Hourglass IX

Welcome to the ninth edition of Hourglass, a blog carnival devoted to the biology of aging!

I want to begin with the first picture-post submission to Hourglass by Mo Costandi, which you can see (and click through to) on the left. Gama sennin, a figure from japanese mythology, "is said to live forever, able to change himself into a toad. He is one of the immortal sages (...) who are associated with longevity and medicine. He is also the creator and manufacturer of magical pills, and whomsoever manages to secure them is able to extend his lifetime."


~Hara Hachi Bu~

Speaking of Japanese culture, "Hara hachi bu" is how the Okinawa, reknown for their long life-span, call the practice of eating only until you are 80% full. And well, what do you know, one of the few methods which reliably extend healthy life span (at least in model organisms) is calorie restriction. While I'm not sure whether it is really that much easier to eat nothing for 2 days per week as opposed to chronically reducing one's intake by about 30%, Lloyd and Peggy Morris tell us how that particular regime has been working out for them in Out and About. Meanwhile Reason is a bit pissed off at how calorie restriction has recently been portrayed in popular media, namely at Oprah's show, and rightfully so. To quote: "A theory on popular media: the more popular it is, the less the information it provides bears any semblance to accuracy, truth, or scientific fact".


~I have full faith in the future of medicine~

This is the tongue-in-cheek reply people who comment on my smoking usually get. While I’m aware that it’s probably not quite what the authors of the next two posts had in mind, this attitude may just be the next best thing to quitting (albeit by a long margin.. ;).

For one, optimists live longer, and are specifically less likely to die from heart disease, who would have guessed? The reasons for this are unknown, but Ward Plunet at Brain Health Hacks points to a number of possible explanations. For example, optimists are more likely to stick to medical advice and may also benefit from a bigger social circle as compared to their grumpy pessimistic counterparts.

And in another post at Fight Aging!, Reason urges us to abandon our evolutionarily conserved short-sightedness and truly think forward. This is a very valid point imho. While one shouldn’t underscore the impact of a healthy lifestyle on life expectancy, it is just as important to keep in mind that the real changes in terms of extending healthy life span will be due to new advances in technology and medicine, and we need to actively push the appropriate areas of research instead of relying on carrot juice alone.

So how about trying to optimistically and proactively look into the future? As a starting point one might want to take a look back for inspiration, at what has been achieved in aging research to date. Paul House has created a Science of Aging timeline, and encourages people to add referenced entries to it. It still looks like early days, but I am pretty sure this could become a great interactive tool for exploring aging research as soon as some more people contribute to it. So if you can think of a cool milestone in biogerontology, please add it to the timeline.


~Experiences after reproduction don't influence the evolutionary process~

as Martin Wiseman (a big shot in cancer research) said in a lecture I recently attended (the lecture was useless btw). This is a bit of a bummer, as it means that characteristics that would extend life span are not necessarily evolutionarily selected for. This might be the case regarding amyloidosis, a clogging of blood vessels and other body tissues over time with various proteins, which Reason speculates might be the ultimate killer if heart disease, cancer or being eaten by bears 'fail' to do the trick. Our bodies might simply not have had the need to get rid of those protein deposits until quite recently. At Fight Aging!, recent advances in our understanding amyloidosis and CPHPC, a promising drug which clears amyloid deposits by preventing them from being protected by a protein called SAP, are described.

Abnormal protein deposits also pose a real problem in several neurodegenerative diseases by the way, for example in Parkinson's disease (hello alpha-synuclein, I'm looking at you!) or Alzheimer's disease. Another example is Huntington's disease, in which abnormal mutated huntingtin accumulates in brain cells. Recently researchers found that acetylation of huntingtin might impact positively on its clearance, and without a doubt learning how to "convince the body to clear its own biochemical waste" could be helpful in fighting a multitude of aging-related diseases (or even 'normal' protein accumulation associated with aging - see above).


~In effect, aging occurs because (...) genes evolved to treat the body as disposable~

as postulated by Thomas Kirkwood in his review: Understanding ageing from an evolutionary perspective (a great piece!) Alas, biogerontologists essentially have to try and fight our bodies' propensity to die once their use has been fulfilled. Funnily enough, even the 'blueprint of life' itself gets damaged over time.

Several types of DNA damage have been implicated with aging, and mitochondrial DNA seems to be no exception. In his post on mitochondrial DNA replication and premature aging at Ouroboros, Mark Walsh elaborates on a recent paper by Bailey et al (free full access :) who studied mutant mice that had a proofreading-deficient mitochondrial DNA polymerase (POLG). In these mice, linear mtDNA, and point-mutations were more common. Also, DNA replication appeared to stall at specific location in the mitochondrial genome, leading an upregulation of replication and possibly additional stresses on the cell as a whole. Interestingly, the human progeroid disorder Werner's syndrome is caused by mutations in the WRN helicase, which is involved in nuclear DNA replication and repair. If all this made little sense, I urge you to check out the original post, where it's all explained much more coherently.

Aging is also associated with a wide variety of changes in gene expression and a plethora of studies have tried to pinpoint those, up to now largely in vain, due to the vast inter- and intrapersonal variation in gene expression. Kristen Fortney at Ouroboros writes about a recent effort by Magalhães et al to mine 27 existing microarray studies in rodents and humans for gene expression changes associated with aging. A total of 73 genes were found to be differentially expressed in relation to aging, and as Kristen notes: "Genes emerge as significant here only if they demonstrate a strong age-associated profile across a range of very different conditions (...) The advantage is that those genes (...) are likely to be the really interesting ones – components of a common aging program that operates in multiple tissues."

Okay, so this is the end of Hourglass IX; I hope you enjoyed reading! Please make sure to check out previous editions, think about contributing or hosting even - more info can be found here.

I'm going to end with a quote I found on Paul's website, the best part of which is the date, imho:

~These bodies which now we wear belong to the lower animals; our minds have already outgrown them; already we look upon them with contempt. A time will come when Science will transform them by means which we cannot conjecture, and which, even if explained to us, we could not now understand, just as the savage cannot understand electricity, magnetism, steam. Disease will be extirpated; the causes of decay will be removed; immortality will be invented~. -Winwood Reade, 1872, from his book The Martyrdom of Man