— September 1, 2026 · Higher Vitamin B12 in Both Mothers and Fathers Linked to Fewer Birth Defects in a Shanghai Cohort

Table of Contents

1. At a Glance
2. What Was Done
3. What Was Found, Number by Number
4. How B12 and Folate Work Together
5. How B12 and Folate Are Measured
6. How It Fits With Earlier Research
7. What It Cannot Show
8. What the Researchers and the Journal Said
9. What Remains Unknown
10. Sources and Primary Documents
11. Key Research Papers
12. Connections

At a Glance

• Paper — Chen H, Chen X, Zhang Y, et al.; SPCC (Shanghai Preconception Cohort) Group. “Periconception Parental Red Blood Cell Folate, Vitamin B12, and Birth Defects in Offspring: A Prospective Cohort Study.” Annals of Internal Medicine, published online September 1, 2026 (DOI 10.7326/ANNALS-25-05243; PubMed 42673604).
• Who — 20 researchers led by Hongyan Chen (first author) and Guoying Huang (senior author) at the Children’s Hospital of Fudan University and the Shanghai Key Laboratory of Birth Defects, with a statistician from the Liverpool School of Tropical Medicine in the United Kingdom.
• Funding — public research funds: the National Key Research and Development Program of China, the National Natural Science Foundation of China and the Chinese Academy of Medical Sciences.
• Design — prospective cohort study; blood levels measured before the outcome was known.
• Size — 3,032 couples sampled within 4 months before conception (73 pregnancies with a birth defect) and 17,765 women sampled at 4 months’ gestation or earlier (327 with a birth defect).
• Mothers’ B12 before conception — predicted birth defects fell from 49.6 to 16.2 per 1,000 pregnancies, lowest (<148 pmol/L) to highest (≥590 pmol/L) group.
• Fathers’ B12 before conception — a similar but weaker fall, from 55.5 to 24.0 per 1,000 pregnancies.
• Mothers’ red blood cell folate after conception — 16.5 per 1,000 at 906 to 1,131 nmol/L vs 25.7 per 1,000 below 453 nmol/L, with little further reduction at higher levels.
• Limit named by the authors — residual confounding (other differences between families that the analysis could not fully remove).

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What Was Done

The cohort. According to the cohort’s published description in BMJ Open (2019), married couples in Shanghai have been encouraged since 2010 to attend a free preconception health examination, and the Shanghai Preconception Cohort recruits from those clinics. It enrolled women and men who were permanent residents and came to preconception clinics at 28 maternity institutions in 10 districts of Shanghai between March 2016 and December 2018, along with women in early pregnancy before 14 weeks. At that time it counted 8,045 preconception couples, 3,054 women who came alone and 15,615 women in early pregnancy, with 12,402 births recorded. The cohort was first set up to study congenital heart disease and later widened to other childhood outcomes. Its stated goal is to follow the children for 18 years. A “Cohort Profile Update” describing the cohort’s work on “parental one-carbon metabolism and offspring health” appeared in the International Journal of Epidemiology in August 2026.

Two groups were analysed.

• Couples before conception: 3,032 couples in whom both partners had blood biomarkers measured within four months before the pregnancy began. Among their pregnancies, 73 had a birth defect.
• Women in early pregnancy: 17,765 women whose blood was sampled at four months of pregnancy or earlier. Among their pregnancies, 327 had a birth defect.

What was measured. Two blood markers: vitamin B12 (in picomoles per litre, pmol/L) and red blood cell folate (in nanomoles per litre, nmol/L). Red blood cell folate is the amount of folate held inside red cells; the same research team has called it “the gold-standard biomarker of folate exposure.” Folate here means the vitamin as measured in the blood, from any source. It is not the same thing as folic acid, the synthetic form used in supplements and fortified flour.

What counted as a birth defect. The abstract states that birth defects were “ascertained among live births, stillbirths, and abortions due to fetal abnormalities.” Counting pregnancies that ended because of a detected abnormality matters: a study that counted only live births would miss affected pregnancies that ended before birth.

How the numbers were produced. The team used weighted logistic regression to estimate a “standardized predicted prevalence” of birth defects for each band of vitamin level. In plain terms, these are model-based estimates of how many pregnancies per 1,000 would be affected at each vitamin level once other measured differences between families are balanced out. They are not simply the raw counts in each group.

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What Was Found, Number by Number

All figures are predicted birth defects per 1,000 pregnancies, as printed in the abstract. The abstract does not print confidence intervals, odds ratios or a breakdown by type of defect, so none are given here.

Vitamin B12 before conception

• Mothers: from 49.6 per 1,000 in the lowest B12 group (below 148 pmol/L) to 16.2 per 1,000 in the highest (590 pmol/L or more). The authors describe this as a dose-response pattern: the higher the level, the lower the predicted rate.
• Fathers: “a similar but attenuated pattern,” from 55.5 to 24.0 per 1,000 between the lowest and the highest category.

In the authors’ words: “Higher preconception parental levels of vitamin B12 were associated with lower predicted prevalences of birth defects in dose-response analyses.”

Red blood cell folate before conception

For both parents, red blood cell folate measured before conception “showed imprecise patterns of lower predicted prevalence.” The numbers pointed in the direction of fewer defects at higher folate, but they were too uncertain to draw a firm line. The couples group included 73 affected pregnancies in all.

Red blood cell folate after conception (mothers)

• 16.5 per 1,000 at 906 to 1,131 nmol/L, compared with 25.7 per 1,000 below 453 nmol/L.
• Above about 1,131 nmol/L there was “little further reduction.”

The lower edge of that band, 906 nmol/L, is the same figure the World Health Organization adopted in 2015 as the population threshold for red blood cell folate in women of reproductive age for the prevention of neural tube defects (see earlier research).

Vitamin B12 after conception (mothers)

• The predicted rate “changed little across lower categories but was lower at higher levels”: 11.8 per 1,000 at 590 pmol/L or more, compared with 20.4 per 1,000 at 148 to 294 pmol/L.

The authors’ conclusion

“Periconception parental vitamin B12 and postconception maternal RBC folate were associated with lower predicted prevalences of birth defects.” Periconception means the weeks around conception, before and just after.

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How B12 and Folate Work Together

Vitamin B12 and folate are partners in what biochemists call one-carbon metabolism: the chain of reactions that hands small chemical units from one molecule to another to build DNA and to switch genes on and off. A 2019 review in the Journal of Inherited Metabolic Disease describes the main steps.

• Two B12-dependent enzymes. In the body, B12 serves as a helper (a cofactor) for just two enzymes: methionine synthase and methylmalonyl-CoA mutase.
• Where folate and B12 meet. Methionine synthase takes a one-carbon unit from a form of folate (5-methyltetrahydrofolate) and uses it to turn homocysteine into the amino acid methionine. Methionine is then made into S-adenosylmethionine, which the review calls “the most important cellular methyl-donor.” Methyl groups from it are used to mark DNA and so help control which genes are active.
• DNA building blocks. Folate-carried one-carbon units are also needed to make thymidine and purines, the building blocks of new DNA. A growing embryo, whose cells divide very quickly, needs a steady supply.
• The second enzyme. Methylmalonyl-CoA mutase works inside mitochondria, where it is needed to break down certain (branched-chain) amino acids. Raised methylmalonic acid in the blood is one of the recognised markers of B12 shortage (see the next section).

Because methionine synthase uses both vitamins in the same reaction, the review notes that its disruption affects the folate pathway inside cells as well as methylation. The animated methylation cycle page on this site shows the loop step by step.

Why fathers might matter

The Shanghai paper reports an association; it does not test how a father’s vitamin level could reach the embryo. Laboratory work has offered one possible route. In a 2013 study in Nature Communications, male mice fed a folate-deficient diet throughout life sired offspring with more birth defects, including craniofacial and musculoskeletal malformations, than males fed a folate-sufficient diet, and their sperm showed differences in DNA methylation at genes involved in development. The authors proposed that the sperm epigenome (the chemical marks laid on sperm DNA and its packaging proteins) carries information about the father’s diet. A 2018 review in The Lancet on health “around the time of conception” listed paternal factors alongside maternal nutrition as influences on offspring health and called for “new guidance on parental preparation for pregnancy, beginning before conception.” Neither paper studied vitamin B12 in human fathers.

Where vitamin B12 comes from in food

A 2007 review of B12 sources in Experimental Biology and Medicine states that “the usual dietary sources of vitamin B12 are animal foods, meat, milk, egg, fish, and shellfish.” The same review reports that the gut’s intrinsic-factor absorption system is estimated to saturate at about 1.5 to 2.0 micrograms per meal, that measured absorption averaged 42% from fish and 56% to 89% from sheep meat, and that B12 in eggs “seems to be poorly absorbed (< 9%)” compared with other animal foods. It also reports that most edible blue-green algae sold as supplements contain mainly pseudovitamin B12, a look-alike that is inactive in humans. Fish such as sardines and salmon, and whole eggs, have their own pages on this site.

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How B12 and Folate Are Measured

A blood vitamin level is only as meaningful as the test behind it, and the B12 numbers in this study come from one particular test.

• Total serum B12. The study reports B12 in pmol/L, the usual unit for a standard B12 blood test. This measures all of the B12 in the serum, whichever carrier protein it is bound to.
• Holotranscobalamin (“active B12”). This measures only the B12 bound to the carrier protein transcobalamin; the Ontario researchers described it as “a sensitive indicator of B12 status.” A 2017 expert primer in Nature Reviews Disease Primers lists low total B12 and low transcobalamin-bound B12 among the diagnostic markers. An Ontario study used this active B12 test (see below).
• Methylmalonic acid and homocysteine. The same primer lists abnormally raised methylmalonic acid and homocysteine as functional signs of B12 shortage, because both build up when the B12-dependent enzymes slow down. It also states that “the exact cut-offs to classify clinical and subclinical deficiency remain debated.”
• Red blood cell folate. The RBC folate test measures folate held inside red cells, as distinct from the serum folate level in the fluid part of the blood. The WHO guideline below sets thresholds for both.

The assay used in this cohort. The cohort’s 2019 description states that red blood cell folate, serum folate, homocysteine, vitamin D, vitamin B12 and ferritin were all measured with electrochemiluminescence assays on one automated analyser. The description notes that this method is “different from the widely used microbiological assay” for folate and that comparison with other populations “needs caution.” Whether the 2026 analysis used the same method could not be confirmed from the abstract. The practical point is that the cut-points in the paper (148, 294, 453, 590, 906 and 1,131) may not line up exactly with numbers from a different laboratory.

The 2017 primer estimates that subclinical B12 deficiency affects between 2.5% and 26% of the general population, depending on the definition used, and names women of reproductive age as a group at high risk where intake of animal-derived foods is restricted. The site’s B12 deficiency page covers the symptoms and causes.

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How It Fits With Earlier Research

Folic acid and neural tube defects: the trials

Neural tube defects, such as spina bifida and anencephaly, form in the first month of pregnancy when the neural tube fails to close. Two randomised trials from the early 1990s settled the role of folic acid.

• The Medical Research Council Vitamin Study (1991). 1,817 women who had already had an affected pregnancy, at 33 centres in seven countries. Among 1,195 completed pregnancies there were 27 neural tube defects: 6 in the folic acid groups and 21 in the other groups, a relative risk of 0.28 (95% CI 0.12 to 0.71), which the authors called “a 72% protective effect.” A mixture of seven other vitamins showed no significant effect (relative risk 0.80, 95% CI 0.32 to 1.72).
• The Hungarian trial (1992). Women planning a pregnancy, most of them a first pregnancy, took a multivitamin containing 0.8 mg of folic acid or a trace-element tablet. There were no neural tube defects in the multivitamin group and six in the trace-element group (P = 0.029). Congenital malformations overall were 13.3 vs 22.9 per 1,000 (P = 0.02). Cleft lip with or without cleft palate was not reduced.

Maternal vitamin B12 and neural tube defects: the case-control studies

• Ontario, Canada (2007). In a population where flour had been fortified with folic acid since mid-1997, researchers measured holotranscobalamin at 15 to 20 weeks of pregnancy in 89 women carrying a fetus with a neural tube defect and 422 unaffected controls. Women in the lowest quarter of active B12 had an adjusted odds ratio of 2.9 (95% CI 1.2 to 6.9) compared with the highest quarter, which the authors described as “almost a tripling in the risk.”
• Ireland (2009). Three separate groups of Irish women, sampled at about 15 weeks of pregnancy at a time when supplements and fortification were rare. In all three, women in the lowest B12 quarter had “between two and threefold higher adjusted odds ratios” of an affected pregnancy than those in the highest; levels below 250 ng/L carried the highest risk. The authors wrote: “We suggest that women have vitamin B12 levels of >300 ng/L (221 pmol/L) before becoming pregnant.”
• Meta-analysis (2012). Nine published studies with 567 cases and 1,566 controls gave a pooled odds ratio of 2.41 (95% CI 1.90 to 3.06) for a neural tube defect with low maternal B12.

These studies looked at neural tube defects only, and at mothers only. The Shanghai paper extends the question to birth defects as a whole, to blood taken before conception, and to fathers.

Folate thresholds and guidelines

• A modelled threshold (2014). A Bayesian model built from two large Chinese studies estimated 25.4 neural tube defects per 10,000 births (95% uncertainty interval 20.8 to 31.2) at a red blood cell folate of 500 nmol/L, falling to about 6 per 10,000 at 1,180 nmol/L. Risk was “substantially attenuated” above about 1,000 nmol/L.
• World Health Organization (2015). The WHO set the population target for red blood cell folate in women of reproductive age at above 400 ng/mL (906 nmol/L) “to achieve the greatest reduction of NTDs,” a strong recommendation based on low-quality evidence. The guideline adds that this threshold “cannot predict the individual” risk, because low folate does not explain every case.
• US Preventive Services Task Force (2023). The Task Force “recommends that all persons planning to or who could become pregnant take a daily supplement containing 0.4 to 0.8 mg (400 to 800 µg) of folic acid,” an A-grade recommendation. It estimates that about 3,000 US pregnancies are affected by neural tube defects each year. The statement concerns folic acid; it makes no recommendation about vitamin B12.

The same team’s earlier heart-defect study (2022)

In the same journal in 2022, the Shanghai group compared 197 mothers of babies with congenital heart disease with 788 matched mothers of unaffected babies. Median red blood cell folate was 714 nmol/L in the case mothers and 788 nmol/L in the controls. Each 100 nmol/L higher was linked to an adjusted odds ratio of 0.93 (95% CI 0.89 to 0.99), and a level of 906 nmol/L or more (vs below 906) to an adjusted odds ratio of 0.61 (95% CI 0.40 to 0.93). A genetic (Mendelian randomization) analysis using the MTHFR C677T variant gave an odds ratio of 0.75 (95% CI 0.61 to 0.92) per 100 nmol higher. The authors wrote that higher folate targets than those set for neural tube defects “may be needed and warrant further study.” The 2026 paper adds vitamin B12 and fathers to that line of work.

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What It Cannot Show

• Association, not cause. Nobody in the study was given B12 or folic acid by random assignment. Parents with higher vitamin levels may differ in many other ways (diet as a whole, income, health, age, other supplements). The authors name “residual confounding” as the study’s limitation: differences the statistical adjustment could not remove.
• Few cases in the couples group. The before-conception findings, including the fathers’ result, rest on 73 pregnancies with a birth defect among 3,032 couples. Small numbers make each category’s estimate less certain. The abstract does not print confidence intervals, so the size of that uncertainty cannot be reported here.
• Predicted, not counted. The figures are model-based standardised estimates, not the raw proportion of affected pregnancies in each group.
• Birth defects grouped together. “Birth defects” covers many different conditions with different causes. The abstract does not say which defects drove the pattern, or whether B12 relates to neural tube defects, heart defects or other conditions separately.
• One city, one population. All participants lived in Shanghai. Diet, supplement habits, folic-acid fortification policy and typical vitamin levels differ between countries, so the same numbers may not hold elsewhere.
• One laboratory method. The cohort used electrochemiluminescence assays, and its own description warns that comparisons with other populations need caution. The study’s cut-points may not transfer directly to results from another laboratory.
• Total B12 only. The abstract reports total serum B12. It does not mention holotranscobalamin, methylmalonic acid or homocysteine, the other markers the 2017 primer lists for judging B12 status.
• Couples who plan. The cohort recruited couples who attended preconception clinics. People who plan a pregnancy and attend check-ups may differ from those who do not.

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What the Researchers and the Journal Said

The authors. The abstract’s conclusion reads: “Periconception parental vitamin B12 and postconception maternal RBC folate were associated with lower predicted prevalences of birth defects.” The American College of Physicians, which publishes the journal, issued a press release for the paper on August 31, 2026, at 5 p.m. US Eastern time, for publication the next day. It quotes the authors: “These findings support the potential importance of both paternal and maternal nutrition during the periconceptional period and early pregnancy.”

The editorial. The journal paired the study with an editorial by Cuilin Zhang and Jing Zhu titled “Both Paternal and Maternal Nutrition Status Matter: An Exemplar From Folate and Vitamin B12 in Association With Risks for Birth Defects.” The editorial’s text was not available to this site, so its arguments are not summarised here.

News coverage. The study was reported the same day by medical news services. Some reports attributed details to the paper, such as which defects were tracked, how long babies were followed, or advice from a patient summary, that do not appear in the abstract. Those details could not be checked against the paper and are not repeated here.

Guideline bodies. The two guideline documents described above, from the WHO (2015) and the US Preventive Services Task Force (2023), concern folate, folic acid and neural tube defects in women. Neither sets a vitamin B12 level for either parent.

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What Remains Unknown

• Would raising B12 change anything? Only a randomised trial of B12 before conception, in mothers, fathers or both, could show whether raising a low level lowers the rate of birth defects. The abstract reports no such trial.
• Which defects? Whether the B12 pattern holds for neural tube defects, heart defects, clefts or other conditions separately is not reported in the abstract.
• How could a father’s B12 matter? Animal work points to the sperm epigenome as one possible route, but this has not been shown in people for B12.
• What level? The paper reports bands, not a target. For mothers’ B12 the lowest predicted rates were in the top band, which was open-ended (590 pmol/L or more), so the abstract gives no figure for higher levels.
• Other markers. Whether active B12 (holotranscobalamin), methylmalonic acid or homocysteine would show the same pattern is untested in this cohort as reported.
• Other populations. Whether the findings hold in countries with mandatory folic-acid fortification of flour, or among people who eat little or no animal food, is not known from this study.

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Sources and Primary Documents

Every figure attributed to the 2026 study comes from its published abstract (the full text is behind a paywall). Cohort details come from the cohort’s open-access 2019 description. Background figures come from the abstracts or full texts of the papers listed under Key Research Papers.

1. Chen H, Chen X, Zhang Y, Li M, Yao Q, Wang D, et al.; SPCC (Shanghai Preconception Cohort) Group (2026). Periconception Parental Red Blood Cell Folate, Vitamin B12, and Birth Defects in Offspring: A Prospective Cohort Study. Annals of Internal Medicine, published online September 1, 2026. — doi:10.7326/ANNALS-25-05243 · PubMed PMID: 42673604
2. Zhang C, Zhu J (2026). Both Paternal and Maternal Nutrition Status Matter: An Exemplar From Folate and Vitamin B12 in Association With Risks for Birth Defects. Annals of Internal Medicine, published online September 1, 2026 (editorial). — doi:10.7326/ANNALS-26-03045 · PubMed PMID: 42673601
3. Wang D, Zhang Y, Jiang Y, Ye Y, Ji M, Dou Y, et al.; SPCC group (2019). Shanghai Preconception Cohort (SPCC) for the association of periconceptional parental key nutritional factors with health outcomes of children with congenital heart disease: a cohort profile. BMJ Open 9(11):e031076. — doi:10.1136/bmjopen-2019-031076 · PubMed PMID: 31767586
4. Zhang Y, Yao Q, Chen X, Dou Y, He W, He Y, et al.; SPCC (Shanghai Preconception Cohort) Group (2026). Cohort Profile Update: the Shanghai Preconception Cohort on parental one-carbon metabolism and offspring health. International Journal of Epidemiology 55(5):dyag200. — doi:10.1093/ije/dyag200 · PubMed PMID: 42727088
5. Chen H, Zhang Y, Wang D, Chen X, Li M, Huang X, et al.; SPCC (Shanghai Preconception Cohort) Group (2022). Periconception Red Blood Cell Folate and Offspring Congenital Heart Disease: Nested Case-Control and Mendelian Randomization Studies. Annals of Internal Medicine 175(9):1212-1220. — doi:10.7326/M22-0741 · PubMed PMID: 35994746

Press release: American College of Physicians, “Higher vitamin B12 levels in both parents are associated with lower risk of birth defects,” August 31, 2026 (via Newswise). News report: HealthDay, September 1, 2026.

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Key Research Papers

Background papers on folate, vitamin B12 and birth defects, in the order they appear above. Each entry was checked against its PubMed record before it was written down.

1. MRC Vitamin Study Research Group (1991). Prevention of neural tube defects: results of the Medical Research Council Vitamin Study. Lancet 338(8760):131-137. — PubMed PMID: 1677062
2. Czeizel AE, Dudás I (1992). Prevention of the first occurrence of neural-tube defects by periconceptional vitamin supplementation. New England Journal of Medicine 327(26):1832-1835. — PubMed PMID: 1307234
3. Ray JG, Wyatt PR, Thompson MD, Vermeulen MJ, Meier C, Wong PY, Farrell SA, Cole DE (2007). Vitamin B12 and the risk of neural tube defects in a folic-acid-fortified population. Epidemiology 18(3):362-366. — PubMed PMID: 17474166
4. Molloy AM, Kirke PN, Troendle JF, Burke H, Sutton M, Brody LC, Scott JM, Mills JL (2009). Maternal vitamin B12 status and risk of neural tube defects in a population with high neural tube defect prevalence and no folic acid fortification. Pediatrics 123(3):917-923. — PubMed PMID: 19255021
5. Wang ZP, Shang XX, Zhao ZT (2012). Low maternal vitamin B12 is a risk factor for neural tube defects: a meta-analysis. Journal of Maternal-Fetal and Neonatal Medicine 25(4):389-394. — PubMed PMID: 21627554
6. Crider KS, Devine O, Hao L, Dowling NF, Li S, Molloy AM, Li Z, Zhu J, Berry RJ (2014). Population red blood cell folate concentrations for prevention of neural tube defects: Bayesian model. BMJ 349:g4554. — PubMed PMID: 25073783
7. Cordero AM, Crider KS, Rogers LM, Cannon MJ, Berry RJ (2015). Optimal serum and red blood cell folate concentrations in women of reproductive age for prevention of neural tube defects: World Health Organization guidelines. MMWR Morbidity and Mortality Weekly Report 64(15):421-423. — PubMed PMID: 25905896
8. US Preventive Services Task Force; Barry MJ, Nicholson WK, Silverstein M, Chelmow D, Coker TR, Davis EM, et al. (2023). Folic Acid Supplementation to Prevent Neural Tube Defects: US Preventive Services Task Force Reaffirmation Recommendation Statement. JAMA 330(5):454-459. — PubMed PMID: 37526713
9. Green R, Allen LH, Bjørke-Monsen AL, Brito A, Guéant JL, Miller JW, et al. (2017). Vitamin B12 deficiency. Nature Reviews Disease Primers 3:17040. — PubMed PMID: 28660890
10. Froese DS, Fowler B, Baumgartner MR (2019). Vitamin B12, folate, and the methionine remethylation cycle — biochemistry, pathways, and regulation. Journal of Inherited Metabolic Disease 42(4):673-685. — PubMed PMID: 30693532
11. Lambrot R, Xu C, Saint-Phar S, Chountalos G, Cohen T, Paquet M, Suderman M, Hallett M, Kimmins S (2013). Low paternal dietary folate alters the mouse sperm epigenome and is associated with negative pregnancy outcomes. Nature Communications 4:2889. — PubMed PMID: 24326934
12. Fleming TP, Watkins AJ, Velazquez MA, Mathers JC, Prentice AM, Stephenson J, et al. (2018). Origins of lifetime health around the time of conception: causes and consequences. Lancet 391(10132):1842-1852. — PubMed PMID: 29673874
13. Watanabe F (2007). Vitamin B12 sources and bioavailability. Experimental Biology and Medicine 232(10):1266-1274. — PubMed PMID: 17959839

PubMed Topic Searches

1. PubMed: Vitamin B12 and neural tube defects
2. PubMed: Paternal vitamin B12 and birth defects
3. PubMed: Red blood cell folate and birth defects
4. PubMed: Holotranscobalamin (active B12) in pregnancy
5. PubMed: Shanghai Preconception Cohort

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Connections

• News Archive
• Vitamin B12 — the vitamin, its forms and its research
• Vitamin B12 Deficiency — symptoms, causes and recovery
• Vitamin B12 Benefits — the deep-dive articles on what B12 does
• Active B12 (Holotranscobalamin) Testing — the test used in the Ontario study
• Vitamin B12 Test — total serum B12 levels and how they are read
• Methylmalonic Acid — the functional test for B12 shortage
• RBC Folate Test — the folate marker measured in this study
• Homocysteine — the amino acid that builds up when B12 or folate is short
• Vitamin B9 (Folate) — folate and folic acid
• Folate and Pregnancy — neural tube defect research
• Folic Acid and Masked B12 Deficiency — how high folic acid can hide a B12 shortage
• Spina Bifida — the best-known neural tube defect
• Congenital Heart Disease — the outcome the Shanghai cohort was built to study
• The Methylation Cycle and Homocysteine — animation of where B12 and folate meet
• Male Infertility — the father’s side of reproductive health

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