Lifespan

Once you recognize that there are universal regulators of aging in everything from yeast to roundworms to mice to humans . . .

. . . and once you understand that those regulators can be changed with a molecule such as NMN or a few hours of vigorous exercise or a few less meals . . .

. . . and once you realize that it’s all just one disease . . .

. . . it all becomes clear

stem cells. Yet the ICE mice were suffering from a loss of body mass, mitochondria, and muscle strength and an increase in cataracts, arthritis, dementia, bone loss, and frailty.

All of the symptoms of aging—the conditions that push mice, like humans, farther toward the precipice of death—were being caused not by mutation but by the epigenetic changes that come as a result of DNA damage signals.

We hadn’t given the mice all of those ailments. We had given them aging.

And if you can give something, you can take it away.

Here’s the vital takeaway: we could age mice without affecting any of the most commonly assumed causes of aging. We hadn’t made their cells mutate. We hadn’t touched their telomeres. We hadn’t messed with their mitochondria.

Researchers began to cautiously agree: address these hallmarks, and you can slow down aging. Slow down aging, and you can forestall disease. Forestall disease, and you can push back death.

Take stem cells, which have the potential to develop into many other kinds of cells: if we can keep these undifferentiated cells from tiring out, they can continue to generate all the differentiated cells necessary to heal damaged tissues and battle all kinds of diseases.

Cloning gives us the answer as to whether or not mutations cause aging. If old cells had indeed lost crucial genetic information and this was the cause of aging, we shouldn’t be able to clone new animals from older individuals. Clones would be born old.

I had the pleasure of meeting the Harman family in 2013. His wife told me that Professor Harman had been taking high doses of alpha-lipoic acid for most of his life to quench free radicals. Considering that he worked tirelessly on his research well into his 90s, I suppose, at the very least, it didn’t hurt.

Even gerontologists, doctors who specialize in aging, often don’t ask why we age—they simply seek to treat the consequences.

Prolonged vitality—meaning not just more years of life but more active, healthy, and happy ones—is coming

The best way to do this might be the simplest—a brisk walk in a T-shirt on a winter day in a city such as Boston will do the trick. Exercising in the cold, in particular, appears to turbocharge the creation of brown adipose tissue.52 Leaving a window open overnight or not using a heavy blanket while you sleep could help, too.

Even if we eat a low-protein, vegetable-rich diet, we may live longer, but we won’t maximize our lifespans—because putting our bodies into nutritional adversity isn’t going to maximally trigger our longevity genes.