Is there a Conspiracy to Make You Die Early?

Healthy Life Extension

Funding Aging Research

Is there a Conspiracy to Make You Die Early?

posted on April 17th, 2012

Dear Future Centenarian,

The answer is¦ Yes and No.

I am NOT a conspiracy theorist. But I do understand a bit about human nature. And the pursuit of self interest, which may account for the vast majority of progress throughout history, can be a double-edged sword.

Self interest motivates us to innovate and achieve. However, once many of us attain a certain level of comfort, and especially vast wealth and power, we tend to forget how we got there and drift into a defensive mode. That™s one reason why behemoth corporations, governments and other organizations fall way behind in innovation when compared to young hungry individuals and companies.

Mature people and companies tend to grow conservative and lower their risk thresholds as they age and prosper. This stifles innovation. That™s one reason most breakthroughs are achieved by young people and small start-up companies.

And once people and companies become financially comfortable, they adopt a subconscious¦ and sometimes conscious tendency to suppress competition. It™s called œprotecting their turf. Governments and mega corporations are especially guilty of this.

Think of it this way. You go to school for 12-20 years, get a good job or grow a thriving business. You get married, have children, take out a mortgage on your new home and get used to a certain standard of living. Now, along comes an upstart competitor or technology that threatens your livelihood.

You may own an established local retail store when a big discount chain applies to build an outlet in your neighborhood. You know the consumers will get a wider selection at lower prices. The chain will also create local jobs. This is all good for the economy. Right? So what does human nature drive you to do?

You try to block their entry to the market every way you can.

Even though your innovations thirty years ago, when you were young and hungry, knocked off your established competitors, you fight to protect your turf now that the shoe is on the other foot. And you™re not above using political influence to do it.

Now magnify this by thousands of times.

You™re the Chairman of a multinational multibillion dollar drug company. When it started up, it developed an amazing drug that saved countless lives. Now however, it spends more on marketing and political lobbying than on R&D. It currently makes most of its profits on patented cancer drugs.

So here comes a new technology developed by a lone individual with a twenty times better cure rate at half the cost¦ and it doesn™t have any sickening side-effects.

Wow! What a boon to humanity. Finally, millions of patients would live who would have otherwise died. And none of the patients would get sick from the treatment.

As a compassionate human being, you™re thrilled. Right? Wrong.

You exert all your financial and political power to make sure the technology never reaches the market.

Now imagine a drug that rejuvenates the aged and keeps the young from deteriorating.

Goodbye to almost all heart disease, stroke, cancer and every other age-related disease. And goodbye to hundreds of billions of dollars that are diverted from big pharma.

Besides the fact that in addition to hundreds of millions of lives being preserved, trillions of dollars will eventually be generated for the world™s economy by those people continuing to be productive. How much resistance do you think there would be to this drug™s approval?

So ask yourself. œIs there a conspiracy to make you suffer and die early?

As you can see, research is not our only challenge. But we™ll clear this hurdle too.

More Life,
David Kekich


Transdifferentiation is showing up more often of late - the ability to switch somatic cells directly between types without having to go through an intermediate stage of reprogramming into stem cells. It should in theory make obtaining specific cells for research and therapy a cheaper and more reliable process in the future: "it has become possible to directly convert cells of the body into one another - without the time-consuming detour via a pluripotent intermediate stage.

However, this method has so far been rather inefficient. [Scientists] have now developed the method to the point that it can be used for biomedical applications. [Researchers] are interested in the biomedical utilization of artificially produced human nerve cells for disease research, cell replacement, and the development of active substances. By blocking the so-called SMAD signaling pathway and inhibiting glycogen synthase kinase 3 beta (GSK3ß), they increased the transformational efficiency [of skin cells to neurons] by several times - and were thus able to even simplify the means of extraction.

Using only two instead of previously three transcription factors and three active substances, [the] researchers were able to convert a majority [of] skin cells into neurons. In the end, their cell cultures contained up to more than 80% human neurons. We were able to demonstrate how the genes typical for skin fibroblast were gradually down-regulated and nerve-cell-specific genes were activated during the cell transformation. In addition, the nerve cells thus obtained were functionally active, which also makes them interesting as a source for cell replacement."

LONGEVITY RISK Thursday, April 12, 2012
A look at why, in this age of biotechnology and great uncertainty over the degree to which life spans will be extended in the next few decades, it is unwise to trust your financial future to large pension and welfare institutions.

Any significant progress over the present very modest baseline of incidental life extension through general advances in medicine will likely bring down much of the existing system in the years ahead - which of course suggests that big centralized pension systems should be avoided like the plague, but that won't happen. If today's politics are any guide, politicians will continue to aggressively devalue their national currencies, taking wealth from their broader population to pay for what cannot be afforded until such time as the house of cards cannot be propped up any longer.

The lesson to be taken away here: expect to provide for your own financial security in later life, and act accordingly now: "Here's the issue: governments have done their analysis of the aging issue largely based on best guesses of population developments in the future. These developments include further drops in fertility and some further increase in longevity. The trouble is that in the past, longevity has been consistently and substantially underestimated. We all live much longer now than had been expected 30, 20, and even just 10 years ago. So there is a good chance in the future people will live longer than we expect now.

We call this longevity risk - the risk we all live longer than anticipated. Why is that a risk, you may ask. We all like to live longer, healthy lives. Sure, but let's now return to those pension worries. If you retire at 65 and plan your retirement finances expecting to live another 20 years (assuming you have enough savings for at least that period), you would face a serious personal financial crisis if you actually live to 95, or - well in your 100s.

You could rely on your social security system at that point, but the program is also counting on people not living much beyond their mid-80s in most countries. Your personal financial problem multiplies by the size of the population, and, for society as a whole, becomes a very large problem." An example of how the present politics and systems of wealth transfer reward irresponsibility at all levels until such time as growth in collective irresponsibility sinks the whole venture.

Researchers are comparing the biochemistry of long-lived species to better understand the roots of large differences in life span: "The team looked at the genome of more than 30 mammalian species to identify proteins that evolve in connection with the longevity of a species.

They found that a protein, important in responding to DNA damage, evolves and mutates in a non-random way in species that are longer-lived, suggesting that it is changing for a specific purpose. They found a similar pattern in proteins associated with metabolism, cholesterol and pathways involved in the recycling of proteins.

Findings show that if certain proteins are being selected by evolution to change in long-lived mammals like humans and elephants, then it is possible that these species have optimized pathways that repair molecular damage, compared to shorter-lived animals, such as mice. The genetic basis for longevity differences between species remains a major puzzle of biology. A mouse lives less than five years and yet humans can live to over 100 for example. If we can identify the proteins that allow some species to live longer than others we could use this knowledge to improve human health and slow the aging process."

This is work performed on cells rather than organisms, but it still might be added to the great weight of existing evidence to suggest that calorie restriction improves most aspects of health: "Heart cells starved of nutrients are less likely to be damaged during periods of decreased blood flow and sudden influxes of blood, known as ischemia and reperfusion, and are also less likely to get out of synch with their cellular neighbors, the damaging phenomenon called arrhythmia.

Scientists learned that starved heart cells maintain normal calcium cycling and basic mitochondrial function far longer than non-starved cells during periods of extreme stress. The findings [add] to a growing body of scientific evidence that suggests the consumption of less energy - while maintaining balanced nutrition - can benefit tissues by enhancing cell performance and reducing DNA damage associated with the aging process.

We are connecting several loose facts about calorie restriction and heart function, in particular, arrhythmias. We have shown why nutrient restriction protects the cells from ischemia and reperfusion. Normal function means less risk of arrhythmias, during which heart cells stop communicating properly with each other, and which can cause further damage, even sudden cardiac death. The scientists studied cultured heart cells originally derived from young rats. The cells were grown in a 2 cm-by-2 cm monolayer, to allow ease of study.

The researchers mapped intracellular calcium ions and mitochondrial membrane potential with the help of fluorescent tags. Ischemia was simulated by placing a 1.8 cm-by-1.8 cm cover slip over the center of the cell culture, which limited oxygen and nutrient flow to that portion of the culture. Reperfusion was simulated by the removal of the cover slip. These experiments are not yet telling us whether we can emulate the effects of nutrient restriction in humans to lessen the damage of ischemia-reperfusion. But we have shown one way nutrient restriction may be acting to reduce heart tissue damage, a subject of interest to many laboratories."

A review paper: "With the improvement of medical care and hygienic conditions, there has been a tremendous increment in human lifespan. However, many of the elderly (older than 65 years) display chronic illnesses, and a majority requires frequent and longer hospitalization.

The robustness of the immune system to eliminate or control infections is often eroded with advancing age. Nevertheless, some elderly individuals do cope better than others. The origin of these inter-individual differences may come from genetic, lifestyle conditions (nutrition, socio-economic parameters), as well as the type, number and recurrence of pathogens encountered during life.

The theory we are supporting is that chronic infections, through life, will induce profound changes in the immune system probably due to unbalanced inflammatory profiles. Persistent viruses such as cytomegalovirus are not eliminated and are a driven force to immune exhaustion. Because of their age, elderly individuals may have seen more of these chronic stimulators and have experienced more reactivation episodes ultimately leading to shrinkage of their repertoire and overall immune robustness." Evidence in recent years suggests that this issue can be addressed by selectively destroying immune cells devoted to largely useless causes such cytomegalovirus - a goal that becomes ever more practical as targeted cell-killing therapies move closer to the clinic.

Some species of sea urchin, you may recall, age so slowly that it is hard to talk about life expectancy or pin down the likely age of a particular specimen with any ease. As for lobsters, another near-ageless collection of species, there isn't actually all that much research taking place into the biology of aging and longevity in these animals.

Here is an example, however: "The life history of sea urchins is fundamentally different from that of traditional models of aging and therefore they provide the opportunity to gain new insight into this complex process. Sea urchins grow indeterminately, reproduce throughout their life span and some species exhibit negligible senescence. Using a microarray and qRT-PCR, age-related changes in gene expression were examined in three tissues (muscle, esophagus and nerve) of the sea urchin species Strongylocentrotus purpuratus.

The results indicate age-related changes in gene expression involving many key cellular functions such as the ubiquitin-proteasome pathway, DNA metabolism, signaling pathways and apoptosis. Although there are tissue-specific differences in the gene expression profiles, there are some characteristics that are shared between tissues providing insight into potential mechanisms that promote lack of senescence in these animals. As an example, there is an increase in expression of genes encoding components of the Notch signaling pathway with age in all three tissues and a decrease in expression of the Wnt1 gene in both muscle and nerve. The interplay between the Notch and Wnt pathways may be one mechanism that ensures continued regeneration of tissues with advancing age contributing to the general lack of age-related decline in these animals."

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