A recent study conducted by researchers at Kobe University Graduate School of Medicine, and published in the Journal of Psychiatric Research, reveals compelling evidence that alcohol dependence accelerates biological aging. By examining various epigenetic markers, the researchers found that individuals with alcohol dependence showed accelerated aging processes, which decelerated after a three-week treatment program.
Alcohol dependence is a chronic condition characterized by an inability to control alcohol consumption despite its negative impact on health and daily life. This condition not only exacerbates existing chronic diseases but also leads to premature deaths worldwide. According to estimates, approximately 2.5 million people die annually due to alcohol-related causes, highlighting the critical need for effective interventions and a deeper understanding of its consequences.
Alcohol dependence is known to increase the risk of several severe health issues, including liver diseases, cardiovascular disorders, and cognitive impairments. Persistent heavy drinking leads to widespread damage throughout the body, manifesting in numerous ways such as cerebral gray matter atrophy, which impacts brain function and accelerates cognitive decline.
Despite this understanding, there are still many questions about the specific biological mechanisms through which alcohol dependence harms health. This gap in knowledge provided a significant impetus for the researchers to explore the potential connections using advanced scientific tools.
One key area of interest in recent years has been the study of biological aging through the lens of epigenetics, particularly DNA methylation patterns. Epigenetic changes can provide insights into how lifestyle factors, such as alcohol consumption, influence the aging process at a molecular level.
Epigenetic clocks, which predict biological age based on genome-wide DNA methylation patterns, have emerged as powerful tools in aging research. These clocks can indicate the pace of biological aging and are associated with various health outcomes, including all-cause mortality and the development of age-related diseases.
For their study, the researchers utilized a publicly available DNA methylation dataset (GSE98876) from the Gene Expression Omnibus database. This dataset included samples from 24 patients with alcohol dependence and 23 healthy controls. All participants were men, primarily German, with one Polish participant in the patient group. The patients’ data were collected before and after a three-week alcohol treatment program at the Clinic for Psychiatry and Psychotherapy in Tuebingen, Germany.
The DNA methylation profiles were obtained from blood samples, specifically focusing on CD3+ T cells, which are a type of immune cell. Using this data, the researchers evaluated six different epigenetic clocks: HorvathAge, HannumAge, SkinBloodAge, PhenoAge, GrimAge, and GrimAge2. They also examined DNA methylation-based telomere length (DNAmTL) and the DunedinPACE measure, which quantifies the pace of biological aging.
The researchers discovered that individuals with alcohol dependence exhibited accelerated aging processes compared to healthy controls. These findings were consistent across multiple epigenetic clocks.
The most significant finding was related to the DunedinPACE clock, which indicated that patients with alcohol dependence experienced a faster pace of biological aging. This clock measures the rate of aging based on a comprehensive set of biomarkers related to various bodily functions, including cardiovascular, metabolic, renal, hepatic, pulmonary, and immune systems. The accelerated aging observed in these patients aligns with known health risks associated with chronic alcohol consumption, such as liver disease, kidney dysfunction, and cardiovascular problems.
The results also showed that a treatment program had a beneficial effect on decelerating the biological aging process. After undergoing a three-week alcohol treatment program, patients showed a significant deceleration in biological aging as measured by the GrimAge and GrimAge2 clocks.
These clocks incorporate specific biomarkers that predict mortality and disease risk, and their findings suggest that treatment can mitigate some of the aging effects associated with alcohol dependence. The study also found that telomere length, a marker of cellular aging, increased in patients after the treatment program, further indicating a reversal of some aging-related changes.
The study also highlighted changes in specific biomarkers associated with aging and health outcomes. Levels of beta-2-microglobulin (B2M) and Cystatin C, which are linked to renal function and cognitive decline, significantly decreased after the treatment program. This decrease aligns with improvements in renal function and cognitive health observed in patients abstaining from alcohol.
Overall, the study’s findings provide strong evidence that alcohol dependence accelerates biological aging, but also highlight the potential for treatment programs to mitigate some of these effects.
The study, “Accelerated epigenetic aging in alcohol dependence,” was authored by Toshiyuki Shirai , Satoshi Okazaki, Ikuo Otsuka, Masao Miyachi, Takaki Tanifuji, Ryota Shindo, Shohei Okada, Haruka Minami, Tadasu Horai, Kentaro Mouri, and Akitoyo Hishimoto.
