Longevity News Digest
How to Keep œStuff from Aging You
Â Dear Future Centenarian,Â
Did you ever start a day where everything was carefully planned? Where you had each hour allocated to get everything done that needed to get done¦ only to see it all unravel in no time with your first unexpected interruption?
What? You say this is your NORMAL day?
It is for most of us. The culprit is always¦ STUFF.
Look what happened to me the other day for example:
I was reviewing my bills and noticed FedEx charged me $189 for a 3rdÂ day delivery letter. Then almost simultaneously, my inflatable wheelchair cushion sprung a leak. This rarely happens, but when it does, finding and then patching it is tedious and time-consuming.
Â œFor the want of a nail¦ One little nail “ and POOF “ a perfectly good kingdom.
Maybe your stuff won™t topple states, but it sure can blow your day. And it usually goes on day-after-day.
Where distractions like this used to throw me off balance, I just got my back-up cushion, and made myself a note to make the three phone calls needed to take care of these items. Then I assigned these tasks along with a few more that accumulated that day into a designated time slot.
Why bring this up in a longevity newsletter? Simple.
Stuff undermines our health and longevity. We may not be dodging saber-toothed tigers anymore, but contemporary stuff can be just as deadly.
Didn™t you ever miss workouts because something popped up at the last minute that just had to get done? How about the times you grabbed some fast food because you œjust didn™t have time to go to the organic food market¦ or even to eat at a decent restaurant that serves healthier meals?
When was the last time you went sleep deprived because you had to get some stuff done before morning?
And finally, stuff heaps stress on you¦ UNLESS¦ you know how to manage it. The best way to stop it from interrupting your schedule flow is to schedule time for the unknown stuff you know is headed your way.
Expect the unexpected. Hardly a day goes by without some. Instead of being surprised and frustrated by it, get used to it and learn to accept it by now. Find a midday or day-end time slot for these unavoidable parts of life.
Except for the occasional emergencies, just dump the rest of it into that slot and tend to it all at once in its own time. If you don™t allocate time for it, it has to steal time from something else.
Not planning for and managing interruptions is why we let stuff knock us out of our flow.
Â If you don™t control your stuff, it will control you.
Â More Life,
Â Latest Headlines from Fight Aging!
Larger Animals and Cancer RatesÂ - Monday, July 21, 2014
Larger animals have more cells in their bodies, and cancer occurs when one cell suffers the right combination of mutations to run amok, so why is it that animals such as whales do not have higher cancer rates? Here researchers propose a partial answer to that question.
Â Acquired Inheritance in Response to StarvationÂ - Monday, July 21, 2014
In recent years researchers have discovered that the metabolic response to calorie restriction can extend into following generations, passed along via epigenetic and other mechanisms.
Â The metabolism of descendant individuals is altered from the norm even when they never experience calorie restriction themselves. Data on this effect is harder to establish for humans in comparison to short-lived laboratory species, but it does exist.
Â Mechanisms Linking Peridontitis and AtherosclerosisÂ - Tuesday, July 22, 2014
Chronic infection and inflammation of the gums, peridontitis, is associated with increased risk of atherosclerosis, a clogging of the arteries.
Â This is because inflammation spreads beyond the mouth, and the process of inflammation in artery walls over the long term contributes to the production of plaques of dead cells and metabolic waste. Here researchers look into the details of this link between the two conditions.
Â Telomere Length is ComplicatedÂ - Tuesday, July 22, 2014
Telomeres are lengths of repeated short DNA sequences that cap the ends of chromosomes. The process of cell division shortens telomeres, and they form a part of the cell division counter that gives most somatic cells an expiration date after which they cease dividing. Telomeres are lengthened by the activity of the enzyme telomerase, which is more active in some cells than others - such as in stem cells, which need long telomeres so that they can divide to produce fresh new long-telomere somatic cells to keep tissues healthy and well-maintained.
Â When researchers measure telomere length in some specific group of cells, they are taking a snapshot of the blurred results of numerous processes in many cells, such as telomerase activity and pace of cell replacement by stem cells, that are themselves affected by near every aspect of health and environment.
Â The most common measure of average telomere length in white blood cells is very dynamic, for example, rising and falling based on day to day health, even though over a lifetime it tends to decrease. But simple measures of average length tend not to capture these effects well, and the precise details of how a telomere length snapshot is taken make the difference between a result that is meaningless, and has no correlation to health, and a result that does tend to correlate with age, health, and future life expectancy.
Â So we have results like this one in which researchers run a rigorous study and find no correlation whatsoever between telomere length and mortality risk. You can compare that with animal studies that used a variety of techniques for telomere measurement and number crunching, such as proportion of very short telomeres versus average length, that do show good correlations with life expectancy and health.
Â The sum of all this seems to me that rushing out to have your telomere length measured by one of the new services started in recent years is premature.
Â Speculating on a Viral Cause of Parkinson's DiseaseÂ - Wednesday, July 23, 2014Â
Parkinson's disease is characterized by the progressive loss of a small population of dopamine-generating neurons in the brain.
Â This loss happens to everyone, but progresses much faster and further in Parkinson's sufferers, for reasons that are still not fully understood. Here is a speculative paper in which researchers suggest that there are viral and autoimmune mechanisms at work.
Â More Physically Aged People Have a Lower Life ExpectancyÂ - Wednesday, July 23, 2014
Aging is no more than damage at the level of cells and tissues and the evolved reactions of biological systems to that damage, not all of them helpful.
Â The pace of damage accumulation is largely determined by lifestyle and environmental factors such as burden of infectious disease and available medical technology over most of a human life span. Only in very old age do common genetic differences rise in importance. Thus if you find that someone at a given chronological age is more frail and is suffering from more evident age-related conditions than their peers, you would expect them to have a shorter remaining life expectancy, since they are more damaged. That is the way it works.
Â Immune Surveillance of Mitochondrial DNA Deletions?Â - Thursday, July 24, 2014
Regular readers will know that mitochondrial DNA damage is thought to be an important contributing cause of aging. It can lead to dysfunctional mitochondria that overtake cells and turn them into exporters of damaging reactive compounds, harming both surrounding tissues and important proteins that circulate widely in the body.
Â This is a fascinating paper that suggests the immune system has evolved to detect the presence of mitochondrial DNA deletions and destroy the cells that harbor those damaged mitochondria.
Â Assuming this holds up there are several ways one could interpret this mechanism: firstly that mitochondrial DNA damage is less important than thought because there are more processes controlling it; or secondly that it is more important because it will lead to increased inflammation and immune system activation, which is a serious issue in later life; and either way thirdly that the age-related decline of the immune system should be considered more important because here is yet another fundamental aspect of aging that it influences.
Advocacy for Longevity Science Can Take Many FormsÂ - Thursday, July 24, 2014
Advocacy for the cause of longevity science doesn't have to mean writing or getting up in front of people to give presentations. There are many ways in which you can go about changing the way in which the rest of the world thinks about aging, so as to grow support for rejuvenation research.
Here, for example, delivery of the message is via a simple game about achieving actuarial escape velocity, the point past which advances in medical science add more than one year of additional future life expectancy for each year that passes, thus enabling indefinite healthy life spans.
Â At the moment the present approach to medicine produces a gain of one year every decade in life expectancy at 60, so there is a great deal of work yet to accomplish. That work will only happen rapidly enough to benefit most of those reading this today in an environment of widespread public understanding and support, but that doesn't exist yet either. Hence the need for advocacy.
Â Stemness of Central Memory T CellsÂ - Friday, July 25, 2014
This research suggests that some aspects of re-engineering an age-damaged immune system to restore its performance may be easier than expected. It is also supportive of work on immune cell transplant therapies as cancer treatments that has taken place over the past few years, as well as a range of other existing and potential immune therapies.
Â Restoring Function in Spinal Cord InjuryÂ - Friday, July 25, 2014
Researchers are making progress on a variety of ways to encourage nerve regrowth in mammals where it normally doesn't occur, such as in the aftermath of spinal injuries.
Â DISCLAIMER:Â News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please seeÂ www.fightaging.org/
Â David A. Kekich
Maximum Life Foundation
Â "Where Biotech, Infotech and Nanotech
Â Â Â Â Meet to Reverse Aging by 2033"