Do you remember the exciting, romantic moment in the movie “Last of The Mohicans” where Hawkeye (Daniel Day Lewis) urges the girl, “Just stay alive!” He would come and find her and rescue her.

It’s like that. “Just stay alive, for Heaven’s sake!”

I’ve been saying for years it’s crazy to let yourself go. Science is moving so fast, it could be any day we have a breakthrough that will stop aging permanently. You’ll be able to choose when you head for the exit!

What a shame it would be to pass away just a short time before the new aging reality became available to everybody.

The latest news could be the front edge of the major breakthrough I’ve been waiting for. Scientists have discovered a “mutant protein” that ages us. If we can master that one protein, who knows what the future life of Mankind will bring?

The mutant protein is known to be involved in the rare premature aging condition known as progeria. This unlucky disease ages a child so rapidly, they die around 12- 13 years old, wrinkled, crumpled and like a very old man or woman (pro- for and geriatric, get it?). So the rogue protein is called progerin: kind of logical.

Thing is, research scientists have found progerin affects normal cells too; just at a much slower rate. But it still gets us in the end.

In the new research, investigators focused on the interaction between progerin and telomeres, the protective caps on the ends of chromosomes. As telomeres shorten, DNA misfires, and cells die.

In the current study, the scientists looked at millions of test-tube cells taken from seven healthy people, aged 10 to 92. They evaluated the cells in the lab for a year. They found the cells actually produce more and more progerin as they age.

I called progerin a “mutant protein”; that’s because it’s a mutated version of a normal cellular protein called lamin A. Lamin A is encoded by a normal LMNA gene. Its job is to help maintain the nucleus of the cell, which holds genetic information.

When progerin takes over from Lamin A protein, telomeres are told to slowly destruct and we know that this process, in itself, is a major component of aging. Telomere loss might be THE anti-aging mechanism, even ahead of inflammation and mitochondrial slow-down.

The bad news is that we, as normal non-progeria cases, still produce small and ever increasing amounts of progerin. But if we can block that, we’re done with aging!

Meantime, the best advice I can give you is hang in there. Take serious care of yourself and, for now, give up all thoughts of dying!

Reference:

The Journal of Clinical Investigation, published online June 13, 2011

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