Here are a few recent longevity news tidbits derived from studies published in geriatrics journals. Two of the news reports confuse cause and effect and project a probably-incorrect message.
· Seniors can use computerized brain exercises to improve their memory and ability to think faster(ref). My comment is sure, and the best computer brain exercise for me is researching how to live a lot longer.
· The news article in the Tehran Times is entitled Daily naps may raise older women’s death risk. ‘White women who took a daily siesta were 44 percent more likely to die from any cause, 58 percent more prone to dying from heart problems, and nearly 60 percent more likely to die from non-cardiovascular or non-cancer causes.(ref)’ However, I point out that people who are quite sick may take more naps than those who are healthy. So, napping itself may not cause increased mortality but may be the result of mortality-inducing illnesses.
· Specific personality traits are associated with children of centenarians and their longevity including low neuroticism, high extraversion and high agreeableness. Apparently these traits enable much better management of stress(ref). My comment is yes and that these characteristics are not only inherited but to some extent can be learned even by us old folks.
· The news item is entitled Keep Hold of Those Car Keys: Driving May Be Good for Your Health. A study in Florida of 660 older people, aged aged 63 to 97, showed that people who kept driving were four to six times more likely to still be alive after a three-year period than their counterparts who stopped driving(ref). I comment again that it is important not to confuse cause with effect. Most of the people who stopped driving were probably a lot sicker to start with than those who kept driving. Stopping driving itself was probably the effect of sicknesses and not the cause of the increased mortality.
Hi Vince
See this link
http://www.redorbit.com/news/science/108380/p16_and_arf_activation_of_teenage_proteins_in_old_age/
what is P16 and ARF? Can you throw some light on these ?
Res: P16/INK4a is sometimes called a tumour suppressor pathway. It plays a key role along with ARF in the initiation and maintenance of cellular senescence. And as the reference you cited points out, P16/INK4a and ARF tend to be upregulated with aging. P16(INK4a) leads to cell cycle arrest and senescence, not apoptosis. From an anti-aging viewpoint having more of it around with advancing age is a mixed blessing in that 1. increasing amounts of it can halt damaged cells from turning cancerous by accelerating premalignant cells becoming senescent and 2. at the same time it inhibits the differentition of somatic stem cells thereby inhibiting tissue renewal. Some think increasing amounts of P16(INK4a)have a lot to do with accelerating aging through turning off stem cell tissue renewal. If you go to my Anti-Aging Firewalls treatise and search on the page for P16 you will find multiple mentions of it and its actions. The treatise is at http://www.vincegiuliano.name/Antiagingfirewalls.htm
As the article you cited points out, much is to be learned about what promotes the expression of P16/INK4a, particularly its relationship to telomere lengths and what are the effects of telomerase activation if any on expression of P16/INK4a? These topics are high on my research watch-list.