How to Put a Stop to Biological Aging – Video
Why do some people live long, healthy lives?
What you will learn about
Why are some people able to live healthy past 100? Certainly, no one wants to live longer, sicker, but what if you felt great and had a sharp mind, would it sound more appealing?
Currently, medicine is increasing the number of old people who are sick – we’ve extended the time we are old, frail, and ill – not fun.
Ideally, we would live longer, during the healthy phase of life by delaying the onset of deterioration and disease.
Stable data about aging
There are stable data about aging that are true whether you are a single-celled yeast, a fly, worm, mouse, or human.
The biggest truth is that calorie restriction extends lifespan and reduces age-related diseases such as cancer, heart disease, type 2 diabetes and obesity. Study after study confirms it.
The only problem is that we don’t like to feel hungry. You can convince yourself it’s “good for you” for only so long before hunger wins out.
Is calorie restriction our only alternative to living a long, healthy life? Fortunately, not.
How to intelligently hack our anti-aging pathways
If you made an analogy of aging to a car, you could speak of premature aging like a car with no brakes. It’s fun and fast, but you’re going to crash at some point and that’s the end of the car. And what if we defined “premature aging” as any disease or disability occurring before the age of 100?
Continuing with the car analogy, the safe, long-lasting car would be able to speed up, slow down, and stop whenever we wanted it to. We would treat it well and it in turn would keep us safe and alive for a long time.
Let’s look at the science of aging and disease
The first aging enzyme we’re going to talk about is called mTOR (this stands for Target of Rapamycin). mTOR is an enzyme that has been likened to a “speeding car without brakes”, hence my car example above.
mTOR is further called a “master determinant of lifespan and aging”. For those of you who enjoy a little historical background, it was given its name when rapamycin was discovered on Easter Island, known by the locals as Rapa Nui. A bacterium was discovered on Easter Island that prolongs life. It does so by inhibiting the mTOR enzyme.
Slowing the velocity of aging
Is there a way to get the brakes of anti-aging pumping and slow mTOR’s effects?
Yes, and that brings us full circle to fasting. A “braking mechanism” that’s been built into us is caloric restriction. mTOR is inhibited when there’s very little food coming in.
During such times of calorie restriction, growth, and cell division slow down significantly. The body instead enters a conservation mode and initiates a process called autophagy, or self-eating. That sounds a little gross, but it’s not actually. In fact, it’s wonderful and healthy.
Your body “self cleans” at times of calorie restriction
Autophagy kicks in when calories are scarce. At such times the body tries to find fuel sources within. Smartly, it goes after death, dying, and malfunctioning cells, as well as malfunctioning parts of cells and organs. It’s like Spring cleaning inside your cells and body, getting rid of unnecessary junk – a healthy self-cleanse.
Understanding autophagy explains why calorie restriction is associated with longer lifespan. If you effectively cleanse yourself of defective cells and parts of organs somewhat regularly, of course your body will live longer.
The body is so clever that when food becomes available again, stem cells are produced that can then become fresh new cells to replace the old sick ones. This is a beautiful anti-aging, regenerative procedure. And one, that has been stimulated, historically, in man by caloric restriction. Of course, that was when food was often scarce; long before the 24-hour grocery stores of today.
Do we have to be hungry in order to not age?
But we’re back to the pesky problem of being hungry again. Fear not, there is a solution.
It turns out that it didn’t have to be ALL calories that were reduced to turn off mTOR, just certain ones, and in most of the pathways we’re going to discuss it revolves around protein calories.
mTOR is stimulated by protein intake; therefore, a reduction of protein without calorie restriction can provide similar effects.
Dr. Longo’s work, detailed in his book “The Longevity Diet” reviews this. In fact, he recommends protein consumption not exceed 10% on a daily basis for this reason.
Proper protein consumption is a key
A 2013 study published in Biochemistry Journal found reducing protein without changes in calories was demonstrated to positively regulate longevity, metabolic fitness and stress resistance.
The second factor of aging is IGF-1, short for insulin-like growth factor, is a hormone similar to insulin (hence its name) that is similar to mTOR in that it assists growth early in life but can contribute to a shortened lifespan and diseases of aging, such as cancer, later in life.
Like mTOR, IGF-1 levels can be controlled by reducing protein intake.
Clearly, IGF-1 isn’t our friend, at least not as an adult. It does have benefits when you are a child because it helps you grow. It was in fact its association with growth that gave us our first clues about the enzyme.
Short people in Ecuador answer a mystery
There is a group of individuals in Ecuador who are very short, under 4 feet tall when fully grown. They do not develop diabetes or cancer, despite a poor diet, and researchers feel they may be protected against heart disease and Alzheimer’s as well.
Science loves a mystery, and this was a good one. In fact; it opened the door to understanding the action of IGF-1, a hormone that causes growth when young, but, like that car without brakes, keeps you speeding along to early aging and disease as life continues.
There are only 350 people in the world with the condition, called Laron Syndrome, and they are all descendents of a single ancestor who had the gene mutation. The natives can’t bind the hormone IGF-1 and therefore cannot grow. The result? Short stature, but also protection against many degenerative diseases.
Obviously, such a genetic mutation is extremely rare, so the big question is, how do we decrease the production of mTOR and IGF-1 with a “normal” diet?
Are plant proteins and animal proteins different?
Research has revealed that plant protein doesn’t raise IGF-1 and mTOR levels nearly as much as animal protein.
Why would plant protein be better tolerated?
Was there something unique in animal protein that stimulated these pro-aging pathways more acutely? It appears that the amino acid composition was a factor. Specifically, two amino acids, leucine and methionine.
Leucine, a branch-chain amino acid, is found predominantly in animal products such as eggs, dairy and meats such as red meat, chicken, and fish, but is much less prevalent in plant foods. It fuels pro-cancer, pro-aging pathways like mTOR.
Of the top 50 foods containing the most leucine, all but soy protein isolate and spirulina are derived from animals. The next plant-based food found on the list is soy protein concentrate in 211th place, out of robust 1,000 foods. Tofu places 286th, firm tofu is 981st.2
The various rankings of soy are worth mentioning as whole organic soybeans and tofu are the best choices when consuming soy, with soy protein isolate something you should steer clear of.
All amino acids are not the same
A quick tutorial on branch-chain amino acids: Leucine is one of 3, the others are isoleucine and valine. There are millions of dollars spent on the purchase of brain chain amino acids in the form of powders and supplements to enhance muscle protein synthesis.
Branch chain amino acids are thoughts to boost muscle growth and exercise performance. Unfortunately, they appear to have a dark side when it comes to aging and cancer.
A 2016 study published in Cell Reports addressed the fact that protein-restricted, high carbohydrate diets improved metabolic health (diabetes, obesity and heart disease) in rodents and humans, but the authors wondered if there were precise protein components responsible vs a generalized low protein diet.
Protein components that speed up the aging process
They proved that feeding mice and humans a diet low in branched chain amino acids was sufficient to improve glucose tolerance, fasting blood glucose levels and weight (fat mass) quickly – in just 6 weeks. The results were just as effective as when they used a generalized protein restricted diet.
Instead of a drastic reduction in dietary protein as performed in earlier studies, a modest reduction was used in tandem with a severe reduction in specific amino acids, in this case, the branch-chain variety.
What do people who live to 100+ have in common?
In support of this, you can observe populations that regularly live over 100 years, centenarians, and you will find they tend to eat minimal animal protein.
Those from Okinawa ate about 10% protein with almost no cholesterol because their diet was predominantly planted. They ate animal foods very occasionally. The same can be said for the Adventists from Loma Linda, CA, who also enjoy incredible longevity.
The second amino acid found much lower in plant-based foods is methionine. Foods very low in methionine are thought to be beneficial in preventing cancer and extending lifespan.
Methionine is predominantly found in animal protein. When looking at foods highest in Methionine based on levels per a 200 calorie serving, the first non-animal food to appear is in 208th place, sesame seed flour, defatted. With partial fat, sesame flour ranks 919th out of 1,000 foods. Soy protein isolate is 896th on the list.
As you can see, plant sources of methionine are extremely low. The top 207 sources of methionine in food, are all animal-based.
Eggs, cheese, chicken, tuna, beef, and bacon head the list. Legumes such as peas, beans (including soy), and lentils are excellent sources of plant protein and low in methionine.
Beans are low in a certain amino acid that promotes aging
Interestingly, beans with their low methionine levels, have been criticized as imbalanced when evaluating their amino acid status.
But with the knowledge that low methionine diminishes free radicals (aging) in internal organs, increases longevity and lowers markers of degenerative disease – the “imbalance” of low methionine in high-protein beans is really a strength of these foods and perhaps their cancer-fighting secret.
A study supported the link between cancer and methionine. It was found that trying to grow cancer cells in a medium with little to no methionine would often result in the cancer cells ceasing to grow. They would not only stop growing and dividing but they would die.3
The line of study graduated from the petri dish to animals and researchers discovered that if mice were implanted with tumors and fed a methionine restricted diet, their tumors grew more slowly and were less likely to spread as compared to those on a regular diet. The low-methionine fed mice also survived longer.
The types of cancer that appear to require methionine to survive include:
- breast cancer
- bladder cancer
- pancreatic cancer
- lung cancer
- brain tumors
- stomach cancer
- leukemia
- lymphoma
- head and neck cancer
- melanoma
- sarcomas
How does methionine, an amino acid, increase cancer risk?
Methionine’s negative effects follow the same mechanism as IGF-1 and mTOR. Namely, it supports building and growth.
Methionine is an amino acid used as a building block for proteins in particular that are essential for cell development and growth. That’s great when you’re young and growing in height and weight, but not as an adult.
Cancer cells rapidly divide and “need” methionine, whereas normal adult cells grow slower and require less of the amino acid.
A 2012 study in Cancer Treatment and Prevention supported the methionine cancer link. The authors had this to say: “Selective killing of methionine dependent cancer cells in co-culture with normal cells has been demonstrated using culture media deficient in methionine.” Interpretation: you can put cancer cells in a petri dish with normal cells and feed them a diet lacking methionine. The cancer cells will die and the normal cells will survive. This beats chemotherapy which kills cancer and healthy cells alike.
The researchers go on to say: “Several animal studies utilizing a methionine restricted diet have reported inhibition of cancer growth and extension of a healthy life-span.” This is self-explanatory – they graduated from a petri dish to animals and saw the same results. Exciting!
“In humans, vegan diets, which can be low in methionine, may prove to be a useful nutritional strategy in cancer growth control. Again, self-explanatory.
An added benefit found in this study was the diet of low methionine also increased something called FGF21 (fibroblast growth factor 21), another longevity hormone.
Longevity hormones “like” a certain diet
Prior studies found the same result – a strong association with the positive effects that vegan and Mediterranean diets have on metabolism with a direct link to the production of the longevity hormone FGF21.
FGF21 is also a growth factor – are you starting to see a pattern here with stimulating growth factors and shortening lifespan? It has beneficial effects on weight, type 2 diabetes, immune function, and longevity, and excitingly was increased in not only rodents but humans as well.
Prior studies that severely reduced dietary protein too saw such results, but these clever researchers accomplished the same feat simply by reducing branch chain amino acids to the level found in low overall protein diets. Patients were able to consume a moderate amount of protein, only methionine was restricted.
We can lessen cancer and extend lifespan without aging
The good news is this continues to support the concept that we can turn off the protein-driven aging, disease and cancer pathways without starving.
Therefore, protein diet quality, specifically amino acid makeup, is critical in avoiding degenerative diseases including cancer. With our understanding of the restriction of branch chain amino acids, leucine in particular, and methionine, both so abundant in animal protein, it clears up why researchers have discovered plant-based proteins having a lower risk for metabolic diseases when compared to the same amount of protein from an animal source.
It’s the amino acid profile that’s distinctly different.
It’s pretty easy when you sum it all up
The pathways we’ve discussed can either reverse aging and decrease the incidence of disease or exactly the opposite, depending on whether they’re active or not.
To experience anti-aging and disease protection, it was discovered we had to reduce protein intake, specifically certain amino acids.
Our final pathway is one turned on by sugar consumption. It’s called the PKA (Protein Kinase A) pathway, or the sugar pro-aging pathway. This pathway is fundamental to the ability of cancer cells to resist dying in the face of glucose starvation, so we definitely don’t want it active.
It appears the reduction of both protein and sugar in the diet can prevent PKA from protecting cancer cells and instead, make them vulnerable to destruction, everyone’s goal.
The pathways we’ve discussed explain why calorie restriction is so successful in extending lifespan. The good news is that there is an alternative to starvation while still enjoying longevity and disease prevention effects.
The perfect health hack
If that’s not the perfect “health hack”, I don’t know what is – Longevity and disease prevention without starving.
I wanted to share the good news that anti-aging pathways are very amenable to activation with some easy dietary changes.
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