Eat Less and Live Longer
Dietary Restriction and Its Effect on the Body
What’s up with all of this talk on eating less?
Is there real science to back up dietary restriction??
So what does “dietary restriction” imply?
Ha yes, you guessed it: eating less.
And usually it entails eating less than you think you need. It’s about actively knowing that you don’t need as much as your body tricks you into believing.
So, that makes it a little hard to deal with… Restricting food is a very tricky subject.
But regardless of how “easy” or not dietary restriction is, the science supporting that it is healthy is undeniable.
We believe it is actually healthy in two ways:
==> 1. Overeating is a very real disorder and addiction. Restricting the substance and avoiding the abuse will directly lead to a life of better control and true happiness.
==> 2. Decreasing the amount of food energy input will directly lead to less electronic reduction of the ETC. (That is the electron transport chain.)
That might sound new to you if you are not a total Bio-nerd like we are.
The ETC is the mechanism by which your body creates the energy you need for everything (ATP).
Less electronic reduction means less ROS production.
==> Less ROS production is generally good.
Do you remember what reactive oxygen species (ROS) are?
We’ve talked about them the last few weeks, so you might not need a reminder. But just in case… you can check out our commentary on the subject here.
And thus begins Part 3 of the trilogy of figuring out why you age.
What is it about eating that causes you to age? Eating is necessary for life, right?
Absolutely. But not in such large amounts as we are used to in America.
So let’s jump into the subject, shall we?
Summary of Part 3
- Eating less puts less strain on the ETC (less ROS production)
- Eating less does not mean less energy production of the ETC
- Rather, it means less free radical leak
- Protein restriction (specifically methionine) has been shown to increase longevity
- The story is NOT about total calories
- Intermittent fasting — gorging yourself in-between — is better than frequent eating of the same calories.
Again, there is no “new” piece of research for this post. But if you are interested, as always, the link is below!
==> The Cell Aging Regulation System (CARS) – conducted by Gustavo Barja at the University of Madrid.
While this whole article is about ROS production and what it implies for the body, there is much more depth as to how ROS is produced.
We specifically go over how eating less is related back to ROS and how this is beneficial for you.
And it turns out that some sources of calories are better than others.
It is not all about “calories in” and “calories out” — like the current medical industry would have you believe.
There is so much to dive into with this research article, but we only wanted to highlight what we found as most valuable.
Less Food = Less ROS
This concept is seems very simple at first. And, indeed, it is.
But to fully “understand” it all requires a lifetime of dedication. The overall, birds-eye view is the best way to convey the message.
Simply put, Complex I is a protein that helps with the regulation of electron flow.
It is from normal electron flow that you generate energy in the form of ATP.
Anyway, if you overload the ETC, your electrons start to “bounce back” to Complex I. That is why it’s the location of ROS production.
Remember that ROS is the precursor to free radical species.
Lost electrons at the ETC = ROS production.
This leads us to a very important point that we reiterated last week:
==> Faster living (meaning more O2 consumption and reduction) does not mean faster dying.
Rather, it is the loss of electrons that matter.
Free Radical Leak
Biology is a very confusing and debated world, so we are here giving very impartial judgments.
For right now, let’s assume they are bad — like our article says.
They suggest (and logically so) that free radicals come from overloading Complex III, not from higher oxygen consumption.
The reduction of O2 is not the problem — the food is.
And it turns out that if you are eating a whole lot, you do not necessarily get more ATP.
Your body seems to know how much it really needs, so it will send that excess backwards.
But if you are eating less, then you are giving your Complex III less of an opportunity to “bounce back” electrons to Complex I to create ROS.
Your mitochondria are acting more efficiently.
Now there is no excess electrons to send back. They are all becoming part of ATP synthesis.
But, it seems to be even more detailed than simply eating less.
It matters how you are accomplishing that and what substrate you are specifically restricting.
Protein (Methionine) Restriction
This article goes into a large amount of detail about protein restriction and how it is beneficial. We are just going to give a quick summary for you.
They found that methionine restriction brought about much higher rates of longevity.
It also had a direct correlation with less incidence of disease.
Pretty much, they are suggesting there is a quality to the food. Longevity depends on what type you are restricting.
Restricting this protein works in many ways (according to the article):
==> decreases blood glucose, insulin IGF-1, triglycerides, and leptin.
The decrease in serum glucose levels is the most logical mechanism.
We know that protein metabolism will result in the creation of glucose in the blood.
So… decrease protein = decrease glucose (which is good). This one is a little easier to see.
The decrease in IGF-1 (insulin-like growth factor) is also beneficial. It has been shown to be related to cancers.
It has an over-expression in highly cancerous environments.
We do not want to get too caught up in the details though…
So for right now, just understand that this article claims protein restriction is the specific part of dietary restriction that “works.”
Not Just About the Calories
Not all calories are created equal.
No, sadly our bodies are not equal opportunity employers. They prefer certain calories to others.
But more interesting is the fact that it is more related to timing than anything.
Even the exact same calorie sources taken at different times can have different effects. Pretty cool, huh?
==> The important finding: extended periods of low food intake had the best results.
“[Intermittent fasting] increases longevity even in mouse strains that gorge the days that they receive food.” 
So… Pretty much, we have been tricked into believing that snacking is better than gorging. Interesting…
It makes sense from our point of view and commentary on the article.
If you are going to have a huge spike in insulin, then you might as well get it over with in one fell swoop.
It is not good for you to have extended periods of hyperinsulinemia. But that is a topic for another time…
This article suggests that a “pro-aging program” is kicked in place when food intake is high (and insulin thus spikes).
And it looks like it is an all-or-nothing kind of mechanism.
It is either “on” or it is “off.”
That would explain why it’s better to eat all at once rather than continually snack throughout the day.
This is very important because it goes against all common advice. We have never seen the real evidence that snacking is better than gorging.
It seems counter-intuitive, but gorging and then intermittent fasting is better than snacking. Maybe not “good”… But better.
The article ends by saying that: “Putting all the food in a single early meal, or perhaps, in two big meals… would be an adequate option.” 
Saturated fat is the best option then!!
100% – without a doubt.
How did we come to that conclusion? Well, as we will see in future research blogs, fats are more satiating.
You simply do not each as much of them because they are more “filling.”
Also, they imitate the mechanisms of dietary restriction very well.
They also produce more efficient mitochondria, and they result in a smaller double bond index (leading to less peroxidation).
We do not want to ruin that surprise completely though… We will get there soon enough.
To health, love and happiness!
 Ifland, J. et al. 2009. Refined food addiction: A classic substance use disorder. Medical Hypotheses 72:518–526.
 Barja, G., et. al. 2017. The Cell Aging Regulation System (CARS). Reactive Oxygen Species 3(9):148–183.
 Liu, Y., Fiskum, G., Schubert, D. 2002. Generation of reactive oxygen species by the mitochondrial electron transport chain. Journal of Neurochemistry 80:780–787.
 Li G. 2013. The Positive and Negative Aspects of Reactive Oxygen Species in Sports Performance. Current Issues in Sports and Exercise Medicine.
 Scialo F, et al. 2018. Mitochondrial ROS Produced via Reverse Electron Transport Extend Animal Lifespan. Cell Metabolism. 23(4):725-735.
 Ross, B. D., Hems, R. & Krebs, H. A. 1967. The rate of gluconeogenesis from various precursors in the perfused rat liver. Biochemical Journal 102:942–951.
 LeRoith, D., Roberts, CT. 2003. The insulin-like growth factor system and cancer. Cancer Letters 195:127-137.
 Crofts, C. 2015. Hyperinsulinemia: A unifying theory of chronic disease? Diabesity 1(4):34-43.