Category Archives: Longevity Medicine

From QFinance: "Big business and governments are already grappling with the uncomfortable side effects of increasing longevity. According to actuaries, the present generation has gained the equivalent of 12 minutes an hour or a 20% increase in average lifespan by comparison with the previous generation. The impact of this is felt first and foremost in the pensions arena, with businesses having to run harder just to stand still as far as their pension scheme deficits are concerned. But it is felt too by governments across Europe as they struggle to pay out meaningful state pension benefits against the headwind imposed by the fact that the ratio of those in work to those on pension is getting more and more out of balance. The impact of increased longevity is felt too in the health systems, where the diseases and ailments of old age take an increasing toll on a country's medical resources. These problems might seem fairly intractable, or at least extremely difficult and challenging in their own right, but it could be just the tip of the iceberg, according to the renowned longevity specialist Dr Aubrey de Grey, Chief Scientist at the charity SENS, which specializes in promoting research that aims to 'defeat ageing.' Dr de Grey is famous for asserting that the first person to enjoy a four-digit lifespan is probably already in his or her middle years. Before I give a rapid summary of his reasoning - those interested in learning more can watch a video of one of his presentations at the SENS website - it is worth saying that if de Grey is right, then instead of exacerbating the pensions problem, as I suggested earlier, it will probably make the problem vanish like a puff of smoke. Provided society stays reasonably open, people will have more than enough time to acquire independent means. The magic of compound arithmetic will be very much in their favor. Start small, watch it grow, where's the hurry?"

View the Article Under Discussion: http://www.qfinance.com/blogs/anthony-harrington/2010/05/05/the-challenge-of-longevity

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

An open access paper from Impact Aging: "The Mitochondrial Free Radical Theory of Aging (MFRTA) is currently one of the most widely accepted theories used to explain aging. From MFRTA three basic predictions can be made: long-lived individuals or species should produce fewer mitochondrial Reactive Oxygen Species (mtROS) than short-lived individuals or species; a decrease in mtROS production will increase lifespan; and an increase in mtROS production will decrease lifespan. It is possible to add a further fourth prediction: if ROS is controlling longevity separating these parameters through selection would be impossible. These predictions have been tested in Drosophila melanogaster." Where I think the researchers go wrong here lies in not accounting for how differences in mitochondrial composition might affect the level of damage caused by a given amount of ROS. There is a strong argument that species life span differences have a lot to do with how resilient mitochondria are to damage. But read the paper anyway; it's a good introduction to thinking about the mitochondrial free radical theory of aging.

View the Article Under Discussion: http://www.impactaging.com/papers/v2/n4/full/100137.html

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

As this Independent article shows, the public view of longevity science extends little beyond the goal of slowing aging espoused by mainstream researchers, and conflates the fakery and fraud of "anti-aging" cosmetics companies with real science: "We spend millions of pounds each year on anti-ageing tonics, potions, vitamins and creams, trying to stave off the ravages of the years. But our genetic inheritance trumps all other factors in determining how well we age and how long we live. By unravelling the genetic determinants of longevity, scientists believe they will be able to manipulate them to add not only years to life, but also life to years. An elixir of youth remains a distant dream but medicines to help us live longer and better are moving closer. At a conference this week, Turning Back the Clock, organised by the Royal Society, researchers described the progress that has been made in the science of ageing. At least 10 gene mutations have been identified that extend the lifespan of mice by up to half, and in humans several genetic variants have been linked with longevity. They include a family of genes dubbed the sirtuins, which one Italian study found occurred more commonly in centenarian men than in the general population. A subsidiary of drug giant GlaxoSmithKline is now looking at sirtuins, and their association with a range of age-related diseases including type 2 diabetes and cancers."

View the Article Under Discussion: http://www.independent.co.uk/news/science/has-the-elixir-of-youth-come-of-age-1971341.html

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Another consequence of the overeating and lack of exercise that leads to metabolic syndrome and diabetes: "In people with insulin resistance or full-blown diabetes, an inability to keep blood sugar levels under control isn't the only problem by far. A new report [shows] that our arteries suffer the effects of insulin resistance, too, just for entirely different reasons. ... Earlier studies showed that in the context of systemic insulin resistance, blood vessels become resistant, too. Doctors also knew that insulin resistance and the high insulin levels to which it leads are independent risk factors for vascular disease. But it wasn't clear if arteries become diseased because they can't respond to insulin or because they get exposed to too much of it. Now comes evidence in favor of the former explanation. ... mice prone to atherosclerosis fare much worse when the linings of their arteries can't respond to insulin. The animals' insulin-resistant arteries develop plaques that are twice the size of those on normal arteries. Insulin-resistant blood vessels don't open up as well, and levels of a protein known as VCAM-1 go up in them, too. VCAM-1 belongs to a family of adhesion molecules [which sit on the endothelium and bind] white blood cells. ... Those cells can enter the artery wall, where they start taking up cholesterol, and an early plaque is born. ... The results provide definitive evidence that loss of insulin signaling in the endothelium, in the absence of competing systemic risk factors, accelerates atherosclerosis."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-05/cp-yam042810.php

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Autophagy is important in determining life span, probably because of its role in clearing out damaged mitochondria (a process known as mitophagy) before they can cause other forms of harm. Here is evidence for that view in the form of a link between Parkinson's disease and autophagy: "Mutations that cause Parkinson's disease prevent cells from destroying defective mitochondria ... Defects in the ubiquitin ligase Parkin are linked to early-onset cases of this neurodegenerative disorder. The wild-type protein promotes the removal of impaired mitochondria by a specialized version of the autophagy pathway called mitophagy, delivering mitochondria to the lysosomes for degradation. Mitochondria are often dysfunctional in Parkinson's disease ... cells expressing mutant forms of Parkin failed to clear their mitochondria after the organelles were damaged. Different mutations blocked mitophagy at distinct steps: mitochondria accumulated in the perinuclear region of cells expressing Parkin lacking its ubiquitin ligase activity, for example. The researchers found that ubiquitination of defective mitochondria by Parkin normally recruits the autophagy proteins HDAC6 and p62 to clear these mitochondrial aggregates. ... The clearance of defective mitochondria is therefore similar to the removal of damaged proteins, another autophagic process that goes wrong in Parkinson's disease resulting in the accumulation of toxic protein aggregates. Both pathways rely on microtubules, HDAC6, and p62, [providing] a common link between the two main features of the neurodegenerative disorder."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-05/rup-mtc050610.php

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Autophagy is important in determining life span, probably because of its role in clearing out damaged mitochondria (a process known as mitophagy) before they can cause other forms of harm. Here is evidence for that view in the form of a link between Parkinson's disease and autophagy: "Mutations that cause Parkinson's disease prevent cells from destroying defective mitochondria ... Defects in the ubiquitin ligase Parkin are linked to early-onset cases of this neurodegenerative disorder. The wild-type protein promotes the removal of impaired mitochondria by a specialized version of the autophagy pathway called mitophagy, delivering mitochondria to the lysosomes for degradation. Mitochondria are often dysfunctional in Parkinson's disease ... cells expressing mutant forms of Parkin failed to clear their mitochondria after the organelles were damaged. Different mutations blocked mitophagy at distinct steps: mitochondria accumulated in the perinuclear region of cells expressing Parkin lacking its ubiquitin ligase activity, for example. The researchers found that ubiquitination of defective mitochondria by Parkin normally recruits the autophagy proteins HDAC6 and p62 to clear these mitochondrial aggregates. ... The clearance of defective mitochondria is therefore similar to the removal of damaged proteins, another autophagic process that goes wrong in Parkinson's disease resulting in the accumulation of toxic protein aggregates. Both pathways rely on microtubules, HDAC6, and p62, [providing] a common link between the two main features of the neurodegenerative disorder."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-05/rup-mtc050610.php

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/