Sub-optimal status of one or more of the interrelated B-vitamins (folate, B12, B6 and riboflavin) is common among older adults1, and considerable observational evidence links low B-vitamin status (and/or elevated concentrations of the related metabolite, homocysteine) with a higher risk of agerelated diseases2,3. These nutrients are interlinked though their roles in one-carbon metabolism, but very few studies have investigated the major contributors to status of all four B-vitamins or the trends in B-vitamin biomarkers with advancing age. The aim of this study, therefore, was to investigate the contribution of fortified foods and supplements to dietary intakes and biomarkers of B-vitamins in older adults.

From a total sample of community-dwelling older adults (n = 5,186; ≥ 60 years) initially recruited to the Trinity-Ulster-Department of Agriculture (TUDA) study from 2008–2012, an eligible subset (n = 953) was re-investigated between 2016 and 2019. Dietary intake was assessed using a 4-day food diary (over four consecutive days) in combination with a food-frequency questionnaire. Mean daily energy and B-vitamin intakes were calculated using a customised version of the nutritional software package Nutritics (V.4). Non-fasting blood samples were collected at initial sampling and at follow-up to measure corresponding B-vitamin biomarkers. Statistical differences between categories of fortified food consumption and supplement use were assessed using ANCOVA (with adjustment for relevant covariates), while relationships between dietary and corresponding biomarker variables were examined using Pearson correlation coefficients.

As dietary intakes of fortified foods increased (from 0 to > 7 portions per week), biomarkers of each B-vitamin improved in a stepwise manner (P<0.001), and there was a corresponding decrease in plasma homocysteine concentrations (P<0.001), and the highest B-vitamin biomarkers were observed in those taking B-vitamin supplements. Although mean values for B-vitamin biomarkers generally compared favourably with normal ranges, deficient status of individual B-vitamins at initial sampling (2008 – 2012) was identified in: serum folate (8%), vitamin B12 (8%), vitamin B6 (8%), riboflavin (23%). Non-consumers of fortified food or supplements were at greatest risk of deficiency for each B-vitamin. Dietary intakes from foods were significantly correlated with corresponding biomarkers for serum folate (r = 0.458, P<0.001), plasma pyridoxal-5-phosphate (PLP; r = 0.192, P 0.002) and erythrocyte glutathione reductase activation coefficient (EGRac; r =−0.197, P 0.001), whereas no significant correlation was observed for vitamin B12 intake with status.

In conclusion, regular consumption of fortified foods is an effective means to improve intakes and status of folate and related B-vitamins, reduce homocysteine concentrations and lower the prevalence of B-vitamin deficiency. These results emphasise the importance of fortified foods and supplements in contributing to status and highlight potential opportunities for the food industry to develop a wider range of foods fortified with sufficient levels of B-vitamins to optimise status and support healthy ageing.

Findings from animal models suggest early exposure to polyunsaturated fatty acids (PUFAs) during pregnancy may influence developmental plasticity including adiposity(1). Birth cohort studies examining associations between offspring weight and maternal n-3 PUFA status or maternal fish intakes, the richest dietary source of n-3 PUFAs have been few and have yielded inconsistent findings. Some have reported lower weight at birth and throughout childhood with increasing maternal fish intakes and n-3 PUFA status(2), whilst others have observed positive or null associations(3,4). These have focused on the first few years of life and have been conducted within low fish-consuming populations. Our study provides novel data by examining associations between maternal fish consumption and prenatal PUFA (n-3 & n-6) status and offspring weight at birth and throughout childhood (7 & 13 years) in a high fish-eating population.

Pregnant women were enrolled in the Seychelles Child Development Study Nutrition Cohort 2 between 2008-2011. Serum PUFAs were quantified in maternal blood collected at 28-weeks’ gestation and in cord blood collected at delivery using gas-chromatography tandem mass spectrometry. Maternal fish consumption was assessed at 28-weeks’ gestation using a Fish Use Questionnaire. Childbirth weight (kg) was measured at delivery and classified according to WHO growth standards(5) (n = 1185). Child height (m), weight (kg), waist and hip circumference (cm) were recorded at 7 (n = 1167) and 13 (n = 878) years. Statistical analysis was conducted using logistic and multiple linear regression adjusting for child sex, gestational age, maternal age, BMI, alcohol use, socioeconomic status, and parity. Models at 7 & 13 years were additionally adjusted for child height and fish intakes.

Women were consuming on average 8.49 ± 4.51 fish meals/week during pregnancy. No significant associations were found between maternal fish intakes and anthropometric outcomes at birth, 7 & 13 years. No significant associations were observed between maternal PUFAs and offspring weight at birth. At both 7 & 13 years, however, higher maternal total n-6 PUFAs were associated with increased child weight [7yr; β = 0.070, p = 0.003, 13yr; β = 0.097, p = 0.004], waist circumference [7yr; β = 0.086, p = 0.003, 13yr; β = 0.105, p = 0.004], and hip circumference [7yr; β = 0.062, p = 0.027, 13yr; β = 0.090, p = 0.013]. No significant associations were found between cord n-6 PUFAs and birth weight. In quartile analysis, cord docosahexaenoic acid (DHA; C22:6n-3) concentrations <0.071mg/ml were associated with a higher risk of large for gestational age (LGA; >90th percentile) when compared to cord DHA concentrations >0.129mg/ml [OR 4.17, p = 0.017]. There were no significant associations between cord PUFAs and anthropometric outcomes at 7 & 13 years.

These findings suggest lower cord DHA, an n-3 PUFA, may be associated with higher risk of LGA at birth whilst higher n-6 PUFAs during pregnancy may be associated with adiposity development throughout childhood. Future work is needed to determine the potential long-term metabolic consequences of such associations.

Maternal thyroid hormones facilitate optimal foetal neurodevelopment; however, the exact role of the thyroid hormones on specific cognitive outcomes is unknown. The present study aimed to investigate associations between maternal thyroid function and neurodevelopmental outcomes in the Seychelles Child Development Study (SCDS) Nutrition 2 cohort (n 1328). Maternal free thyroid hormones (fT3, fT4 and fTSH) were assessed at 28 weeks’ gestation with a range of child cognitive outcomes analysed at 20 months. Dietary iodine intake was analysed for a subset of women through a Food Frequency Questionnaire. Linear regression analysis was used to test associations between serum concentrations of maternal thyroid hormones and child neurodevelopment outcomes. Thyroid hormones were analysed as continuous data and categorised as quintiles. 95% of mothers had optimal thyroid function based on fTSH concentrations. Overall, the present study shows that maternal thyroid function is not associated with neurodevelopmental outcomes in this high fish-eating population. However, a positive association, using quintiles for fT3, was reported for the Mental Developmental Index, between Q3 v. Q4 (β 0⋅073; P 0⋅043) and for Q3 v. Q5 (β value 0⋅086; P 0⋅018). To conclude, mothers in our cohort, who largely have optimal thyroid function and iodine intakes, appear able to regulate thyroid function throughout pregnancy to meet neurodevelopmental needs. However, it is possible that minor imbalances of fT3, as indicated from our secondary analysis, may impact offspring neurodevelopment. Further investigation of the relationship between maternal thyroid function and infant neurodevelopment is warranted, particularly in populations with different dietary patterns and thereby iodine intakes.

The association of MeHg exposure through fish consumption on human autoimmunity remains unclear. Fish also contain n-3 long chain polyunsaturated fatty acids (LCPUFA) that are known to regulate inflammation and mitigate autoimmune disease symptoms. We studied the association of low-level exposure to methylmercury (MeHg) through fish consumption in the SCDS. We examined this association at age 19 years in the SCDS Main Cohort (n = 497). We measured MeHg exposure at 3 time points [prenatal, weighted average (6 months to 19 years) and concurrent (19 years) and LCPUFA status and a panel of 13 autoimmune markers at age 19 years. The autoimmune markers included antinuclear antibodies (ANA), anti-dsDNA and anti-RNP, and total (non-specific) immunoglobulins (Ig) IgG, IgA, and IgM. A combined ANA variable was also calculated based on being within or above reference range for any of the ANA markers; 56% of the subjects met this criterion. Multivariable regression models adjusted for prenatal MeHg, sex and waist circumference, with and without adjustment for LCPUFA, were fit for the three MeHg exposure metrics and each immune marker. Mean (SD) prenatal, weighted average and concurrent MeHg was 6.84 (4.55), 7.46 (2.82), and 10.23 (6.02) ppm, respectively. Combined ANA was positively associated with concurrent MeHg following adjustment for the n6:n3 LCPUFA ratio (β = 0.036, 95%; CI: 0.001, 0.073). Prenatal and average MeHg exposures were not significantly associated with any individual ANA. IgM was negatively associated with concurrent (β = -0.016, 95%CI: -0.016, -0.002), and average (β = -0.042, 95%CI: -0.042, -0.009) MeHg exposure in the models adjusted for n-3, n-6 LCPUFA and when separately adjusted for the n6:n3 LCPUFA ratio. Total (19-year) n-3 PUFA status was negatively associated with anti-RNP (β = -20.355, 95%CI: -36.89, -4.34) and IgG (β = -1.384, 95%CI: -2.682, -0.087). Total n-3 LCPUFA was associated with lower markers of autoimmunity. MeHg exposure at 19 years was associated with higher ANA and lower IgM but only following adjustment for LCPUFA. The clinical significance of these findings is unclear and further research is warranted to determine if these associations precede autoimmune disease development.

Optimal maternal polyunsaturated fatty acid (PUFA) status is essential for foetal development. The desaturase enzymes, encoded by the fatty acid desaturase (FADS) genes, are involved in the endogenous synthesis of long chain (LC)PUFA and influence maternal LCPUFA concentrations. The minor allele of various FADS SNPs has been associated with increased maternal concentrations of the precursors linoleic acid (LA) and α-linolenic acid (ALA), and lower concentrations of the LCPUFA arachidonic acid (AA) and docosahexaenoic acid (DHA); however, there is limited research to date on the influence of FADS genotype on cord PUFA status. The aim of the current study was to investigate the influence of maternal and child genetic variation on cord blood PUFA status in a high fish-eating cohort.

Cord blood samples collected from mother-child pairs (n = 1088) taking part in the Seychelles Child Development Study (SCDS) Nutrition Cohort 2 (NC2) were analysed for total serum PUFA. Maternal (n = 1088) and child genotype (n = 592) were determined for the FADS SNPs rs174537, rs174561, rs174575, and rs3834458. Regression analysis determined associations between maternal and child FADS genotype and cord PUFA status. In all regression models, the major allele homozygote genotype for each SNP was used as the reference group.

Directions of significant associations were as predicted. In mothers, the minor allele homozygote genotype for SNPs rs174537, rs174561 and rs3834458 was associated with lower cord DHA and lower total n-3 PUFA when compared to the major allele homozygous genotype (p < 0.05 for all). The heterozygous genotype was associated with increased concentrations of LA compared to the reference genotype for rs174561 (p = 0.021) and rs383448 (p = 0.023). In children, the heterozygous genotype was associated with lower AA concentrations and lower cord n-6:n-3 ratio for all SNPs (p < 0.05 for all) compared to those with the major allele homozygous genotype. A lower cord AA:LA ratio was also observed for children heterozygous for rs174547, rs174561 and rs174575 (p < 0.05 for all). Contrary to expected, there were no associations between cord PUFA concentrations and child minor allele homozygous genotype.

The current study indicates that variation in maternal and child FADS genotype influences cord PUFA concentrations, despite the high intake of preformed dietary LCPUFA from fish in this population. The sample size for minor allele homozygous children was likely too small to observe any statistically significant associations in the current analysis. Further research is needed to determine whether increased dietary intake can compensate for lower PUFA status as a result of FADS genotype.

Vitamin B12 deficiency is common among older adults, even with dietary intakes well in excess of current recommendations. Severe clinical B12 deficiency (i.e. pernicious anaemia) leads to irreversible neurological damage, but once diagnosed, can be treated effectively with B12 injections. A much more common cause of low vitamin B12 status in older adults is food-bound malabsorption owing to atrophic gastritis. This in turn leads to reduced gastric acid secretion, thus limiting B12 absorption from food (given the essential role of gastric acid in releasing B12 from food proteins). Proton pump inhibitor (PPI) drugs reduce gastric acid secretion, similar to atrophic gastritis, thus there is a concern that these medications may lead to vitamin B12 malabsorption. Therefore, the aim of this study was to investigate biomarker status of vitamin B12 in relation to atrophic gastritis and PPI usage. Data were accessed from The Trinity Ulster Department of Agriculture (TUDA) Ageing Cohort Study, a cross-sectional study of community-dwelling adults (n 5186, ≥ 60 years) recruited across Northern Ireland and the Republic of Ireland (2008–2012). TUDA participants were classified into 3 groups; ‘healthy’ controls, atrophic gastritis and PPI users. Vitamin B12 status was assessed using a total of four biomarkers: serum total B12; serum holotranscobalamin, holoTC; plasma methylmalonic acid, MMA; plasma homocysteine. Atrophic gastritis was identified using pepsinogen analysis (via ELISA), with a pepsinogen I : II ratio of < 3 considered indicative of atrophic gastritis. Based on results from all four biomarkers, participants with atrophic gastritis were found to have significantly lower B12 status compared to healthy controls: e.g. mean (95% CI) serum total vitamin B12, 188 (156, 218) pmol/L vs. 262 (252, 272) pmol/L P < 0.001; holoTC, 46.0 (38.1, 53.8) pmol/L vs. 60.3 (57.8, 62.8) pmol/L P < 0.001; plasma MMA, 0.65 (0.52, 0.78) μmol/L vs. 0.37 (0.32, 0.42) μmol/L P = 0.001. No differences in B12 biomarker concentrations were observed between PPI users and healthy controls. Regular consumption of fortified foods (i.e. ≥ 5 portions per week) compared to non-regular consumption (i.e. 0–4 portions per week) impacted positively on B12 biomarker status in all participants. This effect however appeared insufficient to restore normal vitamin B12 status in those with atrophic gastritis. These results show that older adults with atrophic gastritis have significantly lower vitamin B12 biomarker status, particularly in those who did not regularly consume fortified foods. Further investigations of the effect of atrophic gastritis and PPI usage on B12 status are warranted.

The common C677T polymorphism in the MTHFR gene encoding the folate-metabolising enzyme methylenetetrahydrofolate reductase is implicated in hypertension and hypertension in pregnancy. Hypertension affects up to 15% of all pregnancies and has been identified as a leading cause of maternal and neonatal morbidity and mortality worldwide. We previously reported higher systolic and diastolic blood pressure (BP) in non-pregnant women with the variant MTHFR 677TT genotype compared to CT/CC genotypes. In addition, randomised controlled trials (RCTs) in non-pregnant hypertensive adults from our Centre demonstrated that supplemental riboflavin (co-factor for MTHFR) lowers BP specifically in those with the TT genotype. However, the role of this common folate polymorphism and its interaction with riboflavin during pregnancy remains unclear. The aim of this study was to investigate the impact of MTHFR genotype and riboflavin status on BP in pregnancy. Data were generated from the ongoing Optimal Nutrition for the Prevention of Hypertension (OptiPREG) project. Pregnant women were recruited at the end of the first trimester from antenatal clinics in Northern Ireland and in the Republic of Ireland. Participants were screened for MTHFR genotype and BP was measured according to current clinical guidelines. Biomarker status of riboflavin was determined using the erythrocyte glutathione reductase activation coefficient (EGRac), a functional assay with higher EGRac values representing a lower status. Overall, 117 (11.6%) participants were identified with the variant MTHFR 677TT genotype. Both systolic and diastolic BP decreased from 8th to 16th gestational week (GW), however, this typical BP pattern was not observed in the TT genotype group. After adjusting for maternal age, GW and body mass index, women with the TT genotype at 12th GW had higher mean systolic (P 0.035) and diastolic (P 0.034) BP. When the results at the 12th GW were stratified by riboflavin status, the BP phenotype owing to this polymorphism was evident only among women with lower status (i.e. EGRac > 1.30), with mean (SEM) systolic BP of 120.4 (3.1) mmHg compared to 112.6 (2.5) mmHg in those with higher status (EGRac ≤ 1.30) within the TT genotype group; in contrast, low versus high riboflavin status had no impact on BP in CT/CC genotype groups. These results suggest that MTHFR genotype influences BP during pregnancy and that riboflavin can exert an important modulating effect on BP in women with TT genotype. An RCT is required to fully investigate the role of MTHFR genotype and its interactive effect with riboflavin in BP during pregnancy.

Up to now hardly any quantitative research regarding diagnosis of personality disorders in the environment of Consultation-Liaison Psychiatry and Psychosomatic Medicine is available.

The data of 3032 patients aged 17-65 years seen between 1988 and 1997 at the Mount Sinai Hospital in New York, NY, were recorded and analyzed using the Micro-Cares Database System.

19,7% (N=598) of patients exhibited a personality disorder. Out of those 7,7% distributed to Cluster A (Odd or Eccentric Behavior), 54,3% to Cluster B and 38,0% to Cluster C.

89% of patients with personality disorders showed at least one additional specific psychiatric disorder.

Patients with a personality disorder had a lower incidence of somatic disease, but exhibited a higher level in psychosocial impairment and a higher comorbidity in substance abuse. During the previous year they used psychiatric treatment more often and were in need of a more intense social and psychotherapeutical treatment.

The age group of 17-40 year old patients with a personality disorder was hospitalized shorter and had less of a lag between hospitalization and time of psychiatric consultation.

More reasons for a psychiatric consultation were given when patients with a personality disorder were referred.

In the environment of Consultation-Liaison Psychiatry and Psychosomatic Medicine every 5th to 6th patient requires a specific, psychiatric, psychotherapeutic or social treatment because of a personality disorder.

The classification of personality disorders into clusters did not yield an additional benefit.

It is not clear whether psychiatric comorbidity in medically ill patients contributes to longer lengths of hospital stay (LOS), and whether interventions carried out by psychiatric consultation-liaison (c-l) services lead to a reduction of LOS. Furthermore, the lagtime paradigm, i.e. the notion that the earlier a psychiatric consultation takes place, the shorter LOS of the resp. patients are, has been questioned. To study if different degrees of somatopsychic comorbidity have effects upon Lagtime and LOS of patients seen by a c-l-psychiatric service. Patients consecutively referred to a c-l-service in Berlin during a one year study period were categorized into six groups of different somatopsychic comorbidity using a count-approach based upon ICD-10 psychiatric, and ICD-9 somatic diagnoses. The groups with more psychiatric than somatic diagnoses show shorter LOS and shorter Lagtimes. Patients with only psychiatric diagnoses overall show the shortest average LOS and Lagtime. For the groups, however, with more somatic than psychiatric diagnoses, LOS and lagtimes are longer. In the groups with equal numbers of psychiatric and somatic diagnoses, there is a trend with higher numbers of somatic diagnoses showing longer LOS and Lagtimes. On the other hand, in both groups with 2 and more somatic diagnoses, a trend can be seen toward shorter LOS and Lagtimes in such patients with more than 1 psychiatric diagnosis. Psychiatric comorbidity in medically ill patients does not sufficiently explain differences in LOS and Lagtime of patients seen in psychiatric c-l-services, but a complex interplay of somatopsychic comorbidity has to be taken into account.