Folic acid, homocysteine and one-carbon metabolism: A review of the essential biochemistry

European Journal of Cardiovascular Prevention & Rehabilitation

Volumn 5, Issue 4, 1998, Pages 223-227

  Scott, John M ^a   Weir, Donald G ^a  

^a TRINITY COLLEGE DUBLIN   (Ireland)

Author keywords

[No Author keywords available]

Indexed keywords

FOLIC ACID; HOMOCYSTEINE;

AMINO ACID METABOLISM; ASSAY; BIOCHEMISTRY; FOLIC ACID DEFICIENCY; HUMAN; METHYLATION; PRIORITY JOURNAL; REVIEW; VITAMIN DEFICIENCY; VITAMIN METABOLISM;

CARDIOVASCULAR DISEASES; FEMALE; FOLIC ACID; FOLIC ACID DEFICIENCY; HOMOCYSTEINE; HUMANS; NEURAL TUBE DEFECTS; PREGNANCY; VITAMIN B 12 DEFICIENCY;

EID: 0032443019     PISSN: 17418267     EISSN: 17418275     Source Type: Journal    
DOI: 10.1177/174182679800500403     Document Type: Article

References (6)

1. Scott JM, Weir DG. The role of folic acid/folate in pregnancy: Prevention is ∗ better than cure. In: Bonne J (editor): Recent Advances in Obstetrics and Gynaecology. Edinburgh: Churchill Livingstone; 1998. pp. 1–20. Summarises the history of the research that showed that folic acid can prevent the majority of cases of spina bifida and ther forms of neural tube defects.
2. Scott JM, Weir DG. Folate/vitamin B12 interrelationships. Essays in ∗ Biochemistry London: Portland Press 1994; 28: 63–72. Biochemical background to folic acid and folate metabolism with specific reference to how it overlaps with vitamin B12 metabolism.
3. Weir DG, Scott JM. Biochemical basis of neuropathy in cobalamin ∗ deficiency. In: Singh W (editor): Clinics and haematology. London: Balliere's Tindall; 1996. pp. 479–497. Explains how vitamin B12 deficiency causes neuropathy.
4. Scott JM, Weir DG. Homocysteine and cardiovascular disease. Q J Med 1996; 89: 561–563. A good summary of the evidence that elevated plasma homocysteine may be a risk factor for cardiovascular disease, putting the evidence at a biochemical and clinical level into context.
5. Molloy AM, Daly S, Mills JL, Kirke PN, Whitehead AS, Ramsbottom D, et al∗ Thermolabile variant of 5,10-methylenetetrahydrofolate reductase associated with low red cell folates: Implications for folate intake recommendations. Lancet 1997; 349: 1591–1593. Introduces the concept that a very common genetic variant alters folate metabolism and nutrition. This may suggest that risk of cardiovascular disease from plasma homocysteine exists in people on what would traditionally be considered to be a good diet because they have a genetic variant that renders them less able to metabolise and retain an important nutrient.
6. Daly LE, Kirke PM, Molloy A, Weir DG, Scott JM. Folate levels and neural ∗ tube defects. Implications for prevention. JAMA 1995; 274: 1698–1702. Article concerning the change in risk of spina bifida and other neural tube defects, showing a tenfold increase in risk over what would traditionally be considered the normal range of folate status. Shows an example of a clinical condition where risk varies in the normal range as may happen in the case of the levels of plasma homocysteine seen in apparently normal people, causing an increased risk of cardiovascular disease and stroke.