My Birthday? Your Gift

Healthy Life Extension

Funding Aging Research

One Wealthy Friend Would Make a 20 Year Difference

posted on May 29th, 2012

Dear Future Centenarian,

d Happy Birthday to me d

Remember when you were a kid? You really looked forward to your birthdays, right? Wow, one year closer to getting your driver™s license! After that¦ independence! It seems we all wanted to look older too.

How things change as we age! I can only think of two good things. We™re still breathing and (hopefully) we™ve acquired some wisdom.

It™s my birthday, so I™m wishing for more of those two, and I™m giving you a gift.

It took me years to crack the code on helping you think, work and stress less on you way to extended youth and vitality. I almost make it a no-brainer. If you haven™t started on your way to your open-ended health span yet, make 2012 your year.

I have rewritten and retitled Life Extension Express. I eliminated 30 pages, added 46 and made hundreds of updates and edits. This labor of love is all you need to launch you on your easiest path to super wellness and extreme longevity. The new title is Smart, Strong and Sexy at 100?

Between the covers, you™ll discover exactly how and why open-ended youth may finally be in store for you. Then you™ll see what you can do for yourself that will help ensure you will be able to take advantage of emerging technologies designed to literally rejuvenate you “ every cell in your body!

Yes, this ages-old dream can finally become reality¦ and in your lifetime! But you need to help yourself, and this book will guide you every step of the way.

Book launch is scheduled for June. Price is $17.95 for the paperback and $9.87 for the Kindle version.

But for the next 48 hours (starting midnight Pacific May 29th) you get Smart, Strong and Sexy at 100? Kindle edition for¦ $0.00 !

That™s right, you pay ZERO, but don™t be late. At midnight, May 30th¦ it™s game over.

How cool is that?

œBummer, I don™t have a Kindle yet. NO problem¦ you don™t need a Kindle device to read it.

One more thing: You could do yourself, me and everyone who could benefit from this information a huge favor. I™m sure you™ll think it™s reasonable.

You could help spread the word if you liked it and post a review on Amazon. But please, if you find it did not meet your high expectations, get back to me 1st, before you post less than a 4 star review. I really appreciate it.

And I™ll do what I can to make it even better and get you an updated version as soon as it™s ready.

So all I ask is that you write a review about Smart, Strong and Sexy at 100?

Now before I give you the links, I want to share that the book evolved over the past 11 years. And it was written with you in mind.

So here is all you need to do: You don™t have to pay anything.

Simply follow the instructions below:

1) Go to and enter your Amazon account details. If you don™t have an account, create a free account.

2) After you have done step #1, go to the link below to get your free book Smart, Strong and Sexy at 100? You will not be billed if the price shows $0.00.  

That™s it.

In case it won™t download for you, see the instructions after the P.P.S.

Thanks so much and¦ More life,

P.S. This year is going to be a breakthrough one for you. You will get the best of ancient wisdom, current knowledge and emerging technologies integrated in the most profound and simple manner absolutely free.

P.P.S Don™t forget to leave a review on Amazon. That will help spread the word and be a big help to me too.If you do that, you won™t feel guilty over not paying for the book J. Click this link for your review:


Instructions only in case it doesn™t download:

Step 1

Simply download the free Kindle Reader App, from the links below and install it (easy) on your PC, Mac, iPhone, iPad, Black Berry, Android (Tablet & Smartphone) or Windows Phone 7, from one of these links, depending on your device¦ ...Tablets & Smartphones ¦Windows Phone 7

Step 2

Click on the top left black download image on that page to start the download and follow the really simple instructions. Anybody can do this.

Or if you know you are browsing with Firefox version 6+, Chrome 11+, or Safari 5+, simply open the below link (Kindle CloudReader) by clicking here¦

Step 3

Same for all. If you have already a Kindle Reader App or you installed it just now or are on the Kindle Cloud Reader you just opened¦

Click in the upper right corner on Kindle Store and then copy/paste or type this B00865MDJC into the search field and click œGo or hit œEnter. You will be taken to the right place. Click on the œBuy button (you will not be billed if the price shows $0.00), when you do that and you will get Smart, Strong and Sexy at 100? directly delivered to your device/app within minutes.

Or shut down/close your Kindle app and click on this link instead¦

and then click on the œBuy button (you will not be billed if the price shows $0.00.


A theory that has emerged in recent years points to forms of amyloidosis as the final limiting process for human life span.

Extremely long-lived people, who have survived or evaded all the common fatal age-related conditions, appear to die because of amyloid buildup. The evidence is good enough for the SENS Foundation to start funding work on a therapy - like all the mechanisms of aging, this is something that can be fixed through appropriate use of biotechnology. Here's a little more on the topic (and a link to a PDF format research paper):

"Supercentenarians are persons who have lived beyond the age of 110. Currently there are only about 80 such known individuals in the world whose age is verified. These people represent the limit of human lifespan. For a variety of reasons not fully understood but including lifestyle choices, genetic variants, and chance, these individuals have escaped the usual causes of death including cancer, heart disease and stroke. However, eventually they too die, with the world record holder being Jeanne Calment who survived until age 122.

In a newly published review Drs. Stephen Coles and Thomas Young of the UCLA Gerontology Research Group point out what it may be that is killing supercentenarians: amyloidosis. Amyloidosis is a disease state hallmarked by the deposition of fibers of abnormally clumped masses of transthyretin. The protein transthyretin normally acts to carry thyroid and other hormones. Mutations in the gene make the fibers abnormally sticky and they tend to clump into long fibers which are deposited in multiple organs.

Through early onset amyloidosis leads to disease, it is of interest that supercentanarians all seem to have significant amounts of it.  Though not proven, it is possible the amyloid is killing them. These persons have already escaped the typical causes of death. However, they have lived for so long, the normally innocuous amounts of amyloid that increase with age may actually become toxic to them because they have lived so many years. Where this line of reasoning gets exciting is that experimental drugs exist which may eliminate amyloid."

An example of the way in which the machinery of cells is very intertwined, components reused by evolution in many different mechanisms: "This was certainly an unexpected finding. It is rather uncommon for one gene to have two very different and very significant functions that tie together control of aging and inflammation.

The two, if not regulated properly, can eventually lead to cancer development. It's an exciting scientific find. For decades, the scientific community has known that inflammation, accelerated aging and cancer are somehow intertwined, but the connectionamong them has remained largely a mystery. What was known [was] that a gene called AUF1 controls inflammation by turning off the inflammatory response to stop the onset of septic shock. But this finding, while significant, did not explain a connection to accelerated aging and cancer.

When the researchers deleted the AUF1 gene, accelerated aging occurred, so they continued to focus their research efforts on the gene. The current study reveals that AUF1, a family of four related genes, not only controls the inflammatory response, but also maintains the integrity of chromosomes by activating the enzyme telomerase to repair the ends of chromosomes, thereby simultaneously reducing inflammation, preventing rapid aging and the development of cancer.

[Researchers are now] examining human populations for specific types of genetic alterations in the AUF1 gene that are associated with the co-development of certain immune diseases, increased rates of aging and higher cancer incidence in individuals to determine exactly how the alterations manifest and present themselves clinically."

The underlying infrastructural methods and technologies for working with stem cells are consistently improving - which lowers cost, thus allowing more research and development to take place. Here is an example: "researchers have proven that a special surface, free of biological contaminants, allows adult-derived stem cells to thrive and transform into multiple cell types.

Their success brings stem cell therapies another step closer. An embryo's cells really can be anything they want to be when they grow up: organs, nerves, skin, bone, any type of human cell. Adult-derived 'induced' stem cells can do this and better. Because the source cells can come from the patient, they are perfectly compatible for medical treatments. We turn back the clock, in a way. We're taking a specialized adult cell and genetically reprogramming it, so it behaves like a more primitive cell.

Before stem cells can be used to make repairs in the body, they must be grown and directed into becoming the desired cell type. Researchers typically use surfaces of animal cells and proteins for stem cell habitats, but these gels are expensive to make, and batches vary depending on the individual animal. Human cells are often grown over mouse cells, but they can go a little native, beginning to produce some mouse proteins that may invite an attack by a patient's immune system.

[A] polymer gel created by [researchers] in 2010 avoids these problems because researchers are able to control all of the gel's ingredients and how they combine. [Researchers] had shown that these surfaces could grow embryonic stem cells, [but] the polymer surface can also support the growth of the more medically promising induced stem cells, keeping them in their high-potential state. To prove that the cells could transform into different types, the team turned them into fat, cartilage and bone cells.

They then tested whether these cells could help the body to make repairs. Specifically, they attempted to repair five-millimeter holes in the skulls of mice. The weak immune systems of the mice didn't attack the human bone cells, allowing the cells to help fill in the hole. After eight weeks, the mice that had received the bone cells had 4.2 times as much new bone, as well as the beginnings of marrow cavities. The team could prove that the extra bone growth came from the added cells because it was human bone."

Changes in the stem cell niche are a good part of the age-related decline in stem cell activity, which explains why old stem cells can perform like young stem cells if put into a young environment, and vice versa.

Here researchers compensate for one of those niche changes: "Stem cells reside within a microenvironment of other cells - the niche - that is known to play a role in stem cell function. For example, after a tissue is injured, the niche signals to stem cells to form new tissue. It is believed that stem cells and their niche send signals to each other to help maintain their potency over a lifetime.

But while the loss of tissue and organ function during aging has been attributed to decreases in stem cell function, it has been unclear how this decline occurs. [There are] a number of possible scenarios, such as whether the loss of tissue function is due to a decrease in the number of stem cells, to the inability of stem cells to respond to signals from their niche, or to reduced signaling from the niche.

Researchers discovered that as the stem cell niche [in flies] ages, the cells produce a microRNA (a molecule that plays a negative role in the production of proteins from RNA) known as let-7. This microRNA is known to exist in a number of species, including humans, and helps time events that occur during development. This increase in let-7 leads to a domino effect that flips a switch on aging by influencing a protein known as Imp, whose function is to protect another molecule, Upd, which is secreted from a key area of the niche.

In short, Upd promotes the signaling that keeps stem cells active and in contact with the niche so that they can self-renew. And as aging advances, increasing expression of let-7 ultimately leads to lower Upd levels, decreasing the number of active stem cells in the niche. What leads to accumulation of let-7 in the niche of aged flies still remains an open question. The researchers also demonstrated they could reverse this age-related loss of stem cells by increasing expression of Imp."

Researchers are working on creating regeneration in mammals where it does not normally happen: "Researchers have long tried to get the optic nerve to regenerate when injured, with some success, but no one has been able to demonstrate recovery of vision.

A team [now] reports a three-pronged intervention that not only got optic nerve fibers to grow the full length of the visual pathway (from retina to the visual areas of the brain), but also restored some basic elements of vision in live mice. [the mice were able to] regain some depth perception, the ability to detect overall movement of the visual field, and perceive light. Previous studies [have] demonstrated that optic nerve fibers can regenerate some distance through the optic nerve, but this is the first study to show that these fibers can be made to grow long enough to go from eye to brain, that they are wrapped in the conducting 'insulation' known as myelin, that they can navigate to the proper visual centers in the brain, and that they make connections (synapses) with other neurons, allowing visual circuits to re-form.

[Researchers] combined three methods of activating the growth state of neurons in the retina, known as retinal ganglion cells: stimulating a growth-promoting compound called oncomodulin, [elevating] levels of cyclic adenosine monophosphate (cAMP) and deleting the gene that encodes the enzyme PTEN. These interventions have a synergistic effect on growth of optic nerve fibers. The eye turns out to be a feasible place to do gene therapy. The viruses used to introduce various genes into nerve cells mostly remain in the eye. Retinal ganglion cells are easily targetable."

Ongoing work in regenerative medicine: "scientists have succeeded in taking skin cells from heart failure patients and reprogramming them to transform into healthy, new heart muscle cells that are capable of integrating with existing heart tissue. The research [opens] up the prospect of treating heart failure patients with their own, human-induced pluripotent stem cells (hiPSCs) to repair their damaged hearts.

As the reprogrammed cells would be derived from the patients themselves, this could avoid the problem of the patients' immune systems rejecting the cells as 'foreign'. Recent advances in stem cell biology and tissue engineering have enabled researchers to consider ways of restoring and repairing damaged heart muscle with new cells, but a major problem has been the lack of good sources of human heart muscle cells and the problem of rejection by the immune system.

Recent studies have shown that it is possible to derive hiPSCs from young and healthy people and that these are capable of transforming into heart cells. However, it has not been shown that hiPSCs could be obtained from elderly and diseased patients. In addition, until now researchers have not been able to show that heart cells created from hiPSCs could integrate with existing heart tissue. [Researchers] took skin cells from two male heart failure patients (aged 51 and 61) and reprogrammed them by delivering three genes or 'transcription factors'.

Crucially, this reprogramming cocktail did not include a transcription factor called c-Myc, which has been used for creating stem cells but which is a known cancer-causing gene. The resulting hiPSCs were able to differentiate to become heart muscle cells (cardiomyocytes) just as effectively as hiPSCs that had been developed from healthy, young volunteers who acted as controls for this study.

Then the researchers were able to make the cardiomyocytes develop into heart muscle tissue, which they cultured together with pre-existing cardiac tissue. Within 24-48 hours the tissues were beating together. The tissue was behaving like a tiny microscopic cardiac tissue comprised of approximately 1000 cells in each beating area. Finally, the new tissue was transplanted into healthy rat hearts and the researchers found that the grafted tissue started to establish connections with the cells in the host tissue."

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