How DNA damage contributes to aging
You might think of your DNA as something that never changes, but actually, our DNA is subject to constant damaging events from our environment and other factors. It’s estimated that an individual cell can suffer up to one million DNA changes per day.
Our bodies have built-in mechanisms to repair damage, but over time, the ability to repair damage decreases. Scientists think this damage — and this decrease in the ability to repair damage — may be an crucial component of aging.
Because DNA holds the genetic information for each cell, its stability is essential for living a long and healthy life. If not repaired, this repeated damage can lead to mutations and disease. This repeated damage underlies most of the degenerative diseases that cause premature death, including atherosclerosis, cancer, and Alzheimer’s disease.
Causes of DNA damage
One common example of DNA damage is skin cancer, which is caused by excessive exposure to UV radiation from the sun. Tobacco smoke also causes DNA damage in lung cells, leading to lung cancer. Free radicals, potentially dangerous byproducts of normal metabolic processes, can also cause damage that leads to impaired cell performance and cell death, and also contributes to chronic inflammation.
DNA is also often subject to damage during the process of cell division. Every day, billions of cells in our bodies die and are replaced by new ones, which are formed when a cell divides and passes its genetic information to the two new cells, known as daughter cells. Each strand of DNA has caps on the ends known as telomeres, which help protect our chromosomes. Each time a cell divides, the telomeres get shorter, until they are eventually unable to do their job. This leaves cells at risk of serious damage. Telomere shortening can also occur as a result of stress, smoking, lack of exercise, obesity, and a poor diet.
When telomeres get too short, a cell will do one of three things:
- Continue to divide, forming abnormal daughter cells that can lead to cancer
- Stop replicating by dying, a process known as apoptosis
- Stop replicating by turning itself off, turning into what is known as a senescent cell
Although senescent cells are turned off, they continue to function on some levels and to interact with other cells. Senescent cells are potentially dangerous, as they can release molecules that increase the risk of disease, particularly cancer.
Protecting against DNA damage
Fortunately, you can take steps to protect your DNA from the constant onslaught of damage. The body’s ability to repair DNA is one of our biological processes that are influenced by diet. Studies have found that people who eat a diet high in fruit and vegetables have lower rates of cancer and other diseases related to DNA damage. Foods such as lemons, persimmons, apples, strawberries, celery, and broccoli are particularly effective at protecting DNA.
A group of plant compounds known as xanthophylls have also shown protective effects against DNA damage. Xanthophylls, which are found in yellow and orange vegetables, as well as dark leafy greens, seem to limit DNA damage and strengthen the body’s repair mechanisms.
Periodic prolonged fasting may also strengthen the body’s natural repair process. New research indicates that constantly eating — as most Americans are prone to do — puts too much strain on the digestive system, and prevents our bodies from transitioning into repair mode. Fasting — or even replacing meals with plant-based soups that are easier to digest — can remove this digestive burden and allow the body’s repair and rejuvenation processes to work more effectively.
One such approach is the ProLon fasting mimicking diet — or fasting with food — which was developed based on research from the Longevity Institute at the University of Southern California. ProLon is a five-day diet plan that is low in both protein and total calories. All of the foods required for the diet — which include nut bars, olives, and plant-based soups — are included in the ProLon kit. In clinical studies, ProLon was shown to help maintain healthy levels of a marker associated with increased mortality and DNA damage in human cells.