You've probably called them negative: you've blamed them for your weight, bad habits, or thinning hair. 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 about 20,000 genes, which are pieces of DNA that contain instructions for cells. There are two copies of each - one inherited from each of our parents.
Scientists know that some genes predispose us to a higher risk of poor health. 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 the way our genes are expressed and can effectively turn certain genes 'on' or 'off' - similar to light switches in your home.
Ultimately, this means that in many cases you can turn off the genes associated with disease and boost the genes associated with longevity.
"Studies have shown that longevity in humans is about 25 percent heritable. What it means is that how long we live is largely (75 percent) determined by the environment and only 25 percent by our genes," says Prof. Joao Pedro Magalhaes, head of the Genomics of Aging and Rejuvenation Lab at the University of Birmingham.
"When you exercise, it causes changes in your body that in turn affects the way your genes are expressed. The same goes for nutrition."
It is "very difficult" to draw a line between changes in lifestyle, a change in gene expression and the knock-on effect on longevity, notes Prof. Magalhaes. However, there is promising research.
Calorie restriction
"There is a gene called mTOR that regulates how our cells sense nutrients and - depending on that - decide whether they want to grow or not," explains Dr. Nick Ktistakis, group leader at the Babraham Institute, where researchers study the aging process.
"Reducing the activity of mTOR has been shown to extend the lifespan of many organisms, and this would likely be the case in humans as well. So reducing mTOR activity is good for longevity," he says.
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One way to effectively eliminate mTOR is to cut back on calories, according to research in animals, which involved cutting their diets by up to half.
However, scientists admit that the "sheer willpower" required for people to follow suit makes this unfeasible and warn somewhat obliquely that the approach could cause dangerous side effects, such as too much weight loss.
That's why 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 disables mTOR. "There's a lot of work being done with these drugs to see if they can affect lifespan," says Dr. Ktistakis.
"Rapamycin is one of the most robust life-extending drugs because it extends the lifespan in rodents (up to 15 percent) and is currently being tested in dogs. [It] is one of the most active areas of research in longevity pharmacology," says Prof. Magalhaes.
However, separate studies have supported evidence that cutting calories lasts longer. A study by a team at Columbia University found that people who reduced their food intake by 25 percent for two years slowed their biological aging by two to three percent. That conclusion was reached after they took blood samples from the volunteers to monitor chemical tags that regulate the expression of genes linked to longevity.
The researchers noted that while dramatic calorie reduction is "probably not for everyone," simply following intermittent fasting (eating very little or nothing at all for a set period of time, such as one or two days a week) or time-restricted eating (every day consuming food within a fixed time frame, such as 10am and 6pm) can yield similar results.
Excercise
Scientists are also excited about a gene called FOXO3. Studies dating back more than a decade show that it activates autophagy - the process by which cells remove old and damaged parts, which is essential for extending a healthy lifespan.
While, as with all genes, everyone has two copies of it, three in ten people in Britain have one 'supercharged' version, while one in ten have two - meaning they have a FOXO3 gene with a have a 'jet engine', according to Dr. Craig. Willcox, professor of public health and gerontology at Okinawa International University in Japan. Only a genetic test can reveal which version someone has.
"Our studies have shown that FOXO3 is central to an aging hub. It integrates signals from dozens of other genes that influence the aging process. Think of it as a superintendent gene that controls the aging process and protects against age-related diseases," he says.
Research has shown that FOXO3 protects against cardiovascular disease - one of the leading causes of death in Britain - and against cardiovascular and metabolic diseases, including heart attacks, diabetes and non-alcoholic fatty liver disease.
Exercise can engage FOXO3 by alerting it "to get to work" and counterbalance the stress that physical activity puts on the body, Dr. Willcox explains. In response, FOXO3 activates the release of antioxidants that reduce inflammation.
How quickly the gene is activated depends on a person's genes and lifestyle. But it will likely happen slowly over time, "just like exercise will change your body shape over time," he says. "The most important point when making lifestyle changes is persistence and continuity," adds Dr. Willcox.
Sleep
Other studies show that sleep is essential.
When scientists at the University of Rochester compared how genes were regulated in dozens of animals, they found that in the species that lived the longest, genes related to inflammation and the process of converting food into energy were dimmed.
Instead of the expression of these genes being predetermined, whether they were turned up or down was actually determined 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 shorten lifespan in humans, despite their research focusing on animals.
Drink green tea and eat broccoli, oranges and berries
"AMPK is often thought of as the 'master switch' of our metabolism and also seen as a central intersection for many nutrient-responsive pathways associated with longevity," says Dr. Harpal Bains, the medical director of the Longevity Institute. targeted 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 genetic expression," adds Dr. Bains.
Calorie restriction and exercise also turn up the dial on this gene, she says.
"Caloric restriction is definitely not about eating as little as possible," notes Dr. Harpal. "This would be unhealthy because it would cause nutrient deficiencies and leave us without enough fuel - not good for our lifespan at all. Instead, it's more about not overeating: we should aim to feel 80 percent full at every meal."
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