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As individuals seek increasingly individualised nutrition and lifestyle guidance, numerous apps and nutrition programmes have emerged. However, complex individual variations in dietary behaviours, genotypes, gene expression and composition of the microbiome are increasingly recognised. Advances in digital tools and artificial intelligence can help individuals more easily track nutrient intakes and identify nutritional gaps. However, the influence of these nutrients on health outcomes can vary widely among individuals depending upon life stage, genetics and microbial composition. For example, folate may elicit favourable epigenetic effects on brain development during a critical developmental time window of pregnancy. Genes affecting vitamin B12 metabolism may lead to cardiometabolic traits that play an essential role in the context of obesity. Finally, an individual’s gut microbial composition can determine their response to dietary fibre interventions during weight loss. These recent advances in understanding can lead to a more complete and integrated approach to promoting optimal health through personalised nutrition, in clinical practice settings and for individuals in their daily lives. The purpose of this review is to summarise presentations made during the DSM Science and Technology Award Symposium at the 13th European Nutrition Conference, which focused on personalised nutrition and novel technologies for health in the modern world.
B-vitamins affect brain function through multiple pathways. Given limited evidence on the relationship between dietary intake of these vitamins and psychological disorders, we examined dietary intake of vitamin B6-9-12 in relation to psychological disorders among Iranian women.
Cross-sectional study. Dietary intake was assessed using a valid and reliable FFQ. To assess psychological disorders, we used a version of the Depression Anxiety Stress Scale-21 validated in Iran.
Ten public health centres in southern Tehran, Iran.
A total of 447 female participants aged 20–50 years.
The median values of vitamin B6 (pyridoxine), B9 (folate) and B12 (cobalamin) were 1·30 mg/d, 313·89 µg/d and 3·99 µg/d, respectively. After adjustment for potential confounders, dietary vitamin B6 intake was associated with lower odds of depression (OR: 0·54; 95 % CI: 0·31, 0·95; Ptrend: 0·03). However, there was a positive association between dietary vitamin B12 intake with the odds of depression (OR: 2·05; 95 % CI: 1·17, 3·60; Ptrend: 0·01) and psychological distress (OR: 2·00; 95 % CI: 1·17, 3·41; Ptrend: 0·01). No association was found between vitamin B9 with any psychological disorders.
Women with higher dietary intakes of vitamin B6 had lower likelihood of depression. However, women with higher dietary intake of vitamin B12 had higher odds of depression and psychological distress. Future prospective studies in different populations are needed to clarify whether B-vitamin deficiency is a cause or consequence of psychological disorders.
To investigate homocysteine (Hcy) and folate levels, prevalence of hyperhomocysteinaemia (HHcy) and folate deficiency, which are affected by lifestyles in urban, agricultural and stock-raising populations.
This is a cross-sectional study.
Urban, agricultural and stock-raising regions in Emin, China.
Totally 1926 subjects – 885 (45·9 %) from urban, 861 (44·7 %) from agricultural and 180 (9·4 %) from stock-raising regions – were obtained using multistage stratified random sampling. Inclusion criteria encompassed inhabitants aged ≥15 years who resided at the current address for ≥6 months and agreed to participate in the study. Surveys on health behaviour questionnaires and physical examinations were conducted and blood samples collected.
The folate level of subjects from the stock-raising region was the lowest, followed by those from the agricultural region, and the highest in those from the urban region (3·48 v. 6·50 v. 7·12 ng/ml, P < 0·001), whereas mean Hcy showed no significant difference across regions. The OR for HHcy in stock-raising regions was 1·90 (95 % CI 1·11, 3·27) compared with the urban region after adjusting for all possible covariates. The OR for folate deficiency in stock-raising and agriculture regions was 11·51 (95 % CI 7·09, 18·67) and 1·91 (95 % CI 1·30, 2·82), respectively, compared with the urban region after adjusting for all possible covariates.
HHcy and folate deficiency are highly prevalent in stock-raisers, which is of important reference for HHcy control in Xinjiang, with a possibility of extension to others with approximate lifestyles.
The occurrence of anorectal malformations (ARM) is thought to be reduced with sufficient folate intake. However, there is no apparent evidence. We focused on enzyme cofactors for one-carbon metabolism, including folate (vitamin B9), vitamin B6 and vitamin B12, and explored the association between maternal combined intake of these B vitamins and the risk of ARM. Using baseline data from a Japanese nationwide birth cohort study between 2011 and 2014, we analysed data of 89 235 women (mean age at delivery = 31·2 years) who delivered singleton live births without chromosomal anomalies. Information on dietary intake was obtained via a FFQ focused on early pregnancy and used to estimate B vitamin intake. We also collected information on the frequency of folic acid supplement use. ARM occurrence was ascertained from medical records. We identified forty-three cases of ARM diagnosed up to the first month after birth (4·8 per 10 000 live births). In terms of individual intake of the respective B vitamins, high vitamin B6 intake was non-significantly associated with reduced odds of ARM. Compared with women in the low combined B vitamin intake group, the OR of having an infant with ARM was 0·4 (95 % CI 0·2, 1·0) in the high intake group (folate ≥400 μg/d, and upper half of vitamin B6 and/or vitamin B12). In conclusion, our cohort analysis suggested an inverse association between the combined intake of one-carbon metabolism-related B vitamins in early pregnancy and ARM occurrence.
Strong evidence suggests that older adults at risk of cognitive decline benefit from healthy lifestyle strategies to prevent or delay cognitive disorders. In particular, nutrition has been shown to preserve cognitive functions. Nutritional interventions, whether with single nutrients or following dietary patterns, have all shown protective effects against cognitive decline. In particular, higher levels of vitamins C, D, E, K, and the B family were associated with a better cognitive status. Likewise, fruit and vegetable consumption and omega-3 intake were protective against declined cognition. Regarding dietary patterns, the Mediterranean-type diet, DASH, and MIND diets are all positively associated with slower rates of cognitive decline and decreased risk of incident Alzheimer’s disease and dementia. Nevertheless, intervention trials with vitamins or omega-3 supplements have not demonstrated conclusive evidence for preventing cognitive decline in healthy older adults, or for preventing loss or restoring function in patients with mild to moderate decline. Nutritional recommendations for older adults should emphasize dietary intakes of nutrients and food groups following those recommendations, as well as adoption of the Mediterranean, DASH, or MIND diets, in order to decrease risk of cognitive decline.
The uncertainty surrounding high intakes of folic acid and associations with cognitive decline in older adults with low vitamin B12 status has been an obstacle to mandatory folic acid fortification for many years. We estimated the prevalence of combinations of low/normal/high vitamin B12 and folate status and compared associations with global cognitive function using two approaches, of individuals in a population-based study of those aged ≥50 years in the Republic of Ireland. Cross-sectional data from 3781 men and women from Wave 1 of The Irish Longitudinal Study on Ageing were analysed. Global cognitive function was assessed by the Mini Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA). Prevalence estimates for combinations of vitamin B12 (plasma vitamin B12 < or ≥258 pmol/l) and folate (plasma folate ≤ or >45·3 nmol/l) concentrations were generated. Negative binomial regression models were used to investigate the associations of vitamin B12 and folate status with global cognitive function. Of the participants, 1·5 % (n 51) had low vitamin B12 (<258 pmol/l) and high folate (>45·3 nmol/l) status. Global cognitive performance was not significantly reduced in these individuals when compared with those with normal status for both B-vitamins (n 2433). Those with normal vitamin B12/high folate status (7·6 %) had better cognitive performance (MMSE: incidence rate ratio (IRR) 0·82, 95 % CI 0·68, 0·99; P = 0·043, MoCA: IRR 0·89, 95 % CI 0·80, 0·99; P = 0·025). We demonstrated that high folate status was not associated with lower cognitive scores in older adults with low vitamin B12 status. These findings provide important safety information that could guide fortification policy recommendations in Europe.
There is limited evidence on the interaction by alcohol dehydrogenase 2 (ADH1B) (rs1229984) and aldehyde dehydrogenase 2 (ALDH2) (rs671) regarding the associations of alcohol and a methyl diet (low folate and high alcohol intake) with cancer risk, partly because of rare polymorphisms in Western populations.
In a case–control study, we estimated the ORs and 95 % CIs to evaluate the associations of ADH1B and ALDH2 genotypes with colorectal cancer (CRC) and the joint association between methyl diets and ADH1B and ALDH2 polymorphisms with CRC risk using logistic regression models.
A hospital-based case–control study.
In total, 1001 CRC cases and 899 cancer-free controls admitted to two university hospitals.
We found that alcohol intake increased the risk of CRC; OR (95 % CI) was 2·02 (1·41, 2·87) for ≥60 g/d drinkers compared with non-drinkers (Ptrend < 0·001). The associations for two polymorphisms with CRC were not statistically significant. However, we found a potential interaction of ALDH2 with methyl diets and CRC. We observed a 9·08-fold (95 % CI 1·93, 42·60) higher risk of CRC for low-methyl diets compared with high-methyl diets among individuals with an A allele of ALDH2, but the association was not apparent among those with ALDH2 GG (Pinteraction = 0·02).
Our data support the evidence that gene–methyl diet interactions may be involved in CRC risk in East Asian populations, showing that a low-methyl diet increased the risk of CRC among individuals with an A allele of ALDH2.
B vitamins (including folate, vitamin B2, vitamin B6 and vitamin B12) and methionine are essential for methylation reactions, nucleotide synthesis, DNA stability and DNA repair. However, epidemiological evidence among Chinese populations is limited. The objective of this study was to evaluate B vitamins and methionine in relation to colorectal cancer risk in a Chinese population. A case–control study was conducted from July 2010 to April 2019. A total of 2502 patients with colorectal cancer were recruited along with 2538 age- (5-year interval) and sex-matched controls. Dietary data were collected using a validated FFQ. Multivariable logistic regression was used to assess OR and 95 % CI. The intake of folate, vitamin B2, vitamin B6 and vitamin B12 was inversely associated with colorectal cancer risk. The multivariable OR for the highest quartile v. the lowest quartile were 0·62 (95 % CI 0·51, 0·74; Ptrend < 0·001) for folate, 0·46 (95 % CI 0·38, 0·55; Ptrend < 0·001) for vitamin B2, 0·55 (95 % CI 0·46, 0·76; Ptrend < 0·001) for vitamin B6 and 0·72 (95 % CI 0·60, 0·86; Ptrend < 0·001) for vitamin B12. No statistically significant association was found between methionine intake and colorectal cancer risk. Stratified analysis by sex showed that the inverse associations between vitamin B12 and methionine intake and colorectal cancer risk were found only among women. This study indicated that higher intake of folate, vitamin B2, vitamin B6 and vitamin B12 was associated with decreased risk of colorectal cancer in a Chinese population.
B vitamins involved in one-carbon metabolism have been implicated in the development of inflammation- and angiogenesis-related chronic diseases, such as colorectal cancer (CRC). Yet, the role of one-carbon metabolism in inflammation and angiogenesis among CRC patients remains unclear. The objective of this study was to investigate associations of components of one-carbon metabolism with inflammation and angiogenesis biomarkers among newly diagnosed CRC patients (n 238) in the prospective ColoCare Study, Heidelberg. We cross-sectionally analysed associations between twelve B vitamins and one-carbon metabolites and ten inflammation and angiogenesis biomarkers from pre-surgery serum samples using multivariable linear regression models. We further explored associations among novel biomarkers in these pathways with Spearman partial correlation analyses. We hypothesised that pyridoxal-5’-phosphate (PLP) is inversely associated with inflammatory biomarkers. We observed that PLP was inversely associated with C-reactive protein (CRP) (r –0·33, Plinear < 0·0001), serum amyloid A (SAA) (r –0·23, Plinear = 0·003), IL-6 (r –0·39, Plinear < 0·0001), IL-8 (r –0·20, Plinear = 0·02) and TNFα (r –0·12, Plinear = 0·045). Similar findings were observed for 5-methyl-tetrahydrofolate and CRP (r –0·14), SAA (r –0·14) and TNFα (r –0·15) among CRC patients. Folate catabolite acetyl-para-aminobenzoylglutamic acid (pABG) was positively correlated with IL-6 (r 0·27, Plinear < 0·0001), and pABG was positively correlated with IL-8 (r 0·21, Plinear < 0·0001), indicating higher folate utilisation during inflammation. Our data support the hypothesis of inverse associations between PLP and inflammatory biomarkers among CRC patients. A better understanding of the role and inter-relation of PLP and other one-carbon metabolites with inflammatory processes among colorectal carcinogenesis and prognosis could identify targets for future dietary guidance for CRC patients.
Depression is among the most prevalent mental disorders worldwide, and a substantial proportion of patients do not respond adequately to standard antidepressants. Our understanding of the pathophysiology of depression is no longer limited to the chemical imbalance of neurotransmitters, but also involves the interplay of proinflammatory modulators in the central nervous system, as well as folate metabolism. Additional factors such as stress and metabolic disorders also may contribute. Multiple inflammatory, metabolic, and genetic markers have been identified and may provide critical information to help clinicians individualize treatments for patients to achieve optimal outcomes. Recent advancements in research have clarified underlying causes of depression and have led to possible new avenues for adjunctive treatment. Among these is L-methylfolate, a medical food that is thought to enhance synthesis of monoamines (serotonin, norepinephrine, and dopamine), suppress inflammation, and promote neural health. Clinical studies that assessed supplemental use of L-methylfolate in patients with usual care-resistant depression found that it resulted in improved outcomes. Patients with selective serotonin reuptake inhibitor-resistant depression, and particularly subgroups with biomarkers of inflammation or metabolic disorders or folate metabolism-related genetic polymorphisms (or ≥2 of these factors), had the best responses. Considering this, the goals of this review are to 1) highlight recent advances in the pathophysiology of major depressive disorder as it pertains to folate and associated biomarkers and 2) establish the profiles of patients with depression who could benefit most from supplemental use of L-methylfolate.
Folic acid (FA) supplementation is recommended in the periconceptional period, for the prevention of neural tube defects. Limited data are available on the folate status of New Zealand (NZ) pregnant women and its association with FA supplementation intake. Objectives were to examine the relationship between plasma folate (PF) and reported FA supplement use at 15 weeks’ gestation and to explore socio-demographic and lifestyle factors associated with PF. We used data and blood samples from NZ participants of the Screening for Pregnancy Endpoints cohort study. Healthy nulliparous women with singleton pregnancy (n 1921) were interviewed and blood samples collected. PF was analysed via microbiological assay. Of the participants, 73 % reported taking an FA supplement at 15 weeks’ gestation – of these, 79 % were taking FA as part of/alongside a multivitamin supplement. Of FA supplement users, 56 % reported consuming a daily dose of ≥800 μg; 39 % reported taking less than 400 µg/d. Mean PF was significantly higher in women reporting FA supplementation (54·6 (se 1·5) nmol/l) v. no FA supplementation (35·1 (se 1·6) nmol/l) (P<0·0001). Reported daily FA supplement dose and PF were significantly positively correlated (r 0·41; P<0·05). Younger maternal age, Pacific and Maori ethnicity and obesity were negatively associated with PF levels; vegetarianism was positively associated with PF. Reported FA supplement dose was significantly associated with PF after adjustment for socio-demographic, lifestyle confounders and multivitamin intake. The relationship observed between FA supplementation and PF demonstrates that self-reported intake is a reliable proxy for FA supplement use in this study population.
The functional effects of folate within C1 metabolism involve interrelationships with vitamin B12, vitamin B6 and riboflavin, and related gene–nutrient interactions. These B vitamins have important roles throughout life, from pregnancy, through childhood, to middle and older age. Achieving optimal nutritional status for preventing folate-related disease is challenging, however, primarily as a result of the poor stability and incomplete bioavailability of folate from natural food sources when compared with the synthetic vitamin form, folic acid. Thus, in European countries, measures to prevent neural tube defects (NTD) have been largely ineffective because of the generally poor compliance of women with folic acid supplementation as recommended before and in early pregnancy. In contrast, countries worldwide with mandatory folic acid fortification policies have experienced marked reductions in NTD. Low vitamin B12 status is associated with increased risk of cognitive dysfunction, CVD and osteoporosis. Achieving optimal B12 status can be problematic for older people, however, primarily owing to food-bound B12 malabsorption which leads to sub-clinical deficiency even with high dietary B12 intakes. Optimising B-vitamin intake may be particularly important for sub-populations with impaired folate metabolism owing to genetic characteristics, most notably the 677C→T variant in the gene encoding the enzyme methylenetetrahydrofolate reductase (MTHFR). This common folate polymorphism is linked with several adverse health outcomes, including stroke, however, recent evidence has identified its novel interaction with riboflavin (the MTHFR cofactor) in relation to blood pressure and risk of developing hypertension. This review addresses why and how the optimal status of folate-related B vitamins should be achieved through the lifecycle.
Gestational nutrition is widely recognized to affect an offspring’s future risk of lifestyle-related diseases, suggesting the involvement of epigenetic mechanisms. As folic acid (FA) is a nutrient essential for modulating DNA methylation, we sought to determine how maternal FA intake during early pregnancy might influence tumor sensitivity in an offspring. Dams were maintained on a FA-depleted (FA(−)) or normal (2 mg FA/kg; FA(+)) diet from 2 to 3 days before mating to 7 days post-conception, and their offspring were challenged with chemical tumorigenesis using 7,12-dimethylbenz[a)anthracene and phorbol 12-myristate 13-acetate for skin and 4-nitroquinoline N-oxide for tongue. In both squamous tissues, tumorigenesis was more progressive in the offspring from FA(−) than FA(+) dams. Notably, in the skin of FA(−) offspring, the expression and activity of cylindromatosis (Cyld) were decreased due to the altered DNA methylation status in its promoter region, which contributed to increased tumorigenesis coupled with inflammation in the FA(−) offspring. Thus, we conclude that maternal FA insufficiency during early pregnancy is able to promote neoplasm progression in the offspring through modulating DNA methylation, such as Cyld. Moreover, we propose, for the first time, “innate” utero nutrition as the third cause of tumorigenesis besides the known causes—hereditary predisposition and acquired environmental factors.
Studies on the nutritional status of vegetarians in Spain are lacking. Prevention of vitamin B12 deficiency is the main concern, as dietary sources are of animal origin. The present study aimed to evaluate vitamin B12 and folate status of Spanish vegetarians using classical markers and functional markers. Participants were adult and healthy lacto-ovo vegetarians (forty-nine subjects) and vegans (fifty-four subjects) who underwent blood analyses and completed a FFQ. Serum vitamin B12, homocysteine (Hcy), methylmalonic acid (MMA), erythrocyte folate and haematological parameters were determined. The effects of the type of plant-based diet, and the intake of supplements and foods were studied by a FFQ. Mean erythrocyte folate was 1704 (sd 609) nmol/l. Clinical or subclinical vitamin B12 deficiency was detected in 11 % of the subjects (MMA>271 nmol/l) and 33 % of the participants showed hyperhomocysteinaemia (Hcy>15 µmol/l). Regarding plant-based diet type, significantly higher Hcy was observed in lacto-ovo vegetarians compared with vegans (P = 0·019). Moreover, use of vitamin B12 supplements involved an improvement of vitamin B12 status but further increase in erythrocyte folate (P = 0·024). Consumption of yoghurts was weakly associated with serum vitamin B12 adequacy (P = 0·049) and that of eggs with lower Hcy (P = 0·030). In conclusion, Spanish vegetarians present high folate status but vitamin B12 subclinical deficiency was demonstrated using functional markers. The lack of influence of dietary sources on functional markers and the strong effect of vitamin B12 supplement intake emphasise the need of cobalamin supplementation in both lacto-ovo vegetarians and vegans.
Periconceptional folic acid (FA) is known to have a protective effect in the prevention of neural tube defects (NTD), leading to global recommendations for FA supplementation before and in early pregnancy. Maternal folate throughout pregnancy may have other roles in offspring health, including neurodevelopment and cognitive performance in childhood. Folate is essential for C1 metabolism, a network of pathways involved in several biological processes including nucleotide synthesis, DNA repair and methylation reactions. The evidence reviewed here shows a conclusive role for offspring health of maternal folate nutrition in early pregnancy and probable benefits in later pregnancy. Folate-mediated epigenetic changes in genes related to brain development and function offer a plausible biological basis to link maternal folate with effects in offspring brain, albeit this research is in its infancy. Mandatory FA fortification of food has proven to be highly effective in decreasing NTD cases in populations where it has been implemented, but this policy is controversial owing to concerns related to potential adverse effects of over-exposure to FA. In the absence of population-wide fortification, and given the generally poor compliance with current FA recommendations, optimising folate status of mothers in very early pregnancy for protection against NTD remains challenging. Thus, current policy in the UK, Ireland and elsewhere in Europe for the prevention of NTD (based on periconceptional FA supplementation only), has proven to be largely ineffective. This review addresses the evidence and the controversies that surround this area, as well as identifying the challenges in translating policy into practice.
Conotruncal heart defects are considered to be one of the most common types of birth defect worldwide. Genetic disturbances in folate metabolism such as Thymidylate synthase may increase risk for conotruncal heart defects. We evaluated two common Thymidylate synthase polymorphisms, including the 28 bp tandem repeat in the promoter enhancer region of the 5′-untranslated region and the 6 bp deletion in the 3′-untranslated region, as risk factors of conotruncal heart defects including various subtypes of malformations, in a total of 193 mothers with conotruncal heart defect in offspring and 234 healthy controls in the Chinese population. Logistic regression analyses revealed that mothers who were homozygotes with deletion (−/−) had a 1.8-fold (odds ratio: 1.8; 95% confidence interval: 1.0–3.0, p = 0.040) increased risk for conotruncal heart defect in offspring, respectively, when compared with mothers carrying the wild type (+/+) genotype. Consistently, individuals carrying the genotype −/− of the Thymidylate synthase 6 bp deletion also had higher plasma homocysteine levels compared to the mothers carrying the genotype +/+ in the control and conotruncal heart defect groups (p = 0.006 and p = 0.004, respectively). However, our results showed that Thymidylate synthase 28 bp tandem repeat polymorphism was not associated with risk for conotruncal heart defect and plasma homocysteine level. In conclusion, our data suggest that the maternal Thymidylate synthase 6 bp deletion polymorphism might be associated with plasma homocysteine level and risk for conotruncal heart defect in offspring.
To simulate effects of different scenarios of folic acid fortification of food on dietary folate equivalents (DFE) intake in an ethnically diverse sample of pregnant women.
A forty-four-item FFQ was used to evaluate dietary intake of the population. DFE intakes were estimated for different scenarios of food fortification with folic acid: (i) voluntary fortification; (ii) increased voluntary fortification; (iii) simulated bread mandatory fortification; and (iv) simulated grains-and-rice mandatory fortification.
Ethnically and socio-economically diverse cohort of pregnant women in New Zealand.
Pregnant women (n 5664) whose children were born in 2009–2010.
Participants identified their ethnicity as European (56·0 %), Asian (14·2 %), Māori (13·2 %), Pacific (12·8 %) or Others (3·8 %). Bread, breakfast cereals and yeast spread were main food sources of DFE in the two voluntary fortification scenarios. However, for Asian women, green leafy vegetables, bread and breakfast cereals were main contributors of DFE in these scenarios. In descending order, proportions of different ethnic groups in the lowest tertile of DFE intake for the four fortification scenarios were: Asian (39–60 %), Others (41–44 %), European (31–37 %), Pacific (23–26 %) and Māori (23–27 %). In comparisons within each ethnic group across scenarios of food fortification with folic acid, differences were observed only with DFE intake higher in the simulated grains-and-rice mandatory fortification v. other scenarios.
If grain and rice fortification with folic acid was mandatory in New Zealand, DFE intakes would be more evenly distributed among pregnant women of different ethnicities, potentially reducing ethnic group differences in risk of lower folate intakes.
Public health authorities recommend all fertile women to increase their folate intake to 400 µg/d by eating folate-rich foods or by taking a folic acid supplement to protect against neural tube defects. In a previous study it was shown that folate-rich foods improved folate blood status as effectively as folic acid supplementation. The aim of the present study was to investigate, using NMR metabolomics, the effects of an intervention with a synthetic folic acid supplement v. native food folate on the profile of plasma metabolites. Healthy women with normal folate status received, in parallel, 500 µg/d synthetic folic acid from a supplement (n 18), 250 µg/d folate from intervention foods (n 19), or no additional folate (0 µg/d) through a portion of apple juice (n 20). The metabolic profile of plasma was measured using 1H-NMR in fasted blood drawn at baseline and after 12 weeks of intervention. Metabolic differences between the groups at baseline and after intervention were assessed using a univariate statistical approach (P ≤ 0·001, Bonferroni-adjusted significance level). At baseline, the groups showed no significant differences in measured metabolite concentrations. After intervention, eight metabolites, of which six (glycine, choline, betaine, formate, histidine and threonine) are related to one-carbon metabolism, were identified as discriminative metabolites. The present study suggests that different folate forms (synthetic v. natural) may affect related one-carbon metabolites differently.
We aimed to evaluate clinical note documentation of valproate prescribing and establish the level of knowledge among women of child-bearing potential regarding valproate-associated adverse effects, including teratogenesis, in a regional Irish mental health service.
Of the 42 women prescribed sodium valproate, 21.4% (n = 9) had some documentation in relation to associated risks and 33.3% (n = 14) described an awareness of these risks from consultation with their treating mental health team. On clinical interview, 9.5% (n = 4) of individuals with clear documentation of the risks of teratogenesis described no such awareness. Augmentation with lithium was associated with greater awareness of the teratogenic risks of valproate (P = 0.011).
A clear description of the teratogenic risks of valproate and potential management strategies, including advice regarding contraception and supplementation with folic acid, should be clearly documented and provided repeatedly and in context to all women of child-bearing age who are prescribed valproate.
Mandatory fortification of staple grains with folic acid and/or vitamin B12 (B12) is under debate in many countries including Ireland, which has a liberal, but voluntary, fortification policy. Older adults can be at risk of both deficiency and high folate status, although little is known on the actual prevalence and the major predictors. Population prevalence estimates from older adults (n 5290 ≥50 years) from the Irish Longitudinal Study on Ageing (TILDA) (Wave 1) are presented here. Measures included plasma total vitamin B12 and folate, whereas predictors included detailed demographic, socio-economic, geographic, seasonal and health/lifestyle data. The prevalence of deficient or low B12 status (<185 pmol/l) was 12 %, whereas the prevalence of deficient/low folate status was 15 %. High folate status (>45 nmol/l) was observed in 8·9 %, whereas high B12 status was observed in 3·1 % (>601 pmol/l). The largest positive predictor of B12 concentration was self-reported B12 injection and/or supplement use (coefficient 51·5 pmol/; 95 % CI 9·4, 93·6; P=0·016) followed by sex and geographic location. The largest negative predictor was metformin use (−33·6; 95 % CI −51·9, −15·4; P<0·0001). The largest positive predictor of folate concentration was folic acid supplement use (6·0; 95 % CI 3·0, 9·0 nmol/l; P<0·001) followed by being female and statin medications. The largest negative predictor was geographic location (−5·7; 95 % CI −6·7, −4·6; P<0·0001) followed by seasonality and smoking. B-vitamin status in older adults is affected by health and lifestyle, medication, sampling period and geographic location. We observed a high prevalence of low B12 and folate status, indicating that the current policy of voluntary fortification is ineffective for older adults.