Smoking and health: association between telomere length and factors impacting on human disease, quality of life and life span in a large population-based cohort under the effect of smoking duration

Abstract

Reactive oxygen species (ROS) are of primary importance as they cause damage to lipids, proteins, and DNA either endogenously by cellular mechanism, or through exogenous exposure to environmental injury factors, including oxidation insult factors, such as tobacco smoke. Currently 46.3 million adults (25.7 percent of the population) are smokers. This includes 24 million men (28.1 percent of the total) and more than 22 million women (23.5 percent). The prevalence is highest among persons 25-44 years of age. Cigarette smokers have a higher risk of developing several chronic disorders. These include fatty buildups in arteries, several types of cancer and chronic obstructive pulmonary disease (lung problems). As peripheral leukocytes have been the main target of human telomere research, most of what is known about human telomere dynamics in vivo is based on these cells. Leukocyte telomere length (TL) is a complex trait that is shaped by genetic, epigenetic, and environmental determinants. In this article, we consider that smoking modifies leukocyte TL in humans and contributes to its variability among individuals, although the smoking effect on TL and its relation with other metabolic indices may accelerate biological aging and development of smoking-induced chronic diseases in a large human population-based cohorts with smoking behavior. Recent studies confirmed that individuals with shorter telomeres present a higher prevalence of arterial lesions and higher risk of cardiovascular disease mortality. This study originally suggests that efficient therapeutic protection of TL and structure in response to stresses that are known to reduce TL, such as oxidative damage or inflammation associated with tobacco smoking, would lead to better telomere maintenance. Recently, we have discovered the potential use of telomere-restorative imidazole-containing dipeptide (non-hydrolized carnosine, carcinine) based therapy for better survival of smokers. We conclude that a better therapeutic or nutritional maintenance of TL may confer healthy aging in smokers and exceptional longevity in regularly ROS-exposed human survivors.

Telomere length in circulating leukocytes is associated with lung function and disease

“…The recent large, population-based study by RODE et al [18] revealed that having ever smoked and the cumulative pack-years smoked were associated with telomere length in 46 396 adults. This is in line with previous population-based findings [26]. However, in clinical studies, these effects were not seen [14,17,20].…”

Hormone-brain-aging relationships, broadly reactive with imidazole-containing dipeptides: targeting of telomere attrition as an aging biomarker and dynamic telomerase activity flirting

“…The results indicate that carnosine can reduce telomere shortening rate possibly by protecting telomere from damage [170]. Based on our own studies, we have suggested that the reduction in telomere shortening rate and damages in telomeric DNA made an important contribution to the life-extension effect of carnosine and carcinine [9,10]. Cumulatively, in this article, we propose that patented specific oral formulations of nonhydrolyzed carnosine and carcinine provide a powerful tool for targeted inhibition of cumulative oxidative stress and inflammation associated with telomere shortening in age-related diseases and during smoking behavior ( Figure 8, Table 1) [9,10,15,132,135,143,171].…”

“…Both are states of heightened oxidative stress, which increases the rate of telomere erosion per replication, and inflammation, which enhances WBC turnover [9,10,98,99]. Obese adults have shorter telomeres than their normal-weight counterparts, while this phenomenon is not present in childhood [98].…”

“…The results have implications for current models of how telomeric sequences are lost in normal somatic cells and suggest that peripheral blood leukocytes are an excellent tissue to investigate how this process is controlled [44]. [10]. Telomere shortening occurs concomitant with organismal aging ( Figure 6), and it is accelerated in the context of human diseases associated with mutations in telomerase, such as some cases of dyskeratosis congenita, idiopathic pulmonary fibrosis, and aplastic anemia [41].…”

“…However, in this work, we raise a new therapeutic concept, making it clinically possible that slowing down the rate of telomere shortening could slow down the human aging process in specific tissues where proliferative senescence is known to occur, with the demonstrated evidence of telomere shortening appeared to be a hallmark of oxidative stress and disease [7][8][9][10].…”