Longer Life or Better Life?

Healthy Life Extension

Funding Aging Research

Longer Life Better Life


posted on April 4th, 2012

Dear Future Centenarian,

This question is called a "false alternative." When asked "Which do you want?", most people's knee jerk reaction is to immediately make a choice. Don't be trapped by false alternatives. Choose both options in this case.

Or in the case of negative choices, such as "death or taxes?", why not choose neither? Learn to stay out of the reactive mode, and choose what you want, regardless of the question or the apparent authority of the questioner.

Back to the first question. The truth is, the longer we live, the better life should be... after a point.

That point will be reached soon. At least when we make some more research breakthroughs. When that happens, disease will be erased, visual signs of aging will be a thing of the past, you'll have more energy and an overall improvement in wellness, and you'll even be able to get away with many of the fun habits that shorten you life today. Meanwhile, there is a lot you can do for a much better life now as well as a slightly longer life as well.

Who doesn't want a better life? It's easy to have. Regardless of choices thrown at you, you can choose to look and feel younger and better any time you want. The steps you need to take will also translate to more active years.

Now here's your biggest benefit: While you are improving almost every aspect of your life, you are continually increasing your super longevity odds.

Here's why: Longevity research progress is speeding up. It's getting fast now and will continue to accelerate. In fact, the rate of progress is nearly doubling every year. That means, twenty years from now, progress in the following year will equal as much as has been accomplished during those preceding twenty years.

This is absolutely profound. Think about it for a moment. Every extra year you add to your lifespan could DOUBLE your chances of open-ended youth. A major breakthrough 21 years from now won't do you any good if you
depart before then.

So you™ve got a huge WIN/WIN. You quality of life improves while you double your survival chances every extra year you tack on to your life.

Here's all you need to do for the time-being:

Incorporate the 7 easy steps into your life as detailed in Life Extension Express.

1. Nutrition
2. Exercise
3. Supplements
4. Anti-Aging Medicine
5. Stress Reduction
6. Lifestyle
7. Attitude

Long Life,

David A. Kekich
____________________________

LATEST HEADLINES FROM FIGHT AGING!

A TRANSCRIPT OF "ELIXIR OF LIFE" Friday, March 30, 2012 http://www.fightaging.org/archives/2012/03/a-transcript-of-elixir-of-life.php
An Australian program featuring researchers Aubrey de Grey and David Sinclair: "It feels like science fiction, but it's actually true. And we're really at the cutting edge, it's a really exciting time in the field right now. There's no such thing as ageing gracefully. I don't meet people who want to get Alzheimer's disease, or who want to get cancer or arthritis or any of the other things that afflict the elderly. Ageing is bad for you, and we better just actually accept that. As far as I'm concerned, ageing is humanity's worst problem, by some serious distance.

Now if you think that's an overstatement, consider this: world-wide, a hundred and fifty thousand people die each day, two-thirds of them from aging. That means potentially one hundred thousand people could be saved every day with therapies that combat ageing. Aging is simply and clearly, the accumulation of damage in the body. That's all that aging is. What it's going to take is development of thoroughly comprehensive regenerative medicine for aging.

That means medicine which can repair the molecular and cellular damage that accumulates in our bodies throughout life, as side effects of our normal metabolic processes. We do not know what humanity of the future is going to want to do. If thirty or fifty years from now people don't have the problems that we thought they might have, but we didn't develop those therapies, so those people have to die anyway, after a long period of decrepitude and disease, then they're not going to be terribly happy are they? That's why we have a moral obligation to develop these technologies as soon as possible."

INVESTIGATING INTESTINAL BACTERIA AND AGING IN NEMATODES Thursday, March 29, 2012 http://www.fightaging.org/archives/2012/03/investigating-intestinal-bacteria-and-aging-in-nematodes.php
There's a range of research to indicate that gut bacteria are important in the relationship between metabolism and aging, though the situation in higher animals is probably far more complex than in nematode worms: "A powerful approach to understanding complex processes such as aging is to use model organisms amenable to genetic manipulation, and to seek relevant phenotypes to measure.

Caenorhabditis elegans is particularly suited to studies of aging, since numerous single-gene mutations have been identified that affect its lifespan; it possesses an innate immune system employing evolutionarily conserved signaling pathways affecting longevity. As worms age, bacteria accumulate in the intestinal tract. However, quantitative relationships between worm genotype, lifespan, and intestinal lumen bacterial load have not been examined. We hypothesized that gut immunity is less efficient in older animals, leading to enhanced bacterial accumulation, reducing longevity.

To address this question, we evaluated the ability of worms to control bacterial accumulation as a functional marker of intestinal immunity. We show that as adult worms age, several C. elegans genotypes show diminished capacity to control intestinal bacterial accumulation. We provide evidence that intestinal bacterial load, regulated by gut immunity, is an important causative factor of lifespan determination; the effects are specified by bacterial strain, worm genotype, and biologic age, all acting in concert. In total, these studies focus attention on the worm intestine as a locus that influences longevity in the presence of an accumulating bacterial population. Further studies defining the interplay between bacterial species and host immunity in C. elegans may provide insights into the general mechanisms of aging and age-related diseases."

MORE VISCERAL FAT MEANS MORE INFLAMMATION Thursday, March 29, 2012 http://www.maxlifesolution.com/inflammex/
Yet another study showing a correlation between chronic inflammation and abdominal fat: "Obesity-related increases in multiple inflammatory markers may contribute to the persistent subclinical inflammation common with advancing age. We used factor analysis to identify inflammatory factor(s) and examine their associations with adiposity in older adults at risk for disability.

[Inflammatory markers] were measured in 179 participants from the Lifestyle Interventions and Independence for Elders Pilot (Mean ± SD age 77 ± 4 years, 76% white, 70% women). Body mass index, waist circumference, and total fat mass were assessed by anthropometry and dual-energy x-ray absorptiometry. Greater total and abdominal adiposity are associated with higher levels of an inflammatory factor related to CRP, IL-1ra, and IL-6 in older adults, which may provide a clinically useful measure of inflammation in this population.

[The associations were determined] after adjusting for age, gender, race/ethnicity, site, smoking, anti-inflammatory medications, comorbidity index, health-related quality of life, and physical function. These associations remained significant after further adjustment for grip strength, but only waist circumference remained associated with inflammation after adjusting for total lean mass." Waist circumference is a better correlation with the amount of visceral fat packed around the organs in comparison to body mass index.

EXCESS BODY FAT DAMAGES THE MIND Wednesday, March 28, 2012 http://www.fightaging.org/archives/2012/03/excess-body-fat-damages-the-mind.php
There is plenty of evidence to show that being overweight for any great length of time in life causes harm, either fairly directly by boosting levels of chronic inflammation, or because that fat tissue is associated with a lack of exercise and consequent development of vascular dementia, or for a range of other possible reasons.

Here is another study on this topic: "High midlife body mass index (BMI) has been linked to a greater risk of dementia in late life, but few have studied the effect of BMI across midlife on cognitive abilities and cognitive change in a dementia-free sample. We investigated the association between BMI, measured twice across midlife (mean age 40 and 61 years, respectively), and cognitive change in four domains across two decades in the Swedish Adoption/Twin Study of Aging.

Latent growth curve models fitted to data from 657 non-demented participants showed that persons who were overweight/obese in early midlife had significantly lower cognitive performance across domains in late life and significantly steeper decline in perceptual speed, adjusting for cardio-metabolic factors. Both underweight and overweight/obesity in late midlife were associated with lower cognitive abilities in late life. However, the association between underweight and low cognitive abilities did not remain significant when weight decline between early and late midlife was controlled for.

There is a negative effect on cognitive abilities later in life related to being overweight/obese across midlife. Moreover, weight decline across midlife rather than low weight in late midlife per se was associated with low cognitive abilities." The weight decline association shows up in a range of studies on weight and health; one common conclusion is that it reflects the impact that more serious medical conditions - related to weight or otherwise - can have on people.

LOWER LDL FROM AN EARLY AGE IS BETTER FOR LONG TERM HEALTH Tuesday, March 27, 2012 http://www.fightaging.org/archives/2012/03/lower-ldl-from-an-early-age-is-better-for-long-term-health.php
Some people have an objectively better metabolism than others when it comes to longevity - perhaps better mitochondrial DNA, perhaps less LDL cholesterol, for example: "Coronary atherosclerosis - a hardening of the arteries due to a build-up of fat and cholesterol - can lead to heart attacks and other forms of coronary heart disease (CHD).

Lowering low-density lipoprotein (LDL), or 'bad' cholesterol, reduces the risk of CHD. By the time most people begin treatment to lower LDL, CHD has often been quietly developing for decades. Because coronary atherosclerosis begins early in life, lowering LDL at a younger age may produce even greater reductions in the risk of CHD.

Researchers sought to test this hypothesis by using genetic data to conduct a series of 'natural' randomized controlled trials involving over one million study participants. Researchers used a novel study design called a Mendelian randomized controlled trial (mRCT) to study the effect of nine single-nucleotide polymorphisms (SNPs), or single-letter changes in DNA sequence, each of which is associated with lower levels of LDL cholesterol. Because each of these SNPs is allocated randomly at the time of conception, inheriting one of these SNPs is like being randomly allocated to a treatment that lowers LDL cholesterol beginning at birth. The researchers found that all nine SNPs were associated with a consistent 50-60 percent reduction in the risk of CHD for each 1 mmol/L (38.67 mg/dl) lower lifetime exposure to LDL cholesterol. "

A REPORT ON HAIR REPIGMENTATION Monday, March 26, 2012 http://www.fightaging.org/archives/2012/03/a-report-on-hair-repigmentation.php
Hair color - and loss - is one of the aspects of aging that people care about too much in comparison to its effects on health. There are far more important degenerations to consider. Nonetheless, here is a report suggesting that better control over the cell signaling could restore lost hair color by directing pigment cells to get back to work:

"We report the first case of progressive hair repigmentation associated with the use of lenalidomide in an elderly patient with multiple myeloma. The influence of lenalidomide on follicular melanogenesis may involve removing the inhibitory influences of some cytokines such as IL-1, IL-6 and TNF-α. In addition, certain endocrine effects of lenalidomide on the hypophyseal-adrenal axis could explain its action on hair pigmentation.

We further hypothesize that lenalidomide may be capable of stimulating migration and/or differentiation of melanocytes to promote repigmentation of gray hair follicles. Pending the clarification of how hair repigmentation occurs with lenalidomide, our observation materializes the concept that hair graying may not be an irreversible process." This sort of brute force approach is, however, far less desirable than working to fix the underlying levels of cellular damage that lead to changed signaling and the decline of melanocyte activity in the first place.

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