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As far back as 1935, research showed the effect of dietary restriction on longevity.

It’s become a well-known phenomenon.

And unfortunately, some erroneously  claim that it is “the only way scientifically proven to increase longevity.”

This is too simplistic because the results depend on what the person restricts.

Researchers showed that neither the restriction of carbohydrates or fats (besides PUFA) significantly increases longevity.

Only the restriction of protein does.

But not just any protein.

One amino acid, in particular, has an effect on longevity that eclipses all others.

The first reports of methionine restriction in increasing longevity came in 1992 with a publication from Upstate New York.

He used two large groups of rodents and fed one group 0.86% methionine and one group 0.17%.
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Everything else was identical, except for a slight increase the amino acid glutamate to offset the decrease in methionine.

In this way, the total protein was the same in both diets.

With only this one small dietary change, the rats lived 30% longer.

And researchers cannot blame this result on “caloric restriction” since the low-methionine groups ate MORE food per gram body weight.

They ate more and lived longer, something that we all would probably like to do.

However, the magnitude of lifespan extension seen in rats fed 0.17% methionine in our studies was considerably greater than that attained with protein restriction.

This was big news in 1992.

But such a dramatic effect from lowering just one amino acid invited skepticism from the scientific community.

Although, this skepticism was put to rest a few years later when another researcher replicated the effect.

He used the same percentages of methionine that Orentreich had, .17% and .86%, and he even used the same rat strain.

And he noticed a 42% increase in average lifespan and a 44% increase in maximum lifespan in the low-methionine group.

Plus, the low-methionine animals weighed less.

And just like Orentreich’s rats, they actually ate more food per body weight.

These data suggest that life-long Met restriction results in an actual delay of the biological aging process in F344 rats.

He also measured glutathione levels in multiple organs.

Ostensibly, he did this because he believed that free radical protection could explain this difference in longevity.

Glutathione is a powerful antioxidant, and they body can make it from methionine.

But he found paradoxical results with methionine and glutathione levels.

And so had other researchers who followed this line of thought.

But they found increased levels in the blood of the low-methionine group but decreased in the liver and kidneys.

Blood GSH levels of these old animals were increased with Met restriction to 267% of control levels.

Although glutathione may play a role, methionine most likely decreases lifespan by an entirely different mechanism.

One that involves S-adenosyl methionine (SAM).

This is a normal molecule in metabolism, and it can silence DNA.

So it can silence genes, and the silencing of some genes can lead to cancer.

And researchers notice these changes in DNA in aging.

They reviewed this mechanism in 2006.

He reviewed all of the prior studies on methionine and this type of DNA damage — called methylation.

Special enzymes can show the damage because they affect DNA at only the damaged spots.

But they found little evidence of either increased or decreased DNA damage with methionine.

No significant dietary effects on genome-wide DNA methylation were found.

Although the DNA methylation theory is plausible and may play a role, the life-shortening effects of methionine most likely stem from SAM’s other function.

S-adenosyl methionine (SAM) also produces amino acid groups called polyamines.

It does this by donating its molecular “tail” to another amine, forming longer chains.

Recently, researchers found that these polyamines are biologically active in a way that might explain methionine’s toxicity.

They cultured cells for over a week with spermidine, one of the simplest polyamines.

And to explain the cell’s response to additional polyamines further, the researcher used a polyamine-synthesis-inhibitor called DFMO.

This prevented the creation of other polyamines within the cell, so dosing could be more precise and predictable.

Interestingly, the polyamine inhibitor (DFMO) greatly decreased markers for adipogenesis.

Adipogenesis is the process used to create fat cells.

And added polyamines greatly increased genes for adipogenesis enzymes.

This is probably why in every rat study, the high-methionine rats always weighed more.

In the present study, we have obtained clear evidence that spermidine plays an important role in the maintenance of the expression of some adipocyte specific genes.

They weighed quite a bit more. 

And other studies noticed this as well.

Just a small change in methionine content can increase weight, most likely through the production of polyamines.

And the reduction in longevity could simply be a consequence of that.

Besides decreasing longevity, one of the studies reported changes in blood glucose and insulin levels in the high-methionine group.

Because it produces polyamines, methionine is the most dangerous amino acid.

Early researchers on dietary-restriction had blamed it all on calories.

But a string of newer studies published since the early ‘90s show us what they overlooked.

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Matt Cook is editor-in-chief of Daily Medical Discoveries. Matt has been a full time health researcher for 26 years. ABC News interviewed Matt on sexual health issues not long ago. Matt is widely quoted on over 1,000,000 websites. He has over 300,000 daily newsletter readers. Daily Medical Discoveries finds hidden, buried or ignored medical studies through the lens of 100 years of proven science. Matt heads up the editorial team of scientists and health researchers. Each discovery is based upon primary studies from peer reviewed science sources following the Daily Medical Discoveries 7 Step Process to ensure accuracy.