Category Archives: Longevity Medicine

Research suggests that changes in messenger RNA (mRNA) translation - a step in the complex process by which proteins are built from the blueprint of a gene - are important in the metabolic determination of longevity. This appears to be one of the ways in which the TOR gene, and thus rapamycin, influences longevity: "Appropriate regulation of mRNA translation is essential for growth and survival and the pathways that regulate mRNA translation have been highly conserved throughout eukaryotic evolution. Translation is controlled by a complex set of mechanisms acting at multiple levels, ranging from global protein synthesis to individual mRNAs. Recently, several mutations that perturb regulation of mRNA translation have also been found to increase longevity in three model organisms: the budding yeast Saccharomyces cerevisiae, the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. Many of these translation control factors can be mapped to a single pathway downstream of the nutrient responsive target of rapamycin (TOR) kinase. [This suggests] that mRNA translation is an evolutionarily conserved modifier of longevity and [could] influence aging and age-associated disease in different species."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20886753

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This open access PDF editorial is illustrative of the mainstream scientific examination of human longevity. Demographic studies lead to genetic studies - to identify long-lived populations and then the genetic roots that make them different: "It is now evident from various socio-demographic studies that a greater portion of the population survives into old age, above the seventh decade of life. Projections for Europe estimate that in 1995 13.3% of the population was over the age of 65, whereas by 2015 this figure is expected to rise to 16.3%. However, the factors that promote living after the seventh or eighth decade of life remain unknown. Therefore, a question may arise: what is the 'formula' that allows some elders to avoid chronic diseases, such as cancer and cardiovascular disease? ... Clearly, longevity is a complex attribute determined by factors, such as exposure to disease, variability in sleeping patterns, smoking habits, physical activity and diet, that have a direct effect on longevity, in addition to their indirect emotional and cognitive influence on physiological pathways." This sort of work will continue for many decades, with little sense of urgency and equally little effect upon our lives. It is a world removed from the engineering approach to extending life span advocated by the SENS Foundation, amongst others.

View the Article Under Discussion: http://www.hellenicjcardiol.org/archive/full_text/2010/5/2010_5_479.pdf

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Via FuturePundit, the estimates for recent research funding: "The U.S. invested $139 billion last year in health research from all public and private sources, according to Research!America's latest annual estimate. That amount represents only 5.6% of the $2.47 trillion overall U.S. health spending in 2009 [which] varies no more than 0.2% from 2005 levels. ... We are all growing old. We are all aging and our parts are breaking down and wearing out. A portion of those billions of dollars flows toward science technologies that will eventually put an end to aging. Human bodies will become as repairable as cars. Replacement organs, cell therapies, gene therapies, and even nanobots will, at some point in the 21st century, halt and reverse the process of aging. Will you still be alive when that day is reached?" As has always been the case, funding for research is a tiny percentage of the flows of money in our culture. Funding for aging research is a tiny fraction of the figures given above, and funding for engineered longevity is in turn a tiny fraction of aging research. To fully realize the Strategies for Engineered Negligible Senescence in mice in the laboratory would probably cost in the vicinity of $1-2 billion over a decade or two. Food for thought.

View the Article Under Discussion: http://www.futurepundit.com/archives/007557.html

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From the Australian: "Generating new body organs in the lab is the stuff of Hollywood fantasy. But judging by the latest experimental findings, science fiction may soon be science fact. ... Already, a bio-printer is cranking out three-dimensional tissues and Australian researchers are hard at work growing spare parts, with designer tissues proving their stuff in animal - and even human - trials. ... In animal experiments, [researchers have] made breast, fat, muscle and even pancreatic tissue that secretes insulin. They've also created tissue of a specialised immune system organ, the thymus, opening the way for multiple applications in immunology. That's because the thymus schools T-cells that help the immune system identify and fight infections and foreign cells. Using mice bred with no immune system, [researchers] found that after the mice received newly grown tissue they developed effective immune responses. ... the institute is engaged in a small number of human clinical trials with fat and breast tissue. The goal is to establish whether tissue can be created and used to replace tissue removed due to cancer. The trials have about six months to run. While creating living tissue is important, the larger aim is creation of functioning human organs."

View the Article Under Discussion: http://www.theaustralian.com.au/news/health-science/tailor-made-living-tissue-is-hot-off-the-press/story-e6frg8y6-1225935870396

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Mitochondrially targeted antioxidants - such as gene engineering of increased amounts of catalase - are shown to extend life in mice, but here researchers find no such effect (or a negative effect) in flies: "The simultaneous overexpression of multiple copies of Mn superoxide dismutase (SOD) and ectopic catalase (mtCat) transgenes in the mitochondria of the fruit fly, Drosophila melanogaster, was shown previously to diminish the life span. The hypothesis tested in the present study was that this effect was due primarily to the presence of one or the other transgene. An alternative hypothesis was that both transgenes have additive, negative effects. Crosses were performed between five pairs of transgenic lines containing single-copy insertions of either mtCat, Mn SOD, or P element vector control transgenes at unique loci, and the life spans of progeny containing two mtCat, Mn SOD or vector insertions were determined. Increasing amounts of mitochondrial catalase activity tended to be associated with decreases in mean life span. Overexpression of two copies of the genomic Mn SOD transgene had no effect on life span. The results do not support the hypothesis that enhanced mitochondrial SOD or catalase activity promotes longevity in flies." This suggests that it's possible to set up a situation in mammals wherein mitochondrially targeted antioxidants are harmful to life span, but I'm not aware of any examples.

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20923705

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CALERIE is the largest present study of calorie restriction in humans: "In a robust and consistent manner, sustained caloric restriction (CR) has been shown to retard the aging process in a variety of animal species. Nonhuman primate studies suggest that CR may have similar effects in longer-lived species. The CALERIE (Comprehensive Assessment of the Long-term Effects of Reducing Intake of Energy) research program is the first systematic investigation of CR in nonobese human beings. In the phase 2 study, it is hypothesized that 2 years of sustained CR, involving a 25% reduction of ad libitum energy intake, results in beneficial effects similar to those observed in animal studies. ... The study is a multicenter, parallel-group, randomized controlled trial. A sample of 225 participants [is] being enrolled with 2:1 allocation to CR. ... An intensive dietary and behavioral intervention was developed to achieve 25% CR and sustain it over the 2 years. Adherence is monitored using a doubly labeled water technique. Primary outcomes are resting metabolic rate and core temperature, and are assessed at baseline and at 6-month intervals. Secondary outcomes address oxyradical formation, cardiovascular risk markers, insulin sensitivity and secretion, immune function, neuroendocrine function, quality of life and cognitive function. ... The results will provide insight into the detrimental changes associated with the human aging process and how CR mitigates these effects."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20923909

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