Effect of alcohol use disorder on cellular aging

Abstract

Rationale Human telomeres consist of tandem repeats at chromosome ends which protect chromosomal DNA from degradation. Telomere shortening occurs as part of natural aging; however, life stressors, smoking, drug use, BMI, and psychiatric disorders could disrupt cell aging and affect telomere length (TL). In this context, studies have evaluated the effects of alcohol consumption on TL; however, results have been inconsistent, which may reflect diverse drinking cut-offs and categorizations. Objectives To help clarify this, the present study addresses the association of TL with alcohol use disorder (AUD), drinking behaviors, lifetime stress, and chronological age. Methods TL was quantified as the telomere to albumin ratio (T/S ratio) obtained from peripheral blood DNA using the quantitative PCR assay, from 260 participants with AUD and 449 non-dependent healthy controls (HC) from an existing National Institute on Alcohol Abuse and Alcoholism (NIAAA) database. Results AUD participants showed shorter TL compared to HC with both, age, and AUD, as independent predictors as well as a significant AUD with age interaction effect on TL. TL was also associated with impulsiveness in AUD participants. We did not observe an association between TL and chronicity of alcohol use, alcohol doses ingested, or childhood trauma exposures in either AUD or HC, although very few HC reported a history of childhood trauma. Conclusion Our results support previous findings of telomere shortening with chronic alcohol exposures and show both an effect of AUD on TL that is independent of age as well as a significant AUD by age interaction on TL. These findings are consistent with accelerated cellular aging in AUD.

Leukocyte telomere length is inversely associated with arterial wave reflection in 566 normotensive and never-treated hypertensive subjects

“…Moderate beer consumption may even provide some benefit against cardiovascular disease [30]. While a meta-analysis reported that the results concerning alcohol consumption and LTL are unclear [31], a disorder with heavy alcohol use was associated with telomere shortening [32]. In the present study, moderate alcohol consumption category was associated with shorter telomeres, while low alcohol intake category was associated with lower proportion of short telomeres.…”

The Effect of Alcohol on Telomere Length: A Systematic Review of Epidemiological Evidence and a Pilot Study during Pregnancy

“…To do that, the authors compared 260 patients with alcohol use disorder and 449 healthy controls. Yet, drinking behaviors were not associated with relative TL in both groups [ 42 ]. Finally, the present systematic review identified the study by Tannous and colleagues that compared relative TL in blood samples from 24 patients with alcohol use disorder and 25 controls.…”

“…Interestingly, newborns from drinking women exhibited shorter relative TL than those born from non-drinking women (Figure 2B). [40] No association between alcohol consumption and relative TL Smoking status was associated with relative TL Liu et al, 2013 [41] No association between alcohol intake and relative TL No relationships of folate, choline, methionine, riboflavin, vitamin B6, vitamin B12, and polymorphisms involved in one-carbon metabolism with relative TL Martins de Carvalho et al, 2019 [42] Alcohol use disorder was associated with lower relative TL. However, drinking behaviors were not associated with relative TL A significant interaction between age and alcohol use disorder on relative telomere length was evident Needham et al, 2013 [43] No association between alcohol use and relative TL…”

The association of telomere length with substance use disorders: a systematic review and meta‐analysis of observational studies

“…As shown in Table 1, all studies applied a case–control design. The most represented countries were the United States with three studies [51–53] and Japan with two studies [54,55]. Case samples presented mean ages ranging between 26.2 and 74.5 years (mean = 47.4), whereas control samples ranged from 33.3 to 75.1 (mean = 55.1).…”

“…Three studies included men only [55–57] and one study with two analysis units included women only [58]. Related to the type of substance used, five studies investigated alcohol [52–55,57], one alcohol and cocaine [51], one cocaine [58], one tobacco and marijuana [56], one a mixture of cocaine, heroin, methamphetamine and morphine [59] and one study did not describe the substances consumed by those diagnosed with SUD [60].…”