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1999; Waterland and Jirtle, 2003) A number of mouse models involve a genetic deletion that results either in nonviable embryos or some sort of a severe phenotype that can be rescued with nutrition. Thus, care is warranted related to the possibility that epigenetic effects modify genetic insults that exist in the human population. Dr. Stover believes that certain reprogramming events probably are common, can be modified by nutrition, and influence a number of folate-associated diseases.

Concluding Remarks

In conclusion, Dr. Stover emphasized the need to consider genetic variation, determine relevant parameters, and determine whether or not individual recommendations for B vitamin requirements are needed. Furthermore, there is a need for better understanding of epigenetic effects. In investigating new indicators for both the EAR and UL, a disease prevention approach could involve targeting the molecular antecedents of disease. Promising ones might include molecular antecedents for cancer and for other diseases with mutation rates that can be measured in the population. However, since this approach probably would result in increasing the RDA, attention also would need to be given to new concerns for ULs, including epigenetic effects and genetic rescue.


A number of comments made during the discussion relate to the DRI paradigm. Those comments appear at the end of Chapter 13, “Wrap-Up.”

Dr. Appel asked about homocysteine as a surrogate for folate intake. In particular, findings in recently published clinical trials indicated that decreases in serum homocysteine concentration were not accompanied by a reduction in adverse health outcomes. In some cases, there was the appearance of potential harm. Considering this, how could homocysteine serve as a useful surrogate for folate intake? Dr. Stover responded that those findings were from secondary prevention trials and that primary prevention trials are needed because that probably is where homocysteine is exerting its effects.

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