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Nutritional advice to increase soluble fibre intake does not change plasma folate or homocysteine in men with angina: a randomised controlled trial

Published online by Cambridge University Press:  02 January 2007

Pauline AL Ashfield-Watt ,
Zoë E Clark ,
Pat Breay ,
Paul C Zotos ,
Sara B Cale ,
Michael L Burr  and
Ian FW McDowell
Pauline AL Ashfield-Watt
Affiliation:
Cardiovascular Sciences Research Group (Departments of Medical Biochemistry and Centre for Applied Public Health Medicine), Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, UK
Zoë E Clark
Affiliation:
Cardiovascular Sciences Research Group (Departments of Medical Biochemistry and Centre for Applied Public Health Medicine), Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, UK
Pat Breay
Affiliation:
Cardiovascular Sciences Research Group (Departments of Medical Biochemistry and Centre for Applied Public Health Medicine), Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, UK
Paul C Zotos
Affiliation:
Cardiovascular Sciences Research Group (Departments of Medical Biochemistry and Centre for Applied Public Health Medicine), Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, UK
Sara B Cale
Affiliation:
Cardiovascular Sciences Research Group (Departments of Medical Biochemistry and Centre for Applied Public Health Medicine), Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, UK
Michael L Burr
Affiliation:
Cardiovascular Sciences Research Group (Departments of Medical Biochemistry and Centre for Applied Public Health Medicine), Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, UK
Ian FW McDowell*
Affiliation:
Cardiovascular Sciences Research Group (Departments of Medical Biochemistry and Centre for Applied Public Health Medicine), Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, UK
*
*Corresponding author: Email [email protected]
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Abstract

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Objective:

To study the effect of advice to increase dietary soluble fibre, including fruit and vegetables, on plasma folate and homocysteine in men with angina.

Design:

Data were collected on a subset of subjects from the Diet and Angina Randomised Trial (DART II). In a randomised (2 × 2) factorial design, subjects received advice on either, neither or both interventions to: (1) increase soluble fibre intake to 8.0 g day−1 (fruit, vegetables and oats); (2) increase oily fish intake to 2 portions week−1. Those who received soluble fibre advice were compared with those who did not. Subjects were genotyped for C677T variant 5,10-methylenetetrahydrofolate reductase (MTHFR).

Setting/subjects:

Seven hundred and fifty-three male angina patients were recruited from general practice.

Results:

Plasma homocysteine concentrations were at the upper end of the normal range (median 11.5, 25% 9.4, 75% 14.0 μmol l−1). Baseline intake of fruit and vegetables was positively correlated with plasma folate (rs = 0.29, P < 0.01). Smokers had lower intakes of fruit and vegetables, lower plasma folate and higher homocysteine (all P < 0.01). Homozygotes for variant MTHFR had higher homocysteine concentrations at low plasma folate (P < 0.01). Reported intakes of fruit and vegetables and estimated dietary folate increased in the intervention group (ca. +75 g day−1, P < 0.01 and ca. +20 g day−1, P < 0.05, respectively). However, neither plasma folate (baseline/follow-up 4.5 vs. 4.4 μg l−1, P = 0.40) nor homocysteine (baseline/follow-up 11.7 vs. 11.7 μmol l−1, P = 0.31) changed.

Conclusions:

Plasma homocysteine, a cardiovascular risk factor, is influenced by MTHFR genotype, plasma folate and smoking status. Dietary advice successfully led to changes in fruit and vegetable intake, but not to changes in plasma folate or homocysteine, possibly because the fruits and vegetables that were chosen were not those richest in folate.

Keywords

Fruit and vegetablesAnginaFolateHomocysteine
Type
Research Article
Information
Public Health Nutrition , Volume 5 , Issue 1 , February 2002 , pp. 47 - 53
Copyright
Copyright © CABI Publishing 2002

References

1Ness, AR, Powles, JW. Fruit and vegetables, and cardiovascular disease: a review. Int. J. Epidemiol. 1997; 26: 1–13.CrossRefGoogle ScholarPubMed
2Cummings, JH, Bingham, SA. Diet and the prevention of cancer. Br. Med. J. 1998; 317: 1636–40.CrossRefGoogle ScholarPubMed
3Verhoef, P, Stampfer, MJ, Rimm, EB. Folate and coronary heart disease. Curr. Opin. Lipidol. 1998; 9: 17–22.CrossRefGoogle ScholarPubMed
4Kim, Y-I. Folate and carcinogenesis: evidence, mechanisms, and implications. J. Nutr. Biochem. 1999; 10: 66–88.CrossRefGoogle ScholarPubMed
5MRC Vitamin Study Research Group. Prevention of neural tube defects: results of the Medical Research Council Vitamin Study. Lancet 1991; 338: 131–7.CrossRefGoogle Scholar
6Boushey, 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: 1049–57.CrossRefGoogle ScholarPubMed
7Department of Health. Dietary Reference Values for Food Energy and Nutrients for the UK. Report on Health and Social Subjects No. 41. London: HMSO, 1991.Google Scholar
8Clark, ZE, Bowen, DJ, Whatley, SD, Bellamy, MF, Collins, PW, McDowell, IF. Genotyping method for methylenetetrahydrofolate reductase (C677T thermolabile variant) using heteroduplex technology. Clin. Chem. 1998; 44: 2360–2.Google ScholarPubMed
9Harmon, DL, Woodside, JV, Yarnell, JW, McMaster, D, Young, IS, McCrum, EE, Gey, KF, Whitehead, AS, Evans, AE. The common ‘thermolabile’ variant of methylene tetrahydrofolate reductase is a major determinant of mild hyperhomocysteinaemia. QJM 1996; 89: 571–7.CrossRefGoogle Scholar
10Selhub, J, Jacques, PF, Wilson, PW, Rush, D, Rosenberg, IH. Vitamin status and intake as primary determinants of homocysteinemia in an elderly population. JAMA 1993; 270: 2693–8.CrossRefGoogle Scholar
11Tucker, KL, Selhub, J, Wilson, PW, Rosenberg, IH. Dietary intake pattern relates to plasma folate and homocysteine concentrations in the Framingham Heart Study. J. Nutr. 1996; 126: 3025–1.CrossRefGoogle ScholarPubMed
12Committee on Medical Aspects of Food Policy. Nutritional Aspects of Cardiovascular Disease. Report of the Cardiovascular Review Group. London: HMSO, 1994.Google Scholar
13World Health Organization (WHO). Diet, Nutrition and the Prevention of Chronic Diseases. Report of the WHO Study Group. Technical Report Series 797. Geneva: WHO, 1990.Google Scholar
14Kuo, K, Still, R, Cale, S, McDowell, I. Standardization (external and internal) of HPLC assay for plasma homocysteine. Clin. Chem. 1997; 43: 1653–5.CrossRefGoogle ScholarPubMed
15Ho, Y, Ochiai, J, Saski, R, Suzuki, S, Kusuhara, Y, Morimitsu, Y. Serum concentrations of carotenoids, retinol and α-tocopherol in healthy persons determined by high performance liquid chromatography. Clin. Chim. Acta 1990; 194: 131–4.Google Scholar
16Still, RA, McDowell, IF. Clinical implications of plasma homocysteine measurement in cardiovascular disease. ACP Broadsheet No. 152: March 1998. J. Clin. Pathol. 1998; 51: 183–8.CrossRefGoogle ScholarPubMed
17Nygard, O, Vollset, SE, Refsum, H, Brattstrom, L, Ueland, PM. Total homocysteine and cardiovascular disease. J. Intern. Med. 1999; 246: 425–54.CrossRefGoogle ScholarPubMed
18Guttormsen, AB, Ueland, PM, Nesthus, I, Nygard, O, Schneede, J, Vollset, SE, Refsum, H. Determinants and vitamin responsiveness of intermediate hyperhomocysteinemia (> or =40 micromol/liter). The Hordaland Homocysteine Study. J. Clin. Invest. 1996; 98: 2174–83.CrossRefGoogle ScholarPubMed
19Brattstrom, L, Wilcken, DE, Ohrvik, J, Brudin, L. Common methylenetetrahydrofolate reductase gene mutation leads to hyperhomocysteinemia but not to vascular disease: the result of a meta-analysis. Circulation 1998; 98: 2520–6.CrossRefGoogle Scholar
20Kluijtmans, LA, Kastelein, JJ, Lindemans, J, Boers, GH, Heil, SG, Bruschke, AV, Jukema, JW, van den Heuvel, LP, Trijbels, FJ, Boerma, GJ, Verheugt, FW, Willems, F, Blom, HJ. Thermolabile methylenetetrahydrofolate reductase in coronary artery disease. Circulation 1997; 96: 2573–7.CrossRefGoogle ScholarPubMed
21Jacques, PF, Sulsky, SI, Sadowski, JA, Phillips, JC, Rush, D, Willett, WC. Comparison of micronutrient intake measured by a dietary questionnaire and biochemical indicators of micronutrient status. Am. J. Clin. Nutr. 1993; 57: 182–9.CrossRefGoogle ScholarPubMed
21Ashfield-Watt, PAL, Pullin, CH, Whiting, JM, Clark, ZE, Moat, SJ, Newcombe, RN, Burr, ML, Lewis, ML, Powers, HJ, McDowell, IFW. Methylenetetrahydrofolate reductase (C677T) genotype modulates blood folate and homocysteine responses to a folate rich diet or low dose folic acid supplement: a randomised controlled trial. Am. J. Clin. Nutr. 2001 [in press].Google Scholar
23Bingham, SA, Gill, C, Welch, A, Day, K, Cassidy, A, Khaw, KT, Sneyd, MJ, Key, TJA, Roe, L, Day, NE. Comparison of dietary assessment methods in nutritional epidemiology: weighed records v. 24h recalls, food-frequency questionnaires and estimated-diet records. Br. J. Nutr. 1994; 72: 619–43.CrossRefGoogle Scholar
24Hu, FB, Rimm, E, Smith-Warner, SA, Feskanich, D, Stampfer, MJ, Ascherio, A, Sampson, L, Willett, WC. Reproducibility and validity of dietary patterns assessed with a food-frequency questionnaire. Am. J. Clin. Nutr. 1999; 69: 243–9.CrossRefGoogle ScholarPubMed
25Hu, FB, Rimm, EB, Stampfer, MJ, Ascherio, A, Spiegelman, D, Willett, WC. Prospective study of major dietary patterns and risk of coronary heart disease in men. Am. J. Clin. Nutr. 2000; 72: 912–21.CrossRefGoogle ScholarPubMed
26Brouwer, IA, van Dusseldorp, M, Thomas, CM, Duran, M, Hautvast, JG, Eskes, TK, Steegers-Theunissen, RP. Low-dose folic acid supplementation decreases plasma homocysteine concentrations: a randomised trial. Am. J. Clin. Nutr. 1999; 69: 99–104.CrossRefGoogle Scholar
27Cuskelly, GJ, McNulty, H, Scott, JM. Effect of increasing dietary folate on red-cell folate: implications for prevention of neural tube defects. Lancet 1996; 347: 657–9.CrossRefGoogle ScholarPubMed
28Brouwer, IA, van Dusseldorp, M, West, CE, Meyboom, S, Thomas, CM, Duran, M, het Hof, KH, Eskes, TK, Hautvast, JG, Steegers-Theunissen, RP. Dietary folate from vegetables and citrus fruit decreases plasma homocysteine concentrations in humans in a dietary controlled trial. J. Nutr. 1999; 129: 1135–9.CrossRefGoogle Scholar
29Ministry of Agriculture, Fisheries and Food (MAFF)/Royal Society of Chemistry (RSC). Cereals and Cereal Products. Third Supplement McCance & Widdowson's The Composition of Foods, 4th ed. London: RSC, 1988.Google Scholar
30Ashfield-Watt, PAL, Knowles, RM, Cale, SB, Payne, N, McDowell, IFW. A folate enriched diet lowers plasma homocysteine in patients with hyperlipidaemia: a randomised controlled trial. Br. J. Cardiol. 2001; 8: 28–35.Google Scholar
31Department of Health. Folic Acid and the Prevention of Disease. Report of the Committee on Medical Aspects of Food and Nutrition Policy. Report on Health and Social Subjects No. 50. London: The Stationery Office, 2001.Google Scholar