The relationship between serum cobalamin concentration and mean red cell volume at varying concentrations of serum folate

Metz, J.; McNeil, Alan; Levin, Matthew A.

doi:10.1111/j.1365-2257.2004.00631.x

Cited by 25 publications

(16 citation statements)

References 6 publications

(7 reference statements)

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“…Our results are in agreement with previous reports from both voluntary and mandatory fortification settings which found no changes in anemia indicators and no evidence of deteriorating vitamin B-12 status among those with improved folate status (16,17). Our analyses are also consistent with a U.S. Veterans Affairs hospital-based report which found no significant differences in the proportion of adults with low serum vitamin B-12 (<258 pmol/L) without anemia from before to after fortification (14).…”

Section: Discussionsupporting

confidence: 93%

The Prevalence of Low Serum Vitamin B-12 Status in the Absence of Anemia or Macrocytosis Did Not Increase among Older U.S. Adults after Mandatory Folic Acid Fortification

Hamner

et al. 2014

The Journal of Nutrition

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Whether folic acid fortification and supplementation at the population level have led to a higher prevalence of vitamin B-12 deficiency in the absence of anemia remains to be examined among a nationally representative sample of older U.S. adults. We assessed the prevalence of low vitamin B-12 status in the absence of anemia or macrocytosis before and after fortification among adults aged >50 y using cross-sectional data from the NHANES 1991–1994 (prefortification) and 2001–2006 (postfortification). We compared the prefortification and postfortification prevalence of multiple outcomes, including serum vitamin B-12 deficiency (<148 pmol/L) and marginal deficiency (148–258 pmol/L) with and without anemia (hemoglobin <130 g/L for men, <120 g/L for women) and with and without macrocytosis (mean cell volume >100 fL) using multinomial logistic regression, adjusting for age, sex, ethnicity, body mass index, C-reactive protein, and vitamin B-12 supplement use. Prefortification and postfortification serum vitamin B-12 deficiency without anemia [4.0 vs. 3.9%; adjusted prevalence ratio (aPR) (95% CI): 0.98 (0.67, 1.44)] or without macrocytosis [4.2 vs. 4.1%; aPR (95% CI): 0.96 (0.65, 1.43)] remained unchanged. Marginal deficiency without anemia [25.1 vs. 20.7%; aPR (95% CI): 0.82 (0.72, 0.95)] or without macrocytosis [25.9 vs. 21.3%; aPR (95%CI): 0.82 (0.72, 0.94)] were both significantly lower after fortification. After fortification, higher folic acid intake was associated with a lower prevalence of low serum B-12 status in the absence of anemia or macrocytosis. Results suggest that the prevalence of low serum B-12 status in the absence of anemia or macrocytosis among older U.S. adults did not increase after fortification. Thus, at the population level, we found no evidence to support concerns that folic acid adversely affected the clinical presentation of vitamin B-12 deficiency among older adults.

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Section: Discussionsupporting

confidence: 93%

The Prevalence of Low Serum Vitamin B-12 Status in the Absence of Anemia or Macrocytosis Did Not Increase among Older U.S. Adults after Mandatory Folic Acid Fortification

Hamner

et al. 2014

The Journal of Nutrition

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“…6,7,51 However, post-fortification empirical evidence did not bear out those fears. 44,52–54 Likewise, subsequent concerns that additional folic acid might increase the incidence of colorectal cancer were not confirmed. 55,56 …”

Section: Discussionmentioning

confidence: 99%

Retrospective Assessment of Cost Savings From Prevention

Grosse

Berry

Tilford

et al. 2016

American Journal of Preventive Medicine

103

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Introduction Although fortification of food with folic acid has been calculated to be cost saving in the U.S., updated estimates are needed. This analysis calculates new estimates from the societal perspective of net cost savings per year associated with mandatory folic acid fortification of enriched cereal grain products in the U.S. that was implemented during 1997–1998. Methods Estimates of annual numbers of live-born spina bifida cases in 1995–1996 relative to 1999–2011 based on birth defects surveillance data were combined during 2015 with published estimates of the present value of lifetime direct costs updated in 2014 U.S. dollars for a live-born infant with spina bifida to estimate avoided direct costs and net cost savings. Results The fortification mandate is estimated to have reduced the annual number of U.S. live-born spina bifida cases by 767, with a lower-bound estimate of 614. The present value of mean direct lifetime cost per infant with spina bifida is estimated to be $791,900, or $577,000 excluding caregiving costs. Using a best estimate of numbers of avoided live-born spina bifida cases, fortification is estimated to reduce the present value of total direct costs for each year's birth cohort by $603 million more than the cost of fortification. A lower-bound estimate of cost savings using conservative assumptions, including the upper-bound estimate of fortification cost, is $299 million. Conclusions The estimates of cost savings are larger than previously reported, even using conservative assumptions. The analysis can also inform assessments of folic acid fortification in other countries.

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“…About 10-25 % of older adults have biochemical evidence of low vitamin B 12 status, defined by a low serum concentration (<45 pmol/l) of holotranscobalamin, which is a more sensitive test of vitamin B 12 deficiency than conventional vitamin B 12 testing (27) . There have been reports that patients with pernicious anaemia who are treated with folic acid have an accelerated decline in neurological function (32)(33)(34) . Consequently, the amount of folic acid is routinely limited to a maximum of 1000 mg/d because of concerns about the adverse effects of high-dose folic acid in individuals with vitamin B 12 deficiency.…”

Section: Possible Hazards Of Folic Acidmentioning

confidence: 99%

B-vitamins and prevention of dementia

Clarke

2008

Proc. Nutr. Soc.

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Elevated plasma homocysteine (Hcy) concentrations have been implicated with risk of cognitive impairment and dementia, but it is unclear whether low vitamin B 12 or folate status is responsible for cognitive decline. Most studies reporting associations between cognitive function and Hcy or B-vitamins have used a cross-sectional or case-control design and have been unable to exclude the possibility that such associations are a result of the disease rather than being causal. The Hcy hypothesis of dementia has attracted considerable interest, as Hcy can be easily lowered by folic acid and vitamin B 12 , raising the prospect that B-vitamin supplementation could lower the risk of dementia. While some trials assessing effects on cognitive function have used folic acid alone, vitamin B 12 alone or a combination, few trials have included a sufficient number of participants to provide reliable evidence. An individualpatient-data meta-analysis of all randomised trials of the effects on cognitive function and vascular risk of lowering Hcy with B-vitamins will maximise the power to assess the epidemiologically-predicted differences in risk. Among the twelve large randomised Hcy-lowering trials for prevention of vascular disease, data should be available on about 30 000 participants with cognitive function. The principal investigators of such trials have agreed to combine individual-participant data from their trials after their separate publication.Folate: Vitamin B 12 : Homocysteine: Dementia

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The relationship between serum cobalamin concentration and mean red cell volume at varying concentrations of serum folate

Cited by 25 publications

References 6 publications

The Prevalence of Low Serum Vitamin B-12 Status in the Absence of Anemia or Macrocytosis Did Not Increase among Older U.S. Adults after Mandatory Folic Acid Fortification

The Prevalence of Low Serum Vitamin B-12 Status in the Absence of Anemia or Macrocytosis Did Not Increase among Older U.S. Adults after Mandatory Folic Acid Fortification

Retrospective Assessment of Cost Savings From Prevention

B-vitamins and prevention of dementia

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