Healthy Aging

Life is Easy if You Live it the Hard Way

posted on February 2, 2009

A couple of weeks ago, I published Dr. Pete Hilgartner’s interpretation of the first of one of “Kekich’s Credos”. I’m including another in this week’s issue for two reasons. First, Dr. Pete interprets my Credos as they pertain to your health, and second, it’s Super Bowl Sunday. Since I grew up close to Pittsburgh, I’m taking some time off today for the game, and Dr. Pete’s contribution makes it easier to write this edition.

I have edited his interpretation for the sake of brevity.

 

Real regrets only come from not doing your best.  All else is out of your control.  You're measured by results only.  Trade excuses and "trying" for results, and expect half-hearted results from half-hearted efforts.  Do more than is expected of you.  Life's easy when you live it the hard way... and hard if you try to live it the easy way.

Think about the things you regret. Think of the things you wish had gone or wish would be going differently in your life.  Are they things you have control over?  If not, FIDO!  (Forget It and Drive On!) However, if you are regretting things you have or had control over, chances are the statement above is 100% applicable.

We all have some regrets.  We have all done things half way.  OK... so what.

We can decide never to have anything to regret from now on.  The past does not equal the future, so you can simply decide to never create another regret from this day forward. Think of the regrets you may have:

Did you get in shape last year when you promised yourself you would? 

Did you spend a year promising yourself you’d start eating healthier, lose weight or stop smoking?

You get the idea. Take a moment and write down the top three health habit regrets you have.

Do you notice a trend?  Are they all things that you could have created a different outcome for? Is there a pattern of behavior here?  After all, we humans are a reactive lot, programmed to repeat the same habits unless there is a conscious effort to act otherwise. You're decisions lead to the actions, or inactions, which result in your state of health.

You may be loudly protesting, "Nu-Uh!  It's my genes.  It's thanks to my lousy genetics."

Sorry!  It doesn't work that way unless you have a rare genetic mutation like Tay-Sachs syndrome. Modern science has confirmed that the victim mentality that blames everything on faulty genetics is false. It's more related to your lifestyle.  A supportive and healthy lifestyle allows optimal genetic expression. 
   
No Regrets and No Whining!  Just DO IT!

 

Dr. Pete goes on to say more about regrets. But let me substitute a thought regarding the phrase “Life's easy when you live it the hard way... and hard if you try to live it the easy way.”

A prime example is exercise. Spend thirty minutes a day, at least several days a week exercising instead of lying around. At first blush, this might seem like effort, the hard way to live. In reality, that 30 minutes of “work” translates to a quality of life for your remaining 23 ? hours that is so superior to your pre-exercise life, that you can only appreciate it once you make training a habit. You’ll look, feel, sleep, think and function in every way so much better, that it is beyond description. You’ll live longer too, you won’t get sick as often, and you may even dodge a crippling or deadly disease.

A half-hour of “hard” in exchange for 23 ? hours of “easy”. Doesn’t that sound like a great investment?
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THE ARGUMENT FROM GREAT SUFFERING AND DEATH

The death and suffering caused by aging far outstrips everything else that takes place in this world of ours - but, strangely, using this as an argument for greater support of longevity science doesn't seem to have much traction. Sadly, people will accept any situation, no matter how dire, if it is all they know: failure of progress is so often a failure of imagination.

http://www.fightaging.org/archives/001665.php

"Despite all our advances in medicine, sanitation, and other relevant factors, [survival at old age] still tapers off around age 100. Average lifespan has increased, but maximum lifespan has not changed significantly. One reason may be that research to prolong maximum lifespan receives minuscule funding, especially compared with popular endeavors such as cancer research. Many people seem to feel that extending maximum lifespan would be 'wrong' (even at a time of rapidly declining birth rates in many nations) or 'unnatural' (even though our average life expectancy used to be around 40, and has improved through totally unnatural means such as antibiotics)."
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Novel Telomere Extension Method Adds Longevity (January 30 2009) http://pmid.us/19145831
This is an interesting paper. I would be almost inclined to think that the life extension effect has to do with the link between telomerase and mitochondrial damage, but that's very speculative at this point. For all we know, the treatment of mice might have led to accidental calorie restriction and extended life span by that method: "Telomeres become shorter after each cell division, which is one of the mechanisms of gradual ageing. Telomerase is the reverse transcriptase responsible for the extension of telomere length. It is well known that activation of telomerase in the most types of organism's cells is not enough for telomere length stabilization. The reason may be in the telomere 'caps', which cover telomere ends from telomerase action. This experiment shows that telomeres were elongated by the combination of hypoxia activated telomerase and a newly developed pharmacological method removing the telomere cap. Rats from the control group died at the age 1 year 7 months - 1 year 8 months, which is typical for the Wistar rats from our sub-line. Rats from the experimental group died at the age 2 years 4 months."

Resetting a Damaged Immune System (January 30 2009) http://www.eurekalert.org/pub_releases/2009-01/nu-sct012909.php
Scientists can reboot a human immune system by destroying it and then transplanting new stem cells. This is a promising line of research given what happens to the immune system with aging, but the present focus is curing autoimmune disease: researchers "appear to have reversed the neurological dysfunction of early-stage multiple sclerosis patients by transplanting their own immune stem cells into their bodies and thereby 'resetting' their immune systems. [researchers] treated patients with chemotherapy to destroy their immune system. They then injected the patients with their own immune stem cells, obtained from the patients' blood before the chemotherapy, to create a new immune system. We focus on destroying only the immune component of the bone marrow and then regenerate the immune component, which makes the procedure much safer and less toxic than traditional chemotherapy for cancer. After the transplantation, the patient's new lymphocytes or immune cells are self-tolerant and do not attack the immune system. In MS the immune system is attacking your brain. After the procedure, it doesn't do that anymore."

Regenerating Spinal Cord Injury (January 29 2009) http://wwwjp.blackwellpublishing.com/bw/press/pressitem.asp?ref=2061
Researchers are expanding the array of methods demonstrated to repair spinal cord injuries: "transplantation of stem cells from the lining of the spinal cord, called ependymal stem cells, reverses paralysis associated with spinal cord injuries in laboratory tests. The findings show that the population of these cells after spinal cord injury was many times greater than comparable cells from healthy animal subjects. The results open a new window on spinal cord regenerative strategies. The transplanted cells were found to proliferate after spinal cord injury and were recruited by the specific injured area. When these cells were transplanted into animals with spinal cord injury, they regenerated ten times faster while in the transplant subject than similar cells derived from healthy control animals. The presence of these stem cells in the adult human spinal cords suggests that stem cell-associated mechanisms might be exploited to repair human spinal cord injuries."

Linking General Health and Alzheimer's Risk (January 28 2009) http://www.sciencedaily.com/releases/2009/01/090127152835.htm
Another study confirms the link between diabetes and Alzheimer's risk, suggesting once again that Alzheimer's is a lifestyle condition for many, brought on by being overweight and not exercising over the years: "Diabetics have a significantly greater risk of dementia, both Alzheimer's disease - the most common form of dementia - and other dementia, reveals important new data from an ongoing study of twins. The risk of dementia is especially strong if the onset of diabetes occurs in middle age. Our results [highlighted] the need to maintain a healthy lifestyle during adulthood in order to reduce the risk of dementia late in life ... the chances of a diabetic developing Alzheimer's disease may be even greater in real life than in the study, the researchers write. They identify several factors that might have led them to underestimate the risk of dementia and Alzheimer's among those who develop diabetes before the age of 65. Diabetes usually appears at a younger age than dementia does, the researchers note. Diabetes is also associated with a higher mortality rate, which may reduce the size of the sample of older adults. In addition, approximately 30 percent of older adults with diabetes have not been diagnosed. The results of the study implicate adult choices such as exercise, diet and smoking, as well as glycemic control in patients with diabetes, in affecting risk for Alzheimer's disease."

Ouroboros on Mitochondrial Antioxidant SkQ1 (January 28 2009) http://ouroboros.wordpress.com/2009/01/28/skq1-a-mitochondrially-targeted-antioxidant-that-extends-lifespan/
Ouroboros weighs in on SkQ1 research: "Mitochondria produce rreactive oxygen species (ROS) as a byproduct of metabolism.  These ROS are implicated in the mitochondrial free radical theory of aging (MFRTA) as the major cause of aging phenotypes.  If the MFRTA is true, one could delay aging by removing these mitochondrially-produced ROS with enzymes or antioxidants. Although many antioxidant therapies for cancer and other age-related diseases have proved fruitless, these studies did not specifically target antioxidants to the mitochondria. One group recently did just that in mice with catalase, an antioxidant enzyme normally found in peroxisomes. By translocating catalase to the mitochondria, the scientists expanded the lifespan of the animals by five months. Such genetic manipulations such as these are not in the cards when it comes to preventing human aging. Therefore, other mitochondrial targeting strategies must be employed. Accordingly, Vladamir Skulachev's group synthesized an antioxidant attached to a positively charged ion, which they call SkQ1. This compound can readily pass through the cell membrane and travel to the mitochondrial intermembrane space, the only negatively charged region in the cell.  There, SkQ1 will soak up any ROS formed by the electron transport chain. SkQ1 works similarly to the popular MitoQ, but does not have the pro-oxidant properties MitoQ is known to have at higher concentrations. SkQ1 is also better than MitoQ at inhibiting apoptosis induced by hydrogen peroxide."

Calorie Restriction Improves Memory (January 27 2009)
http://www.technologyreview.com/printer_friendly_article.aspx?id=22023
Another metric by which to measure the more rapid impacts of calorie restriction upon health: "The participants [underwent] memory tests before and after going on the diet. At the end of three months, the calorie-restricted group increased its scores by about 20 percent, while the performance in the other groups did not change. In addition to showing a boost in memory, the study also suggests that the same underlying mechanisms uncovered in animals could be at work in humans too. The researchers found that people who cut calories had improvements in several indicators of metabolic health, such as blood levels of insulin and C-reactive protein, a marker of inflammation. In fact, the rise in cognitive test scores correlated with lower insulin levels. In animal studies, high insulin levels and low-grade inflammation - products of being overweight and of high calorie intake - have been shown to hamper cognitive function. Limiting calories in mice boosts a molecule in the brain called BDNF, which has a key role in memory. Regular exercise, along with calorie restriction, also boosts the growth of new brain cells in mice. The current results [suggest] that those pathways from animal studies might also work in humans."

General Interest Article on Sirtris (January 26 2009) http://www.cbsnews.com/stories/2009/01/25/60minutes/printable4752082.shtml

A good example of the very diluted, delayed way in which news of progress in aging research makes its way into the mainstream from CBS News: "Dr. Westphal says we all may soon be taking a drug that just might beat the clock, a simple pill that could delay the inevitable. 'Our goal is to prevent and forestall many of the diseases that strike us as we reach 50, 60, and 70. All with one pill.' Asked if he's suggesting that it's some kind of a rejuvenation drug that would turn a 70-year-old into a 35-year-old, Westphal tells Safer, 'That might be pretty hard to do. But I think if we're on a train heading one direction, we can slow down that train. I think we can slow down these genes that control the aging process.' That quest to put death on hold began in 2003 when Westphal met David Sinclair, a biochemist at Harvard who was studying the genetic components of aging. 'Five years ago I met David. And he had shown that you could extend life span in yeast. That's pretty exciting,' Westphal recalls. Yeasts are one thing. Human beings are more complicated. So Sinclair focused on a gene present in almost all life forms: the sirtuin gene. It's normally inactive, but when it is active, Sinclair believes it triggers a survival mechanism that extends life. Convinced that something in nature could activate that gene, Sinclair randomly tested thousands of compounds and got a hit: resveratrol."

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