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Hourglass #3: the biology of aging

Wel­come to the third edi­tion of Hour­glass, the month­ly vir­tu­al gath­er­ing of blog­gers to Hourglassdis­cuss the Biol­o­gy of Aging.

For today’s edi­tion, let’s imag­ine all par­tic­i­pants sit­ting around a table lead­ing a live­ly Ques­tions & Answers ses­sion, dis­cussing as a group, lis­ten­ing, talk­ing. (And, well, aging.)

Q: What is aging?
Ms. Wikipedia: “Age­ing or aging (Amer­i­can Eng­lish) is the accu­mu­la­tion of changes in an organ­ism or object over time. Age­ing in humans refers to a mul­ti­di­men­sion­al process of phys­i­cal, psy­cho­log­i­cal, and social change. Some dimen­sions of age­ing grow and expand over time, while oth­ers decline. Reac­tion time, for exam­ple, may slow with age, while knowl­edge of world events and wis­dom may expand.”

Aging may not be the sex­i­est  of words in our vocab­u­lary. Unless, of course (as I heard some­where recent­ly but can’t prop­er­ly cred­it), you con­sid­er the most com­mon alter­na­tive.

Q: If the objec­tive of anti-aging research is to extend lifes­pan, isn’t there a risk that we may neglect qual­i­ty of life. After all, would peo­ple real­ly like to spend more years afflict­ed by the dis­eases and the decline that often come with age?
Ed (dragged to the dis­cus­sion by Chris and Alvaro): I have rel­a­tive­ly good news to share. A recent Uni­ver­si­ty of South­ern Den­mark found that the pro­por­tion of elder­ly Danes who man­age to remain inde­pen­dent holds steady at about 30–35 per­cent between the ages of 90 to 100. This means that from soci­ety’s point of view, excep­tion­al long-life won’t lead to excep­tion­al lev­els of dis­abil­i­ty. This pat­tern seems con­sis­tant across dif­fer­ent lifes­pans.

Q: OK, so at least it is not all doom and gloom. Now, can we real­ly expect we will one day be able to extend not only mean but max­i­mum lifes­pan?
Chris: well, poten­tial­ly yes, but first of all we need to bet­ter  under­stand how pre­ma­ture aging resem­bles extend­ed longevi­ty, and the source of tran­scrip­tion­al change as we age, to mea­sure bio­log­i­cal age in a mean­ing­ful way. Giv­en the obser­va­tion that expres­sion of gene X (or hor­mone Z) changes with age, one must next ask: How do we know whether this change reflects a causative fea­ture of aging, a defen­sive response to anoth­er age-relat­ed change, a pas­sive response of no great import, an epiphe­nom­e­non, or an arti­fact of the exper­i­men­tal sys­tem?.

Q: Let’s now dis­cuss the con­cept of “lifes­pan plas­tic­i­ty” and the sta­tus of the research today.
Jake (dragged too): Research on lab organ­isms such as yeast, worms and mice has encour­aged the notion that lifes­pan is plas­tic-this is, it can be extend­ed. Nature just pub­lished a great review of anti-aging sci­ence, com­bin­ing cau­tious opti­mism with a call not to head down too quick­ly to the Nat­ur­al med­i­cine store for resver­a­trol in a pill, for exam­ple. Caloric-restric­tion, and some com­pounds, seem to influ­ence path­ways that reg­u­late over­all metab­o­lism, and have an impact on lifes­pan. How­ev­er, none of the drugs test­ed have shown length­en life span in healthy rodents much less humans. we also don’t know whether inhibit­ing pro-aging path­ways in humans will have the same effect that it has in low­er organ­isms. Fur­ther, we still have to fig­ure out how to dis­tin­guish between dis­ease and what is called intrin­sic aging — or aging not caused by dis­ease.

Q: In short, there is much poten­tial, but more research needs to be done. Now, does exist­ing research sup­port spe­cif­ic inter­ven­tion to expand Healthspan (not just lifes­pan, but lifes­pan in a healthy con­di­tion).
Ward: Exer­cise is an obvi­ous first step. A num­ber of stud­ies have shown how con­sis­tent car­dio­vas­cu­lar exer­cise can have mod­est effects on mean lifes­pan (usu­al­ly in the 8–12%) and also help main­tain func­tion­al abil­i­ty, there­fore con­tribut­ing to longer healthspan.

Q: We should also con­sid­er our Brain Healthspan. After all, “we” are a func­tion of our brains. Any­thing we can do there?
Adri­an: exer­cise helps there too, both by help­ing main­tain cog­ni­tive func­tion and by pro­mot­ing neu­ro­ge­n­e­sis and neu­ron sur­vival.
Alvaro: the brain reserve the­o­ry adds light on the impor­tance of life­long men­tal stim­u­la­tion, but still need to bet­ter under­tand  the neu­ro­bi­ol­o­gy of aging and cog­ni­tive decline. Let’s take a look at some of San­ti­a­go Ramon y Cajal’s rec­ol­lec­tions of his life. On the one hand, was aware of the poten­tial for life­long neu­ro­plas­tic­i­ty. On the oth­er, he could do lit­tle to pre­vent his own cog­ni­tive decline.

Q: Can food also play a role in main­tain­ing brain health as we age?
Pas­cale: For a great in-depth review of the effects of food on the brain you can check out Fer­nan­do Gomez-Pinil­la’s recent arti­cle in Nature Reviews Neu­ro­science, dis­cussing the respec­tive mer­its of Omega‑3 fat­ty acids, folic acid , flavonoids, antiox­i­dant foods. Please note that most of the stud­ies show­ing pos­i­tive effects of these nutri­ents have been con­duct­ed in mice.

Q: Let’s go back to the con­cept of expand­ing Healthspan. Are there pub­lic health impli­ca­tions
Liz: I’d say pre­vent­ing falls among the elder­ly — falls are a lead­ing cause of seri­ous injury and death among the U.S. elder­ly. Juer­gen Blu­dau, chief geri­a­tri­cian at the Brigham and Wom­ens Hos­pi­tal, says the med­ical com­mu­ni­ty needs to do a bet­ter job sup­port qual­i­ty of life, by which he meant two things: as much free­dom from the rav­ages of dis­ease as pos­si­ble, and the reten­tion of enough func­tion for active engage­ment in the world.

Q: Let’s explore future direc­tions for research in the area. What’s the recent deal with autophagy?
Rea­son: You might think of autophagy as a form of self-main­te­nance for your cells: it is the destruc­tion of dam­aged and old­er cel­lu­lar com­po­nents such that new­ly built com­po­nents can take their place. You may expect to see some autophagy-enhanc­ing drugs appear in the next years, once we bet­ter under­stand, for exam­ple, how to manip­u­late the tumor sup­pres­sor pro­tein p53, which has a major impact on organ­is­mal aging.

Q: Oth­er inter­est­ing areas?
Abel: I’d sug­gest pay atten­tion to the prop­er­ties of mus­ca­dine skin extract . Some com­pa­nies are in fact already sell­ing those as dietary sup­ple­ments (i.e., prod­ucts not eval­u­at­ed by the FDA for either effec­tive­ness or safe­ty), despite weak evi­dence.
Lau­ra: we also need to pay more atten­tion to neu­rode­gen­er­a­tive dis­or­der such as Mul­ti­ple Sys­tem Atro­phy (MSA), a rare spo­radic dis­ease with aver­age age of onset at 59 years (+/- 7), and aver­age dura­tion being 7 years.

Q: Fun discussion…but we need to wrap up now. Any vol­un­teer to pro­vide some final words of wis­dom before we go back to our busy dai­ly lives?
Anne: Let’s remem­ber, Exis­tence is won­der­ful. I look for­ward to learn­ing more of what such crea­tures as mole-rats and echid­nas may be able to teach us about them­selves, about aging, and about the curi­ous inter­play between metab­o­lism, chem­istry, activ­i­ty, and all the oth­er process­es that make life pos­si­ble.

Thank you all for your par­tic­i­pa­tion. Please remem­ber that Hour­glass IV will appear on Octo­ber 14th at Exis­tence is Won­der­ful.

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8 Responses

  1. The Hour­glass group blog is a great IDEA lab and Sharp­brains remains the best to go site on all things brainy. How about bios and web­sites of the blog­gers involved?

  2. Hel­lo M.A., that’s a great sug­ges­tion. Chris at Ouroboros is the orga­niz­er behind Hour­glass, so why don’t you reach out to him to dis­cuss options?

  3. marla says:

    Isn’t the cur­rent­ly-avail­able sup­ple­ment called Juvenon an autophagy-enhanc­ing drug?

    I’d love to see more info on Juvenon on your site. Juvenon seems legit­i­mate, but I’m skep­ti­cal.

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