There’s a saying where a mom tells her child that if he doesn’t eat – he won’t grow up, and there’s actually more than one may think in this say.
Growing up takes energy, and energy comes from food. How exactly? By oxidizing the food and producing energy units – ATP. This process takes place in all living creatures’ power plant – the mitochondria.
But there’s also another side, a darker side, in this process. Another mitochondria production – the free radicals, a by-product of ATP synthesis. In short, in addition to their role of regulation, free radicals harm other molecules and drive aging. Saying that we easily figure out the inevitable equation:
Food = Free Radicals = Harm (Mutations) = Diseases and a Shorter Lifespan.
So how exactly can an extremely low-calorie diet form healthy effective diets that produce the least free radicals as possible and encourage longevity, health, and slow down the process of aging?
WHY Calorie Restriction And Aging Are Correlated
During evolution, animals had to develop a way of handling famine, which is to say, only animals who can handle starvation could survive so their successful genes could help their offspring do so as well. What happens in those harsh times is simply a sexual maturity delay, that is to say – wait for the required resources to be available, and then get ready for sex in order to bring offspring, like a sort of an hibernation, which is another technique developed by some animals in order to survive harsh times. But why, one may ask, a sexual maturity delay?
The tradeoff between sex and longevity is based on the energy resources limit we have.
First of all – gestation requires huge amounts of energy (food), so the animal wouldn’t make it through this period while lacking in food. And even if it does, its offspring are likely to die the very first moments they’re born as a result of starvation, so the animal genes don’t survive, which is as worthy as not having offspring at all.
This is how, in short, the system was developed during evolution and why the genes that delay aging are stimulated by famine, e.g insulin hormones remain silent in famine, waiting…
So there’s no wonder that the slower the metabolism, the longer the lifespan and vice versa, and this is where a very low-calorie diet comes into place, and forms the most effective diets in terms of longevity, health, and anti-aging.
HOW Does it Work? Free Radicals
What are they?
Free radicals are molecules that contain electrons that miss their pairs, making them chemically reactive, trying to steal an electron to be stable. But by doing so, they hurt the molecule the electron belongs to, making it a free radical itself, and so on, causing a chain reaction.
Where do they come from?
Some free radicals are the result of pollution and toxins getting inside our body from the outside, but most of them are generated in the mitochondria itself during our cell respiration process, leaking when ATP is produced. During the years as the mitochondria wear out, the free radicals leakage in the mitochondria gets worse.
What do they do?
The first option is as written. They are mainly active in the mitochondria, and they are very reactive, so the moment they go, they start looking for an electron and don’t get far away while attacking the first opportunity in front of them, so most of their damage is in their close environment – the mitochondrial DNA, and also other cell components, such as proteins.
Once the free radicals drive those components crazy, it starts the inflammation state that accumulates mutations in the mitochondrial DNA. These mutations lead to a corrupt functionality of the cell, that is to say, the main road to cancer and age-related diseases.
The second option is using an evolutionary system that drives a cell suicide (as for preventing cancer) as soon as the leak speeds up. Either way doesn’t look promising, no matter what we choose, the aging progress is still on. Moreover – the faster the leak, the shorter both lifespan and ‘healthspan’.
WHAT Can We Do?
The leak rate is determined by the metabolic rate. So we may think – let’s fight them!, but have no mistake about free radicals – they have an important role in regulation, and fighting them with antioxidants is useless since the free radicals are too reactive, and even if it was possible to fight them, it would do as much harm as good (Also, recent studies show antioxidants are mainly active in the nucleus, where fewer mutations are accumulated, and their help in extending life is insignificant if any).
The other option we have is trying to keep the free radicals leak at a low pace. How? Exactly as was described before – calorie restriction.
Calorie Restriction
Calorie restriction always induces more mitochondria which have membranes resistant to damage, and leak fewer reactive free radicals, as free radicals are a by-product of oxidizing food.
Calorie restriction resets the clock of life back to youth, returning the genes to the youthful chemical environment, so calorie restriction improves the efficiency of energy use without lowering functional energy levels.
The Bottom Line
The question we care about the most is how relevant all of this is to us.
In practice, mice that are given calorie restriction diets that contain 60% of the calories of their normal diet, end up with a lifespan of 150% and a much longer health-span. When a calorie restriction diet is tried among nematodes, they live a few times longer than normal.
So in summary, calorie restriction slows down the aging process, thus preserving youth functionality, and protecting old age diseases in correlation to restriction level. A healthy low-calorie diet is essential for forming safe and effective diets in terms of health and longevity.
We notice obesity in humans and other animals with plenty of food accessibility since the body never knows how much to eat precisely, it tends to consume more than its nutritional needs, as our evolution taught us all to stick to the phrase: “Let us eat and drink, for tomorrow we die!”. We mustn’t allow our destructive desires to lead us toward this miserable state of illness.