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Senescent cells and the promise of human regeneration (11/7/11)

November 7, 2011

Learning From Mice

Aging seems inevitable, but thoughts of reversing it propel great excitement.  A group at Mayo Clinic has recently discovered that if a tiny group of cells, called senescent cells, are genetically manipulated to self-destruct, much of aging disappears – in mice.

What the Study Showed

The mice were a specially bred group that usually dies young of heart attacks.  With their senescent cells obliterated, aging did not appear to happen – the mice looked younger, did not wrinkle, were more energetic and muscularly robust.  Results looked best when the mice had their senescent cells knocked out in youth.  Senescent cell depleted middle aged mice looked and acted younger, but still suffered cataracts.

All, however,  died of heart attacks as expected – a cautionary note for those hoping longevity might be prolonged.

Rust and Decay

Many people view aging as slow decay, with increasing biological process errors eventually causing the system to break down – or “weakened” so a new random event kills you.

Sorry. This and other studies strongly argue against that mechanical model.

Here, mice stayed youthful with the knock out of a very small group of cells – not the whole.   The information given by those cells led to aging.  Without them, it did not happen.

Aging as an Information Issue

Bodies do not decay, but rather regenerate in constantly morphing ways.  Change that information flow and organisms live much longer. Programmers of that regeneration include genes like sirtuins; lifestyle changes like calorie depletion; and now removal of specific cell types, like senescent cells.

In theory, this means that aging can be both delayed and reversed. Bodies are constantly remade.  Given the right information, cells should be able to be reprogrammed, as occurs in the lab, into “younger” types.

It may not turn out that way.

Why Programmed Youthfulness Won’t Happen Soon

1. Aging in mice is not like aging in people.  Manipulating the lifespan and organs of a mammal that lives two or three years is very different from that which lives eighty or more.

2. The biological information systems involved are remarkably complex and as of yet hardly understood – even the right questions to ask remains controversial.

3. Cancer has yet to be licked, but as an information issue is related, but perhaps less complicated than aging.  For example, most tumors can be felled in the mouse – translating those results to humans has been vastly less successful.

4. Present theories of aging blame much of it on “inflammation”.  Yet the immune system is weakly comprehended, especially its whole vbody effects.  If lactobacilli in the gut can prevent depression and stress responses in mice (see “What your gut is telling your brain” in the blog archive,) it’s clear we have little clue what the millions of individual bacterial genes in our gut are doing and there are at least 150 more unique bacterial genes working on us than exist in the entire human genome.  And these are huge, diverse information flows across many cells and tissues that were previously thought clear cut and independent in their functions.  Most of the public has no idea that kidney cells, and fat cells in the abdomen,  are also major hormone producers.

What You Can Do

Figuring out technological advances is very difficult.  President Nixon started the “war on cancer” in 1969 with the idea of “curing cancer” in a decade – or two.  Cancer therapy has not turned out to be like putting a man on the moon. We know vastly more about the processes of cancer, but cancer cure rates have only improved incrementally.  Sadly, getting  rid of senescent cells in humans, if it can be done, may have completely different systemic effects than it does in mice.

However, very ordinary activities may delay aging – and particularly death.  Asian American women in Suffolk County New York have an expected lifespan of 95.6 years.  In the 1980’s human survival was expected to “top out” at 85 years. Ten years advance in lifespan inside thirty years is a big number.  And with lots more centenarians around, studying them and what got them living longer and healthier has become easier.

Basic life activities make a big difference.  Long lived populations move their bodies regularly.  They eat foods of considerable variety, emphasizing many plant stuffs; have regular habits, and considerable social engagement.

Elements that delay aging are within reach of most in the population.

So changing the body’s regeneration appears powerfully within individuals capacity. Which gives us a chance to wait for the medical advances that might radically change our lives.

Where’s My Rocket Car?

Neal Stephenson recently asked in a recent article, “where’s my rocket car?”  I remember when growing up putting brightly colored stickers into albums illustrating the “rocket car of 1985.”

Lifestyle moves are predictable and within our power – technology is far less predictable.  We may hope that the information technology revolution soon leads to a revolution in biosystems understanding.

In the meantime, there’s a lot we can do – just by ourselves.

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