Fine Line between Wellness and Death

Longevity News Digest

Funding Aging Research

Fine Line between Wellness and Death

Dear Future Centenarian, 

There™s an extremely narrow margin between almost everything good and bad in life. Ultimately, it shrinks to a black and white difference. The grey area (not in a hair sense) starts disappearing with age.

The good news is, you control that margin. In fact, only you.

It™s a sad fact that only about 5% of any given population rises to the top of the wellness meter. Surprisingly, the differences between this œelite group and the other 95% boil down to unbelievably simple mundane habits. In fact, œhabits is the most appropriate term I can pick.

The œlucky 5% learned, either by accident or design, simple lifestyle steps that they incorporated at some point into their lives. The secret is, these steps became so routine that they barely have to think about them.

They became habits.

A close friend calls the secret to optimal healthy longevity œsustainability.

That means you separate yourself from the 95% who tend to suffer more and die sooner by doing simple things that they don™t, and you do them day-in and day-out.

You move a little more. You eat a little less. You substitute some nourishing foods for some harmful foods. You take your supplements regularly. You take at least a few moments each day to consciously de-stress.

Skipping these no-brainers could literally mean life or death.

You don™t need to be a fanatic about any of it.

How hard is it to take a few flights of stairs instead of an elevator¦ and at least get in some brisk walking every day?

Or to use smaller dishes instead of filling up dinner plates?

Or the lowest effort step “ taking your key supplements every day? I recommend more than one, but InflaGene is one of my top three, especially if you™re over 40.

It™s just as easy to consciously relax or briefly meditate once or twice a day as it is to let stress build.

If you haven™t read your copy of Smart, Strong and Sexy at 100 yet, you may want to give it a quick skim.

Or, I shudder at this thought O¦ you don™t have your copy yet. If not, Amazon now offers it in three formats: hard copy, Kindle and audio book.

More Life,
David Kekich
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Latest Headlines from Fight Aging!

Better Proteostasis in Long-Lived Species - Monday, January 26, 2015
Proteostasis is the desired state of correctly function in maintaining specific protein levels and an absence of damaged or misfolded proteins in cells over time.

Various regulatory systems and quality control mechanisms - such as those associated with proteasomes and lysosomes - are involved in maintaining correct function in this fashion. Like other aspects of cellular biology, proteostasis is negatively impacted over the course of aging, and exceptionally long-lived species seem to have better versions of the mechanisms involved in maintaining this desirable state of continued function.

Read More https://www.fightaging.org/archives/2015/01/better-proteostasis-in-long-lived-species.php

Intermittent Fasting and Hippocampal Biochemistry - Monday, January 26, 2015
Researchers here show that intermittent fasting in older rats beneficially alters one narrow measure of function in the hippocampus, an area of the brain that is well-studied in connection with age-related cognitive decline.

Read More https://www.fightaging.org/archives/2015/01/intermittent-fasting-and-hippocampal-biochemistry.php

On the Decline of Chaperone-Mediated Autophagy in the Liver - Tuesday, January 27, 2015
More than six years ago a research group demonstrated that autophagy can be boosted in the liver to reverse some of the age-related decline in function of that organ.

Old mice were shown to have some measures of liver function little different from young mice. Science is a slow business, however. These researchers are still working their way around this area of study, and at this time there is no significant movement in the direction of translating this and other potential autophagy enhancing treatments into human therapies. This is very much the standard story when it comes to potential treatments for aging, sad to say.

Read More https://www.fightaging.org/archives/2015/01/on-the-decline-of-chaperone-mediated-autophagy-in-the-liver.php

An Early Negative Result for Tau Immunotherapy - Tuesday, January 27, 2015
Immunotherapy is a promising approach for the treatment of Alzheimer's disease, in which immune cells are directed to attack amyloid aggregates or precursor proteins associated with the condition.

More pertinently, this field of research could produce a successful and mature technology platform for targeting all forms of amyloid, and possibly other types of metabolic waste, that should be cleared from the body in order to remove their contributions to degenerative aging. Unfortunately progress is slow and challenging: Alzheimer's is complex, the immune system is complex, and both are incompletely understood. There continue to be many more failures than successes in the process of development.

One more recent line of work is to focus on tau aggregates rather than amyloid. There is evidence to suggest that these neurofibillary tangles are also significant in the progression of Alzheimer's disease, but again understanding of the mechanisms involved is at this point sketchy.

From an engineering point of view forging ahead to build a removal mechanism in advance of full knowledge is a good approach, if it can be done given the present state of knowledge.

It stands a reasonable chance of cutting straight to a viable treatment even in absence of greater knowledge, or at least shedding more light on the situation if it clears tau and yet still fails to improve the outcome for a treated individual. In this case researchers encounter a fairly typical result in this work, which is that they are floundering on unanticipated complexity, but learning as they go.

Read More https://www.fightaging.org/archives/2015/01/an-early-negative-result-for-tau-immunotherapy.php

More on the Klotho Allele Associated with Better Cognition - Wednesday, January 28, 2015
Klotho is one of a range of longevity-associated genes identified in animal studies. You might recall that last year researchers identified a klotho variant associated with better cognitive function in humans. It didn't appear to protect against age-related decline as the researchers hoped, however. Here is more on this topic.

Read More https://www.fightaging.org/archives/2015/01/more-on-the-klotho-allele-associated-with-better-cognition.php

A Historical Analysis of Lifespan for the Privileged - Wednesday, January 28, 2015
The general consensus among researchers is that over the last few centuries of increasing human life expectancy most of the early gains were due to reductions in mortality in youth, such as those caused by infectious disease, malnutrition, and the like.

Over time the ongoing gains in life expectancy have shifted to occur in later life due to other forms of improvement in medicine and related technologies: present trends are as much in adult life expectancy as in life expectancy at birth. This study takes a novel approach to gain a different confirming perspective from the existing data.

Read More https://www.fightaging.org/archives/2015/01/a-historical-analysis-of-lifespan-for-the-privileged.php

Considering Amyloid Beta and Alzheimer's Disease - Thursday, January 29, 2015
Efforts to treat Alzheimer's disease by clearing the amyloid beta (Aβ) deposits and related precursors associated with the progression of the condition have proven to be challenging, beset with failures and complications.

Wherever there is slow progress in this sort of work, there is always the question of whether the problem is just hard, or whether the whole strategy is the wrong direction. Alternative hypotheses and approaches will spring up, and there is a lot of that going on in Alzheimer's research.

Still, the presence of amyloids of various forms are a hallmark of aged tissues, and they should be cleared as a part of the activity of any potential rejuvenation toolkit. The work on clearing Aβ will hopefully contribute meaningfully to the development of a general technology platform to achieve this goal, even if it turns out that Aβ removal isn't the right path for Alzheimer's treatment.

Read More https://www.fightaging.org/archives/2015/01/considering-amyloid-beta-and-alzheimers-disease.php

Executive Dysfunction Predicts Stroke Risk - Thursday, January 29, 2015
There is a large body of evidence to link cognitive decline in aging with corresponding decline in blood vessel integrity. A variety of processes in aging contribute to failing elasticity and structural remodeling of blood vessel walls, which in turn cause deterioration in the whole cardiovascular system as it tries to adapt to changing characteristics of blood flow.

It is probably the case that a fair degree of cognitive deterioration in every individual is caused by physical damage to the brain resulting from issues in the vascular system: many ongoing instances of tiny blood vessels failing, causing blockages or bleeds that harm small areas of brain tissue.

Individually these events are unnoticeable, but over time they add up, and the worse the state of your cardiovascular system the worse the impact on your brain. Thus we should expect to see strong correlations between decline in cognitive function and risk of catastrophic structural failure in the cardiovascular system. The interesting part of this ugly process is that because of the way the brain works, this distribution of physical damage results in very different levels of harm to various different aspects of cognition.

Read More https://www.fightaging.org/archives/2015/01/executive-dysfunction-predicts-stroke-risk.php

What to Do About Modified Low-Density Lipoproteins? - Friday, January 30, 2015
Low-density lipoproteins (LDL cholesterol) are involved in the progressive damage to blood vessel walls that leads to atherosclerosis.

The initial presence of oxidatively damaged LDL can cause a cascade of inflammation responses and further retention of LDL in the inflamed area. Macrophage cells arrive to clean up, some of which are overwhelmed by the amount of LDL to deal with and die.

Their debris attracts more macrophages and changes local cell behavior, and all of this leads to a dysfunctional remodeling of the blood vessel wall and eventual growth of fatty plaques that can block the blood vessel or break off to cause a blockage elsewhere.

One source of damaged LDL is the small population of cells with dysfunctional, damaged mitochondria that exist in older people. Getting rid of those through some form of repair treatment yet to be developed would help the issue. The authors of this open access review paper propose interfering elsewhere in the process, targeting the molecular biochemistry involved in other aspects of damaged LDL behavior in the blood vessel wall.

More Work on DNA Methylation Patterns and Aging - Friday, January 30, 2015
In recent years researchers have made good progress towards a biomarker of age based on patterns of DNA methylation that change over time.

The trick here is pulling out meaningful changes that are characteristically related to aging in much the same way in everyone versus the much larger set of changes that vary widely between individuals. As aging is a process of damage accumulation, some of these epigenetic changes in DNA methylation are responses to that damage, meaning that somewhere in all of this is a methodology to rapidly evaluate potential rejuvenation treatments that are based on repair of damage. That is the real significance of this ongoing field of research.

Read More https://www.fightaging.org/archives/2015/01/more-work-on-dna-methylation-patterns-and-aging.php
______________________

DISCLAIMER:  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
www.MaxLife.org

"Where Biotech, Infotech and Nanotech
     Meet to Reverse Aging by 2033"

 



 

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