A new study from Los Angeles has shown that seniors who have a poor quality of sleep also experience depression and other negative symptoms.

Good sleep is important for everyone, but a new study shows that the necessity of quality sleep is especially crucial when it comes to seniors.  A recent study published in the Journal of the American Geriatrics Society showed that if seniors don’t sleep well each night, it could decrease their overall quality of life.

The research focused on residents of Assisted Living Facilities in Los Angeles.  The study followed up with them for 6 months and traced their sleep patterns and emotional states.  The researchers found that the 65% of seniors that reported that they slept poorly also have increased levels of depression and poor quality of life.

Of the seniors studied, sleep was about 5 hours on average.  The people also reported “trouble sleeping” as defined by the Pittsburgh Sleep Quality index. This includes waking up in the middle of the night, or taking more than 30 minutes to fall asleep.  The Pittsburgh Sleep Quality Index is a free test that measures your quality of sleep. It only takes 5 minutes to complete and can be found here.

Those who reported poor sleep in the Los Angeles study were not only more depressed but also more likely to need help with common everyday activities.  Jennifer Martin, PhD, of the University of California, Los Angeles and VA Greater Los Angeles Healthcare System stated, “We cannot conclude that poor sleep truly causes these negative changes; however, future studies should evaluate ways to improve sleep in ALFs to see if sleeping better might improve quality of life, delay functional decline and reduce risk of depression.”

The study does mention that there are effective methods for improving sleep, for example, bright light therapy.  Other methods for improving sleep include spending time outside during the day, resisting alcohol or caffeine before bed and avoiding smoking.

Sources:
medicalnewstoday.com
sleep.pitt.edu
health.com

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Researchers have regrown teeth in rats by manipulating existing stem cells: "a new technique [can] orchestrate the body's stem cells to migrate to three-dimensional scaffold that is infused with growth factor. This can yield an anatomically correct tooth in as soon as nine weeks once implanted in the mouth. ... These findings represent the first report of regeneration of anatomically shaped tooth-like structures in vivo, and by cell homing without cell delivery. ... By homing stem cells to a scaffold made of natural materials and integrated in surrounding tissue, there is no need to use harvested stem cell lines, or create a an environment outside of the body (e.g., a Petri dish) where the tooth is grown and then implanted once it has matured. The tooth instead can be grown 'orthotopically,' or in the socket where the tooth will integrate with surrounding tissue in ways that are impossible with hard metals or other materials. ... A key consideration in tooth regeneration is finding a cost-effective approach that can translate into therapies for patients who cannot afford or who aren't good candidates for dental implants. Cell-homing-based tooth regeneration may provide a tangible pathway toward clinical translation."

View the Article Under Discussion: http://www.dentistryiq.com/index/display/article-display/0045494294/articles/dentisryiq/industry/2010/05/body_s-stem_cells.html

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

From the Max Planck Institute: "Marriage is more beneficial for men than for women - at least for those who want a long life. Previous studies have shown that men with younger wives live longer. While it had long been assumed that women with younger husbands also live longer, [a new study] has shown that this is not the case. Instead, the greater the age difference from the husband, the lower the wife's life expectancy. This is the case irrespective of whether the woman is younger or older than her spouse. ... The mortality risk of a husband who is seven to nine years older than his wife is reduced by eleven percent compared to couples where both partners are the same age. Conversely, a man dies earlier when he is younger than his spouse. For years, researchers have thought that this data holds true for both sexes. They assumed an effect called 'health selection' was in play; those who select younger partners are able to do so because they are healthier and thus already have a higher life expectancy. ... These theories now have to be reconsidered. It appears that the reasons for mortality differences due to the age gap of the spouses remain unclear."

View the Article Under Discussion: http://www.demogr.mpg.de/en/press/1813.htm

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

A new technique for tissue engineering: "Tissue engineering has long held promise for building new organs to replace damaged livers, blood vessels and other body parts. However, one major obstacle is getting cells grown in a lab dish to form 3-D shapes instead of flat layers. ... To obtain single cells for tissue engineering, researchers have to first break tissue apart, using enzymes that digest the extracellular material that normally holds cells together. However, once the cells are free, it's difficult to assemble them into structures that mimic natural tissue microarchitecture. Some scientists have successfully built simple tissues such as skin, cartilage or bladder on biodegradable foam scaffolds. ... That works, but it often lacks a controlled microarchitecture. You don't get tissues with the same complexity as normal tissues. ... Researchers [have] come up with a new way to overcome that challenge, by encapsulating living cells in cubes and arranging them into 3-D structures, just as a child would construct buildings out of blocks. The new technique, dubbed 'micromasonry,' employs a gel-like material that acts like concrete, binding the cell 'bricks' together as it hardens. ... You can reproduce this in any lab. It's very simple. ... The short-term next step is really looking at different cell types and the viability of tissue growth."

View the Article Under Discussion: http://web.mit.edu/newsoffice/2010/tissue-legos-0513.html

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

Via EurekAlert: "Humans are born with 30,000 cochlear and vestibular hair cells per ear. (By contrast, one retina harbors about 120 million photoreceptors.) When a significant number of these cells are lost or damaged, hearing loss occurs. The major reason for hearing loss and certain balance disorders is that - unlike other species such as birds - humans and other mammals are unable to spontaneously regenerate these hearing cells. ... After years of lab work, researchers [have] found a way to develop mouse cells that look and act just like the animal's inner-ear hair cells - the linchpin to our sense of hearing and balance - in a petri dish. If they can further perfect the recipe to generate hair cells in the millions, it could lead to significant scientific and clinical advances along the path to curing deafness in the future. ... While researchers will ultimately need human hair cells, the mouse version is a good model for the initial phases of experimentation, he said. In addition to using mouse embryonic stem cells, the researchers used fibroblasts that had been reprogrammed to behave like stem cells: These are known as induced pluripotent stem cells, or iPS cells."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-05/sumc-at051010.php

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

From the SENS Foundation: "To date, all successful interventions into the biological aging process in experimental animals have entailed modulation of basic metabolic pathways, generally through genetic or dietary manipulation. Of these, the earliest, most well-studied, and arguably the most robust, is Calorie restriction (CR): the reduction in dietary energy intake, without compromise of essential nutrients. With few exceptions, CR retards the biological rate of aging in nearly every species and strain of organisms in which it has been tested, ranging from rotifers, through small multicellular invertebrates, and most extensively to laboratory rodents; and although inconclusive, recent evidence also supports its effectiveness in dogs and nonhuman primates. Moreover, while necessarily preliminary, a growing body of human research has reported that rigorous CR, when practiced by previously normal-weight adults, results in physiological, functional, and perhaps even structural changes consistent with its translation to the human case. ... But despite the initial attractiveness of the notion; its strong theoretical basis; the high level of scientific interest that it has garnered; the launching of biotech startups originating in CR mimetic research; and the popularization and commercial exploitation of the concept by the dietary supplement industry - despite all of these drivers, the ensuing decade and a half or more of CR mimetic research have thus far been fruitless. Initially-promising compounds have failed to extend lifespan, while surprising findings have preempted the further investigation of what might otherwise have been novel targets for CR mimetics."

View the Article Under Discussion: http://www.sens.org/node/777

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

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/