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As the blueprint of life, the genetic material in the cells exists in the form of deoxyribonucleic acid (DNA), which is a delicate biomolecule requiring protection and preservation in its native state. Eukaryotic chromosomes have telomeres at their ends, which are repetitive hexameric sequences (TTAGGG). Telomeres protect and preserve the integrity of the genome from deterioration, recombination, and fusion by capping and strengthening sticky ends of chromosomes (McGrath et al., 2007). The length of telomeres varies according to the replication activity of the cells. During cell division, telomeres shorten to allow replications of genetic material. McGrath et al. (2007) explain that oxidative stress in the cells shortens telomeres while antioxidants alleviate oxidative stress and prevent shortening of telomeres. Telomerase is an essential enzyme that catalyzes the formation of telomeres at the end of each chromosome to preserve and protect the integrity of a genome.
The length of telomeres has become a molecular marker for most forms of cancers. Studies have established that short telomeres predispose individuals to the occurrence of different forms of cancers such as lung cancer and bladder cancer (McGrath et al., 2007; Mirabello et al., 2009). Since telomeres protect and preserve the integrity of chromosomes, short telomeres do not offer adequate protection and preservation, resulting in the decay, recombination, and fusion of chromosomes. Moreover, since the genetic material of cancerous cells replicate fast, and cell division occurs rapidly, they cause telomeres to shorten and consequently increase the risk of tumorigenesis. Cells have mechanisms for preventing the occurrence of cancer by synthesizing shortened telomeres and maintaining appropriate length using telomerase. When telomeres become very short for telomerase to repair and synthesize, cells triggers the process of senescence, resulting in apoptosis to protect cells from becoming cancerous (McGrath et al., 2007). Thus, the length of telomeres is a molecular marker of some cancers such as lung cancer and bladder cancer among individuals.
Diet and Cancer
Diet and cancer have an intricate relationship because a healthy body and cells are dependent on the nature of the diet people consume. As cancerous cells require a lot of glucose for DNA replication, cell division, and cell growth, reduction of glucose in diet would slow down the growth of cells and prevent the occurrence of cancer. Based on the premise that cancerous cells rely on the process of glycolysis in generating high energy, Ho et al. (2011) undertook a study to determine the effect of diets with low carbohydrate and high protein and high carbohydrate and low protein on the growth and progression of tumors among mice. The findings indicated a marked difference in the growth and progression of cancer between mice fed on a diet with low carbohydrate and high protein and diet with high carbohydrate and low protein. According to Ho et al. (2011), at the age of one year, mice fed on a diet with high carbohydrate and low protein had 50% tumor penetrance while the ones fed on the low carbohydrate and high protein had no tumor, low weight, and low blood glucose. Therefore, the findings suggest that diets with high carbohydrates promote the growth and progression of tumors for they supply glucose required for energy production.
As a common drink, alcohol contributes to the occurrence, development, and progression of liver cancer, throat cancer, esophageal cancer, breast cancer, and gastric cancer amongst other forms of cancers. In the metabolism of alcohol, alcohol dehydrogenase catalyzes the conversion of ethanol into acetaldehyde, which is a toxic compound that damages genetic materials in the mouth, esophagus, liver, and gastric cells, resulting in the formation and development of respective cancers. In their prospective study of 30 years done among 7150 men, Everatt et al. (2012) revealed that alcohol consumption predisposes people to gastric cancer. In an in vitro study, Park et al. (2014) treated diverse cancerous cells with casein and established that it induces the proliferation of the cancerous cells of prostate cancer.
Antioxidants play a central role in the prevention of cancer because they reduce oxidative stress in cells, which often results in the damage of DNA and the occurrence of cancer. Fuchs-Tarlovaky (2013) asserts that persistent and increasing oxidative stress in cells has injurious effects on cellular components such as DNA, lipids, and proteins, resulting in tumorigenesis. Antioxidants in different types of foods reduce oxidative stress in cells by oxidizing free radicals. When compared to casein, an in vivo study on mice revealed that rice protein regulates glutathione (Yang, Chen, Xu, Zhou, & Yang, 2012). Thus, glutathione regulation boosts oxidative capacity and alleviates oxidative damage in cells
A polyphenolic compound in green tea, epigallocatechin-3-gallate, has an anti-proliferative effect on cancerous cells. Ahmad, Feyes, Agarwal, Mukhtar, and Nieminen (1997) treated various cancerous cells with green tea and found out that epigallocatechin-3-gallate does not only cause apoptosis but also arrest cell cycle at G0 and G1 phases. In their review, Niedzwiecki, Roomi, Kalinovsky, and Rath (2016) concluded that a combination of green tea, quercetin, resveratrol curcumin and cruciferex have anti-carcinogenic properties, which are effective in preventing the occurrence, development, and progression of cancer.
Comparison of Western diet with high carbohydrates and Asian diet with high protein and vegetables show different risks and prevalence of cancers in vitro and in vivo studies. The findings of Ho et al. (2011) show that mice fed on a Western diet with high carbohydrate and low protein had 50% tumor penetrance whereas the ones fed on the Asian diet with low carbohydrate and high protein had no tumors. In a related study, Hakkaka, Korouriana, Ronisa, Johnstona, and Badgera (2001) found out that male rats fed on an Asian diet with soy proteins had 12% incidence of colon tumors compared to 50% incidence among rats fed on a Western diet with casein. Park et al. (2014) established that casein induces the proliferation of cancerous cells in prostate cancer. In their study, O’Callaghan et al. (2014) found out that red meat shortens telomeres in colonocytes and increases their DNA damage while resistant starch offers protective effect due to dietary fiber in them.
Protein Diet, Telomere Length, and Cancer
The protein diet has some links with telomere growth and the development of cancer. Protein diet reduces the growth rate of cancerous cells because it denies them glucose for energy production during glycolysis and diminishes the supply of carbon chains for ribose, citrate, and alanine synthesis (Ho et al., 2011). As the functions of telomeres are to cap proteins and prevent them from deterioration, recombination, and fusion, shortened telomeres do not provide adequate protection, resulting in DNA damage and cancer development (McGrath et al., 2007). Normally, rapidly dividing cells such as cancerous cells have shortened telomeres to allow rapid replication of genetic material in the cells. Therefore, shortened telomeres due to the availability of excess glucose and rapid cell division weaken genomic stability and increase predisposition to DNA damage and the development of cancer. Since McGrath et al. (2007) have established that shortened telomeres predispose people to bladder cancer, further research is necessary to establish if short telomeres predispose people to other forms of cancer.
Ahmad, N., Feyes, D. K., Agarwal, R., Mukhtar, H., & Nieminen, A. L. (1997). Green tea constituent epigallocatechin-3-gallate and induction of apoptosis and cell cycle arrest in human carcinoma cells. Journal of the National Cancer Institute, 89(24), 1881-1886.
Everatt, R., Tamosiunas, A., Kuzmickiene, I., Virviciute, D., Radisauskas, R., Reklaitiene, R., … Milinaviciene, E. (2012). Alcohol consumption and risk of gastric cancer: A cohort study of men in Kaunas, Lithuania, with up to 30 years follow-up. BMC Cancer, 12(475), 1-11.
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Hakkaka, R., Korouriana, S., Ronisa, M. J. J., Johnstona, J. M., & Badgera, T. M. (2001). Soy protein isolate consumption protects against azoxymethane-induced colon tumors in male rats. Cancer Letters, 166 (1), 27-32.
Ho, V. W., Leung, K., Hsu, A., Luk, B., Lai, J., Shen, S. Y.,… Nelson, B. H. (2011). A low carbohydrate, high protein diet slows tumor growth and prevents cancer initiation. Cancer Research, 71(13), 4484-4493.
Park, S. W., Kim, J. Y., Kim, Y. S., Lee, S. J., Lee, S. D., & Chung, M. K. (2014). A milk protein, casein, as a proliferation-promoting factor in prostate cancer cells. The World Journal of Men’s Health, 32(2), 76-82.
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McGrath, M., Wong, J. Y., Michaud, D., Hunter, D. J., & De Vivo, I. (2007). Telomere length, cigarette smoking, and bladder cancer risk in men and women. Cancer Epidemiology and Prevention Biomarkers, 16(4), 815-819.
Mirabello, L., Huang, W. Y., Wong, J. Y., Chatterjee, N., Reding, D., David Crawford, E., … & Savage, S. A. (2009). The association between leukocyte telomere length and cigarette smoking, dietary and physical variables, and risk of prostate cancer. Aging Cell, 8(4), 405-413.
Niedzwiecki, A., Roomi, M., Kalinovsky, T., & Rath, M. (2016). Anticancer efficacy of polyphenols and their combinations. Nutrients, 8(9), 1-17.
O’Callaghan, J., Toden, S., Bird, R., Topping L., Fenech, M., & Conlon, A. (2012). Colonocyte telomere shortening is greater with dietary red meat than white meat and is attenuated by resistant starch. Clinical Nutrition, 31(1), 60-64.
Yang, L., Chen, J. H., Xu, T., Zhou, A. S., & Yang, H. K. (2012). Rice protein improves oxidative stress by regulating glutathione metabolism and attenuating oxidative damage to lipids and proteins in rats. Life Sciences, 91(11), 389-394.