Chronic PTSD Alters Gene Activity and Causes Premature Aging

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Chronic PTSD Alters Gene Activity and Causes Premature Aging

Research has linked post-traumatic stress disorder (PTSD) in 9/11 World Trade Center responders to a range of aging-related conditions including memory loss, increased risk of cognitive impairment, and physical functional limitations.

Now, new research shows that 9/11 World Trade Center responders with current PTSD present with accelerated aging at the level of gene activity, also called transcriptional aging, compared to those without PTSD. Notably, this study showed that accelerated aging in gene activity is linked to major domains of PTSD symptoms, including re-experiencing, avoidance, numbing, and hyperarousal.

“This is the first study to establish that transcriptional age acceleration may be associated with chronic PTSD,” stated the authors. “Interestingly, past PTSD showed no accelerated aging, suggesting that biological age may normalize after this disorder is effectively treated.”

PTSD and a propensity for aging

PTSD is a mental health condition that may occur in people that have experienced or witnessed a stressful or terrifying event. This condition can last for extended periods, and events from everyday life may trigger episodes that include intense emotional and physical reactions. Previous research shows that approximately 7% of the US population suffers from some degree of this debilitating condition (1).

Researchers have studied patients with PTSD to understand how the condition affects overall health. PTSD is a complex condition that has many presentations, as no two PTSD patients have the same type of symptoms. However, one thing these patients have in common is a reduced lifespan and a higher propensity for chronic conditions (2). This has led scientists to believe that the trauma experienced by these patients can somehow exert damage at the genetic level that may lead to accelerated aging.

PTSD is a mental health condition that may occur in people that have experienced or witnessed a stressful or terrifying event

Gene activity influences the rate of aging

Most times, the patterns of disease and aging seen in some people do not line up with what is expected in terms of their chronological ages. Scientists are not clear on what causes this discrepancy, but several biological mechanisms may lead to accelerated aging. One such mechanism depends on the proper maintenance of DNA through a process known as DNA methylation. This process protects our DNA from deterioration. DNA methylation preserves the integrity of DNA, which, in turn, allows proper gene expression.

Unfortunately, the process is not perfect, and over-methylation can lead to some protective genes known as tumor suppressor genes becoming inactivated. This can cause unchecked tumor growth and the spread of cancer. Similarly, under-methylation can cause the overproduction of compounds that promote inflammation, such as cytokines, and research shows that chronic inflammation is closely related to accelerated aging (3).

Researchers have developed epigenetic “clocks” that use the process of DNA methylation to assess biological age more effectively. These epigenetic clocks are better predictors of chronic diseases and mortality than chronological age. Another way that researchers can gauge genetic age is by measuring how much genes get activated. This process takes certain gene groups that increase their expression at a known rate, and compares it against an individual’s chronological age to obtain a more accurate picture of biological age.

epigenetic clocks are better predictors of chronic diseases and mortality than chronological age.

PTSD drives accelerated aging

Patients with PTSD interest anti-aging researchers because of the way stressful events can affect the behavior of genes. For this reason, scientists have closely followed first responders from the World Trade Center in the years following the attacks. A group of researchers from Stony Brook University in New York recently published a study in the journal Translational Psychiatry examining the effects of PTSD on aging in a group of World Trade Center first responders (4).

The study included data from over 300 men who had been part of the initial response to the 9/11 terrorist attacks. The researchers separated the participants into three groups: patients currently suffering from PTSD, patients who had recovered from PTSD, and patients who never experienced the symptoms associated with PTSD.

The study examined DNA from each group of participants and measured their epigenetic age by using several epigenetic “clocks”. The research team compared the participants’ epigenetic ages and their genetic activity to their chronological age. Current and previous PTSD status was taken into consideration to see how much of an effect the condition would have on their biological age. 

Results from the study showed that participants with ongoing PTSD had accelerated transcriptional aging compared to participants who did not have PTSD. This adds to the evidence that chronic conditions like PTSD may promote aging through their effects on genes. Interestingly, the study did not find signs of accelerated aging in participants who had PTSD in the past, but who were currently symptom-free. This suggests that PTSD’s aging effects can be reversed with proper treatment for the condition.

The researchers then compared the transcriptional age of participants against the results from different epigenetic clocks. Results showed a strong correlation between PTSD and accelerated aging. Examining the data at a more specific level showed that the aging effects of PTSD were closely related to specific characteristics or “dimensions” used to assess the severity of the condition, such as avoidance and numbing.

Although transcriptional aging increased because of PTSD, further analysis of the data showed PTSD had an even stronger effect on the DNA methylation process. “If validated in other cohorts, these findings should advance understanding of the biological mechanisms underlying premature medical morbidity and mortality in PTSD, and aid in identification of potential gene modifiers that may alter the rate of cellular aging in the general population,” concluded the authors.

Show references

  1. Kessler RC, Berglund P, Demler O, Jin R, Merikangas KR, Walters EE. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication [published correction appears in Arch Gen Psychiatry. 2005 Jul;62(7):768. Merikangas, Kathleen R ] [added]

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