Weight Battle

This study shows centenarians to more often carry a variant gene that affects exonuclease 1 (EXO1), involved in some forms of DNA repair - adding some fuel to the debate over the significance of nuclear DNA damage in aging. At this stage researchers are turning up longevity-associated differences in genes at a much faster rate than progress in understanding how it all ties together and how important specific genetic differences might be. From the paper: "Human longevity is heritable with a genetic component of 25-32%. Variation in genes regulating the levels of somatic maintenance and DNA repair functions is thought to modulate the aging process and to contribute to survival at advanced age. We tested 92 non-synonymous SNPs in 49 DNA repair genes for a possible association with longevity in a sample of 395 German centenarians and 411 controls. The obtained association signal in exonuclease 1 (EXO1) was further investigated by fine-mapping and mutation detection, leading to the identification of the functionally relevant SNP rs1776180. Our detailed analyses revealed that the common allele (C) of this promoter SNP is significantly enriched in female centenarians. This finding replicated in 455 female French centenarians and 109 controls. ... Given the survival advantage that is associated with the C allele of rs1776180, EXO1 can be considered a candidate for a novel longevity-enabling gene."

View the Article Under Discussion: http://pmid.us/19698732
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Via ScienceDaily: "We wanted to uncover the workings of skin health in order to see why older people don't deal well with skin infections and are prone to skin cancers also. ... In the past, the reduction in skin health was put down to potential defects in the white blood cells called T-cells that would usually help to identify and clear infection. However, when experiments were carried out with healthy young individuals under the age of 40 years and older individuals over the age of 70 years in this study, it was shown that in fact there is nothing wrong with the T-cells in the older group; instead it is the inability of their skin tissue to attract T-cells where and when they are needed that is the source of reduced immunity. ... Knowing this now raises the question of whether the same defect also occurs in other tissues during ageing. Is it possible that, for example, lung tissues also fail to give out the right message to T-cells to bring them into the tissue to do their job? This may explain, in part, the higher rates of lung cancer, chest infections and pneumonia in older people, perhaps. ... at least in the test tube, it is possible to make older skin express the missing signals that attract T cells. This indicates that, in principle, the defect is entirely reversible."

View the Article Under Discussion: http://www.sciencedaily.com/releases/2009/08/090827192336.htm
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Excess visceral fat, the insulin resistance of type 2 diabetes and metabolic syndrome, and chronic, damaging inflammation all go together. But why? Looking at the fat tissue tells us that macrophages seem to be involved, but here researchers dive in deeper, finding "in cultured cells and mouse experiments that Fox01 stimulates inflammatory white blood cells called macrophages, which migrate to the liver and adipose, or fat, tissue in insulin-resistant states, to increase production of a cytokine called interleukin-1 beta (IL-1B). The cytokine in turn interferes with insulin signaling. Insulin typically inhibits Fox01, setting up a feedback loop in healthy tissues that helps regulate insulin levels. ... The findings suggest that when there is a lack of insulin or when cells such as macrophages are resistant to its presence, there are no brakes on Fox01's stimulation of IL-1B and its further interference with insulin signaling. That might explain why chronic inflammation often is coupled with obesity and type 2 diabetes." All the more reason to take better care of your health so that you don't find yourself experiencing this firsthand.

View the Article Under Discussion: http://www.sciencedaily.com/releases/2009/08/090826113823.htm
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

The interesting thing about longevity science is that the end result - a much longer, healthier life - is so compelling that even communities traditionally opposed to free and rapid development of new technologies on ideological grounds (such as prioritizing equality so highly that universal poverty and death is preferable to inequality) find their members coming around eventually. See this, for example, from an ethicist steeped in the social justice viewpoint: "A fair system of social cooperation is one that is both rational and reasonable (John Rawls, 2001). Is it rational and reasonable for societies that (1) are vulnerable to diverse risks of morbidity (e.g. cancer, heart disease) and mortality, and (2) are constrained by limited medical resources, to prioritize aging research? In this paper I make the case for answering 'yes' on both accounts. Focusing on a plausible example of an applied gerontological intervention (i.e. an anti-aging pharmaceutical), I argue that the goal of decelerating the rate of human aging would be a more effective strategy for extending the human healthspan than the current strategy of just tackling each specific disease of aging. Furthermore, the aspiration to retard human aging is also a reasonable aspiration, for the principle that underlies it (i.e. the duty to prevent harm) is one that no one could reasonably reject."

View the Article Under Discussion: http://colinfarrelly.blogspot.com/2009/08/annals-of-ny-academy-of-sciences-paper.html
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

By now I'd hope you know that the evidence points to excess visceral fat being very bad for you over the long term. Is it the visceral fat or something else correlated with visceral fat, however? "New findings [suggest] that it's not whether body fat is stored in the belly that affects metabolic risk factors for diabetes, high blood triglycerides and cardiovascular disease, but whether it collects in the liver. ... For years, scientists have noted that where individuals carried body fat influences their metabolic and cardiovascular risk. Increased fat inside the belly, known as visceral fat, is associated with an increased risk of diabetes and heart disease. ... Data from a large number of studies shows that visceral fat is associated with metabolic risk, which has led to the belief that visceral fat might even cause metabolic dysfunction. However, visceral fat tracks closely with liver fat. We have found that excess fat in the liver, not visceral fat, is a key marker of metabolic dysfunction. Visceral fat might simply be an innocent bystander that is associated with liver fat." On the other hand, mouse studies show that surgically removing visceral fat extends life.

View the Article Under Discussion: http://www.innovations-report.de/html/berichte/medizin_gesundheit/fat_liver_belly_a_marker_disease_risk_138380.html
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/