Younger Every Year

Reuters - New prescription drug coverage in the
federal Medicare insurance plan for the elderly drove a boost
in use of pricey brand-name drugs such as statins and ulcer
medications, an analysis released on Tuesday said.

Original post by stephend

We go through life sometimes focusing on some goal, some prize, some future payoff. Maybe it’s a new job at a new company, or moving from an apartment to a condo or home. Maybe it’s not having to deal with a car that always seems to be in need of repair. Or finding a good “healthy” relationship with someone, or repairing an old relationship gone awry. We often seemed focused on the future, planning for the next big thing.
Things are okay with me these days
Got a good job, got a good office
Got a new wife, got a new life
– Billy Joel
When we do this, all too often we miss what we do have, what is right in front of us. We want the new car, the new job, the new life, and don’t give thanks or appreciate the old car, the old job, or the old life.
Every year, we have our annual “Yankee Homecoming” in Newburyport, Mass. It’s an annual festival celebrating the natives coming home to Newburyport. The event was initiated in 1957 by Newburyport native, George Cashman, reportedly to stimulate the economy and lift the spirits of the townspeople. Nowadays the festival encompasses an entire week of arts and crafts people in their booths, good food, and live music. It fills some of the main streets of the tiny little town with bustling activity, thousands of people, and a very good spirit.
Walking through the town today, I couldn’t help but appreciate all of the craftsmanship that goes into so much artistic expression, through jewelry, painting, photography, carvings, clothing and more. There are just so many artistic people out there, so many people with real skill and talent, who create some really interesting items.
Breathing in the fresh summer seaside air and feeling the sun on my face while walking on my two good feet and using my two good eyes, ears, and my one good nose to take in all of the sights and sounds of today’s festival, I just had to stop for a moment and stop worrying about all of the future things I have little or no control over. I had to stop myself from wanting this or that, or thinking I needed something more than I had at just that moment.
I just was, for a moment in time, simply another living being in the middle of the world. Enjoying life for a minute. And not wanting something else.
They say if all you have is your health, you have it all. I have my health and then some, but if we don’t stop to appreciate the things we do have in our lives, our lives will be over before we know it. All of that wanting something else, something more will be for naught.
It’s hard, I can’t stop myself from wanting more, from wanting to make things better here or do that something there. But once in a while we need to stop ourselves, take a deep breath, and just live.
Even if it’s just for a moment. (Source: World of Psychology)

Original post by World of Psychology

An interesting paper on aging in bacteria illustrates some of the present thinking on the evolutionary roots of aging; in this case, that aging seems to be an inevitable consequence of the cellular model of life.

Experimental evolution of aging in a bacterium:

Aging refers to a decline in reproduction and survival with increasing age. According to evolutionary theory, aging evolves because selection late in life is weak and mutations exist whose deleterious effects manifest only late in life. Whether the assumptions behind this theory are fulfilled in all organisms, and whether all organisms age, has not been clear. We tested the generality of this theory by experimental evolution with Caulobacter crescentus, a bacterium whose asymmetric division allows mother and daughter to be distinguished.

…

Our results confirm that late-acting deleterious mutations do occur in bacteria and that they can invade populations when selection late in life is weak. They suggest that very few organisms - perhaps none - can avoid the accumulation of such mutations over evolutionary time, and thus that aging is probably a fundamental property of all cellular organisms.

Inevitable until that cellular life becomes smart enough to develop medicine and learn how to repair itself sufficiently well, in any case. That time is just around the corner.

You might recall that aging in bacteria was demonstrated back in 2005; previously it was thought that bacteria might be effectively immortal. This hypothesis of aging as an inevitable consequence of evolution in cellular life versus present studies of those forms of cellular life that might be immortal will make for good science in the decades ahead - but it is largely irrelevant as to how aging in humans proceeds from here on out. Evolution’s days are all but over, and the invisible hand of the market will take over as technology enables individual humans to shape themselves rather than be shaped.

When people can choose between degenerative aging or no degenerative aging, I imagine there won’t be a great deal of degenerative aging in the world - much the same as for the smallpox/no smallpox choice that became available in recent times, for example.

Technorati tags: aging, evolution (Source: Fight Aging!)

Original post by Fight Aging!

by Dov MichaeliSometimes revolutionary developments come out of the most unexpected corners. There is new branch is medical research called regenerative medicine. The “old” way of treating disease (which we are still practicing today) is through drugs that treat the consequences of the disease. For instance, anti-inflammatory drugs to treat arthritis, or statins to lower cholesterol through inhibition of its synthesis, or chemotherapeutic drugs to kill tumor cells. The bold vision of investigators in the regenerative medicine field is to simply replace the ailing organ with a healthy one. I am not talking about transplantation; I am talking about stem cells that can be programmed to replace an injured muscle, a severed spinal cord, or damaged pancreatic beta cells that can no longer synthesize insulin. This is a breathtaking paradigm shift that promises to revolutionize the way medicine will be practiced in the not so distant future.  Out of left field As our attention was riveted on “the big stuff” of stem cells, a barely noticed report, published in the February issue of The Archives of Dermatology (vol. 143, pp. 155-163, 2007), looked at the mode of action of a dermal filler used in cosmetic medicine to treat facial wrinkles. The report, by a group from the department of Dermatology at the University of Michigan, showed that contrary to the belief that the material (Restylane is made up of a substance called cross-linked hyaluronic acid) acted simply by physical expansion of the skin volume, it actually had a biological effect.  What is a wrinkle? The skin is made up of a thin outer layer of cells called epidermis, and a much thicker layer called dermis. The bulk of the dermis is composed of a protein called collagen, as well as smaller amount jelly-like materials, hyaluronic acid being one of them. Collagen is synthesized by special skin cells called fibroblasts. In a young person the fibroblasts have a stretched appearance and secrete copious amounts of the collagen, enough to make up for the continuous degradation of skin collagen by an enzyme called collagenase. In older people the fibroblasts become more relaxed and rounded, and secrete less collagen, not enough to counteract the losses due to the degradation by collagenase. Slowly but surely, enough collagen is removed, the dermal structure collapses, and we get the dreaded wrinkles. What the investigators found is that the hyaluronic acid in Restylane caused the re-stretching of the fibroblasts, causing them to increase their synthesis of collagen. As a bonus, the material also reduced the activity of the enzyme collagenase. The key to achieving this effect was the repeated injection of the material, 6-12 months apart, until enough stretching of the fibroblasts took place. How long would this effect last? This is still unknown, but the thought is that as long as the injected material is present the fibroblasts would remain stretched and synthesize more collagen.  Why is it exciting? First, if confirmed, it promises to make us look young forever, or at least as long as we live. Isn’t that what all aging boomers look for?  But more importantly, here is the first realization of the regenerative medicine dream: use of the body’s own cells to regenerate damaged organs. I love this study, because out of the limelight of the titanic stem cell struggles a relatively unknown group of dermatologists found a simple, and vastly more practical solution then stem cells to rejuvenation the sagging skin—simply stretch the old fibroblasts.   The study used Restylane only because it was started before a similar product, Juvéderm, was available. In my estimation, both products should work equally well; but the proof will require another study. Here is another interesting aspect of progress in medicine. The material was originally intended as a physical filler; nobody had any grandiose thoughts about profound biological effects. After all, collagen itself was used as a filler to treat wrinkles, and indeed that is all it was—a filler, which degraded with time. Hyaluronic acid, quite unexpectedly, opened new avenues for research in tissue regeneration. Would we be able soon to grow pre-existing brain neurons in Parkinson’s or Alzheimer’s patients by simply injecting ‘brain filling material’? If you asked this question a few months ago you’d be laughed out of the room. It is now totally plausible. Isn’t that exciting? Dov Michaeli MD Ph.D. is in the biotech industry, engaged in drug development. (Source: The Doctor Weighs In)

Original post by The Doctor Weighs In

Dave B and Alvaro have had an interesting (albeit, brief) discussion in their comments about the subject of the hypothetical “cognitive reserve” that stands between each one of us, and the timing of the onset of Alzheimer’s Disease (AD).
First, Dave B said that while he saw ample evidence that most cognitively capable (”highly educated”) individuals that were in his studies at Medical College of Georgia seemed to be far removed from any danger of AD in their immediate future (in strong contrast to individuals in his studies who were poorly educated, and/or were less cognitively active), he saw no clear evidence in the literature that convincingly demonstrated that the onset of Alzheimer’s Disease could be delayed by cognitive training or enrichment.
Alvaro questioned this conclusion by citing studies (there are about a hundred in the literature) that first argued, about a decade ago, that individuals who were more cognitively active were protected by a greater “cognitive reserve” that gave them more protection from an end-of-life collapse into AD than was afforded to cognitively-dormant individuals.
Dave B countered by noting that such claims are generally plagued by the old chicken vs egg problem: Does your larger “cognitive reserve” merely reflect the co-inheritance of a neurology that generally assures that you’re a) with it, and b) you won’t develop AD — and that to the inexorable extent that you sustain or lose ‘a’, you can count on also sustaining or losing ‘b’? That being full of fun and playing lots of games and dancing and seeing the world and developing lots of new fun hobbies and reading like a bandit and doing your sudoku and crossword and jigsaw puzzles and still having fun in life is just exactly the kind of thing that an individual who is very unlikely to develop AD is inclined to do, whether they like it or not?!! He might also have noted that by the usual interpretation of “cognitive reserve”, having a big one does NOT protect you from the onset of Alzheimer’s pathology. To the contrary, it means that the pathology has to progress over a longer period before you meet the behavioral criteria for receiving the Alzheimer’s label. You’ve GOT the pathology. You just have more memory and cognitive ability to lose before anyone notices!
This question of whether brain fitness exercises of the best sort delays the onset of the pathology itself is difficult (and very expensive) to answer, and no “gold standard” study has yet been conducted that provides an unequivocal confirmation that this can be achieved. We have initiated a large study that will ultimately answer this question, but it shall take months to complete it. What ARE we certain of, at this point in time?
1) The cognitive performance abilities (memory, reasoning, fluency, et alia) of most of us (the average individual) peak(s) in the third decade of life, and declines systematically and continuously from that early young-adult epoch, forward to the end of life.
2) The average more-cognitively-competent 25-year-old has a longer path, in forward years, before they cross a performance threshold that would put them measurably “at risk” for AD onset. In this sense, most more-cognitive-competent individuals (irregardless of their formal education) have greater “cognitive reserve”, and a lower probability of collapsing into AD than do less-cognitively-competent individuals, through each passing decade.
3) A cognitively competent youngster can sustain their “edge” (cognitive reserve) by leading an active, rich, mentally-challenging life. If you’re quick of wit and thought and action as a young woman or man, and you stay mentally active and agile in maturity, you’re probably still sitting on a pretty good cognitive reserve!
4) With appropriately designed “brain fitness exercises” like those produced by Posit Science, it is possible to significantly improve one’s cognitive performance abilities, at any age. Such improvements presumably bucks up your “cognitive reserve”, irregardless of the level of protection that you are carrying forward from earlier life, at the time you initiate traing. You’re hypothetically safer, because after training, you have correspondingly farther to decline before your measured performance abilities label you as “at risk” for, or in the clutches of AD.
5) Our collaborators at UCSF, UC Davis and Stanford have tracked the maintenance of such improvements in MCI patients who are at risk for AD onset, and have shown that Posit Science Brain Fitness Program-trained patients are a) can substantially improve their standing, by standard assessment criteria, within this high-risk category; and b) that trained patients sustain their BFP-driven improvements in memory and cognition without further training, over a period of at least several months. Again, we hypothesize that these gains provide them with a greater, on-the-spot “cognitive reserve”, i.e., can be expected to delay symptomatic AD onset.
6) If useful training is not discontinued (as it was in the UCSF/UCD/Stanford study), it should be possible to drive the cognitive abilities of the average older individual a long distance in the direction of ‘greater safety’ (greater ‘cognitive reserve’).
7) In animals, appropriate training CAN substantially delay the onset of the Alzheimer’s pathology itself. It is highly likely that this shall also be true in human populations. We now have markers for pathology in living humans that makes it possible for us to directly determine if this is or is not the case. It shall take a little time, but before too long we’ll know the answer to this key question.
In the meantime, keep working on your “cognitive reserve”, because training-driven improvements can certainly delay your loss of function, and may well save your bacon!
Dave B indicates that if such exercises actually DO delay the onset of AD pathology, then we must consider how they could conceivably delay the hundred-and-and-one complex pathological sequelae that characterize the disease. I agree. That is why the growing number of studies arguing that AD pathology can be delayed by providing animal models in which AD shall develop with “rich environments” are so important. Dave seems to suggest that because there are several hundred aspects of change that affect the older brain as it collapses into AD, it may be impossible to explain how a little brain fitness training can delay them.
I don’t agree, David. It is possible that even a single fundamental change of the right sort (e.g., a slow loss of the ability of the forebrain to produce and release acetylcholine, which shall degrade the brain’s abilty to learn and remember, shall radically alter the dynamics of blood perfusion coupled to brain activity, and can trigger widespread consequences for brain metabolism, homeostasis and immune responses) would have a MYRIAD of pathological consequences. There are several scenarios that might provide that important basis for linking a an unhealthy, unfit brain to those pathological processes that we collectively describe as AD. This particular aspect of the science of aging research has been almost completely neglected. I know that DaveB has the talent and skills to make real progress in this area. As your studies progress, David, keep us all in the know about what you are discovering about this key scientific issue! (Source: On the Brain by Dr. Michael Merzenich, Ph.D.)

Original post by On the Brain by Dr. Michael Merzenich, Ph.D.

I’m in Jacksonville, Florida today, participating in what is a very unusual and special event –– “The Jacksonville Brain Summit”. In an earlier entry, I told you that Jacksonville has adopted a leadership position in their use of the most advanced brain-science-based strategies to improve the academic performance and the mature working skills and performance abilities of its citizenry. There efforts have been inspired by a combination of great leadership and vision from the administration and on the School Board of the Jacksonville public schools, combined with exceptionally strong support from informed leaders in the wider community. This school district (the 19th largest in the US, extending from dense urban through extensive suburban to rural areas across one of the largest territories of any American school district), and this community have made a collective decision to improve their standing in the US and in the world in the most straightforward way in which that can be achieved: by improving the brainpower of its kids and working citizens. A visionary school superintendent (Dr. Joey Wise) and other school and business leaders recognize that one of the keys to improving their city lies with improving the skills and achievements of its greatest resource: the citizens that comprise its diverse community populations. What is exceptional about the Jacksonville effort is the extension and involvement of individuals in this effort far beyond the schoolhouse walls.
“The Jacksonville Brain Summit” was a step designed to further ducate it’s teachers, school administrators, special education professionals and adult education specialists – along with key leaders and influencers in the Northeast Florida region —– about the scientific bases, and the potentially great values of applying brain science-based training strategies to help ALL children and MANY adults in their community increase their learning rates and capacities. The enthusiasm and energy and collective good spirits expressed by the several thousand participants in this 2-day meeting was inspiring. They once again revealed that can-do and determined-to-help attitude that infects the best teachers and administrators, and that permeates every great school and every healthy community in America. Every teacher, every administrator, every good parent, every good citizen WANTS TO HELP the kids in their community rise up in their achievements and goals, far above their current standards. There are few large school districts as committed to this ideal, and as well prepared to achieve it, as Jacksonville, Florida.
You watch along, America. I’m going to help you track the improvements in the student population and in the community of Jacksonville, as they unfold over the next several years. Expect a report on their progress every several months. As I said in my last entry on this subject (and I am now more certain about it than ever), you are going to see this energetic city leapfrog, in educational achievement, right over other comparable cities in the US! (Source: On the Brain by Dr. Michael Merzenich, Ph.D.)

Original post by On the Brain by Dr. Michael Merzenich, Ph.D.

The presence of fish oils reduces the conversion of vegetable oils into inflammation-causing prostanoids. Scientists have provided new evidence that using more fish oil than vegetable oil in the diet… (Source: FuturePundit)

Original post by FuturePundit

Original post by stephend

Your stem cells grow old. Stuart Chambers, Margaret Goodell, and their colleagues investigated the molecular mechanisms underlying aging of stem cells by looking at the gene expression profiles of aging… (Source: FuturePundit)

Original post by FuturePundit

I hear Joe Jackson singing: Everything Everything gives you cancer Everything Everything gives you cancer Theres no cure, theres no answer Everything gives you cancer You want benefits without costs?… (Source: FuturePundit)

Original post by FuturePundit