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Soda and Cell Aging

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Soft drinks, sodas, fruit flavoured drinks, sports drinks and energy drinks are widely termed as sugar-sweetened beverages. In the United States, such products contain the highest concentrations of added sugar in their ingredients. Due to the high rates of consumption of these drinks, the department of public health has raised concerns and thus policies and efforts targeted at reducing consumption. The prevalence of lifestyle diseases especially diabetes, cardiovascular complications, and obesity have increased significantly, indicating a link between the consumption of SSBs and the diseases (Leung et al. 2425).

Although the development of these disorders is not entirely established, the shortening and impairment of the telomere length is a phenomenon that can be utilized in explaining the relationship between SSB use and increased risk of metabolic diseases. Telomeres are located at the end of chromosomes and are responsible for chromosomal stability and protection of genomic DNA from damage. The length of the telomere has a tendency to become shorter during cell cycles. Once the length reaches a particular short length threshold, that cell can no longer divide and instead, it is likely to malfunction. Furthermore, shortening of telomeres has been associated with lifestyle behavior as well as psychological stress (Leung et al. 2425).

The objectives of this research are aimed at determining whether the telomere length of leukocytes provides any relationship between SSB consumption and the risk of developing cardiometabolic disorders. The study involves the examination of cross-sectional relations between SSB consumption, diet soda, and fruit juice and telomere lengths of a nationally representative population made up of healthy adults. At the end of the day, the findings indicated that SSB consumption is linked with shorter telomeres. This observation, therefore, leads to the conclusion that indeed regular consumption of SSBs is likely to affect the development of metabolic diseases possibly through the acceleration of cell aging (Leung et al. 2425).

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