Chronic stress may result in DNA damage that not only causes graying hair but also increases the risk of developing life-threatening diseases, according to a new study.
In a pioneering research just published online in Nature, scientists from Duke University in North Carolina investigated the mechanisms that cause stress-induced damage to DNA, the critical genetic material in humans and nearly all other living organisms. The authors simulated a biological response to prolonged stress in mice by injecting them with adrenaline for four weeks and evaluating the processes involved in damaging the animals’ DNA.
Like cortisol, adrenaline is a natural yet powerful hormone produced by the adrenal gland and secreted under stressful situations. The surge of both cortisol and adrenaline enhances the response to a perceived threat by increasing heart rate, dilating air passages, and contracting blood vessels, thereby temporarily boosting physical function. It is intended to be transient, with a return to homeostasis, or physical and mental equilibrium, necessary to maintain health.
Prolonged stress, however, inhibits the return to a natural state, with elevated hormone levels wreaking havoc by suppressing the immune system and making individuals susceptible to illness, disease and psychological disorders. Additionally, chronic stress has been shown to cause DNA damage as minor as graying hair, with pigment-producing cells being impacted, and as serious as tumor development, growth inhibition, metabolic impairments and miscarriages. Diseases such as peptic ulcers, cardiovascular disorders, migraines, and hypertension have been associated with persistent distress, with medical care professionals estimating that nearly 70% of doctor visits are directly related to ongoing stress.
Generally, when DNA damage occurs, a critical anti-cancer protein known as p53 and often referred to as the ‘guarding of the genome’ is activated. The protein is encoded in a specific gene and suppresses tumors by preventing genome mutations.
In the experiment, the p53 levels of the adrenaline-infused lab mice fell. Researchers hypothesized that the suppression of the protein due to the continuous presence of the stress hormone plays a key role in the destruction of DNA.
The findings also revealed that the molecule beta-arresting 1, a protein embedded in DNA, contributes to the degradation of p53. Mice that lacked the protein, also called ARRB1, showed no signs of genetic impairment and had unchanged p53 levels in two areas of the body: the thymus, which is an organ of the immune system responsible for countering stress, and the testes, in which the offspring’s genetic material may be impacted by stress from the male parent. Future drugs that hinder this molecule might counter the many effects of stress, from the superficial ones of turning grey to the more life-threatening ones of developing cancer.
Co-author Robert Lefkowitz, MD, noted that the findings might explain how persistent stress could lead to a variety of human conditions. By understanding how the chromosomal irregularities develop, scientists can unravel the processes involved in the destruction of DNA and begin developing treatments to interfere with those mechanisms.
The team is conducting further investigations to determine if the findings can be replicated when adrenaline is produced naturally. They plan to trigger an internal release of stress hormones by restraining mice and comparing those outcomes to the results from this study.