Longevity News Digest
How to Avoid Aging
Dear Future Centenarian,
If you’re like me, you hate the toll aging takes on you.
I hate not seeing and hearing as well as I used to. I hate the fact that aging erodes our immune systems. It slows our brains down, weakens us and shortens our lives, etc, etc, etc.
Do you look as good as you used to? Unfortunately, what you see in the mirror reflects what’s going on internally.
I looked at some women’s profiles ranging from those in their 20’s to 70’s on a dating website the other day, and harsh truths hit home.
Allowing for the fudge factor of some of the posted ages being understated and some photos being not so current, I was able to instantly guess nearly all their ages with amazing accuracy.
Here’s the reality:
As we age, we surely and steadily deteriorate. Without strong intervention, you probably look and feel better now than you EVER will. That probably explains why instead of checking me out, no matter how well I take care of myself, I™m transparent to the young babes. Part of the background noise at best.
I hope I got your attention with all this sobering reality, because if I haven™t chased you away with it, good news of rosy youthful futures for many of us is next.
I™ve said it before, and I™ll keep reminding you. For the first time in history, we™re on the path to conquer aging. That means, you may be part of the first generation to never die from anything aging-related.
In fact, it means more.
Not just avoiding dying from aging¦ but rejuvenation. That means one of these days you would have an excellent chance to be fully rejuvenated. Imagine resetting your biological clock to 25 (for example).
If so, you would not only look and function as well as you did at 25¦ but better. (More on that in another letter.)
So the bottom line is, you have a lot at stake in living to see these breakthroughs. And no one has as much control over your survival (and open-ended youthfulness) as YOU do.
How important is this to you?
Important enough to do the following? Actions speak louder than words, so your children shall see.
If you don™t think about this every day, you have other priorities. That™s OK. I™m not here to push anyone to do anything they don™t want to do. I am here to help those eager to live long, strong and well.
So here goes:
Priority #1 is replacing your life-shortening habits with life-extending habits. I boiled strategies the down and wrote extensively about them in Smart, Strong and Sexy at 100. We™re seeing more and more good books on that subject all the time too.
If you™re not financially stable already, do what you can to ensure stability with enough savings to be able to travel offshore for elective life-extending medical treatment when available if necessary, or to get it in your country if it™s approved.
If you have discretionary wealth, invest in some of the more promising longevity technologies and companies. After all, your life hangs in the balance.
If you’re not an investor, donate annually to SENS Research Foundation. www.sens.org Why SENS? Because the aging-repair research they support will be the ONLY chance for rejuvenation for many of us to survive long enough to see the day when our biochemical complexities are understood well enough to control aging.
Join Alcor Life Extension Foundation to arrange for cryonic suspension. That way, if you’re part of the last generation to die from aging, or if a fatal accident victimizes you, you might be revived and repaired in the future. Both my parents are cryonically suspended, and I hope to be reunited with them one day.
Meanwhile, you’re not going to be able to avoid aging until some emerging technologies mature.
But you may very well be able to survive aging until they mature. And survive it in good health with vitality.
Latest Headlines from Fight Aging!
A Demonstration of Tissue Engineering Nerve Grafts – Monday, February 2, 2015
Researchers in the field of tissue engineering are making steady progress towards repair of larger sections of nerve damage caused by injury, here demonstrating a little restoration of function in pigs.
Social Contact Not As Correlated to Life Expectancy as Thought – Monday, February 2, 2015
In this analysis of many independent studies, the authors suggest that more social contact, on its own and independent of all of the other items associated with it, is not as meaningfully associated with greater life expectancy as was thought.
It isn’t hard to speculate on the outcomes that are associated with more gregarious individuals, such as greater wealth, and on how these outcomes impact lifestyle choices and use of medical resources. There is a strong web of correlations between wealth, intelligence, education, and life expectancy.
It is interesting, but like all examinations of natural variations in human longevity at the present time, it is a distraction from efforts that aim to make everyone live far longer in good health. Given the means to repair the causes of aging and prevent age-related disease, all of the small things that presently shift life expectancy a little in one direction or the other will no longer matter in the slightest.
On Clonal Expansion of Mitochondrial Mutations in Aging – Tuesday, February 3, 2015
Mitochondria are the power plants of the cell. Each cell has a herd of them that reproduce like bacteria and have their own DNA, separate from that of the nucleus.
One of the causes of aging is progressive mitochondrial dysfunction caused by forms of DNA damage that (a) deprive mitochondria of necessary proteins for correct function, but also (b) allow the damaged mitochondria a survival advantage during replication.
Thus a fraction of cells become overtaken by damaged mitochondria, and this causes them to export damaging reactive molecules into surrounding tissues. That contributes to, for example, the formation of damaged lipids involved in the progression of atherosclerosis.
This paper looks at the process of clonal expansion whereby damaged mitochondria overtake a cell. The authors focus on point mutations, however.
While point mutations will be carried along in damaged DNA that provides a survival advantage, I think that the existence of mitochondrial mutator mice that have a very high load of point mutations but no premature aging as a result shows that point mutations are not all that important in this process. It is probably deletions and other more serious forms of damage that are significant.
Exploring Laser Treatment for Macular Degeneration – Tuesday, February 3, 2015
Researchers here demonstrate that they can use very short bursts of laser light to somewhat reduce levels of extracellular waste deposits known as drusen present in the aged retina. The mechanisms of action remain to be explored in greater depth, however.
Proposing the Term “Chondrosenescence” – Wednesday, February 4, 2015
In this open access paper, researchers look at some of the interacting effects of aging on the maintenance of cartilage tissues.
Ever More Cancers Until Cancer and Its Causes are Defeated – Wednesday, February 4, 2015
Cancer research is perhaps the field of medical science with the greatest level of funding and public support.
The next generation of therapies presently under development are a great leap ahead in comparison to the present staples of chemotherapy and radiation therapy, making use of new tools in cellular biotechnology and promising accurate targeting of cancer cells for destruction with few side-effects.
This is just as well, as life spans are lengthening now, and will continue to lengthen at an increasingly rapid pace in the future. That additional time brings with it the standard risk of suffering cancer at some point, which is large at this time since more people are living longer in a period of life that has high cancer risk due to the damage of aging.
Overall we should expect incidence of cancer to increase with the present trend towards longer life spans until better medical technologies become widely available, either rejuvenation treatments that repair cellular damage and restore tissue environments to a much lower, youthful risk of cancer, or which can control cancer sufficiently well so that the higher risk doesn’t matter.
The latter will probably emerge first. Either way, robust and reliable ways to control the risks of cancer are a very necessary part of any near future toolkit for rejuvenation and healthy life extension.
Examining the Brains of Those With Exceptional Memory Function in Old Age – Thursday, February 5, 2015
Some people have exceptional memory function in old age, showing far less deterioration than their peers. Researchers here look for differences in the brains of these individuals.
The most actionable of the items discovered so far is the level of metabolic waste in the form of neurofibillary tangles. A range of research groups are presently working on ways to clear these tangles in connection with Alzheimer’s disease and other neurodegenerative conditions, but any resulting practical treatment should clearly be applied to everyone on a regular basis.
A Study on Exercise Levels and Mortality Showing that More is Not Necessarily Better – Thursday, February 5, 2015
Past epidemiological studies have found little or very mixed evidence that more or different types of exercise are better.
There is clearly a big difference between no exercise and regular moderate exercise, but adding more exercise on top of that doesn’t seem to have any reliably greater association with long-term health and lower mortality rates.
On the other hand there are studies to show that elite athletes live significantly longer than the general population, but there it may be the case that a successful career in athletics selects for those who are more robust and more likely to live longer anyway.
Here is a study demonstrating an interesting pattern of association between levels of exercise and mortality.
Considering Dietary AGEs and Alzheimer’s Disease – Friday, February 6, 2015
Advanced glycation end-products (AGEs) are involved in aging, as they can form cross-links that damage tissue structure, and trigger chronic inflammation via the receptor for AGEs.
There are many types of AGE and their influence is not all the same. Some can be broken down rapidly by our biochemistry, and some cannot. They can be manufactured in the body as a form of metabolic waste and also ingested in the diet, so there are two very different characteristics of AGE presence, one class that builds up slowly over time, and another that varies according to intake and ongoing clearance.
Further, the types of AGE involved in the pathology of aging in shorter lived animals such as mice are very different to the important types in we longer-lived humans, something that sabotaged early efforts to build treatments that clear the AGEs that damage tissue. More recent initiatives focus on glucosepane as the important source of cross-links in human tissues.
The degree to which dietary AGEs are significant in aging is a topic for debate. On the whole it looks to be the case that the inflammatory consequences of short-lived AGEs are the more important set of mechanisms for that source.
Mifepristone Extends Life in Flies, and Studies Using It as a Tool Must Be Reevaluated – Friday, February 6, 2015
In aging research inadvertent calorie restriction has been the usual confounding factor in life span studies carried out with short-lived animals.
If the treatment under study happened to cause animals to eat less then there was indeed an extension of life, but due to reduced calorie intake rather than the treatment.
The calorie restriction response is large compared to the results of most interventions under study, and many studies were contaminated because there was no control for calorie intake. There are any number of other ways in which life span studies can be compromised, however.
For example solvents extend life in nematodes, which is a problem for all experiments using them, a list that includes a range of genetic studies of longevity carried out prior to the solvent discovery. Here researchers find a similar problem in fly studies, wherein a part of the methodology of genetic engineering is shown to extend life.
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 see www.fightaging.org/
David A. Kekich
Maximum Life Foundation
“Where Biotech, Infotech and Nanotech
Â Â Â Â Meet to Reverse Aging by 2033”