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Without sucient NAD, the sirtuins don’t work efficiently: they can’t remove the acetyl groups from histones,
they can’t silence genes, and they can’t extend lifespan. And we sure wouldn’t have seen the
lifespan-extending impact of the activator resveratrol.

We and others also noticed that NAD levels decrease with age throughout the body, in the brain, blood,
muscle, immune cells, pancreas, skin, and even the endothelial cells that coat the
inside of microscopic blood vessels.

But because it’s so central to so many fundamental cellular processes, no
researchers in the twentieth century had any interest in testing the eects of
boosting levels of NAD. “Bad stu will happen if you mess with NAD,” they
thought. But not even having tried to manipulate it, they didn’t really know
what would happen if they did.

The benefit of working with yeast, though, is that the worst-case scenario in
any experiment is a yeast massacre.
There was little risk in looking for ways to boost NAD in yeast. So that’s
what my lab members and I did. The easiest way was to identify the genes that
make NAD in yeast. We rst discovered a gene called PNC1, which turns
vitamin B
into NAD. That led us to try boosting PNC1 by introducing four
extra copies of it into the yeast cells, giving them five copies in total. Those yeast
cells lived 50 percent longer than normal, but not if we removed the SIR2 gene.
The cells were making extra NAD, and the sirtuin survival circuit was being

Could we do this in humans? Theoretically, yes. We already have the
technology to do it in my lab, using viruses to deliver the human equivalent of
the PNC1 gene called NAMPT. But turning humans into transgenic organisms
requires more paperwork and considerably more knowledge about safety—for
the stakes are higher than a yeast massacre.
That’s why we once again began searching for safe molecules that would
achieve the same result.
Charles Brenner, who is now the head of biochemistry at the University of
Iowa, discovered in 2004 that a form of vitamin B3
called nicotinamide riboside, or NR, is a vital precursor of NAD. He later found that NR, which is found in
trace levels in milk, can extend the lifespan of yeast cells by boosting NAD and
increasing the activity of Sir2. Once a rare chemical, NR is now sold by the ton
each month as a nutraceutical.

Meanwhile, on a parallel path, researchers, including us, were homing in on a
chemical called nicotinamide mononucleotide, or NMN, a compound made by
our cells and found in foods such as avocado, broccoli, and cabbage. In the body,
NR is converted into NMN, which is then converted into NAD. Give an animal
a drink with NR or NMN in it, and the levels of NAD in its body go up about
25 percent over the next couple of hours, about the same as if it had been fasting
or exercising a great deal.

My friend from the Guarente lab Shin-ichiro Imai demonstrated in 2011 that
NMN could treat the symptoms of type 2 diabetes in old mice by restoring
NAD levels. Then researchers in my lab at Harvard showed we could make the
mitochondria in old mice function just like mitochondria in young mice after
just a week of NMN injections.

In 2016, my other lab at the University of New South Wales collaborated
with Margaret Morris to demonstrate that NMN treats a form of type 2 diabetes
in obese female mice and their diabetes-prone ospring. And back at Harvard,
we found that NMN could give old mice the endurance of young mice and then
some, leading to the Great Mouse Treadmill Failure of 2017, when we had to
reset the tracking program on our lab’s miniature exercise machines because no
one had expected that an elderly mouse, or any mouse, could run anywhere near
three kilometers.

This molecule doesn’t just turn old mice into ultramarathoners; we have used
NMN-treated mice in studies that tested their balance, coordination, speed,
strength, and memory, too. The dierence between the mice that were on the
molecule and the mice that were not was astounding. Were they human, those
rodents would long since have been eligible for senior citizen discounts.
Nicotinamide mononucleotide turned them into the equivalent of contenders
on American Ninja Warrior. Other labs have shown that NMN can protect
against kidney damage, neurodegeneration, mitochondrial diseases, and an
inherited disease called Friedreich’s ataxia that lands active 20-year-olds in

As I write this, a group of mice that were put on NMN late in life are getting
very old. In fact, only seven out of the original forty mice are still alive, but they
are all healthy and still moving happily around the cage. The number of mice
alive that didn’t get the NMN?

Every day I’m asked by members of the public, “Which is the superior
molecule: NR or NMN?” We nd NMN to be more stable than NR and see
some health benets in mouse experiments that aren’t seen when NR is used.
But it’s NR that has been proven to extend the lifespan of mice. NMN is still
being tested. So there’s no denitive answer, at least not yet.
Human studies with NAD boosters are ongoing. So far, there has been no
toxicity, not even a hint of it. Studies to test its eectiveness in muscle and
neurological diseases are in progress or about to begin, followed by super-NADboosting
molecules that are a couple of years behind them in development.

But a lot of people haven’t been content to wait for these studies, which can
take years to play out. And that has given us some interesting leads about where
these molecules, or ones like them, might take us.