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Scientist studying the science of aging in the Longevity Code

The Longevity Code

In his new book, The Longevity Code: Secrets to Living Well for Longer from the Front Lines of Science, medical doctor and researcher Kris Verburgh explains why we age and how we can delay the process through new and imminent scientific breakthroughs.

Scientifically reviewed by Dr. Gary Gonzalez, MD, in October 2024. Written by: Garry Messick.

For millennia, humankind has thought of aging as an inevitable process. After all, what could be more observably apparent than that everyone who survives past a certain age begins to slowly deteriorate, ends up decrepit, and dies?

But the latest science tells us that aging is essentially a disease, and, like any other disease, it can possibly be cured.

In his new book, The Longevity Code: Secrets to Living Well for Longer from the Front Lines of Science, medical doctor and researcher Kris Verburgh examines the reasons why we age and what can be done to not just slow that process, but even reverse it through various means including scientific breakthroughs that currently exist or are very close to being realized.

Dr. Verburgh is a researcher at the Center Leo Apostel for Interdisciplinary Studies at the Free University Brussels and is on the faculty of Singularity University, a Silicon Valley think tank. He has proposed the discipline of nutrigerontology to develop diets and guidelines to reduce the risk of age-related diseases.

What you need to know

Dr. Kris Verburgh, M.D. explains why we age and discusses the groundbreaking research on what we can do about it in his new book The Longevity Code: Secrets to Living Well for Longer from the Front Lines of Science.

In the following interview, Verburgh discusses the reasons aging exists and briefly touches on aspects of his four-step plan to slow and even reverse it.

— Garry Messick

Seniors exercising  

LE: What is the cause of aging?

KV: The average lifespan of an animal species, or the rate at which it ages, is determined by the average time that this animal species can survive in the wild. If an animal species, such as a mouse, frequently dies of external causes, it will also age faster and have a shorter lifespan. If an animal species can survive longer in the wild, it will age at a slower rate and have a longer lifespan, as is the case with turtles. That explains why a mouse is already very old at age 3, while a bat can live to be 30 years old.

In contrast to mice, bats can fly, which is why they can evade danger much faster. Unlike mice, they do not have to live on the ground, where they can fall prey to cats and mouse traps. Thanks to their wings, bats can also cover longer distances and are better able to find food. Every mutation in the past that made it possible for a bat to live longer was useful, because bats are much better able than mice to flee from danger, find food, and survive.

What is true for mice is also true for people. Our lifespan, too, is determined by the length of time that our ancestors could overcome dangers and survive in the wild. In prehistoric times humans often perished by around age 30 from disease, hunger, accidents or violence. A mutation that allowed them to age at a slower rate and live longer (to 200 years, for example) was not useful, because before their third decade they usually had been eaten by a saber-toothed tiger or died from blood poisoning caused by a tooth abscess.

LE: So aging isn’t a simple matter of wear and tear, as was once thought?

KV: The popular notion that aging is a matter of irreparable damage stems from the so-called machine myth. People tend to view the human body or any other organism as a machine that is subject to wear and tear and eventually breaks down. But living beings are not machines. Contrary to machines, living beings can continuously rejuvenate and repair themselves. They do that by extracting energy from their environment (in the form of nutrients, light, and oxygen).

LE: So what can we do to slow down the aging process?

KV: Scientists have learned a lot more about aging in the last decade than in the thousands of years before. New discoveries follow each other with unprecedented speed. To better organize these new insights and knowledge, and to make maximum use of their potential, I have designed a plan for living a longer and healthier life. It can be represented in the form of a staircase, which currently has four steps. Each step contains a method to slow down the aging process and stay young longer.

LE: What’s the first step?

KV: Avoid deficiencies. In the West, millions of people are overweight but still suffer from malnutrition. They consume too many macronutrients, and are malnourished due to a lack of micronutrients. Macronutrients are carbohydrates (sugar), fats, and proteins. These foods supply energy. Micronutrients are healthy substances, such as vitamins, flavonoids, stilbenes, phenolic acids, lignans, and omega-3 fatty acids. Micronutrients are needed for the proper functioning of the body. Much of the food we eat today consists mainly of macronutrients with very few micronutrients.

LE: Can you give an example of an important, neglected micronutrient?

KV: Magnesium is a micronutrient that is lacking in many people. Magnesium binds to all kinds of proteins to make them function better. Like the B vitamins, this mineral is important for our metabolism, including sugar metabolism. Magnesium improves the ability to process sugars. That is important because the older we get, the less the body is able to process sugars, which increases our risk of various aging-related diseases, including type II diabetes, cardiovascular disease, and dementia. Magnesium can also lower blood pressure, which is good for the blood vessels. It can also reduce the risk of heart-rhythm abnormalities, which are an important cause of death in older people.

Seniors exercising  

LE: You write in your book that supplements can be useful, and that studies sometimes erroneously find that certain supplements are not beneficial because they either use too low a dose, or the wrong form of a vitamin, or they ignore the ways vitamins and nutrients work together. Can you give an example of how researchers make these mistakes?

KV: One study found that in people with little vitamin B12 in their blood, there can be six times greater shrinkage of the brain than in people with sufficient vitamin B12. Researchers who gave high doses of vitamins B6, folic acid (B9), and vitamin B12 to a group of elderly people observed in brain scans that there was seven times less brain shrinkage in this group than in a group that did not take supplements. The researchers concluded that “the disease process responsible for cognitive decline can be slowed down significantly and maybe even halted.”

A more recent study, however, in which participants were given high doses of only two types of B vitamins (B9 and B12) did not show an effect on cognition. Does that mean that high doses of B are useless? Not according to scientists like Sudha Seshadri, a professor and Alzheimer’s researcher, who stated, “The second study did not last long enough and the methods used to measure cognition were too crude.” The study lasted two years, while we know that diseases like Alzheimer’s take decades to develop. Also, only two types of B vitamins were used, while there exist many other B vitamins, which all have a synergistic effect in our body by working together.

LE: Your second step to combat aging is to stimulate hormesis—the effect by which harmful things can be healthy in small doses. You mention the highly beneficial drug metformin as an example.

KV: Metformin, as it happens, is mildly toxic to mitochondria, the energy generators that activate the cells in our body. This causes the mitochondria to better protect and repair themselves, making them less prone to aging. This, in turn, causes the body to improve its capacity to process insulin and sugars.

Exercise is also a form of hormesis. The most important reason why exercising is healthy is because it damages the body. An hour of cycling or swimming makes our cells work much harder than they usually do. They become overtaxed and slightly damaged, which you can feel the next day when you wake up with sore muscles. However, this prompts cells to repair and protect themselves for the next time you go for a bike ride or dive into a pool. As the cells keep arming themselves against that kind of damage, they are then also better prepared against other kinds of damage, such as that caused by aging processes. This is one important reason why exercising can decrease the risk of all kinds of aging-related diseases, such as heart disease and dementia.

CRISPR research  

LE: After your third step of reducing growth stimulation that speeds up cell aging, your fourth step for longevity is to not just slow but reverse the aging process. We don’t have space to discuss all the possibilities you mention in your book, but could you briefly outline one of the more interesting scientific advances in this area, the use of CRISPR proteins?

KV: CRISPR proteins are a recent discovery that enables researchers to rewrite genes (pieces of DNA that contain the building instructions for proteins).

Until recently this was a very laborious and time-consuming process. A certain gene had to be made in the laboratory (a piece of DNA that could cure a disease caused by absence of that gene or a poorly functioning gene). This gene had to be inserted into a virus and that virus was injected into a person. The virus then infected cells and planted the gene somewhere at random in your DNA. Since this is a completely random process it could, for example, cause cancer if the gene was planted in an area of DNA that controls cell growth.

Via CRISPR proteins, this can all be done very fast and very precisely. They are designed to search out and rewrite specific genes in the DNA. Scientists have succeeded in curing mice of a metabolic disease simply by injecting CRISPR proteins into the tail. These proteins rewrote the DNA of the mice so that they no longer suffered from this genetic disease.

LE: How does CRISPR technology relate to the fight against aging?

KV: In the future, it may be possible to rewrite genes that play a role in aging. Some people may object that this would be very difficult, since they believe that many thousands of genes are involved in the aging process, and it would be difficult to change all these genes. But that does not seem to be necessary. Often only one gene needs to be changed to extend the lifespan, as has been shown in numerous experiments with lab animals. Changing only one gene, such as the gene that controls insulin metabolism, could allow a mouse to live, for instance, 50% longer. These genes are often master genes that can influence the activity of other genes. You would need to change only these master genes.

Besides altering the genome with technologies like CRISPR, there also seems to be promise in modifying the epigenome. The epigenome determines which genes are active or not. Scientists managed to reprogram the epigenome in mice, thereby rejuvenating them. The grey fur of the mice turned shiny black again, and their organs and muscles could regenerate themselves far better. Many other fascinating experiments show that aging can be reversed, at least in animals.

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LE: To sum up, what should the average person do to achieve longevity?

KV: In the future, we will see the advent of promising new technologies that can substantially slow down, or even reverse aging. However, the best method we currently have to live as long as possible is our lifestyle. It is not a coincidence that a healthy lifestyle reduces the risk of both age-related diseases and overweight, for aging and overweight are two sides of the same coin. And for those who want to become really old, a healthy lifestyle is the best way to achieve it. They may be able to profit from LEV, longevity escape velocity, to achieve a much longer life. Each time, they will live long enough to profit from the latest life-extending technology. To put it in the words of Bill Maris, the former Google investing maverick, “I just hope to live long enough not to die.”

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