Hyperhomocysteinemia is a risk factor for colorectal adenoma in women
Homocysteine is involved in a one-carbon transfer reaction, which is important for DNA synthesis and methylation. High level of plasma homocysteine, biochemical marker of folate status, is known to be a risk factor for cancer. However, it is inconclusive as to whether plasma homocysteine concentrati...
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| Published in | Journal of Clinical Biochemistry and Nutrition Vol. 51; no. 2; pp. 132 - 135 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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Japan
SOCIETY FOR FREE RADICAL RESEARCH JAPAN
01.09.2012
the Society for Free Radical Research Japan |
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| Online Access | Get full text |
| ISSN | 0912-0009 1880-5086 1880-5086 |
| DOI | 10.3164/jcbn.D-11-00025 |
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| Abstract | Homocysteine is involved in a one-carbon transfer reaction, which is important for DNA synthesis and methylation. High level of plasma homocysteine, biochemical marker of folate status, is known to be a risk factor for cancer. However, it is inconclusive as to whether plasma homocysteine concentration can predict colorectal adenoma. We conducted a case-control study to determine whether hyperhomocysteinemia is a risk factor for adenoma. Data from 1,039 subjects who underwent a colonoscopy and plasma homocysteine concentration determination during health examinations at single center over a two-year period were analyzed. The subjects were classified into two groups (422 adenoma and 617 controls). Subjects defined as having advanced adenomas were those with more than three adenomas, over 1 cm in size, high grade dysplasia, or villous components. Male, old age, high body mass index, low high-density lipoprotein-cholesterol, smoking, fasting glucose, and past history of colon polyps were significantly associated with adenoma according to multiple logistic regression. According to subgroup analysis by gender, plasma homocysteine concentration was not associated with adenoma in males; however, a high plasma homocysteine concentration significantly increased the risk of adenoma as well as advanced adenoma in females. Hyperhomocysteinemia is a risk factor for colorectal adenoma in women. |
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| AbstractList | Homocysteine is involved in a one-carbon transfer reaction, which is important for DNA synthesis and methylation. High level of plasma homocysteine, biochemical marker of folate status, is known to be a risk factor for cancer. However, it is inconclusive as to whether plasma homocysteine concentration can predict colorectal adenoma. We conducted a case-control study to determine whether hyperhomocysteinemia is a risk factor for adenoma. Data from 1,039 subjects who underwent a colonoscopy and plasma homocysteine concentration determination during health examinations at single center over a two-year period were analyzed. The subjects were classified into two groups (422 adenoma and 617 controls). Subjects defined as having advanced adenomas were those with more than three adenomas, over 1 cm in size, high grade dysplasia, or villous components. Male, old age, high body mass index, low high-density lipoprotein-cholesterol, smoking, fasting glucose, and past history of colon polyps were significantly associated with adenoma according to multiple logistic regression. According to subgroup analysis by gender, plasma homocysteine concentration was not associated with adenoma in males; however, a high plasma homocysteine concentration significantly increased the risk of adenoma as well as advanced adenoma in females. Hyperhomocysteinemia is a risk factor for colorectal adenoma in women. Homocysteine is involved in a one-carbon transfer reaction, which is important for DNA synthesis and methylation. High level of plasma homocysteine, biochemical marker of folate status, is known to be a risk factor for cancer. However, it is inconclusive as to whether plasma homocysteine concentration can predict colorectal adenoma. We conducted a case-control study to determine whether hyperhomocysteinemia is a risk factor for adenoma. Data from 1,039 subjects who underwent a colonoscopy and plasma homocysteine concentration determination during health examinations at single center over a two-year period were analyzed. The subjects were classified into two groups (422 adenoma and 617 controls). Subjects defined as having advanced adenomas were those with more than three adenomas, over 1 cm in size, high grade dysplasia, or villous components. Male, old age, high body mass index, low high-density lipoprotein-cholesterol, smoking, fasting glucose, and past history of colon polyps were significantly associated with adenoma according to multiple logistic regression. According to subgroup analysis by gender, plasma homocysteine concentration was not associated with adenoma in males; however, a high plasma homocysteine concentration significantly increased the risk of adenoma as well as advanced adenoma in females. Hyperhomocysteinemia is a risk factor for colorectal adenoma in women. Homocysteine is involved in a one-carbon transfer reaction, which is important for DNA synthesis and methylation. High level of plasma homocysteine, biochemical marker of folate status, is known to be a risk factor for cancer. However, it is inconclusive as to whether plasma homocysteine concentration can predict colorectal adenoma. We conducted a case-control study to determine whether hyperhomocysteinemia is a risk factor for adenoma. Data from 1,039 subjects who underwent a colonoscopy and plasma homocysteine concentration determination during health examinations at single center over a two-year period were analyzed. The subjects were classified into two groups (422 adenoma and 617 controls). Subjects defined as having advanced adenomas were those with more than three adenomas, over 1 cm in size, high grade dysplasia, or villous components. Male, old age, high body mass index, low high-density lipoprotein-cholesterol, smoking, fasting glucose, and past history of colon polyps were significantly associated with adenoma according to multiple logistic regression. According to subgroup analysis by gender, plasma homocysteine concentration was not associated with adenoma in males; however, a high plasma homocysteine concentration significantly increased the risk of adenoma as well as advanced adenoma in females. Hyperhomocysteinemia is a risk factor for colorectal adenoma in women.Homocysteine is involved in a one-carbon transfer reaction, which is important for DNA synthesis and methylation. High level of plasma homocysteine, biochemical marker of folate status, is known to be a risk factor for cancer. However, it is inconclusive as to whether plasma homocysteine concentration can predict colorectal adenoma. We conducted a case-control study to determine whether hyperhomocysteinemia is a risk factor for adenoma. Data from 1,039 subjects who underwent a colonoscopy and plasma homocysteine concentration determination during health examinations at single center over a two-year period were analyzed. The subjects were classified into two groups (422 adenoma and 617 controls). Subjects defined as having advanced adenomas were those with more than three adenomas, over 1 cm in size, high grade dysplasia, or villous components. Male, old age, high body mass index, low high-density lipoprotein-cholesterol, smoking, fasting glucose, and past history of colon polyps were significantly associated with adenoma according to multiple logistic regression. According to subgroup analysis by gender, plasma homocysteine concentration was not associated with adenoma in males; however, a high plasma homocysteine concentration significantly increased the risk of adenoma as well as advanced adenoma in females. Hyperhomocysteinemia is a risk factor for colorectal adenoma in women. |
| Author | Park, Sue K. Kim, Young-Ho Kim, Jeong Hwan Kim, Jae J. Lim, Yun Jeong Son, Hee Jung |
| AuthorAffiliation | 1 Department of Internal Medicine, Dongguk University Ilsan Hospital, Dongguk University College of Medicine, Goyang, Korea 4 Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Irwon-Dong 50, Gangnam-gu, Seoul 135-710, Korea 2 Department of Internal Medicine, Konkuk University Hospital, Konkuk University School of Medicine, Seoul, Korea 3 Department of Preventive Medicine, SNU College of Medicine, Seoul, Korea |
| AuthorAffiliation_xml | – name: 4 Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Irwon-Dong 50, Gangnam-gu, Seoul 135-710, Korea – name: 2 Department of Internal Medicine, Konkuk University Hospital, Konkuk University School of Medicine, Seoul, Korea – name: 3 Department of Preventive Medicine, SNU College of Medicine, Seoul, Korea – name: 1 Department of Internal Medicine, Dongguk University Ilsan Hospital, Dongguk University College of Medicine, Goyang, Korea |
| Author_xml | – sequence: 1 fullname: Kim, Young-Ho organization: Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine – sequence: 1 fullname: Park, Sue K. organization: Department of Preventive Medicine, SNU College of Medicine – sequence: 1 fullname: Lim, Yun Jeong organization: Department of Internal Medicine, Dongguk University Ilsan Hospital, Dongguk University College of Medicine – sequence: 1 fullname: Kim, Jae J. organization: Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine – sequence: 1 fullname: Son, Hee Jung organization: Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine – sequence: 1 fullname: Kim, Jeong Hwan organization: Department of Internal Medicine, Konkuk University Hospital, Konkuk University School of Medicine |
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| Cites_doi | 10.1001/archinte.157.20.2299 10.1158/1055-9965.EPI-07-0199 10.1054/bjoc.2000.1582 10.1067/mlc.2001.117161 10.1056/NEJM199905133401901 10.1093/jn/135.11.2703 10.1056/NEJMoa021423 10.1038/nrc1298 10.1038/nrc1144 10.7326/0003-4819-129-7-199810010-00002 10.1001/archinte.163.3.309 10.3164/jcbn.10-70 10.1080/01635589609514489 10.1056/NEJM200006293422606 10.1093/oxfordjournals.epirev.a036154 10.1002/cncr.21950 10.1053/j.gastro.2006.09.010 10.1136/gut.2005.073163 10.1001/jama.274.13.1049 10.1016/S0889-8553(02)00057-2 |
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| Keywords | homocysteine risk factors adenoma |
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| References | 17 Martínez ME, Thompson P, Jacobs ET, et al. Dietary factors and biomarkers involved in the methylenetetrahydrofolate reductase genotype-colorectal adenoma pathway. Gastroenterology 2006; 131: 1706–1716. 16 Boutron-Ruault MC, Senesse P, Faivre J, Couillault C, Belghiti C. Folate and alcohol intakes: related or independent roles in the adenoma-carcinoma sequence? Nutr Cancer 1996; 26: 337–346. 4 Lim YJ, Kwack WG, Lee YS, Hahm KB, Kim YK. Increased pulse wave velocity reflecting arterial stiffness in patients with colorectal adenomas. J Clin Biochem Nutr 2010; 47: 261–265. 21 Fung T, Hu FB, Fuchs C, et al. Major dietary patterns and the risk of colorectal cancer in women. Arch Intern Med 2003; 163: 309–314. 6 Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med 2003; 348: 1625–1638. 13 Moghadasian MH, McManus BM, Frohlich JJ. Homocyst(e)ine and coronary artery disease. Clinical evidence and genetic and metabolic background. Arch Intern Med 1997; 157: 2299–2308. 19 Ryan BM, Weir DG. Relevance of folate metabolism in the pathogenesis of colorectal cancer. J Lab Clin Med 2001; 138: 164–176. 2 Jänne PA, Mayer RJ. Chemoprevention of colorectal cancer. N Engl J Med 2000; 342: 1960–1968. 18 Kim YI. Nutritional epigenetics: impact of folate deficiency on DNA methylation and colon cancer susceptibility. J Nutr 2005; 135: 2703–2709. 15 Lamprecht SA, Lipkin M. Chemoprevention of colon cancer by calcium, vitamin D and folate: molecular mechanisms. Nat Rev Cancer 2003; 3: 601–614. 7 Ahmed RL, Schmitz KH, Anderson KE, Rosamond WD, Folsom AR. The metabolic syndrome and risk of incident colorectal cancer. Cancer 2006; 107: 28–36. 20 Giovannucci E, Stampfer MJ, Colditz GA, et al. Multivitamin use, folate, and colon cancer in women in the Nurses’ Health Study. Ann Intern Med 1998; 129: 517–524. 5 Peipins LA, Sandler RS. Epidemiology of colorectal adenomas. Epidemiol Rev 1994; 16: 273–297. 9 Frezza EE, Wachtel MS, Chiriva-Internati M. Influence of obesity on the risk of developing colon cancer. Gut 2006; 55: 285–291. 12 Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA 1995; 274: 1049–1047. 8 Nilsen TI, Vatten LJ. Prospective study of colorectal cancer risk and physical activity, diabetes, blood glucose and BMI: exploring the hyperinsulinaemia hypothesis. Br J Cancer 2001; 84: 417–422. 11 Jacques PF, Selhub J, Bostom AG, Wilson PW, Rosenberg IH. The effect of folic acid fortification on plasma folate and total homocysteine concentrations. N Engl J Med 1999; 340: 1449–1454. 10 Lim YJ, Choi YH, Kim YH, et al. The association between plasma homocysteine concentration and the risk of rectosigmoid adenoma in heavy alcohol drinkers. Korean J Med 2004; 67: 475–479. 1 Giovannucci E. Modifiable risk factors for colon cancer. Gastroenterol Clin North Am 2002; 31: 925–943. 3 Kim JH, Lim YJ, Kim YH, et al. Is metabolic syndrome a risk factor for colorectal adenoma? Cancer Epidemiol Biomarkers Prev 2007; 16: 1543–1546. 14 Bingham S, Riboli E. Diet and cancer—the European prospective investigation into cancer and nutrition. Nat Rev Cancer 2004; 4: 206–215. 11 12 13 14 15 16 17 18 19 1 2 3 4 5 6 7 8 9 20 10 21 17087956 - Gastroenterology. 2006 Dec;131(6):1706-16 12711737 - N Engl J Med. 2003 Apr 24;348(17):1625-38 16721800 - Cancer. 2006 Jul 1;107(1):28-36 21103036 - J Clin Biochem Nutr. 2010 Nov;47(3):261-5 11528369 - J Lab Clin Med. 2001 Sep;138(3):164-76 12578511 - Arch Intern Med. 2003 Feb 10;163(3):309-14 16251634 - J Nutr. 2005 Nov;135(11):2703-9 9758570 - Ann Intern Med. 1998 Oct 1;129(7):517-24 11161410 - Br J Cancer. 2001 Feb 2;84(3):417-22 17684126 - Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1543-6 7563456 - JAMA. 1995 Oct 4;274(13):1049-57 8910915 - Nutr Cancer. 1996;26(3):337-46 7713180 - Epidemiol Rev. 1994;16(2):273-97 9361570 - Arch Intern Med. 1997 Nov 10;157(20):2299-308 14993902 - Nat Rev Cancer. 2004 Mar;4(3):206-15 12894248 - Nat Rev Cancer. 2003 Aug;3(8):601-14 16239255 - Gut. 2006 Feb;55(2):285-91 12489270 - Gastroenterol Clin North Am. 2002 Dec;31(4):925-43 10320382 - N Engl J Med. 1999 May 13;340(19):1449-54 10874065 - N Engl J Med. 2000 Jun 29;342(26):1960-8 |
| References_xml | – reference: 16 Boutron-Ruault MC, Senesse P, Faivre J, Couillault C, Belghiti C. Folate and alcohol intakes: related or independent roles in the adenoma-carcinoma sequence? Nutr Cancer 1996; 26: 337–346. – reference: 18 Kim YI. Nutritional epigenetics: impact of folate deficiency on DNA methylation and colon cancer susceptibility. J Nutr 2005; 135: 2703–2709. – reference: 5 Peipins LA, Sandler RS. Epidemiology of colorectal adenomas. Epidemiol Rev 1994; 16: 273–297. – reference: 13 Moghadasian MH, McManus BM, Frohlich JJ. Homocyst(e)ine and coronary artery disease. Clinical evidence and genetic and metabolic background. Arch Intern Med 1997; 157: 2299–2308. – reference: 3 Kim JH, Lim YJ, Kim YH, et al. Is metabolic syndrome a risk factor for colorectal adenoma? Cancer Epidemiol Biomarkers Prev 2007; 16: 1543–1546. – reference: 12 Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA 1995; 274: 1049–1047. – reference: 14 Bingham S, Riboli E. Diet and cancer—the European prospective investigation into cancer and nutrition. Nat Rev Cancer 2004; 4: 206–215. – reference: 15 Lamprecht SA, Lipkin M. Chemoprevention of colon cancer by calcium, vitamin D and folate: molecular mechanisms. Nat Rev Cancer 2003; 3: 601–614. – reference: 20 Giovannucci E, Stampfer MJ, Colditz GA, et al. Multivitamin use, folate, and colon cancer in women in the Nurses’ Health Study. Ann Intern Med 1998; 129: 517–524. – reference: 4 Lim YJ, Kwack WG, Lee YS, Hahm KB, Kim YK. Increased pulse wave velocity reflecting arterial stiffness in patients with colorectal adenomas. J Clin Biochem Nutr 2010; 47: 261–265. – reference: 17 Martínez ME, Thompson P, Jacobs ET, et al. Dietary factors and biomarkers involved in the methylenetetrahydrofolate reductase genotype-colorectal adenoma pathway. Gastroenterology 2006; 131: 1706–1716. – reference: 11 Jacques PF, Selhub J, Bostom AG, Wilson PW, Rosenberg IH. The effect of folic acid fortification on plasma folate and total homocysteine concentrations. N Engl J Med 1999; 340: 1449–1454. – reference: 2 Jänne PA, Mayer RJ. Chemoprevention of colorectal cancer. N Engl J Med 2000; 342: 1960–1968. – reference: 1 Giovannucci E. Modifiable risk factors for colon cancer. Gastroenterol Clin North Am 2002; 31: 925–943. – reference: 8 Nilsen TI, Vatten LJ. Prospective study of colorectal cancer risk and physical activity, diabetes, blood glucose and BMI: exploring the hyperinsulinaemia hypothesis. Br J Cancer 2001; 84: 417–422. – reference: 10 Lim YJ, Choi YH, Kim YH, et al. The association between plasma homocysteine concentration and the risk of rectosigmoid adenoma in heavy alcohol drinkers. Korean J Med 2004; 67: 475–479. – reference: 19 Ryan BM, Weir DG. Relevance of folate metabolism in the pathogenesis of colorectal cancer. J Lab Clin Med 2001; 138: 164–176. – reference: 7 Ahmed RL, Schmitz KH, Anderson KE, Rosamond WD, Folsom AR. The metabolic syndrome and risk of incident colorectal cancer. Cancer 2006; 107: 28–36. – reference: 6 Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med 2003; 348: 1625–1638. – reference: 21 Fung T, Hu FB, Fuchs C, et al. Major dietary patterns and the risk of colorectal cancer in women. Arch Intern Med 2003; 163: 309–314. – reference: 9 Frezza EE, Wachtel MS, Chiriva-Internati M. Influence of obesity on the risk of developing colon cancer. Gut 2006; 55: 285–291. – ident: 13 doi: 10.1001/archinte.157.20.2299 – ident: 3 doi: 10.1158/1055-9965.EPI-07-0199 – ident: 8 doi: 10.1054/bjoc.2000.1582 – ident: 19 doi: 10.1067/mlc.2001.117161 – ident: 11 doi: 10.1056/NEJM199905133401901 – ident: 18 doi: 10.1093/jn/135.11.2703 – ident: 6 doi: 10.1056/NEJMoa021423 – ident: 14 doi: 10.1038/nrc1298 – ident: 15 doi: 10.1038/nrc1144 – ident: 10 – ident: 20 doi: 10.7326/0003-4819-129-7-199810010-00002 – ident: 21 doi: 10.1001/archinte.163.3.309 – ident: 4 doi: 10.3164/jcbn.10-70 – ident: 16 doi: 10.1080/01635589609514489 – ident: 2 doi: 10.1056/NEJM200006293422606 – ident: 5 doi: 10.1093/oxfordjournals.epirev.a036154 – ident: 7 doi: 10.1002/cncr.21950 – ident: 17 doi: 10.1053/j.gastro.2006.09.010 – ident: 9 doi: 10.1136/gut.2005.073163 – ident: 12 doi: 10.1001/jama.274.13.1049 – ident: 1 doi: 10.1016/S0889-8553(02)00057-2 – reference: 16239255 - Gut. 2006 Feb;55(2):285-91 – reference: 8910915 - Nutr Cancer. 1996;26(3):337-46 – reference: 7713180 - Epidemiol Rev. 1994;16(2):273-97 – reference: 9361570 - Arch Intern Med. 1997 Nov 10;157(20):2299-308 – reference: 7563456 - JAMA. 1995 Oct 4;274(13):1049-57 – reference: 12711737 - N Engl J Med. 2003 Apr 24;348(17):1625-38 – reference: 17684126 - Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1543-6 – reference: 10874065 - N Engl J Med. 2000 Jun 29;342(26):1960-8 – reference: 10320382 - N Engl J Med. 1999 May 13;340(19):1449-54 – reference: 16251634 - J Nutr. 2005 Nov;135(11):2703-9 – reference: 11161410 - Br J Cancer. 2001 Feb 2;84(3):417-22 – reference: 14993902 - Nat Rev Cancer. 2004 Mar;4(3):206-15 – reference: 12578511 - Arch Intern Med. 2003 Feb 10;163(3):309-14 – reference: 21103036 - J Clin Biochem Nutr. 2010 Nov;47(3):261-5 – reference: 16721800 - Cancer. 2006 Jul 1;107(1):28-36 – reference: 17087956 - Gastroenterology. 2006 Dec;131(6):1706-16 – reference: 9758570 - Ann Intern Med. 1998 Oct 1;129(7):517-24 – reference: 12489270 - Gastroenterol Clin North Am. 2002 Dec;31(4):925-43 – reference: 12894248 - Nat Rev Cancer. 2003 Aug;3(8):601-14 – reference: 11528369 - J Lab Clin Med. 2001 Sep;138(3):164-76 |
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| Title | Hyperhomocysteinemia is a risk factor for colorectal adenoma in women |
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