Should the United States Fund a “War on Aging?”

Healthy Life Extension

Funding Aging Research

Should the United States Fund a "War on Aging?"

posted on May 15th, 2012

Dear Future Centenarian,

For purely pragmatic and philosophical reasons, I normally oppose government intervention and tax dollars to fund most programs. Without elaborating, governments usually accomplish the opposite of what they say they intend doing.

The war on aging may be an exception though”not because of my passion for the program, but because it makes economic and humanitarian sense. It would be hard¦ not impossible¦ but hard for them to screw it up.

Look how successful we were with the Manhattan Project to develop the atomic bomb and the Apollo Project to land on the moon when the pressure was on. The benefits of solving aging will dwarf those derived from any and all prior projects.

Slowly but surely, scientists and doctors are beginning to understand why people inevitably age and die. Slowly but surely, progress is occurring in the field of life extension. Much work remains to be done, but in a country that declares, "life" as the first inalienable right in its Constitution, pursuit of open-ended life extension should be a national priority!

As I said, I'm usually not in favor of asking for government help. But if we want to solve the healthcare crisis that is sinking our economy, we need an Apollo or Manhattan type Project to fast-track this. (See

It could rescue the 100,000 people who die every day from aging. Most suffer and linger for years, draining economies with unnecessary medical expenses and turning our most experienced and productive citizens into terminally ill liabilities.

You can encourage the presidential candidates to make extreme life extension a priority by clicking on the following link and vote for a top science question they should answer:

œShould the United States fund a War on Aging?"


This is co-sponsored by The National Academy of Sciences along with other prestigious organizations. So it should get the attention of the candidates.

BTW, I mentioned this in last week™s letter, but I gave you the wrong link. Oops!

Please vote now. It will take you 30 seconds.

Meanwhile, we are doing our best in the private sector until politicians come to their senses.

More Life,
David Kekich


Singularity Hub looks at the tissue engineering of teeth: "For years, researchers have investigated stem cells in an effort to grow teeth made for a person's own cells. Toward this end, [scientists] have developed methods to control adult stem cell growth toward generating dental tissue and 'real' replacement teeth.

[The] researchers' approach is to extract stem cells from oral tissue, such as inside a tooth itself, or from bone marrow. After being harvested, the cells are mounted to a polymer scaffold in the shape of the desired tooth. The polymer is the same material used in bioreabsorable sutures, so the scaffold eventually dissolves away. Teeth can be grown separately then inserted into a patient's mouth or the stem cells can be grown within the mouth reaching a full-sized tooth within a few months.

So far, teeth have been regenerated in mice and monkeys, and clinical trials with humans are underway, but whether the technology can generate teeth that are nourished by the blood and have full sensations remains to be seen. Teeth present a unique challenge for researchers because the stem cells must be stimulated to grow the right balance of hard tissue, dentin and enamel, while producing the correct size and shape."

Following on from a recent post on the involution of the thymus in adults, the process by which it ceases to generate immune cells and atrophies, here is a another paper that considers some of the possible paths to interventions that maintain the thymus into old age.

Given experiments in mice showing that transplant of a young thymus extends life, this seems worthy of further investigation: "The thymus is the primary organ for T-cell differentiation and maturation. Unlike other major organs, the thymus is highly dynamic, capable of undergoing multiple rounds of almost complete atrophy followed by rapid restoration. The process of thymic atrophy, or involution, results in decreased thymopoiesis and emigration of naïve T cells to the periphery.

Multiple processes can trigger transient thymic involution, including bacterial and viral infection(s), aging, pregnancy and stress. Intense investigations into the mechanisms that underlie thymic involution have revealed diverse cellular and molecular mediators, with elaborate control mechanisms. This review outlines the disparate pathways through which involution can be mediated, from the transient infection-mediated pathway, tightly controlled by microRNA, to the chronic changes that occur through aging."

An update on the LysoSENS research project from the SENS Foundation, which aims to discover and adapt bacterial enzymes to break down the damaging buildup of unwanted metabolic byproducts in the aging body:

"SENS Foundation-funded research shows that expression of a modified microbial enzyme protects human cells against 7-ketocholesterol toxicity, advancing research toward remediation of the foam cell and rejuvenation of the atherosclerotic artery. Atherosclerotic cardiovascular disease is the principal cause of ischaemic heart disease, cerebrovascular disease, and peripheral vascular disease, making it the root of the leading cause of morbidity and mortality worldwide. Atherosclerosis begins with the entrapment and oxidation of low-density lipoprotein (LDL) cholesterol in the arterial endothelium.

As a protective response, the endothelium recruits blood monocytes into the arterial wall, which differentiate and mature into active macrophages and engulf toxic oxidized cholesterol products
(oxysterols) such as 7-ketocholesterol (7-KC). Although initially protective, this response ultimately leads to atherosclerotic plaque: oxidized cholesterol products accumulate in the macrophage lysosome, and impair the processing and trafficking of native cholesterol and other materials, leading macrophages to become dysfunctional and immobilized. More and more of these disabled "foam cells" progressively accumulate in the arterial wall, generating the fatty streaks that form the basis of the atherosclerotic lesion.

Rejuvenation biotechnology can be brought to bear against this disease of aging through the identification, modification, and therapeutic delivery of novel lysosomal enzymes derived from microbes to the arterial macrophage - enzymes which are capable of degrading oxidized cholesterol products. SENS Foundation-funded researchers have been making steady progress in the identification and characterization of candidate enzymes for several years now, and a new report represents a substantial advance in the research: the rescue of cellular oxysterol toxicity by an introduced microbial lysosomal enzyme."

Extensive studies of the genetics of human longevity are growing more common - the flow of data is becoming a flood. Here is an example: "we chose to investigate 1,200 individuals of the Danish 1905 birth cohort, which have been followed since 1998 when the members were 92-93 years old.

The genetic contribution to human longevity has been estimated to be most profound during the late part of life, thus these oldest-old individuals are excellent for investigating such effect.
The follow-up survival data enabled performance of longitudinal analysis, which is quite unique in the field of genetic epidemiology of human longevity. However, this study explores the genetic contribution to survival during the ninth decade of life, hence, in order to investigate the genetic contribution to survival in younger elderly we also included 800 individuals of the Study of Middle-aged Danish twins (MADT).

The analyses of the data set verified the association [with longevity of] SNPs in the APOE, CETP and IL6 genes, [and] pointed to new candidate genes of human longevity: especially SNPs in the INS, RAD52 and NTHL1 genes appeared promising. As part of these investigations, replication studies of the single-SNP level findings were conducted in German case-control samples of 1,613 oldest-old (ages 95-110) and 1,104 middle-aged individuals and in a Dutch prospective cohort of 563 oldest-old (age 85+).

Interesting aspects of the study were that the majority of the rare alleles of the identified SNPs were longevity variants, not mortality variants, indicating that at least in our study population, longevity is primarily affected by positively acting minor alleles. Furthermore, the genotype data generated were used for a number of replication studies on variation in the FOXO3A, TERT and TERC genes. These studies were performed in response to new data being published on the association of genetic variation in the genes with longevity (FOXO3A and TERT) and with telomere length (TERT and TERC). Our studies verified a role of TERC in human telomere length and of FOXO3A in human longevity (survival from middle age to old age), while a novel role of TERC in human longevity was found."

Tissue engineering is steadily advancing into the easier areas of growing replacement parts: "Other groups have tried to tackle nose replacement with implants but we've found they don't last. They migrate, the shape of the nose changes.

But our one will hold itself completely, as it's an entire nose shape made out of polymer. Inside this nanomaterial are thousands of small holes. Tissue grows into these and becomes part of it. It becomes the same as a nose and will even feel like one. When the nose is transferred to the patient, it doesn't go directly onto the face but will be placed inside a balloon inserted beneath the skin on their arm. After four weeks, during which time skin and blood vessels can grow, the nose can be monitored, then it can be transplanted to the face.

At the cutting edge of modern medicine, [researchers] are focusing on growing replacement organs and body parts to order using a patient's own cells. There would be no more waiting for donors or complex reconstruction - just a quick swap. And because the organ is made from the patient's own cells, the risk of rejection should, in theory, be eliminated. We seed the patient's own cells on to the polymer inside a bioreactor. This is a sterile environment mirroring the human body's temperature, blood and oxygen supply. As the cells take hold and multiply, so the polymer becomes coated. The same methods could be applied to all parts of the face to reconstruct those of people who have had severe facial traumas."

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