Increase Your Longevity

Four Good Things Happened Last Week

posted on May 25, 2010

We’re on a roll.

It was a very good week. Sometimes I get antsy over progress just inching along. Then sometimes, it takes off like a rocket. That’s what happened last week. We made four leaps forward in our war on aging.

By now, you should be familiar with the term “caloric restriction”, or CR. CR, or dietary restriction, means ingesting a nutritious diet while cutting calories drastically. Most people should be taking in about 2000 calories a day, depending on your ideal body weight and your level of activity. But the average American wolfs down about 3300, and the rest of the developed world is almost as bad.

CR means reducing your caloric intake by about 20-40% from what you should be taking in. So that means cutting back to 1200-1600 calories a day if your ideal body weight maintenance dose is 2000. CR is the only proven method to extend maximum lifespan in mammals. It also extends average lifespan and dramatically reduces your propensity to get nicked by most of the diseases we associate with aging.

The problem is, CR has its downsides. Practitioners are often hungry, cold, underweight, have diminished sex drives, reduced bone mass and more, and have to be on guard about what they eat. It’s a Spartan way to exist, even though the rewards outweigh the negatives.

But what if scientists could find a way to trick your body into thinking it was caloric-restricted while you got to eat a normal diet? Then you could have your cake and eat it too.

Well, one of last week’s good things was finding out about a compound that might be able to give you the same benefits of CR without most of the annoying effects. And we also know of another compound that needs a little more analysis which may do the same. And that one may be a supplement, so no waiting ten years for FDA approval. That was Good Thing #1.

Then I had a call with a doctor on an entirely different subject. One thing led to another, and I learned one of his partners is doing incredible things offshore with adult stem cell treatments. The stem cell practitioner may have discovered some overlooked insights into aging. I will find out more soon.

Third, one of the companies I have been tracking for some time made a major breakthrough that could help many of us in the near future. I will have lots of details in about a month. Reading between the lines tells me it could add several years to many of our lifetimes. Who knows, that may be all some of us need to live long enough to see full age reversal.

Finally, I got a call from another international company with the interest and the ability to invest major funds into the life extension sector.

Not bad for one week, right? Oh, did I say one week? Actually, this all happened in a flurry in one DAY, Monday of last week. What a way to start the week!

We wrapped up the week with the dramatic announcement that Craig Venter’s lab built a synthetic cell, and we saw progress on a possible reversal for dementia. Avoiding and reversing dementia is integral to our program. Our chances of getting Alzheimer’s by 85 are about 50/50. Quantity of life is pointless without quality, and we are hard at work on getting you both. 

Long Life,
David Kekich
____________________________

LATEST HEALTHY LIFE EXTENSION HEADLINES

ANOTHER STUDY LINKING FAT AND DEMENTIA RISK (May 21 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4734
Via EurekAlert!: "excess abdominal fat places otherwise healthy, middle-aged people at risk for dementia later in life. [The study] included 733 community participants who had a mean age of 60 years with roughly 70% of the study group comprised of women. Researchers examined the association between Body Mass Index (BMI), waist circumference, waist to hip ratio, CT-based measures of abdominal fat, with MRI measures of total brain volume (TCBV), temporal horn volume (THV), white matter hyperintensity volume (WMHV) and brain infarcts in the middle-aged participants. Our results confirm the inverse association of increasing BMI with lower brain volumes in older adults and with younger, middle-aged adults and extends the findings to a much larger study sample. Prior studies were conducted in cohorts with less than 300 participants and the current study includes over 700 individuals. More importantly our data suggests a stronger connection between central obesity, particularly the visceral fat component of abdominal obesity, and risk of dementia and Alzheimer's disease. The association between VAT and TCBV was most robust and was also independent of BMI and insulin resistance. Researchers did not observe a statistically significant correlation between CT-based abdominal fat measures and THV, WMHV or BI."

THE COST OF EXCESS FAT TISSUE (May 20 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4733
Another paper looks at some of the consequences of becoming obese. In a more fair and productive world, medical costs would be an individual responsibility rather than being socialized as they are at present: "The prevalence of adult obesity has increased in recent decades. It is important to predict the long-term effect of body weight, and changes in body weight, in middle age on longevity and Medicare costs in older ages.
We predicted longevity and lifetime Medicare costs via simulation for 45-year-old persons by body weight in 1973 and changes in body weight between 1973 and 1983. Obese 45-year-olds had a smaller chance of surviving to age 65 and, if they did, incurred significantly higher average lifetime Medicare costs than normal-weight 45-year-olds ($163,000 compared with $117,000). Those who remained obese between ages 45 and 55 in 1973 to 1983 incurred significantly higher lifetime Medicare costs than those who maintained normal weight. Chronic obesity in middle age increases lifetime Medicare costs relative to those who remained normal weight. As the survival of obese persons improves, it is possible that Medicare costs may rise substantially in the future to meet the health care needs of today's obese middle-aged population."

TRANSFORMING BRAIN CELLS (May 20 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4732
From the Technology Review: "Support cells in the brain called astroglia can be turned into functioning neurons. Researchers found that they could transform the cells into two different classes of neurons, and that the neurons could form connections with one another in a dish. Although the research is at an early stage, the finding suggests that scientists could someday recruit existing cells in the brain to repair the brain and spinal cord after a stroke, injury, or neurodegenerative disease. The addition of one specific gene generated excitatory neurons, which promote activity in other cells. By adding a different gene, they generated inhibitory neurons, which dampen cell activity. In principle, [you] could generate other types of neurons if you choose the appropriate factors. The study adds to growing evidence that certain cell types can be transformed directly into other cell types without first being converted into stem cells. One of the next challenges is to determine whether these reprogrammed neurons can survive and function in a living brain. Fortunately, the brain seems to have a ready source of astroglia. When the brain is injured, these cells proliferate, similar to the way the skin repairs itself after a wound. The researchers found they could also derive neurons from injury-induced astroglia taken from the brains of adult mice."

H+ MAGAZINE ON SWITCHING MEMORY BACK ON (May 19 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4731
From h+ Magazine: "A new study [sheds] some light on how 'memory disturbances' in an aging mouse brain are associated with altered 'hippocampal chromatin plasticity' - the combination of DNA, histones, and other proteins that make up the chromosomes associated with the hippocampus. Specifically, the study describes an acetyl genetic switch that produces memory impairment in aging 16-month-old mice. Because the acetyl wasn't present in young 3-month-old mice, the study concludes that it acts as a switch for a cluster of learning and memory genes. When young mice are learning, an acetyl group binds to a particular point on the histone protein. The cluster of learning and memory genes on the surrounding DNA ends up close to the acetyl group. This acetyl group was missing in the older mice that had been given the same tasks. By injecting an enzyme known to encourage acetyl groups to bind to any kind of histone molecule, [researchers] flipped the acetyl genetic switch to the 'on' position in the older mice and their learning and memory performance became similar to that of 3-month-old mice. [Researchers hope] that the study of hippocampal chromatin plasticity and gene regulation in mice will help them to identify therapeutic strategies to encourage neuroplasticity (the formation of new neural networks in the brain), to improve learning behavior, and to recover seemingly lost long-term memories in human patients."

STEM CELL INDUCED REGENERATION IN THE LUNG (May 18 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4729
Researchers here demonstrate that comparatively simple stem cell transplants may be effective in regenerating lung injuries: "Human stem cells administered intravenously can restore alveolar epithelial tissue to a normal function in a novel ex vivo perfused human lung after E. coli endotoxin-induced acute lung injury (ALI). ALI is a common cause of respiratory failure in the intensive care units, often leading to death. It can be caused by both direct injury such as aspiration and pneumonia, and indirect injury such as sepsis and from trauma. Yearly, ALI affects approximately 200,000 patients in the US and has a 40 percent mortality rate despite extensive investigations into its causes and pathophysiology. Innovative therapies are desperately needed. We found that intravenous infusion of [stem cells] preferentially homed to the injured areas of the lung, which means that the cells find their way from the bloodstream to the sites in the lung of injury. In addition to having restored function of alveolar epithelial cells, lungs treated with [stem cells] showed a reduction in inflammatory [cytokine] levels suggesting a favorable shift away from a proinflammatory environment in the injured alveolus."

AN INTERVIEW WITH A TISSUE ENGINEER (May 18 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4728
From the Guardian: "The human body has tremendous capacity to repair itself after disease or injury. Skin will grow over wounds, while cells in our blood supply are constantly being manufactured in our bone marrow. But there is a limit to the body's ability to replace lost tissue. Cartilage cells are notoriously poor at regrowing after injury, for example. As a result, accidents and illnesses - including cancers - often leave individuals with disfiguring wounds or life-threatening damage to tissue. The aim of Molly Stevens, a nanoscience researcher at Imperial College, London, and founder of the biotech firm Reprogen, is a simple but ambitious one. Working with a team of chemists, cell biologists, surgeons, material scientists and engineers, she is developing techniques that will help the body repair itself when it suffers damage. This is the science of regenerative medicine. One approach that we have had considerable success with involves taking quite straightforward materials including simple polymers and using them to boost bone growth in a person. We made them into gels that we could inject into bones. The key to this technique lies with the fact that our bones are covered in a layer of stem cells. We inject our material under that layer and that wakes up those stem cells. They start to multiply and produce lots of new bone."

ANOTHER STEP FORWARD FOR TOOTH REGENERATION (May 17 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4727

Researchers have regrown teeth in rats by manipulating existing stem cells: "a new technique [can] orchestrate the body's stem cells to migrate to three-dimensional scaffold that is infused with growth factor. This can yield an anatomically correct tooth in as soon as nine weeks once implanted in the mouth. These findings represent the first report of regeneration of anatomically shaped tooth-like structures in vivo, and by cell homing without cell delivery. By homing stem cells to a scaffold made of natural materials and integrated in surrounding tissue, there is no need to use harvested stem cell lines, or create a an environment outside of the body (e.g., a Petri dish) where the tooth is grown and then implanted once it has matured. The tooth instead can be grown 'orthotopically,' or in the socket where the tooth will integrate with surrounding tissue in ways that are impossible with hard metals or other materials. A key consideration in tooth regeneration is finding a cost-effective approach that can translate into therapies for patients who cannot afford or who aren't good candidates for dental implants. Cell-homing-based tooth regeneration may provide a tangible pathway toward clinical translation."

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