But fasting in general also helps to increase longevity, as well.
A Quick Mitochondrial Overview
In order to follow the biochemical explanation below, we have to briefly revisit the mitochondria.
These organelles power the cells. They are the culmination of several biochemical pathways beginning with either glucose or fatty acids, stripping them down into essentially electrons, and these funnel into the mitochondrial electron transport chain. If conditions are right (i.e. if the body needs more energy), the mitochondria takes this fuel and turns it into ATP, the body’s energy currency. A small percentage of the electrons flowing into the mitochondria will leak out into the surrounding tissues and create oxidative stress, but at a low level this is actually beneficial, as it sends a feedback signal to the mitochondria to speed up production.
If the body has all the energy it needs, though, then the mitochondria get the signal that they need to slow down production, as there’s nowhere for it to go. This is fine, if input is likewise low. But, if we’re eating a cheeseburger while sitting on the couch all day, there’s a mismatch between energy and production. On a mitochondrial level, this means that those electrons going into the electron transport chain won’t make it to their end point, and will instead leak out into the surrounding tissues. The most immediate consequence of this will be damage to the mitochondria themselves.
Eventually, this will lead to decreased mitochondrial efficiency, and mitochondrial dysfunction. Since mitochondrial dysfunction is still the prevailing theory of aging, this is significant.
The Feedback Signals from Used ATP
Two molecules are important for our purposes in the fasting/ATP/longevity story. These are AMPK and PPARα.
Once ATP is stripped of phosphates, it becomes AMP, which then sends a feedback signal for the body to break down more energy stores (fat) in order to make more ATP. It does this via activating the enzyme AMPK, or adenosine monophosphate–activated protein kinase.
Meanwhile, peroxisome proliferator-activated receptor alpha, or PPARα, boosts ATP production efficiency, and coordinates its efforts with AMPK, since they’re working toward the same end, but from different angles.
This fat-burning, energy-producing state is optimal for mitochondrial function. Just as overeating and lack of exercise contributes to mitochondrial damage, the opposite—caloric restriction, fasting, or intermittent fasting, as well as exercise—turns on AMPK and PPARα.
This means more than just weight loss. On the mitochondrial level, it also means less oxidative damage, and thus, less inflammation.
How Adiponectin Plays A Role
I wrote here on the “good” hormone produced by fat cells called adiponectin, which helps with fat burning.
It turns out that lower adiponectin impairs PPARα activity, too. Again, this means less efficient ATP production, and potentially more oxidative damage to the mitochondria.
Eating well, losing weight, sleeping well, and specific antioxidant support can help boost adiponectin production.
Nicotinamide: The Anti-Aging Vitamin
Vitamin B3, or niacinamide, also known as niacin or nicotinamide, play several roles in the ATP story. But fasting will regenerate the oxidized (and most useful) NAD+ form of the vitamin, via peroxisomes.
NAD+ in turn activates AMPK, which will signal the body to break down more stored energy for ATP production. This in turn means less oxidative stress on the mitochondria.
Enhancing healthy longevity is another great reason to incorporate fasting, or intermittent fasting, into your lifestyle.
And don’t neglect regular exercise while you’re at it!