Scientists in recent years have developed ways to measure biological age by tracking chemical changes in DNA that occur naturally as people age but occur at different times in different people.
In a new study, Yale researchers used one such clock, appropriately named “GrimAge,” to ask two questions: How much does chronic stress accelerate that biological clock?
And are there ways to slow it down and extend a healthy lifespan?
According to their findings, published in the journal Translational Psychiatry, stress does indeed make life’s clock tick faster—but that individuals can help manage the effects by strengthening their emotion regulation and self-control.
Rajita Sinha, the Foundations Fund Professor of Psychiatry at Yale, a professor of neuroscience and professor at the Yale Child Study Center, and one of the authors of the study, has spent decades studying stress and the myriad and pernicious ways that it erodes our mental and physical health.
It can influence metabolism, accelerating obesity-related disorders such as diabetes. Stress also saps our ability to regulate emotions and to think clearly.
A Yale team led by Sinha and Zachary Harvanek, a resident in the Yale Department of Psychiatry, decided to explore whether stress also accelerates aging in a relatively young and healthy population. Other co-authors included Ke Xu, an associate professor of psychiatry, and Nia Fogelman, an associate research scientist in psychiatry at Yale.
For their study, they enrolled 444 people, ages 19 to 50, who provided blood samples used to evaluate the age-related chemical changes captured by GrimAge as well as other markers of health. The participants also answered questions designed to reveal stress levels and psychological resilience.
However, stress didn’t affect everyone’s health to the same degree. Subjects who scored high on two psychological resilience measures – emotion regulation and self-control – were more resilient to the effects of stress on aging and insulin resistance, respectively.
“These results support the popular notion that stress makes us age faster,” Harvanek said, “but they also suggest a promising way to possibly minimize these adverse consequences of stress through strengthening emotion regulation and self-control.”
In other words, the more psychologically resilient the subject, the higher the likelihood they would live a longer and healthier life, he said.
“We all like to feel like we have some agency over our fate,” Sinha said.
It is a known fact that over the past decades, human life expectancy has greatly increased (Costantini et al., 2018). As a result, the population is aging, and this determines the development of geriatric medicine. Since aging is the main risk for the development of age-associated diseases, the field of geriatrics and geroscience has been developing very actively recently. The main goal of studies is to avoid age-related diseases before it is too late. Recently, the number of publications on anti-aging technologies and interventions has been increasing. This topic is certainly very popular not only in the medical community but also in society (Scapagnini et al., 2016).
Aging may be a complex process that happens under the influence of genetic, epigenetic, and environmental factors. Changes in an aging organism occur at the molecular, cellular, and tissue levels (Khan et al., 2017). In this regard, the question naturally arises on what factors possibly influence it. The most promising and effective approaches are nutritional strategies, physical activity, and hormone therapy (Scapagnini et al., 2016). In addition, these approaches can be used not only as anti-aging strategies but also as preventive directions. Preventive technologies will slow down aging and have a greater impact on quality of life than disease-specific approaches.
In order to understand the basis for development the directions of preventive and anti-age medicine, it is necessary to understand what basic pathological processes underlie the aging process. Some of these processes that determine aging include inflammation, cellular senescence, and senescence-associated secretory phenotype (SASP) development, altered glucose tolerance, and insulin resistance (IR) following dysregulated nutrient sensing and impaired cell–cell communication (De Souto Barreto et al., 2020). All these pathophysiological processes underlie age-associated neurodegenerative disorders.
It is predicted over the subsequent years that the incidence of age-related neurodegenerative diseases will increase dramatically. One of the most important factors in brain aging is the extremely high energy demand of neurons for maintaining neuronal work and preserving mental abilities (Davinelli et al., 2016).
With age, there is an increase in systemic inflammation, the inflamm-aging, and peripheral immunosenescence. Due to reciprocal interactions between the nervous and immune systems, chronic aseptic inflammation within central nervous system (CNS), called neuro-inflamm-aging, develops. Immunosenescence and inflamm-aging accompany brain aging and the loss of mental, cognitive, and other complex behaviors characteristic of Alzheimer’s disease (AD) and Parkinson’s disease (PD) (Khan et al., 2017; Costantini et al., 2018).
Recently, much research has been focused on the consequences of nutrients, and adiposity- and nutrient-related signals in brain aging and cognitive decline. Previously, it has been shown that insulin signaling affects the molecular cascades that underlie hippocampal functions, cognition, and memory (Spinelli et al., 2019). Our previous results have shown that a significant contribution to the development of brain IR is caused by neuroinflammation due to the overproduction of proinflammatory cytokines, astroglial and microglial activation, and disruption of the processes of reparative neurogenesis (Komleva et al., 2018).
reference link : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7841337/
More information: Zachary M. Harvanek et al, Psychological and biological resilience modulates the effects of stress on epigenetic aging, Translational Psychiatry (2021). DOI: 10.1038/s41398-021-01735-7
