April 13, 2024

How to “turn on” your anti-aging genes – and live longer

You’ve probably referred to them in a negative way – blaming them for your weight, bad habits or hair loss. But while you can’t change the genetic hand you’ve been dealt, you actually have more control over how your genes work than you think.

We are born with around 20,000 genes, which are stretches of DNA that contain instructions for our cells. There are two copies of each – one inherited from each of our parents.

Scientists know that some genes predispose us to a greater risk of health problems. For example, certain genetic variants can increase the risk of becoming obese, developing Alzheimer’s disease and suffering from cancer.

However, lifestyle habits are intertwined with how our genes are expressed and can effectively “turn” certain genes “on” or “off” – similar to the light switches in your house.

Ultimately, this means that, in many cases, it is possible to decrease genes linked to disease and increase those linked to long life.

“Studies have shown that longevity in humans is about 25% hereditary. What this means is that the time we live is mostly (75 percent) determined by the environment and only 25 percent by our genes”, says Prof. João Pedro Magalhães, head of the Aging and Rejuvenation Genomics Laboratory at the University of Lisbon. Birmingham.

“If you exercise, it induces changes in your body that in turn affect how your genes are expressed. The same goes for diet.”

It is “very difficult” to draw a line between changes in lifestyle, a change in genetic expression and the indirect effect on longevity, notes Professor Magalhães. However, there is some promising research.

Calorie restriction

“There is a gene called mTOR that regulates the way our cells perceive nutrients and – depending on this – decide whether to grow or not”, explains Dr. Nick Ktistakis, group leader at the Babraham Institute, where researchers study the process of aging.

“Reducing mTOR activity has been shown to extend lifespan in many organisms, and would likely do so in humans. So reducing mTOR activity is good for longevity,” he says.

One way to effectively turn off mTOR is to reduce calories, according to studies in animals, which have had their diet cut in half.

However, the scientists admit that the “sheer willpower” people would need to follow suit makes this unattainable, and they make the somewhat obvious warning that the approach could trigger dangerous side effects, such as excessive weight loss.

Therefore, researchers are studying a pharmaceutical alternative – a drug called rapamycin. It was originally developed as an immunosuppressant for organ transplant patients, but like calorie restriction, it deactivates mTOR. “A lot of work is being done with these medications to see if they can affect longevity,” says Dr. Ktistakis.

“Rapamycin is one of the most robust life-extending drugs, as it extends lifespan in rodents (up to 15%) and is currently being tested in dogs. [It] It is one of the most active areas of research in longevity pharmacology”, says Prof Magalhães.

However, separate studies have supported the evidence that cutting calories allows for a longer life. A study by a team at Columbia University found that people who reduced their food intake by 25% over two years slowed biological aging by 2 to 3%. This conclusion was reached after collecting blood samples from volunteers to monitor chemical markers that regulate the expression of genes related to longevity.

The researchers noted that while drastic calorie cutting is “probably not for everyone,” simply following intermittent fasting (eating very little or nothing during a set period of time, such as one or two days a week) or eating restricted time. (consuming food within a fixed window each day, such as 10am and 6pm) can trigger similar results.


Scientists are also excited about a gene called FOXO3. Studies dating back more than a decade show that it activates autophagy – the process where cells get rid of old, damaged parts, which is vital for increasing healthy life expectancy.

Although, as with all genes, everyone has two copies of it, three in 10 people in the UK have a “supercharged” version, while one in 10 have two – meaning they have a “supercharged” FOXO3 gene. jet,” according to Dr. Willcox, professor of public health and gerontology at Okinawa International University in Japan. Only a genetic test can reveal which version a person has.

“Our studies have shown that FOXO3 is at the heart of the aging core. It integrates signals from dozens of other genes that affect the aging process. Think of it as an overseer gene that directs the aging process and also protects against age-related diseases,” he says.

Research has shown that FOXO3 protects against cardiovascular disease – one of the leading causes of death in the UK – and cardiometabolic diseases, which include heart attack, diabetes and non-alcoholic fatty liver disease.

Exercise can activate FOXO3, alerting it “that it needs to get to work” and counteracting the stress that physical activity puts on the body, explains Dr. Willcox. In response, FOXO3 triggers the release of antioxidants that reduce inflammation.

How quickly the gene is activated depends on the person’s genes and lifestyle. But it will likely occur slowly over time, “just as physical exercise will change your body shape over time,” he says. “The key to lifestyle change is persistence and continuity,” adds Dr. Willcox.

To sleep

Other studies show that sleep is vital.

When scientists at the University of Rochester compared how genes were regulated in dozens of animals, they found that among the longest-living species, genes linked to inflammation and the process of converting food into energy were downregulated.

Rather than the expression of these genes being predetermined, whether they were increased or decreased was actually dictated by the body’s circadian network – also known as the body’s internal clock.

The team concluded that this meant that an unhealthy sleep schedule or exposure to light at night could increase the expression of genes that reduce people’s lifespans, although the study focused on animals.

Drink green tea and eat broccoli, oranges and berries

“AMPK is often viewed as the ‘master switch’ of our metabolism and also as a central junction for many nutrient response pathways associated with longevity,” says Dr. Harpal Bains, medical director of the longevity-focused Harpal Clinic, In London.

Both green tea and the antioxidant quercetin—found in onions, broccoli, citrus fruits, and berries—can activate AMPK, she says.

“Finding good quality green tea is a fundamentally good way to support longevity, as green tea can support many areas of gene expression,” adds Dr. Bains.

Calorie restriction and exercise also activate this gene, she says.

“Calorie restriction definitely doesn’t mean eating as little as possible,” notes Dr. Harpal. “That would be unhealthy, causing nutritional deficiencies and causing us to have inadequate fuel – which is not good for our longevity. Instead, it’s more about not overeating: we should aim to feel about 80% full at each meal.”

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