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Rapid Responses: Rapid Responses published:
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Prevention is easier than treatment
- Daniel Jabbari (13 May 2009)
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Beware of nutritional yeast
- Hugh Mann (15 May 2009)
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Unforeseen long-term consequences?
- David J R Hutchon (25 May 2009)
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Might glutamine improve the ability of folic acid fortification to prevent congential heart disease?
- Richard G Fiddian-Green (27 May 2009)
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Daniel Jabbari, General Practice SHO Hazeldene House Surgery, Main Road, Great Haywood, Stafford. ST18 0SU
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As Folic Acid is especially important during periods of rapid cell division and growth, therefore, the importance of its role in pregnancy in prevention neural tube defect or Congenital Heart Diseases is not ignorable. It seems that we need to highlight more the role of Folic Acid in pregnancy with education of pregnant women and of course the government policy in adding it to diary products of pregnants could be significantly useful. Leafy vegetables such as spinach, turnip greens, lettuces, dried/fresh beans and peas, fortified cereal products, sunflower seeds and certain other fruits and vegetables are rich sources of folate. Liver and liver products also contain high amounts of folate, as does baker's yeast. Some breakfast cereals (ready-to-eat and others) are fortified with 25% to 100% of the recommended dietary allowance (RDA) for folic acid. Competing interests: None declared |
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Hugh Mann, Physician Eagle Rock, MO 65641 USA
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Although nutritional yeast is a good source of vitamins and minerals, including folic acid, it is nonetheless very high in glutamate, which is a major excitatory neurotransmitter in the central nervous system. As a result of its high glutamate concentration, yeast is moderately addictive and can cause or aggravate asthma and headaches. Despite its nutritional and flavor-enhancing properties, it is best to avoid glutamate in all its forms, including the ubiquitous monosodium glutamate. Competing interests: None declared |
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David J R Hutchon, Consultant Obstetrician Memorial Hospital, Darlington
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Sir, Re Gardiner H M, Fouron J Folic acid fortification and congenital heart disease BMJ 2009;338:b1144 As we changed our diet over the last thousand years, no-one anticipated what the consequences would be for a small proportion of individuals with a sluggish gene which rendered them vulnerable to lower levels of folic acid in their diet.(1) Now that we know the consequences, we are trying to right the problem of abnormal fetal cardiac development by returning the maternal intake of folic acid to normal ‘physiological’ levels using dietary supplements. Normal heart development during pregnancy and normal heart function at birth must be the aim of any health program. In the journal Heart, Gardiner describes “The most dramatic changes in loading (of the heart) occur at birth when there is a sudden increase in distal impedance associated with removal of the placental circulation . . . . .”. (2) Although the control of the removal of the placental circulation is not specified, it is clearly outside the intrinsic control of the newborn. Obstetricians and midwives will recognise this extrinsic control as that of the cord clamp applied before the natural closure of the placental circulation has taken place. Gray’s Anatomy (3) does not include the cord clamp in the physiological description of transitional circulation at birth, and does not describe any dramatic change in heart loading either. True physiological changes at birth allow the simultaneous (although rapid) transfer of circulation from the placenta to the lungs, so there is virtually no change in heart loading. Gardiner’s description is understandable with the present routine practice of immediate or early cord clamping at birth which does lead to the dramatic increase in load described. The cord clamp is also part of many descriptions of physiological transition at birth in textbooks, showing an appalling misunderstanding of normal physiology. (4,5,6,7,8) Clamping the functioning placental circulation is a birth intervention which has become much more prevalent in the last sixty years. The consequences for the neonate were never really properly considered and only now are being considered more thoroughly. (9,10) The cord clamp, first invented exactly 110 years ago, was never intended to occlude the functioning placental circulation. (11) Will we discover in years to come that the dramatic increase in loading of the heart at birth caused by the application of the cord clamp to a functioning circulation can have serious consequences for a small group of vulnerable individuals? When an intervention is routine and commonly applied it is very difficult to realise cause and effect. Furthermore the intervention is never documented to allow a long term retrospective study. While correction of the deficiency of folic acid is proving difficult to achieve as it depends on the compliance of women planning pregnancy, it should be simple enough to stop the practice of immediate (or early) cord clamping which is within the control of the profession. A change in practice would ensure that this unnecessary intervention does not have any unforeseen long-term consequences. We already know that the intervention of immediate or early cord clamping causes harm in both preterm (12) and term neonates (13) by causing hypovolaemia which leads to anaemia. Are we going to allow this practice to continue until we can confirm even more harms of hypovolaemia and the dramatic increase heart loading? Would it not be sensible to return to the practice advised in Williams’ Obstetrics of 1917 (14) and 1939 (15) which keeps close to a physiological transition by advising that the cord should not be clamped until it has ceased to pulsate?
David J R Hutchon FRCOG Competing interests: None declared |
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Richard G Fiddian-Green, FRCS, FACS None
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Although mandatory fortification of grain products with folic acid in Quebec was accompanied by a 6.2% decrease in birth prevalance of congential heart defects per year the absolute reduction prevalence was from some 1.6 severe cases per 1000 births to some 1.25 (1). There remains considerable room for improvement. Folic acid supplements would not be able to support nucleic acid synthesis, rapid cell division and growth were it not for the capacity to generate large amounts of ATP (2) which is also dependent upon the availability of folic acid. The effect of folic acid fortification on ATP synthesis might, therefore, be of primary importance in the decrease in prevalance in congenital heart disease observed in the present study. Support for this hypothesis is provided by the associations between inherited mitochondrial disorders and other congential diseases (3). Replenishment of purine nucleotides, which include ATP which is known to be depleted during the course of a critical illness (4), by de novo synthesis requires aspartate, 10-Formyl-tetrahydrofolate [a derivative of folic acid], glutamine and ribose (5). Of these 10-formyl-tetrahydrofolate and glutamine are of established clinical relevance because of the benefits of folic acid fortification reported in this study (6) and the benefits of glutamine supplements on 6-month survival after a critical illness (7). If folic acid fortification prevents congenital heart disease by enhancing ATP resynthesis, and thereby supporting nucleic acid synthesis, rapid cell division and growth, might glutamine supplements be of additional benefit? If of equal importance the combination of these two supplements might even be expected to decrease the prevalence of congenital heart disease from the former 1.6 severe cases to some 0.75 severe cases per 1000 births. If, however, severe cases of congential heart disease are merely a clearly defined marker of a far more common problem, subclinical degrees of systemic organ dysfunctions, such as being in the lower precentiles in cognitive skills, the benefits to populations and to society in the future could be infinitely larger. 1. Helena M Gardiner and Jean-Claude Fouron Folic acid fortification and congenital heart disease BMJ 2009; 338: b1144 2. A. H. Stouthamer. A theoretical study on the amount of ATP required for synthesis of. microbial cell material . Antonie van Leeuwenhoek, Volume 39, Number 1 / December, 1973 3. S. DiMauro, E. Bonilla, M. Zeviani, S. Servidei, D. C. DeVivo and E. A. Schon. Mitochondrial myopathies. Journal of Inherited Metabolic Disease. Volume 10, Supplement 1 / March, 1987, pp 113-118. 4. C M Grum, R H Simon, D R Dantzker, and I H Fox. Evidence for adenosine triphosphate degradation in critically-ill patients. CHEST November 1985 vol. 88 no. 5 763-767. 5. Jeremy M. Berg, John L. Tymoczko, Lubert Stryer, Neil D. Clarke. Biochemistry. 2002 by W. H. Freeman and Company. 6. R. Griffiths, C. Jones, T. Allan Palmer. Six-month outcome of critically ill patients given glutamine-supplemented parenteral nutrition. Nutrition, Volume 13, Issue 4, Pages 295-302. Competing interests: None declared |
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