Longevity News Digest
Empathy and Longevity
Dear Future Centenarian,Â
When™s the last time you were in a crowded place and thought only about yourself?
We do it all the time. It™s natural. Sometimes we become so self-absorbed with our problems that we feel isolated. But as we develop empathy, we feel more connected. When we™re connected, personal challenges, health or otherwise, are MUCH easier to meet.
Ariela Sarai sent me an interesting exercise to help you on your way. I suggest you practice it. But even if you don™t, read it at least twice. The general message will sink in, and you and those around you will profit.
Latest Headlines from Fight Aging!
Failing to Extend Life Via Altered Levels of Membrane Fatty Acid Unsaturation - Monday, March 17, 2014
The membrane pacemaker hypothesis suggests that composition of cell membranes, especially those of mitochondria, is an important determinant of longevity differences between species - and possibly between individuals within a species as well.
One specific proposed mechanism is the degree to which membranes contain unsaturated fatty acids, as these are more vulnerable to oxidative damage. Oxidative damage is connected to aging, but its role is subtle and complex: look back in the archives for an outline of the mitochondrial free radical theory of aging, for example, in which oxidative damage inside cells is only the initiator for a long chain of consequences.
Here researchers make an attempt to demonstrate the relevance of the membrane pacemaker hypothesis by running a life span study in mice wherein membrane unsaturated fatty acid levels are lowered. They achieve the expected results in mouse biochemistry, changes that look a lot like slowing of aging, but without any resulting extension of life - an outcome that they blame on side-effects of the method used.
ECP Knockdown Extends Life in Flies, Probably via AMPK - Monday, March 17, 2014
Too many ways to modestly slow aging in lower animals are being discovered nowadays to mention them all. These methods generally involve altering levels of one or more proteins, and then observing the resulting effects on metabolism and life span.
As knowledge of the various pathways and mechanisms involved expands, it is becoming clear that most interventions discovered over the past two decades are linked to one another, being just different points of influence in the same larger set of mechanisms. So it isn't unusual at all for a novel method of life extension in laboratory animals to be connected to other, previously discovered methods, and that is the case here.
Examining Mitochondrial DNA Damage With Aging in Human Tissues - Tuesday, March 18, 2014
We age in part because mitochondrial DNA accumulates mutations, probably via oxidative damage. Mitochondria exist as bacteria-like self-replicating herds within our cells, and mitochondrial function is essential to cellular processes.
Mitochondria have their own DNA, distinct from that in the cell nucleus. This DNA is the blueprint for a number of essential portions of protein machinery used within mitochondria: severe mutations such as deletions can remove the ability of a particular mitochondrion to maintain itself and continue to operate correctly.
Cellular quality control should destroy all such damaged mitochondria, but unfortunately some damage can cause forms of dysfunction that evade these quality control processes. This ultimately leads to cells overtaken by clones of a dysfunctional mitochondria, and which themselves become dysfunctional as a result, harming surrounding tissues.
Possible approaches to remove this contribution to degenerative aging include periodic mitochondrial DNA repair or replacement, and the SENS method of adding backup copies of the relevant genes to the cell nucleus. Here is an example of research that supports this view, in which researchers examine the prevalence of mitochondrial DNA mutations with advancing age in human brain tissue, showing that deletion mutations increase significantly with age.
Axon Debris and Declining Nerve Regeneration With Age - Tuesday, March 18, 2014
One aspect of nerve regeneration is the reconstruction of lost or severed axons, the long connecting threads that link neurons in the nervous system. Some of this damage can regenerate naturally, but as for most of the critical functions of our biology this regenerative ability declines with age. Here researchers note a possible cause, the first step towards some form of treatment or reversal of age-related loss of function.
Muscle Stem Cells Aid in Repair of Nerve Damage - Wednesday, March 19, 2014
Here is news of a recent demonstration of the use of stem cells in nerve regeneration.
More Modeling of the Grandmother Hypothesis - Wednesday, March 19, 2014
We humans live for much longer than the other large primates, and the grandmother hypothesis suggests that this longevity evolved because of our greater capacity for culture, cooperation, and communication.
Once we became intelligent enough for older and less physically capable individuals to nonetheless materially assist in the survival of their descendants, longer lives were selected for. As is the case for other theories in the evolution of aging, simulation is used to investigate the grandmother hypothesis and bolster arguments on interpretation and plausibility. Here, the researchers suggest that enhanced longevity in our ancestors in comparison to their primate peers may have predated our species.
Betting Against Longevity, and Concerned About It - Thursday, March 20, 2014
The pension and annuity industries and even some of the individual companies involved are truly massive. Vast sums are at play over the course of decades, and these industries will be greatly impacted by advances in means of extending healthy human longevity.
Those involved are well aware of this: their challenge is not the fact that human lives will grow longer, but rather that there is great uncertainty over the upper limits to that growth. We are no longer in an era in which it is safe to extend the slow upward trend in adult life expectancy: work such as that of the SENS Research Foundation or any of dozens of other scientific groups could contribute to a sudden leap in healthy life span by producing the means of at least partial rejuvenation.
This is a challenge for the annuity and pension giants because in providing their services they have effectively taken on bets against a large increase in life span within our lifetimes. They will be ruined, or more likely they will take on a form of insurance themselves and their counterparties in the broader financial industry will implode. Equally these entities are so large and have so much leverage that they will be able to have politicians bail them out, transferring the cost of being wrong to the public purse. It will be something like the fallout from the US real estate bubble, and another symptom of much that is wrong with the existence of highly centralized, powerful states and governance.
Various entities around the world are taking half-steps in the direction of reducing their financial exposure to increasing longevity - which might be an indication of what people really think about the prospects for greater longevity arising from medical science, if they have enough money at stake to carefully investigate the issue. Cynically, this might be thought of as a shifting of risk onto larger financial parties willing to take it on because they know they can engineer a state bailout at the end of the day. This is an example of the type, not particularly important in and of itself, but representative of the flow of money and responsibilities presently underway in response to changing expectations on the future of human longevity.
Lower Resting Metabolic Rate Correlates With a Lower Risk of Age-Related Conditions and Impairments - Thursday, March 20, 2014
Differences in resting metabolic rate (RMR) between species of mammal correlate well with differences in life span. It has also been found that in our species RMR declines with advancing age, and a higher RMR is predictive of a greater risk of death. This study confirms these associations.
Investigating Osteoblast Deficiencies in Aspects of Osteopenia - Friday, March 21, 2014
Bone density declines with aging, a condition known as osteopenia, and which leads to the serious frailties of osteoporosis.
One of the possible reasons for this is a growing deficiency in osteoblasts, the cells that lay down bone structure, or perhaps a widening mismatch between the behavior of osteoblasts and osteoclasts, the cells responsible for breaking down bone structure when needed. Here, researchers look into some of the details of osteoblast deficiency, and find it is complex, with differing mechanisms between the genders.
REST and Alzheimer's Disease - Friday, March 21, 2014
A popular science piece on a new association in the biochemistry of Alzheimer's disease.
Read More https://www.fightaging.org/archives/2014/03/rest-and-alzheimers-disease.php
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"