To the Editor: Dr. Morris and coworkers have made significant contributions to clinical nutrition, and I am grateful for their endorsement of the importance of scientific evidence in addressing the question posed in my title. The need for balanced, open-minded scientific analysis was the central point of my review. In regard to their specific comments, their reference 2 was not published by the time of submission of the review and was not cited. I did reference an earlier paper (1), which, indeed, showed an association between high blood folate and protection against cognitive decline in those with normal B-12 status, in agreement with a recent randomized controlled trial. However, a subgroup (3.2%) of those with cognitive impairment had high blood folate but low B-12 levels. The authors did not conclude that high folate exacerbated the consequences of B-12 deficiency, and I did not choose to further discuss the folic acid (FA)-cognition relationship beyond citing the references that I could find on both sides of the issue.

I reviewed the evidence against masking the anemia of B-12 deficiency by FA because this led to the Institute of Medicine's setting the tolerable upper level of synthetic FA intake at 1000 μg/d for adults, and at proportionally lower levels for children based on weight. The Morris et al. article (1) cited evidence from four recent publications and their own data that favored the conclusion that FA in doses currently consumed does not mask the anemia of B-12 deficiency.

Blood folate levels have risen since the advent of fortification. However, analysis of data from the source used by the authors (1) indicates that almost all of the participants in the “high folate” group took supplements (2). In this subpopulation, the contribution from fortified grain products falls well below that obtained from taking supplements (2).

An randomized controlled trial has shown that very low oral doses of B-12 can effectively increase serum B-12 in individuals with age-related B-12 malabsorption (3). It seems important to pursue the possibility that the supplement-taking subgroup with high folate-low B-12 have preclinical pernicious anemia and cannot absorb oral B-12 adequately (1,2). Regardless of folate status, they could benefit from parenteral or high-dose oral B-12. Moreover, if low B-12 status is as common as Morris et al. estimate, why are we not mounting a public health campaign to raise B-12 intake in older Americans? The experience and expertise of Morris and workers with B-12 nutrition suggest that they would be effective leaders of such an initiative.

No one wants to harm older Americans while protecting babies, and interested parties should work openly and collaboratively to optimize FA nutrition in individuals of all ages. Posited harms from FA intake should be investigated. But the data show clearly that FA fortification has reduced the rate of serious birth defects. The posited harms carry varying levels of biologic plausibility, but to date none is a proven risk.