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Breakthroughs in Anti-Aging Science Appear in The Scientist

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March 6, 2015

Dear Reader,

It’s been an eventful week. On Monday, people started forwarding me the link for the new issue of The Scientist. The reason is that the issue delves into some of the most important breakthroughs in anti-aging science, which I’ve been talking about for the last several years.

I’ll talk about these biotechnologies in depth this week and next, but I’d like to point out that the simple fact that The Scientist has devoted this issue to the subject of increasing health spans (anti-aging) is, in itself, important. The healthcare industry is in the midst of a transition from the old model of medicine (treating diseases) to the new (delaying or preventing the age-related conditions that cause diseases).

This issue of the magazine is not just making the case for that approach to medicine, it’s highlighting some of the most important new discoveries into the causes of accelerated aging and their solutions. Moreover, it’s quite good.

This transition to “wellness” from traditional reactive healthcare is not simply the logical humane approach to medicine in the 21st century; it is the only way we can possibly deal with the financial problems created by below-replacement birth rates and continually lengthening lifespans.

As I’ve pointed out in several previous articles here, a projection of future tax revenues and expenditures leads to the inevitable conclusion that, within a few decades, government programs that support the aged population will begin to fail badly. As a society, in fact, we won’t be able to pay the costs associated with aging—unless the healthcare model is substantially transformed.

The new model of healthcare, recognized in this issue of The Scientist, proposes to deliver all the benefits enjoyed by the super-agers to the general population. Super-agers are the small minority of the population who have an unusual version of the cholesteryl ester transfer protein (CETP), which controls the makeup of cholesterol.

Somehow, those with homozygous G alleles of the CETP gene tend to avoid all the major killers until the end of their longer-than-normal lives. Then, somewhere around a hundred years old, all at once, they seem to get all of the diseases they previously avoided. They go out quickly and cheaply. If the entire population lived and died this way, we would not have a healthcare crisis, which is the largest component of our budgetary crisis.

In truth, we have to solve this problem. Remember, the American government and many other governments as well are not just broke; though deficit spending is already at historic levels internationally, most governments, including America, are massively in debt.

This would be bad enough, but the underlying demographic transition that created this situation is worsening. More and more people are getting older, while fewer and fewer are born. This means that we can’t simply raise taxes to cover the additional expenses that come with a population that has demographically inverted. Alzheimer’s alone presents an existential threat to Western societies.

Unlike the other major killers, we have thus far made no progress in slowing the rate of increase in AD, our most expensive disease. If you look at the numbers, one thing is clear. If we don’t get a handle on AD and the other major diseases, we are well and truly hosed. By 2050, current trends show spending on Alzheimer’s in the US rising from less than $200 billion a year today to over $1 trillion annually, but there will be far fewer younger workers to pick up the tab. Other medical costs associated with a rapidly aging population will also skyrocket.

The Affordable Health Care Act, even if it stands up to legal and political challenges, has failed to bring enough younger, healthier people into the program to fund healthcare for the aged. This dynamic will continue to worsen.

The good news—spectacularly good news actually—is that the science needed to solve these problems has already yielded remarkable and unexpected breakthroughs. The obstacles to their deployment are significant but they aren’t scientific. They are primarily in the area of institutional and government practices based on the old disease treatment model. In many cases, we see open hostility toward anti-aging strategies of the sort laid out in the current issue of The Scientist.

Regardless, let’s move on and briefly review one of the major topics covered in the current issue. Next week, I’ll discuss several more.

Reducing NF-κB Activation Improves Aging

“It seems that with almost anything that activates NF-κB, if you reduce it, it improves aging,” says Paul Robbins of the Scripps Research Institute in this feature article “How We Age.” I’m personally glad to see this new area of research hitting a more mainstream audience, because I’ve been alone reporting these developments for too long. There have been lots of journal articles supporting this view that NF-κB accelerates aging, but for some reason, nothing in the journals seems to penetrate the public consciousness. The article in The Scientist, by the way, cites this great journal piece.

The reality is that NF-κB over-activation, which is autoimmune syndrome, is a major accelerator of the aging processes. Essentially, the body recognizes normal aging as signs of injury and invasion, prompting an emergency innate immune response. A cytokine storm ensues and aging accelerates.

One alkaloid, which I’ve talked about incessantly here, has been shown in animal as well as human studies to moderate NF-κB and the associated accelerated aging. It’s not on the market at present, but I’m confident that others will be soon simply because the gene target is now known.

My confidence is based on the increased pace of discovery resulting from Moore’s Law and its impact on biological tools. It is orders of magnitude easier today to screen potential molecules for therapeutic activities. If I were a young, smart molecular biologist, like my son, I’d be looking for molecules in nature that mimic the alkaloid known to moderate NF-κB. Another likely target for researchers, which may actually work via a similar mechanism of action, is a widely prescribed drug used to prevent transplant rejection: rapamycin. It also, however, has significant anti-aging impacts.

Pharmaceutical giant Novartis is studying rapamycin at its enormous cutting-edge Novartis Institutes for Biomedical Research with an eye to applying for the first anti-aging drug. This would be historic if the company does, in fact, seek approval of rapamycin or a similar molecule for anti-aging, as opposed to a disease-specific therapy.

The rapamycin molecule, by the way, is naturally occurring in the soil of Easter Island. The name of the drug, in fact, comes from the Polynesian name of the island, Rapa Nui. I find it unlikely that other compounds similar to rapamycin, an antifungal produced by bacteria, won’t be discovered.

It’s possible, however, that rapamycin may work as a true immune suppressant, which could suppress immune reactions even when they’re needed. That’s not optimal, and it means that a compound that prevents over activation of NF-κB, preventing autoimmune inflammation but allowing proper immune responses, would actually be more effective as an anti-aging therapy. We’ll see, and probably pretty soon now that so many people are studying these molecules.

A Last Word from Mister Spock

It was sad to lose Leonard Nimoy. He was a fascinating man who first rejected his Star Trek typecasting and then embraced it. I remember as a teenager when Star Trek first appeared on my family’s black-and-white television. I was already reading science fiction, ranging from the classics like H. G. Wells and Jules Verne to the hard science writers like Arthur C. Clarke, Robert Heinlein, and Isaac Asimov. So Star Trek was somewhat pedestrian. It was, however, science fiction and I was thrilled. For a lot us with mathematical predispositions, Spock’s insistence on logic was liberating and probably had more influence on us than most would admit.

Anyway, I stumbled across a very clever piece written as a kind of tribute to Nimoy by Brett Arends, titled “How to Invest Like Leonard Nimoy’s Mr. Spock.” He did a great job of applying pure Vulcan logic to investing. You can read the whole thing here, but I’ll excerpt a bit below. It’s seriously good advice.

There are no bubbles or crashes on the Vulcan Stock Exchange, because investors never try to run with the herd. Vulcans believe that such an instinct, which once saved primitive man from lions, is a poor guide to sensible behavior in a financial market.

There are no fads on the Vulcan stock market.

Vulcans pay hardly any attention to quarterly earnings statements. Vulcans know that most of the value of a stock is based on the long term, and the last three months, or the next three months, is basically irrelevant.

Vulcans don’t trade stocks often. They know that, the more often they trade, the more likely it is that their emotions will overtake their reason.

And Vulcans never buy stocks because they have already gone up. Nor do they sell them just because they have fallen in price. Vulcans try to buy low and sell high. Anything else, as they say, would be ... highly illogical.


Patrick Cox
Patrick Cox
Editor, Transformational Technology Alert

Mauldin Economics


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