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Erythrocytes, compared with plasma, are considered more robust markers of n-3 (ω-3) polyunsaturated fatty acid (PUFA) intake, because dietary-induced change in fatty acid (FA) composition takes longer to complete. The extent to which this applies to intakes of saturated fatty acid (SFA) or n-6 PUFA is unclear. We compared the pattern of change over time in the fatty acid composition of plasma, erythrocyte, buccal cell, and adipose tissue lipids when changing between diets high in SFA or n-6 PUFA. Twenty-four (n = 7 male) healthy participants were instructed to consume either an SFA-rich (18% energy) or n-6 PUFA-rich (10% energy) diet for 8 wk before crossing over, without washout, to the alternate diet. The FA composition of plasma triacylglycerol (TG), nonesterified FAs, cholesterol ester, total phospholipids, erythrocyte total phospholipids, erythrocyte phosphatidylcholine, and buccal cell total phospholipids was measured every 2 wk and adipose tissue TG every 4 wk during the 16-wk intervention. Linoleic acid composition of plasma, erythrocyte, and buccal cell lipids increased (P < 0.01) during the first 2 wk of the n-6 PUFA diet and remained unchanged during the remaining 6 wk. During the 8-wk SFA diet, the same pattern of change over time occurred for the pentadecanoic acid composition of plasma and erythrocyte lipids; however, the pentadecanoic acid composition of buccal cell lipids did not differ between the diet periods. There were no differences in linoleic or pentadecanoic acid composition of adipose tissue TG. These results suggest plasma and erythrocyte FAs reflect intakes of SFA and n-6 PUFA over a similar period of time.

National data on the blood folate status of New Zealand adults is lacking. The objective of this study was to describe the blood folate status and examine the predictors of blood folate status in a national sample of adults from New Zealand, a country with voluntary folic acid fortification. The 2008/09 New Zealand Adult Nutrition Survey was a nationwide multistage systematic random cross-sectional survey. Serum and erythrocyte folate concentrations were measured by microbiologic assay. The survey included 4721 participants aged ≥15 y, 3359 of whom provided a nonfasting blood sample. Biochemical folate status was measured in 3277 participants. The median serum and erythrocyte folate concentrations were 23 and 809 nmol/L, respectively. The prevalence of biochemical folate deficiency, defined as plasma folate <6.8 nmol/L or erythrocyte folate <305 nmol/L, was 2%. Having breakfast daily compared with never eating breakfast was associated with 53% higher serum and 25% higher erythrocyte folate concentrations; consumers of fortified yeast extract spread had 17% higher serum and 14% higher erythrocyte folate concentrations than nonconsumers; daily users of folate-containing supplements compared with nonusers had 48% higher serum and 28% higher erythrocyte folate concentrations. The prevalence of biochemical folate deficiency in New Zealand adults is low. Participants who ate breakfast more frequently, consumed folate-fortified yeast, or used a daily folate supplement had higher blood folate concentrations.

Daily supplementation with folate increases erythrocyte folate concentrations; however, the time to reach steady-state concentrations has not been empirically demonstrated. Previous predictions of time to steady state or time to 90% steady-state concentration, based on modeling changes in erythrocyte folate during short-term trials, range widely from 40 to 86 wk. We sought to determine the time to steady-state erythrocyte folate concentrations following the initiation of daily folate supplementation using data collected from a 2-y, double-blind, placebo-controlled, randomized trial involving 276 participants aged 65 y or older. The daily supplement contained 1 mg of folate. Erythrocyte folate concentrations were measured, using a microbiological assay, at baseline and at 6, 12, 18, and 24 mo. The mean plasma and erythrocyte folate concentrations in the folate-supplemented group were higher than in the placebo group at 6, 12, 18, and 24 mo (P < 0.001). Adjusted for baseline differences, the difference in erythrocyte folate concentrations between the folate and placebo group at 6 mo was 1.78 μmol/L (95% CI: 1.62-1.95 μmol/L). The difference increased significantly to 2.02 μmol/L (95% CI: 1.85-2.18 μmol/L) at 12 mo. This difference (between the folate and placebo groups) did not significantly change after a further year of folate supplementation; at 18 mo, it was 2.09 μmol/L (95% CI: 1.92-2.27 μmol/L) and at 24 mo it was 1.98 μmol/L (95% CI: 1.18-2.15 μmol/L). Twelve months of daily folate supplementation with 1 mg is sufficient time to cause erythrocyte folate concentrations to reach a new steady state.

There is evidence to suggest that folate, homocysteine, or both affect the (n-3) long chain PUFA composition of tissues; however, this evidence is derived largely from experiments with animals and small observational studies in humans. Results from randomized controlled trials are needed. The objective of this study was to determine whether homocysteine lowering with a B vitamin supplement affects the proportion of (n-3) long-chain PUFA in plasma phosphatidylcholine. We conducted a double-blind, placebo-controlled, randomized clinical trial involving 253 participants, 65 y or older, with plasma homocysteine concentrations of at least 13 micromol/L. Participants in the vitamin group (n = 127) took a daily supplement containing 1000 microg folate, 500 microg vitamin B-12, and 10 mg vitamin B-6 for 2 y. The fatty acid composition of plasma phosphatidylcholine was measured at baseline and at 2 y. Plasma homocysteine concentrations during the course of the study were 4.4 micromol/L lower in the vitamin group than in the placebo group. The proportions of eicosapentaenoic, docosapentaenoic, and docosahexaenoic acids in plasma phosphatidylcholine did not differ between the vitamin and placebo groups at 2 y; the mean differences after adjusting for baseline values and sex were -0.03 (99% CI: -0.22, 0.16), 0.03 (99% CI: -0.03, 0.09), and -0.02 (99% CI: -0.27, 0.24) mol%, respectively. Lowering plasma homocysteine concentrations of older men and women with folate, vitamin B-12, and vitamin B-6 had no effect on the proportion of (n-3) long-chain PUFA in plasma phosphatidylcholine.

An elevated circulating homocysteine concentration is associated with the risk of cardiovascular disease. The mechanism by which an elevated homocysteine increases cardiovascular risk is unclear but may be mediated in part by elevating blood pressure. It is well established that supplements containing folate, vitamins B-12, and B-6 lower homocysteine concentrations. However, the effect of homocysteine-lowering vitamins on blood pressure has not been well studied. We sought to determine whether lowering homocysteine with B vitamins lowers blood pressure in healthy older people with elevated homocysteine concentrations. Two hundred seventy-six healthy older participants (> or = 65 y) with a homocysteine > or = 13 micromol/L were randomized to receive a daily supplement containing folate (1 mg), vitamin B-12 (500 microg), and vitamin B-6 (10 mg), or a placebo, for 2 y. Plasma homocysteine was lower in the Vitamins group than the Placebo group at both 1 [-4.3 micromol/L (95% CI; -4.9, -3.7)] and 2 y [-4.4 micromol/L (95% CI: -5.3, -3.6)]. Systolic and diastolic blood pressures as well as pulse pressure in the Vitamins group did not differ from the Placebo group over the duration of the trial. The mean differences in blood pressures, adjusted for baseline values, did not exceed 1 mm Hg. Supplemental B-vitamins lowered plasma homocysteine but had no effect on blood pressure in older people with elevated baseline homocysteine concentrations.

The dietary-induced changes in the fatty acid composition of plasma, platelet, and erythrocyte lipids were measured as a function of time. Healthy adults consumed a diet rich in saturated fat (18% total energy, TE) for 19 d and then crossed over, without washout, to a diet rich in (n-6) polyunsaturated fat (10% TE) for a further 19 d. The fatty acid composition of plasma and blood cell lipids was measured in blood samples collected from fasting subjects on d 0, 1, 2, 5, 8, 12, and 19 of consuming the diet rich in (n-6) polyunsaturated fats. The linoleic acid composition of all plasma, platelet, and erythrocyte lipids increased to a plateau within 19 d, reaching at least 70% of maximum within 5 d. The maximum increase in linoleic acid composition of erythrocyte phosphatidylcholine was 3.8 mol% at d 12; the increase at d 1 was 2 mol% and at d 5 was 3.2 mol%. The decrease in pentadecanoic acid composition followed a similar time course in all lipids with the exception of plasma phospholipids. Our results show that the time course of dietary-induced changes in erythrocyte fatty acid composition is similar to that in plasma and platelet lipids. These results provide convincing, albeit indirect evidence that the exchange of fatty acids from plasma to erythrocytes and platelets is a major determinant of their membrane fatty acid composition.

New Zealand children, particularly those of Māori and Pacific ethnicity, may be at risk for low vitamin D status because of low vitamin D intakes, the country's latitude (35-46 degrees S), and skin color. The aim of this study was to determine 25-hydroxyvitamin D concentrations and their determinants in a national sample of New Zealand children aged 5-14 y. The 2002 National Children's Nutrition Survey was designed to survey New Zealand children, including oversampling of Māori and Pacific children to allow ethnic-specific analyses. A 2-stage recruitment process occurred using a random selection of schools, and children within each school. Serum 25-hydroxyvitamin D concentration [mean (99% CI) nmol/L] in Māori children (n = 456) was 43 (38,49), in Pacific (n = 646) 36 (31,42), and in New Zealand European and Others (NZEO) (n = 483) 53 (47,59). Among Māori, Pacific, and NZEO, the prevalence (%, 99% CI) of serum 25-hydroxyvitamin D deficiency (<17.5 nmol/L) was 5 (2,12), 8 (5,14), and 3 (1,7), respectively. The prevalence of insufficiency (<37.5 nmol/L) was 41 (29,53), 59 (42,75), and 25 (15,35), respectively. Multiple regression analysis found that 25-hydroxyvitamin D concentrations were lower in winter than summer [adjusted mean difference (99% CI) nmol/L; 15 (8,22)], lower in girls than boys [5 (1,10)], and lower in obese children than in those of "normal" weight [6 (1,11)]. Relative to NZEO, 25-hydroxyvitamin D concentrations were lower in Māori [9 (3,15)] and Pacific children [16 (10,22)]. Ethnicity and season are major determinants of serum 25-hydroxyvitamin D. There is a high prevalence of vitamin D insufficiency in New Zealand children, which may or may not contribute to increased risk of osteoporosis and other chronic disease. There is a pressing need for more convincing evidence concerning the health risks associated with the low vitamin D status in New Zealand children.

The natural diastereoisomer [6S]-5-methyltetrahydrofolate ([6S]-5-MTHF) may be a safer fortificant than folic acid for neural tube defect (NTD) prevention because it is unlikely to mask vitamin B-12 deficiency. An inverse relationship between NTD risk and blood folate concentrations has been reported. In this randomized, placebo-controlled, double-blind trial, we compared the effects of [6S]-5-MTHF and folic acid supplementation for 24 wk on plasma folate and red cell folate (RCF) in women of childbearing age (18-49 y). Women (n = 104) were randomly assigned to receive a supplement containing [6S]-5-MTHF (113 micro g/d), folic acid (100 micro g/d) or placebo. The mean estimated linear increase in plasma folate concentration was 0.3 [95% confidence interval (CI): 0.1, 0.5], and 0.4 (0.2, 0.6) nmol/(L. wk) in the [6S]-5-MTHF and folic acid groups, respectively. The mean estimated linear increase in RCF was 7.4 (95% CI: 4.5, 10.3), and 8.3 (4.4, 12.3) nmol/(L. wk) in the [6S]-5-MTHF and folic acid groups, respectively. There were no differences in the slopes between the [6S]-5-MTHF group and the folic acid group in either plasma folate (P = 0.48) or RCF (P = 0.70). At 24 wk, estimated mean increases in plasma folate concentrations were 6.9 (95% CI: 1.7, 12.2) and 9.2 (3.3, 15.1) nmol/L, and in RCF, 251 (143, 360) and 275 (148, 402) nmol/L, in the [6S]-5-MTHF and folic acid groups, respectively, relative to the placebo group. These data suggest that low dose [6S]-5-MTHF and folic acid supplementation increase blood folate indices to a similar extent. A steady state in the blood indices had not been reached by 24 wk.