicals and damaged components. More autophagy taking place in your cells appears to be all upside based on what we see happening under the hood during calorie restriction, and based on the use of other fairly crude methods of boosting autophagy. It looks very much like increased autophagy increases longevity and improves long term health. Cellular senescence on the other hand is a mixed bag; a mechanism that does bad things to you so as to avoid worse things. A cell that lapses into a senescent state due to damage no longer divides, but just sits there emitting biochemical signals that harm the immediate cellular environment - and also hopefully flag the cell for destruction by the immune system. On the one hand this is very effective at preventing runaway replication of damaged cells, i.e. cancer. On the other hand, these harmful senescent cells start to accumulate rapidly with advancing age and collectively contribute to the malfunctioning of your tissues and organs. Nothing in our cellular biochemistry exists in isolation. Our cells are wondrous rats' nests of interconnected mechanisms, feedback loops, dependencies, and other complex evolved machinery. As it turns...... Read more »
Young, A., Narita, M., Ferreira, M., Kirschner, K., Sadaie, M., Darot, J., Tavare, S., Arakawa, S., Shimizu, S., Watt, F.... (2009) Autophagy mediates the mitotic senescence transition. Genes , 23(7), 798-803. DOI: 10.1101/gad.519709
- August 17, 2009
- 07:17 PM
- 739 views
The AGE-Breaker TRC4186 From Torrent Pharmaceuticals
by Reason in Fight Aging!
Back in late 2006, a lifetime ago in Internet Time, I briefly mentioned the efforts of Torrent Pharmaceuticals. They are one of the few groups doing any sort of serious work on AGE-breakers, compounds aimed at breaking down the advanced glycation endproducts (AGEs) that build up with age and cause all sorts of havoc in our biochemistry. One of the ways in which normal metabolic processes degrade important components in your body (such as kidneys, heart, skin and blood vessels) is through the generation of advanced glycation endproducts (AGEs). Your body needs certain proteins in order to work properly; the creation of AGEs involves taking two or more of these proteins and sticking them together with chemical gunk, preventing them from doing their jobs. This is known as crosslinking; day in and day out, it is taking place in your body. Some AGEs are short-lived but common, growing or declining in population in response to your diet and metabolic peculiarities. Others are very long-lived or impossible for the body to break down; they build up over the years, and eventually there's enough of this gunk to seriously damage you. Problems caused - or not helped - by AGE buildup include...... Read more »
Joshi, D., Gupta, R., Dubey, A., Shiwalkar, A., Pathak, P., Gupta, R., Chauthaiwale, V., & Dutt, C. (2009) TRC4186, a Novel AGE-breaker, Improves Diabetic Cardiomyopathy and Nephropathy in Ob-ZSF1 Model of Type 2 Diabetes. Journal of Cardiovascular Pharmacology, 54(1), 72-81. DOI: 10.1097/FJC.0b013e3181ac3a34
- June 15, 2009
- 11:03 PM
- 738 views
Failing Memory and the Failing Immune System: Reversible?
by Reason in Fight Aging!
You might recall a Rejuvenation Research paper from last year that put forward evidence to suggest that some age-related mental deterioration stems from a declining immune system. Aging is often associated with a decline in hippocampus-dependent spatial memory. Here, we show that functional cell-mediated immunity is required for the maintenance of hippocampus-dependent spatial memory. As you probably know by now, our immune systems have not evolved for perpetual use. Their very structure and function results in an increasing level of disarray and malfunction with advancing age and usage. A failing immune system doesn't just mean greater vulnerability to pathogens, however. It also means damaging chronic inflammation, the accumulation of damaging senescent cells, and an increasing risk of cancer - all of which negatively impact life expectancy and the likely future of your health. Which is not to mention this memory issue, further outlined in a more recent paper: The factors that determine brain aging remain a mystery. Do brain aging and memory loss reflect processes occurring only within the brain? Here, we present a novel view, linking aging of adaptive immunity to brain senescence and specifically to spatial memory deterioration. Inborn immune deficiency, in addition to sudden imposition of immune...... Read more »
Ron-Harel, N., & Schwartz, M. (2009) Immune senescence and brain aging: can rejuvenation of immunity reverse memory loss?. Trends in Neurosciences. DOI: 10.1016/j.tins.2009.03.003
- July 30, 2009
- 07:28 PM
- 727 views
Too Much Methionine Appears to be Bad For Mammals
by Reason in Fight Aging!
I'm sure you all know by now that restricting the amino acid methionine in the diet provides many of the health and longevity benefits of calorie restriction - in mice, at least. This is only the case for methionine, not any of the other essential amino acids that must be obtained through diet, and the resulting changes in biochemistry are not exactly the same as calorie restriction. This suggests that, for example, the loss of visceral fat associated with calorie restriction also plays an important role in extended healthspan and longevity. Per recent research, it looks like too much methionine is a bad thing - all the biochemical measures of damage and good operation that are improved by lowering methionine intake are instead made worse when methionine is supplemented in the diet. This worsened set of metabolic processes occurs in addition to any further unpleasant effects produced by the visceral fat tissue most of us would gain in boosting our methionine intake the easy way - by eating more. Methionine restriction without energy restriction increases, like caloric restriction, maximum longevity in rodents. Previous studies have shown that methionine restriction strongly decreases mitochondrial reactive oxygen species (ROS) production and oxidative damage...... Read more »
Gomez, J., Caro, P., Sanchez, I., Naudi, A., Jove, M., Portero-Otin, M., Lopez-Torres, M., Pamplona, R., & Barja, G. (2009) Effect of methionine dietary supplementation on mitochondrial oxygen radical generation and oxidative DNA damage in rat liver and heart. Journal of Bioenergetics and Biomembranes. DOI: 10.1007/s10863-009-9229-3
- May 18, 2009
- 08:32 PM
- 723 views
Do Broad Commonalities Exist in Cancer?
by Reason in Fight Aging!
This is the age of biotechnology, and many believe that one of the crowning triumphs of the age will be the defeat of cancer. If we're going to greatly extend healthy human longevity, then the defeat of cancer certainly has to be achieved one way or another. I think that the one of the most exciting possibilities in modern cancer research is that a cure for cancer is in fact easy, but we don't yet know how to do it. Let me explain what I mean by "easy." This is an era in which we can order cells around, identify cells by tiny differences in their surface biochemistry, construct viruses to order, and in which researchers are rapidly deciphering and manipulating the most fundamental mechanisms of our biology. In this sort of background, "easy" means that researchers find some common mechanism necessary to all (or even just most) cancers. Scientists will then pile in and develop a way of attacking cancer by disrupting or manipulating that mechanism, and there the story is done. We'll have a robust cancer therapy, and will reap the benefits thereof. "Hard" on the other hand means that there is no common mechanism shared between more...... Read more »
Rebecca J. Critchley-Thorne, Diana L. Simons, Ning Yana, Andrea K. Miyahira, Frederick M. Dirbas, Denise L. Johnson, Susan M. Swetter, Robert W. Carlson, George A. Fisher, Albert Koong.... (2009) Impaired interferon signaling is a common immune defect in human cancer. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.0901329106
- July 9, 2009
- 10:45 PM
- 723 views
Calorie Restriction Produces the Expected Slowing of Aging in Rhesus Monkeys
by Reason in Fight Aging!
Results from a long-running primate study of calorie restriction (CR) are becoming more definitive as the years pass. Two decades in, the reports continue to be consistent with the many, many other CR studies in animals and humans: eating fewer calories while still obtaining adequate nutrition slows down degenerative aging in primates. Studying aging in monkeys takes patience. Mice and rats only live for a couple of years, while these monkeys can live to 40, and the average life span is 27 years. Now that the surviving monkeys have reached their mid- to late 20s, the Wisconsin group could glean how calorie restriction was affecting their life span. Sixty-three percent of the calorie-restricted animals are still alive compared to only 45% of their free-feeding counterparts. For age-related deaths caused by illnesses such as cardiovascular disease and cancer, the voracious eaters died at three times the rate of restricted monkeys: 14 versus five monkeys, respectively. ... Researchers who study aging are split on how much stock to put in the study. Leonard Guarente, a molecular biologist at the Massachusetts Institute of Technology in Cambridge who has studied aging in yeast, believes that not enough monkeys have died yet to make definitive...... Read more »
Colman, R., Anderson, R., Johnson, S., Kastman, E., Kosmatka, K., Beasley, T., Allison, D., Cruzen, C., Simmons, H., Kemnitz, J.... (2009) Caloric Restriction Delays Disease Onset and Mortality in Rhesus Monkeys. Science, 325(5937), 201-204. DOI: 10.1126/science.1173635
- June 20, 2009
- 12:14 AM
- 717 views
A Male-Only Longevity Mutation in Mice
by Reason in Fight Aging!
Researchers are uncovering longevity mutations in mice fairly rapidly these days. The cost of genetic engineering is falling, the concept of extending longevity through altering the processes of metabolism is well established, and so much more experimentation is taking place than in past years. Here is another recent example from the open access PLoS ONE, this time with the unusual twist that it seems to work only for male mice: Mutations that cause a reduction in protein kinase A (PKA) activity have been shown to extend lifespan in yeast. Loss of function of mammalian RIIβ, a regulatory subunit of PKA expressed in brain and adipose tissue, results in mice that are lean and insulin sensitive. It was therefore hypothesized that RIIB null (RIIβ−/−) mice would express anti-aging phenotypes. We conducted lifespan studies using 40 mutant and 40 wild type (WT) littermates of equal gender numbers and found that both the median and maximum lifespans were significantly increased in mutant males compared to WT littermates. The median lifespan was increased from 884 days to 1005 days [and] the 80% lifespan (defined here as 80% deaths) was increased from 941 days to 1073 days. [There] was no difference in either median or...... Read more »
Enns, L., Morton, J., Treuting, P., Emond, M., Wolf, N., McKnight, G., Rabinovitch, P., & Ladiges, W. (2009) Disruption of Protein Kinase A in Mice Enhances Healthy Aging. PLoS ONE, 4(6). DOI: 10.1371/journal.pone.0005963
- July 1, 2009
- 08:22 PM
- 710 views
Subtleties of Calorie Restriction and Evolution
by Reason in Fight Aging!
My attention was drawn today to a recent open access paper that theorizes on how evolution came to produce the calorie restriction response. Given that calorie restriction notably improves health and longevity, why isn't this beneficial metabolic state switched on all the time? Stresses like dietary restriction or various toxins increase lifespan in taxa as diverse as yeast, Caenorhabditis elegans, Drosophila and rats, by triggering physiological responses that also tend to delay reproduction. Food odors can reverse the effects of dietary restriction, showing that key mechanisms respond to information, not just resources. Such environmental cues can predict population trends, not just individual prospects for survival and reproduction. When population size is increasing, each offspring produced earlier makes a larger proportional contribution to the gene pool, but the reverse is true when population size is declining. ... We conclude that the beneficial effects of stress on longevity (hormesis) in diverse taxa are a side-effect of delaying reproduction in response to environmental cues that population size is likely to decrease. The reversal by food odors of the effects of dietary restriction can be explained as a response to information that population size is less likely to decrease, reducing the chance that delaying...... Read more »
Ratcliff, W., Hawthorne, P., Travisano, M., & Denison, R. (2009) When Stress Predicts a Shrinking Gene Pool, Trading Early Reproduction for Longevity Can Increase Fitness, Even with Lower Fecundity. PLoS ONE, 4(6). DOI: 10.1371/journal.pone.0006055
- June 24, 2009
- 08:29 PM
- 708 views
Deciphering the Machine By Pulling Out Cogs and Flipping Switches
by Reason in Fight Aging!
I wanted to point out an example of research into the biochemistry of calorie restriction as an example of how scientists progress in their investigations of cellular biology. If the cell is a machine, then the biotechnology revolution has provided scientist-mechanics with wrenches to pull out cogs and screwdrivers to force the settings on inner switches. It has also bequethed a ream of disordered notes from a thousand other mechanics, and from all this sense and understanding has to eventually emerge. So how do you find out what does what in a cell, and by extension in the entire organism that the cell belongs to? Pulling out pieces to see what they were needed for isn't such a bad strategy, especially guided by educated guesswork and related discoveries made by many other engineers. Good educated guesswork is very possible these days, and the cost of chasing down a dead end (in time and money) is falling all the time - it makes sense to explore and take risks. In this vein, a recent paper shows how scientists added more genes to the list of those needed for longevity produced via calorie restriction in worms, though the story is better told...... Read more »
Carrano, A., Liu, Z., Dillin, A., & Hunter, T. (2009) A conserved ubiquitination pathway determines longevity in response to diet restriction. Nature. DOI: 10.1038/nature08130
- June 5, 2009
- 12:25 AM
- 700 views
Accumulating Mitochondrial DNA Damage: More Harm or Less Repair?
by Reason in Fight Aging!
The mitochondrial free radical theory of aging tells us that accumulating damage to the DNA inside the mitochondria in our cells is a prominent cause of age-related degeneration. Mitochondria are powerplants, thousands to a cell swarming to turn food into the fuel chemical ATP, and their DNA, separate from the DNA in the cell's nucleus, is the blueprint for their assembly and operation. You'll find a simplified layman's explanation of the mitochondrial free radical theory of aging back in the Fight Aging! archives - there are a lot of steps and processes run awry between damaged mitochondrial DNA and the large-scale damage of aging. Damaged mitochondria proliferate in some cells and, like damaged factories, pollute those cell with excess reactive oxygen species (ROS) and free radicals produced as metabolic byproducts. Each damaged cell then tries to maintain itself by exporting more reactive oxygen species and free radicals from its cell membrane structures, spreading the damaging pollution far and wide in the body. We humans are self-repairing systems to some degree, as are the cells we are made up of. When considering an accumulation of damage in a self-repairing system, it isn't as simple as "dents and errors add up over...... Read more »
Soerensen, M., Gredilla, R., Müller-Ohldach, M., Werner, A., Bohr, V., Osiewacz, H., & Stevnsner, T. (2009) A potential impact of DNA repair on ageing and lifespan in the ageing model organism Podospora anserina: Decrease in mitochondrial DNA repair activity during ageing. Mechanisms of Ageing and Development. DOI: 10.1016/j.mad.2009.05.003
- July 7, 2009
- 10:43 PM
- 686 views
Consumers of Drugs of Abuse
by Reason in Fight Aging!
Unintentional poetry can sometimes be found amidst the drudgery of translating literature from one language to another. Spanish to English gifts us with "consumers of drugs of abuse," which serves as the point of attraction to here consider the relationship between aging and damaging ourselves, both proactively and through neglect. The full PDF is also freely available in both Spanish and English, lined up in parallel. The aging or senescence process that follows maturation is characterized by time-related functional decline due to genetic, biochemical, physiological and anatomical degeneration in tissues and organ systems with time. Oxidative damage to mitochondrial DNA (mtDNA) in the heart and brain is inversely related to maximum life span of mammals, suggesting that accumulation of mtDNA damage is involved in the various disorders associated with aging, cancer and neurodegeneration. The suppression of stem/progenitor cell proliferation also contributes to the aging process, by reducing tissue regeneration and repair and ultimately reducing longevity. Another important factor is the intracellular deposition of lipofuscin granules (age pigment), a non-degradable polymeric material accumulated within lysosomes, which ultimately exacerbate oxidative stress levels in senescent cells. Drugs of abuse can strongly contribute to these senescence accelerating factors in the brain. Methylenedioxymethamphetamine ('ecstasy') and...... Read more »
Carvalho F. (2009) How bad is accelerated senescence in consumers of drugs of abuse?. Adicciones, 21(2). DOI: ADICCIONES, 2009 - VOL. 21 NUM. 2 - PAGES. 99-104
- July 8, 2009
- 10:45 PM
- 682 views
Late-Life Administration of Rapamycin Extends Life in Mice
by Reason in Fight Aging!
Rapamycin is a drug of interest because researchers know that the TOR gene (which stands for Target of Rapamycin, so you can probably guess the order of discovery) is involved the big tangled mess of biochemistry relating to the calorie restriction response. Less food while maintaining adequate nutrition modulates the functions of metabolism in ways that lead to longer lives and slower aging. Unless you've spent the past few years living in a basket, you'll know that this is of considerable interest to the gerontological and pharmaceutical research communities, and many efforts are underway to develop means of achieving or bettering this biochemical response without modifying diet. Personally, I think this is all a sideshow of limited benefit in comparison to research that aims to repair and reverse the damage of aging rather than merely slowing it a little. But the sideshow has the main stage and the attention of the tent for now. Sideshow or not, it will produce a vast amount of new information on the way in which our biochemistry works - so it isn't a waste, it's just not very efficient if the end goal is for humans to live much longer in good health than...... Read more »
Harrison, D., Strong, R., Sharp, Z., Nelson, J., Astle, C., Flurkey, K., Nadon, N., Wilkinson, J., Frenkel, K., Carter, C.... (2009) Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature. DOI: 10.1038/nature08221
- July 21, 2009
- 09:36 PM
- 680 views
Induced Pluripotent Cells Demonstrated to Repair Heart Damage
by Reason in Fight Aging!
The research community is rapidly reproducing the past ten years of stem cell technology demonstrations, using induced pluripotent stem (iPS) cells this time around. You'll recall that iPS cells are normal cells - usually skin cells - reprogrammed to act as though they are stem cells. The methodology is well within reach of any laboratory previously working on stem cells, and many research groups have dived into the fray since the first publication of the reprogramming method. Rapid progress has been made in a very short time, a characteristic state of affairs for biotechnology these days. As a recent paper shows, iPS researchers have reached the point of demonstrating regeneration of damaged hearts in mice. Non-scientists might prefer the press release to the original paper: The ultimate goal is to use iPS cells derived from patients to repair injury. Using a person's own cells in the process eliminates the risk of rejection and the need for anti-rejection drugs. One day this regenerative medicine strategy may alleviate the demand for organ transplantation limited by donor shortage, the researchers say. ... The Mayo Clinic team genetically reprogrammed fibroblasts via a "stemness-related" human gene set to dedifferentiate into an iPS cell capable of...... Read more »
Nelson, T., Martinez-Fernandez, A., Yamada, S., Perez-Terzic, C., Ikeda, Y., & Terzic, A. (2009) Repair of Acute Myocardial Infarction With Induced Pluripotent Stem Cells Induced by Human Stemness Factors. Circulation. DOI: 10.1161/CIRCULATIONAHA.109.865154
- September 2, 2009
- 09:47 PM
- 672 views
Yet Another Reason Not to Be Obese: It Accelerates Immune System Aging
by Reason in Fight Aging!
By now, I would hope, the life science horror stories that turn up here on a regular basis will have convinced you that excess body fat is not good for your long term health and longevity. Some of that is the result of the biochemistry of fat tissue en mass, and some of that is the reaction of your metabolism to the sedentary, high-calorie lifestyle required to gain that fat tissue, but the end result isn't pretty. More fat means a lowered life expectancy and a greater risk of all the common age-related diseases - and the decades of suffering in health and wallet that come with them. Being overweight is a choice for 99.9% of people. A seductive, easy choice to slip into in a wealthy society whilst surrounded by an adundance of food, but a choice nonetheless. You might think of doing something about that. In any case, today I thought I'd showcase another motivativational piece of research on the consequences of excess body fat, this time as it relates to the degeneration of your immune system. One of the reasons your immune system fades and fails with age is the involution - or shrinkage and atrophy -...... Read more »
Yang H, Youm YH, Vandanmagsar B, Rood J, Kumar KG, Butler AA, & Dixit VD. (2009) Obesity accelerates thymic aging. Blood. PMID: 19721009
- May 26, 2009
- 10:06 PM
- 670 views
AGEs and RAGE in Alzheimer's Disease
by Reason in Fight Aging!
One of the issues inherent in research of a late stage age-related condition is that a lot of different things are going wrong with the body at the same time. The comparatively few categories of age-related damage have spilled over into hundreds of different types of malfunctions and the further disarray resulting from those malfunctions. By way of an analogy, consider rust in a machine: rust is a simple process, but the way in which the machine eventually breaks down can be a very complicated sequence of failing components and chained consequences. So it is with aging. I noticed a review paper today that explores the role advanced glycation endproducts (AGEs) and their cell receptor (RAGE) might play in Alzheimer's disease. The way to walk into this discussion is with a web of known correlations and research results in mind: The buildup of AGEs is one of the fundamental causes of aging per the Strategies for Engineered Negligible Senescence (SENS) way of looking at things The disarray to biochemical processes due to AGEs is at least partly caused by constant triggering of RAGE AGEs build up faster in diabetes, and we know that risk of diabetes is strongly associated with...... Read more »
Srikanth, V., Maczurek, A., Phan, T., Steele, M., Westcott, B., Juskiw, D., & Münch, G. (2009) Advanced glycation endproducts and their receptor RAGE in Alzheimer's disease. Neurobiology of Aging. DOI: 10.1016/j.neurobiolaging.2009.04.016
- July 29, 2009
- 07:29 PM
- 669 views
Complicating Antioxidants Some More
by Reason in Fight Aging!
We'll start off today's post with a quick refresher on the present state of knowledge regarding antioxidants and life span in laboratory animals. Antioxidants are compounds that neutralize oxidants, such as the reactive oxygen species produced by your mitochondria that are implicated in the damage of aging. In theory, neutralizing those damaging oxidants before they can cause harm to your cellular machinery will lead to a lesser accumulation of cellular and tissue damage over time, and thus a slower rate of aging. Aging, after all, is no more than the accumulation of damage and the body's response to that damage. Oxidant compounds also play important roles in the body's signaling mechanisms, however, so it's far from the case that we can declare all oxidants bad. What do researchers presently know? Many studies show that ingested antioxidants do nothing positive, and might actually be bad for longevity by interfering in beneficial mechanisms like exercise. The body produces a range of different natural antioxidants. Long-lived species seem to maintain the same levels of these compounds throughout life, but there's no correlation between levels of natural antioxidants and life span differences between similar species. Manipulating levels of natural antioxidants through gene engineering has...... Read more »
Jang, Y., Perez, V., Song, W., Lustgarten, M., Salmon, A., Mele, J., Qi, W., Liu, Y., Liang, H., Chaudhuri, A.... (2009) Overexpression of Mn Superoxide Dismutase Does Not Increase Life Span in Mice. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences. DOI: 10.1093/gerona/glp100
- July 24, 2009
- 08:24 PM
- 668 views
Ageless Animals, the Pearl Mussel Edition
by Reason in Fight Aging!
The freshwater pearl mussel (Margaritifera margaritifera) is a very long-lived beast, though as for many of these species its life span is poorly studied. There are too many bivalves and not enough researchers - remember that we live in a world in which we can't even determine lobster ages with any degree of certainty. Like many bivalves, lobster biochemistry doesn't seem to change with age in any usefully measurable way. You might recall research into the longevity of another bivalve, the arctic quahog clam, that suggests its longevity is a matter of excellent natural antioxidants: The ocean quahog Arctica islandica is the longest-lived of all bivalve and molluscan species on earth. Animals close to 400 years are common and reported maximum live span around Iceland is close to 400 years. High and stable antioxidant capacities are a possible strategy to slow senescence and extend lifespan Compare that with this recent open access paper on the pearl mussel wherein the researchers found a different story when looking at superoxide dismutase (SOD) and catalase (CAT): Free radicals are extremely reactive and produce damage and modify cell functions. Furthermore, superoxide dismutase and catalase are believed to play a key role in the enzymatic...... Read more »
CARLOS FERNÁNDEZ, EDUARDO SAN MIGUEL, & ALMUDENA FERNÁNDEZ-BRIERA. (2009) Superoxide dismutase and catalase: tissue activities and relation with age in the long-lived species Margaritifera margaritifera. Biological Research, 42(1), 56-57. DOI: 19621133
- October 13, 2009
- 11:30 PM
- 661 views
Alternate Day Fasting Continues to Look Promising
by Reason in Fight Aging!
Alternate day fasting, or intermittent fasting in general, is known to produce similar health and longevity benefits to the practice of calorie restriction. Intermittent fasting isn't as well researched as calorie restriction - by which I mean to say the evidence for health benefits is "only" very good rather than overwhelming, as in the case of calorie restriction. It's worth noting that there exist intriguing hints that the underlying biological mechanisms by which these benefits are conferred are different for these two strategies, despite the basic similarity: eating less while still obtaining all the necessary nutrients. Over at the Longevity Meme I recently remarked upon a study showing improvement in heart function and overall health with age as a result of suppressing one gene involved in the calorie restriction response: researchers compared aged mice with a functional p110alpha to aged mice with suppressed p110alpha and found that mice with the suppressed gene had: improved cardiac function; less fibrosis (fibrosis causes the heart to lose flexibility); fewer biological markers of aging; and a pattern of cardiac gene expression like that of younger mice. By way of comparison, here is another study showing much the same result, but achieved through alternate day...... Read more »
Castello L, Froio T, Maina M, Cavallini G, Biasi F, Leonarduzzi G, Donati A, Bergamini E, Poli G, & Chiarpotto E. (2009) Alternate-day fasting protects the rat heart against the age-induced inflammation and fibrosis by inhibiting oxidative damage and NF-kB activation. Free radical biology . PMID: 19818847
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