Aging Research

Funding Aging Research

100,203 Perish in World™s Biggest Tragedy


posted on July 28, 2009

Pretty sobering, isn™t it?

Yesterday, about 100,203 lives were snuffed out prematurely. But hardly anyone noticed while the international press clamored to report on the 23 new deaths from the swine flu.

That™s because we™re used to losing 100,000 lives a day, equivalent to over 500 jetliners falling from the sky every day, from a cause we can do something about¦ but don™t.  Aging! That™s 100,000 lives yesterday, the day before, today and tomorrow. Total about 37 million every year.

Nanomedicine expert Robert Freitas points out that each of us carries within us a unique and complex universe of knowledge, skills, wisdom, life experience and human relationships. Almost all this rich treasury of information is forever lost when you die. If the vast content of each person's life can be summarized in just one book, then every year, death from aging robs us of 37 million books, worldwide. So each year, we allow a destruction of knowledge equivalent to three Libraries of Congress.

Natural death also destroys wealth on a grand scale. According to insurance company estimates, there™s an average value of about $2 million dollars for each human life lost, or an economic loss of about $74 trillion dollars”every year. That's almost equal to the entire tangible wealth of the world.

We have accepted the fact that deaths from aging are œnatural, and they are scattered worldwide. So we tend to disregard not only the personal tragedies, but also the treasures society loses in terms of that wisdom, experience, skills and knowledge that disappears with them.

But I promise researchers will not only someday be able to stop aging dead in its tracks... but will also be able to reverse the ravages of aging. In other words, they™ll be able to turn old men and women into healthy mature adults who look and feel like 25 year olds. Seeing this happen in your lifetime is my mission.

While hundreds of billions of dollars are spent on cancer, heart disease and other research... and even more on treatment, we calculate aging can be solved for a fraction of that amount - if it's spent the right way.

And Maximum Life Foundation identified that way. Over the past nine years, we discovered how science can control and even reverse the aging process, maybe within 20 more years. Armed with the law of Accelerating Returns - we can put our assault on aging, the Manhattan œBeach Project, into high gear. We know what it takes to succeed. We're determined to avoid being part of the last generation to die from aging... when we can be the first generation to control our destinies.

Then we will look for headlines like this:

œ100,203 Saved by World™s Biggest Medical Breakthrough

Long life!
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Controlling Cells to Regenerate the Heart (July 24 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4305
If you know exactly how to order cells around, you don't need stem cells to spur healing that would not normally take place: researchers "have devised a method to coax heart muscle cells into reentering the cell cycle, allowing the differentiated adult cells to divide and regenerate healthy heart tissue after a heart attack. The key ingredient is a growth factor known as neuregulin1 (NRG1 for short). To my knowledge, this is the first regenerative therapy that may be applicable in a systemic way. For instance, he added, people might one day go to the clinic for daily infusions of NRG1 over a period of weeks. In principle, there is nothing to preclude this going into the clinic. Based on the all the information we have, this is a promising candidate. The heart had long been considered an organ largely incapable of repairing itself. Heart muscle cells, also known as cardiomyocytes, do proliferate during prenatal development. Recent evidence has shown that adult heart muscle cells can replace themselves at some low level, with perhaps half of the cells in the heart turning over in the course of a lifetime. The new study provides multiple lines of evidence for this turnover ability - including video of the cells in action - and shows that neuregulin1 can ramp up the process."

An Important Proof for iPS Cells (July 24 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4304
Researchers have demonstrated an important proof of the capabilities of induced pluripotent stem (iPS) cells: "Since Shinya Yamanaka of Kyoto University in Japan created the first iPS cells in 2006, researchers have wondered whether they could generate an entire mammalian body from iPS cells, as they have from true embryonic stem cells. The team reports 27 live births. With their best cell line and optimal recipe, they were able to get 22 live births from 624 injected embryos, a success rate of 3.5%. The mice seem to have a high death rate, with some dying after just two days, and others displaying physical abnormalities, details of which the team would not reveal. But some of their mice passed one of the most fundamental tests of health: all 12 mice that were mated produced offspring, and the offspring showed no abnormalities. The team says it now has hundreds of second-generation, and more than 100 third-generation, mice. The team found no tumors in the mice, although they have not systematically looked for them." You might look at this as analogous to early cloning attempts - high failure rates and abnormalities in early efforts are beside the point. The point is that the process works, will be rapidly improved, and some form of induced pluripotent stem cells can eventually be substituted for embryonic stem cells for every application.

Bold Predictions on Artificial Brains (July 23 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4303
You should watch with interest progress towards emulating the human brain in hardware; this is the (long) path to ensuring we can live a lot, lot longer than our biology allows for. The claims in this BBC article are bold, conditional on massive funding and a large research community, but probably not completely out of line: "A detailed, functional [simulated] artificial human brain can be built within the next 10 years, a leading scientist has claimed. Henry Markram, director of the Blue Brain Project, has already simulated elements of a rat brain. He told the TED Global conference in Oxford that a synthetic human brain would be of particular use finding treatments for mental illnesses. It is not impossible to build a human brain and we can do it in 10 years. Over the last 15 years, Professor Markram and his team have picked apart the structure of the neocortical column. The project now has a software model of 'tens of thousands' of neurons - each one of which is different - which has allowed them to digitally construct an artificial neocortical column."

The Mechanisms by Which Excess Fat Harms You (July 22 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4300
Excess fat leads to chronic inflammation and damage over time. From ScienceDaily: "Fat tissue is no longer considered simply a storage place for excess calories, but in fact is an active tissue that secretes multiple compounds, thereby communicating with other tissues, including the liver, muscles, pancreas and the brain. Normal communication is necessary for optimal metabolism and weight regulation. However, in obesity, fat (adipose) tissue becomes dysfunctional, and mis-communicates with the other tissues. This places fat tissue at a central junction in mechanisms leading to common diseases attributed to obesity, like type 2 diabetes and cardiovascular diseases. Fat tissue dysfunction is believed to be caused by obesity-induced fat tissue stress: Cells over-grow as they store increasing amounts of fat. This excessive cell growth may cause decreased oxygen delivery into the tissue; individual cells may die (at least in mouse models), and fat tissue inflammation ensues. Also, excess nutrients (glucose, fatty acids) can also result in increased metabolic demands, and this in itself can cause cellular stress." You might also look at the role of macrophages in fat-induced inflammation.

Building Nerves in the Lab (July 21 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4298
Via EurekAlert!, researchers "report on the first lab-grown motor nerves that are insulated and organized just like they are in the human body. The model system will drastically improve understanding of the causes of myelin-related conditions, such as diabetic neuropathy and later, possibly multiple sclerosis (MS). In addition, the model system will enable the discovery and testing of new drug therapies for these conditions. MS, diabetic neuropathy, and many conditions that are caused by a loss of myelin, which forms protective insulation around our nerves, can be debilitating and even deadly. The [team] plans to use their new model system to explore the origins of diabetic neuropathy. Once the causes of myelin degradation are identified, targets for new drug therapies can be tested with the model. Other planned experiments will focus on how electrical signals travel through myelinated and unmyelinated nerves to reveal how nerves malfunction as well as for spinal cord injury studies." Loss of myelin appears to be important in general degenerative aging as well, so advances in understanding here will probably have wider application in the repair of the aging nervous system.

Calorie Restriction Provides Benefits Even Started Late (July 20 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4296
Here is another example of research showing benefits from late adoption of calorie restriction in mice: "Numerous reports implicate increased oxidative stress in the functional and structural changes occurring in the brain and other organs as a part of the normal aging process. Dietary restriction (DR) has long been shown to be life-prolonging intervention in several species. This study was aimed to assess the potential efficacy of late-onset short term DR when initiated in 21 months old male wistar rats for 3 months on the antioxidant defense system and lipid peroxidation, cellular stress response protein HSP 70 and synaptic marker protein synapsin 1 in discrete brain regions such as cortex, hypothalamus, and hippocampus as well as liver, kidney and heart from 24 month old rats. Age-associated decline in activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione, and elevated levels of lipid peroxidation was observed in brain and peripheral organ as well as increased expression of HSP 70 and reduction in synapsin 1 was observed in brain studied. Late-onset short term DR was effective in partially restoring the antioxidant status and in decreasing lipid peroxidation level as well as enhancing the expression of HSP 70 and synapsin 1 in aged rats.

Late onset short term DR also prevented age-related neurodegeneration [in] hippocampus and cortex regions of rat brain. Thus our current results suggest that DR initiated even in old age has the potential to improve age related decline in body functions."

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