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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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