Higher Plasma Homocysteine Is Associated with Increased Risk of Developing Colorectal Polyps

Abstract

Colorectal adenomas are considered to be precursors of colorectal cancer. B-vitamins (i.e., folate, vitamin B(6) and B(12)) are involved in homocysteine metabolism and play an important role as coenzymes in 1-carbon metabolism, which is thought to have a critical role in the progression of colorectal polyps. The purpose of this study was to examine the effects of B-vitamins and homocysteine on the risk of developing colorectal polyps. Forty-eight participants with colorectal polyps [29 adenomatous polyps (AP), 19 hyperplastic polyps (HP)], and 96 age- and sex-matched healthy controls were recruited. Fasting blood was drawn from each participant to measure hematological parameters, plasma pyridoxal 5'-phosphate (PLP), serum folate and vitamin B(12), and plasma homocysteine. Participants with AP and HP had significantly higher plasma homocysteine levels than did healthy controls. There was no significant difference in serum folate and vitamin B(12) and plasma PLP among the 3 groups. B-vitamins had no significant effect on the risk of colorectal polyps. However, participants with higher plasma homocysteine [odds ratio (OR) = 1.87, 95% confidence interval (CI) = 1.13, 3.08) level exhibited significantly increased risk of colorectal polyps after adjusting for potential confounders. Plasma homocysteine was a strong predictor of the risk of colorectal polyps in participants with adequate B-vitamins status.

The Metabolic Syndrome Is Associated with an Increased Risk of Colorectal Polyps Independent of Plasma Homocysteine

“…Hyperhomocysteinemia, a well-known risk factor for cardiovascular diseases, can increase the production of oxygen free radicals through homocysteine oxidation and can diminish the DNA methylation in critical tissues through a simultaneous increase in intracellular S-adenosylhomocysteine and is thus a risk factor for cancer [46,47]. Although some previous studies did not show that high plasma homocysteine was significantly associated with the development of colorectal polyps [48,49], the present study, in agreement with other studies [19,20,21,22], demonstrated that an increased plasma homocysteine concentration was associated with the development of colorectal polyps. …”

“…In the last decade, much attention has also been paid to the relationship between high plasma homocysteine levels and the risk of colorectal polyps [19,20,21,22]. Besides the many known risk factors (i.e.…”

Colonic Lysine Homocysteinylation Induced by High-Fat Diet Suppresses DNA Damage Repair

“…Moreover, impaired DNA damage repair and genomic instability are common in both CRC (Cancer Genome Atlas Network, 2012;Jasperson et al, 2010;Peltomä ki, 2001;Boland and Goel, 2010;Grady and Carethers, 2008) and hyperhomocysteinemia (HHcy) (Kruman et al, 2000(Kruman et al, , 2002Fenech, 2001;Jensen et al, 2008). Human intestinal dysbacteriosis (Louis et al, 2014) and elevated Hcy levels (Miller et al, 2013;Chiang et al, 2014;Bobe et al, 2010;Kato et al, 1999;Chen et al, 2013) both comprise CRC risk factors, with the colon being one of the major organs in which most microbiome residents and fatty acids are metabolized; an HF diet increases Hcy in both humans (Berstad et al, 2007) and animal models (Fonseca et al, 2000). Furthermore, trimethylamine, a downstream metabolite of fat, is converted to trimethylamine N-oxide almost exclusively by colonic bacterial species (Zeisel et al, 1983), with trimethylamine conversion levels being inversely correlated with Hcy levels (Obeid et al, 2017).…”

Effects of Riboflavin Interactions with 5-Methyltetrahydrofolate and Tetrahydrofolate on Changes in Homocysteine and Folate Derivative Levels, with and without Methionine Addition

“…An association between elevated Hcy and the risk of developing colorectal polyps [15], particularly in subjects with the TT genotype whose MTHFR activity is sensitive to riboflavin status [2], was previously reported. Furthermore, Powers et al studied the effects of folic acid, with and without riboflavin supplementation, on Hcy and 5-MTHF status in healthy subjects and colorectal polyp patients, and demonstrated the plasma 5-MTHF increase to be enhanced by riboflavin supplementation only in subjects with polyps who had the MTHFR CT or the TT genotype [7].…”