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PubMed2000

24-hour history is more closely associated with vitamin A status and provides a better estimate of dietary vitamin A intake of deficient Indonesian preschool children than a food frequency method.

OBJECTIVES: To determine if the Simplified Dietary Assessment to Identify Groups at Risk of Inadequate Intake of Vitamin A developed by the International Vitamin A Consultative Group (IVACG) correctly classified a group of vitamin A-deficient children as being at risk, and to see if a food frequency questionnaire (FFQ) or 24-hour history (24HH) yielded estimated dietary vitamin A intakes most closely associated with vitamin A status. DESIGN: Forty-seven foods were identified as contributing most of the vitamin A to the diet of the study population. For each food, usual portion sizes were determined during a pilot study. Intake was calculated from data collected by FFQ and 24HH. Four modifications of the 24HH analysis were made to determine if this method of analysis could be simplified. SUBJECTS/SETTING: Subjects were 265 Indonesian children with or at high risk of developing xerophthalmia. RESULTS: Mean and median intakes of vitamin A based on the 24HH analysis were 50% and 27% of the US Recommended Dietary Allowance, respectively, which accurately identified the study sample as being at risk. Dietary intake based on the 24HH was significantly associated with serum retinol concentration (P = .01, trend test). Eliciting portion sizes during the 24HH was not necessary once the usual portion sizes consumed by the population were estimated in the pilot study. Mean and median intakes of vitamin A based on the FFQ were 150% and 118% of the Recommended Dietary Allowance, respectively, which suggests that the FFQ overestimated intake. Intake based on the FFQ was not correlated with serum retinol concentration. CONCLUSIONS: Our findings do not support the IVACG recommendation that the FFQ be regarded as more reliable than the 24HH when the 2 methods produce different conclusions, nor the recommendation of some users of the method that the 24HH be dropped from the assessment method.

Child Nutrition Disorders↗

PubMed1993

Supplementation of vitamin K in pregnant women receiving anticonvulsant therapy prevents neonatal vitamin K deficiency.

OBJECTIVE: The null hypothesis of this study is that extra vitamin K administered to pregnant women on a regimen of enzyme-inducing anticonvulsant therapy will not decrease the frequency of symptoms of vitamin K deficiency in their neonates. STUDY DESIGN: A multicenter case-control study was performed on 16 pregnant women on anticonvulsant therapy who received 10 mg of vitamin K1 daily from 36 weeks of pregnancy onward. Concentrations of PIVKA-II (protein induced by vitamin K absence for factor II) and of vitamin K1 were determined in cord blood and compared with those in 20 controls. RESULTS: In none of 17 cord samples was PIVKA-II detectable, compared with 13 of 20 in controls (chi 2, p < 0.001). Median cord vitamin K1 level was 530 pg/ml compared with below detection limit in most controls. CONCLUSIONS: Antenatal vitamin K1 treatment decreases the frequency of vitamin K deficiency in neonates of mothers on anticonvulsant therapy.

Anticonvulsants↗

PubMed2006

Determinants of vitamin D status in adult Crohn's disease patients, with particular emphasis on supplemental vitamin D use.

OBJECTIVE: To investigate determinants (pathophysiologic and physiologic, behavioural and lifestyle) of vitamin D status in Irish Crohn's disease (CD) patients. DESIGN: A cross-sectional observational study. SETTING: Cork City, Ireland (52 degrees N). SUBJECTS: Crohn's Disease patients (n=58; mean age 38.1 years) were recruited from Cork University Hospital. RESULTS: Fifty and nineteen percent of Irish CD patients were vitamin D deficient (defined by serum 25 hydroxyvitamin (OH) D levels <50 nmol/l) during winter and summer, respectively. Multiple regression analysis showed that summer-time serum 25 (OH) D levels were positively associated with use of vitamin D supplements (P=0.033) and negatively associated with smoking (P=0.006) and being male (P=0.063). During winter-time, use of vitamin D supplements (P=0.041) and sun habits (P=0.066) were positively associated, whereas small intestinal involvement (P=0.005) and body mass index (BMI) (P=0.083) were negatively associated with serum 25 (OH) D levels. There was no significant association between other non-pathophysiologic (age, dietary calcium or vitamin D) or pathophysiologic factors (steroid use, resection), and serum 25 (OH) D levels, at either season. Approximately 41 and 60% of the total variation in summer- and winter-time serum 25 (OH) D, respectively, was explained by this model. CONCLUSION: A high proportion of Irish CD patents had some level of vitamin D deficiency (<50 nmol/l) during late-wintertime. Use of regular low-dose supplemental vitamin D, particularly by patients with small intestinal involvement, cessation of smoking and adequate, but responsible, exposure to summer sunlight as well as maintaining BMI in the normal range could help maintain adequate vitamin D levels during wintertime.

Adult↗

PubMed1999

Determination of vitamins D2, D3, K1 and K3 and some hydroxy metabolites of vitamin D3 in plasma using a continuous clean-up-preconcentration procedure coupled on-line with liquid chromatography-UV detection.

A semi-automatic procedure for the continuous clean-up and concentration of several fat-soluble vitamins prior to their separation by HPLC and UV detection is reported. The procedure is based on the use of a minicolumn packed with aminopropylsilica as sorbent located prior to the chromatographic detection system. The overall process was developed and applied to the main liposoluble vitamins (A, D2, D3, E, K1, K3) and several hydroxy metabolites of vitamin D3 [25-(OH)-D3,24,25-(OH)2-D3 and 1,25-(OH)2-D3]. All the analytes were monitored at a compromise wavelength of 270 nm. Calibration graphs were constructed between 0.01 and 100 ng ml-1 for vitamin D2 and D3 and their hydroxy metabolites, between 0.1 and 100 ng ml-1 for vitamin A, K1 and K3 and between 1 and 100 ng ml-1 for vitamin E, with excellent regression coefficients (> or = 0.9901) in all cases. The precision was established at two concentration levels with acceptable RSDs in all instances (between 3.6 and 8.7%). The method was appropriate for the determination of vitamin D2, D3, K1 and K3 and the 24,25-dihydroxy and 25-hydroxy metabolites of vitamin D3 in human plasma. The method was applied to plasma samples spiked with the target analytes and the recoveries ranged between 78 and 109%.

Chromatography, High Pressure Liquid↗

PubMed1997

Effect of injected vitamin A and level of dietary vitamin E on alpha-tocopherol status in gestating swine.

A 2 x 2 trial was conducted to determine the effects of injected vitamin A and dietary level of vitamin E on blood serum and tissue concentrations of alpha-tocopherol during early gestation of gilts. Thirty-two crossbred gilts were fed a corn soybean meal basal diet supplemented with DL-alpha tocopheryl acetate to provide either 25 or 500 IU of vitamin E/kg of diet. Gilts were fed daily 1.9 kg/gilt beginning 7 days before breeding until day 25 of gestation. Sixteen gilts were injected (i.m.) with 350,000 IU of retinol palmitate 7 days before breeding, at the time of breeding (d0), and 7 days after breeding. Blood samples were collected on day -7, 0, 7, and 24, and all gilts were slaughtered on day 25 of gestation. Supplemental vitamin E at 500 IU/kg of diet increased alpha-tocopherol concentrations (P < 0.01) in blood serum in all tissues examined, including reproductive and embryonic, except fat. Vitamin A injections had no effect (P > 0.10) on blood serum alpha-tocopherol concentrations except on day 7 when a small increase (P < 0.06) was noted. Vitamin A injections had no effect (P > 0.10) on tissue alpha-tocopherol concentrations. Increasing dietary level of vitamin E increased blood serum and tissue alpha-tocopherol concentrations, and vitamin A injections had little or no effect on these concentrations during the early gestation of gilts.

Animals↗

PubMed1996

Serum vitamin A, vitamin E, and beta-carotene levels in preeclamptic women in northern nigeria.

We compared the serum levels of beta-carotene, vitamin A (retinol), and vitamin E (alpha-tocopherol) in healthy pregnant women and their counterparts who exhibited the signs and symptoms of preeclampsia or eclampsia, including: systolic blood pressure greater than 160 mm Hg, edema, and proteinuria. The study was conducted in the cities of Maiduguri and Bauchi, which are located in the semi-arid northeastern region of Nigeria. Most of the pregnant subjects: (1) were teenagers, though they ranged in age from 14 to 25 years; (2) had 2 or fewer prior pregnancies; and (3) were predominantly of the Muslim faith and members of the Hausa, Fulani, or Kanuri ethnic groups. Few of the women had received prenatal care. Serum levels of vitamins A and E and betacarotene were quantified using high pressure liquid chromatography. The serum vitamin A levels of the 9 preeclamptic women (15.3 mg/dL) and the 7 eclamptic women (8.3 mg/dL) were significantly reduced (p < 0.01) relative to the serum vitamin A levels of healthy women in the third trimester (24.2 mg/dL). For the healthy pregnant controls, the levels of vitamins A and E and beta-carotene were relatively constant throughout pregnancy. The mean serum beta-carotene levels for both the preeclamptic and eclamptic groups of subjects were half as high as those of healthy control women in the third trimester (p = 0.004). The serum vitamin E levels of the preeclamptic and eclamptic women were 15% and 30% lower, respectively, than those of the corresponding controls (p < 0.01). The serum levels of these three lipids in the healthy pregnant and non-pregnant women we studied are similar to values reported by others for North American and European women of childbearing age. These results support the hypothesis that preeclampsia-eclampsia deplete natural lipid antioxidants and suggest that the reduced levels of vitamin A in such women experiencing hypertension of pregnancy, if they happen to be infected with the HIV-1 virus, may place them at increased risk for mother-child transmission of the virus.

Adolescent↗

PubMed2005

Increased production of functional recombinant human clotting factor IX by baby hamster kidney cells engineered to overexpress VKORC1, the vitamin K 2,3-epoxide-reducing enzyme of the vitamin K cycle.

Some recombinant vitamin K-dependent blood coagulation factors (factors VII, IX, and protein C) have become valuable pharmaceuticals in the treatment of bleeding complications and sepsis. Because of their vitamin K-dependent post-translational modification, their synthesis by eukaryotic cells is essential. The eukaryotic cell harbors a vitamin K-dependent gamma-carboxylation system that converts the proteins to gamma-carboxyglutamic acid-containing proteins. However, the system in eukaryotic cells has limited capacity, and cell lines overexpressing vitamin K-dependent clotting factors produce only a fraction of the recombinant proteins as fully gamma-carboxylated, physiologically competent proteins. In this work we have used recombinant human factor IX (r-hFIX)-producing baby hamster kidney (BHK) cells, engineered to stably overexpress various components of the gamma-carboxylation system of the cell, to determine whether increased production of functional r-hFIX can be accomplished. All BHK cell lines secreted r-hFIX into serum-free medium. Overexpression of gamma-carboxylase is shown to inhibit production of functional r-hFIX. On the other hand, cells overexpressing VKORC1, the reduced vitamin K cofactor-producing enzyme of the vitamin K-dependent gamma-carboxylation system, produced 2.9-fold more functional r-hFIX than control BHK cells. The data are consistent with the notion that VKORC1 is the rate-limiting step in the system and is a key regulatory protein in synthesis of active vitamin K-dependent proteins. The data suggest that overexpression of VKORC1 can be utilized for increased cellular production of recombinant vitamin K-dependent proteins.

Animals↗

PubMed1990

Influence of dietary fats and vitamin E on plasma and hepatic vitamin A and beta-carotene levels in rats fed excess beta-carotene.

Effects of different dietary lipids and excess vitamin E on plasma and hepatic concentrations of beta-carotene were evaluated in rats fed diets containing a large excess (0.2%) of beta-carotene. Male weanling Wistar Kyoto rats were fed beta-carotene-supplemented diets containing various dietary lipids as follows: Group I, a saturated fat (coconut oil); Group II, a monounsaturated fat (olive oil); Group III, a polyunsaturated fat rich in omega-6 fatty acids (safflower oil); Group IV, same as Group III plus vitamin E; and Group V, a polyunsaturated fat rich in omega-3 fatty acids (menhaden oil). All diets contained 2% safflower oil to provide sufficient amounts of linoleic acid (an essential fatty acid). Rats were killed after six weeks of feeding the various diets, and the concentrations of beta-carotene and vitamin A were determined in plasma and liver. Plasma vitamin A levels were not altered by any of the dietary lipids or by an excess of vitamin E. The concentrations of beta-carotene in plasma were the lowest in rats fed the diet containing menhaden oil. The feeding of the diet containing an excess of vitamin E also resulted in a significant decrease in plasma beta-carotene concentration. Similarly, the hepatic beta-carotene concentration was also reduced to about one-half in rats fed the diet containing an excess of vitamin E. Liver beta-carotene concentration was higher in Groups II and III than in the other three dietary groups. Hepatic vitamin A concentrations were also affected by the type of dietary fat.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1981

Effect of vitamin E on prothrombin levels in warfarin-induced vitamin K deficiency.

Rats rendered lightly vitamin K deficient with warfarin (0.01 mg/100 g, IP) and given the equivalent of 1000 units of vitamin E/kg IM for 7 days, showed a marked reduction in functional factor II activity, but normal factor II levels using Echis venom on coagulation analysis. In 12 humans receiving warfarin, vitamin E was administered in doses of 100 or 400 units/day orally for 4 wk. The results in these patients showed no significant change in the prothrombin time, factor II coagulant activity, or factor II antigen (by electroimmunoassay). However, by using a ratio of factor II coagulant activity to immunoreactive protein, significant reduction was observed when compared to pretreatment ratios. These data suggest that vitamin E acts at the step mediated by vitamin K and not in the synthesis of the factor II precursor. Although the administration of high doses of vitamin E in animals, and possibly humans, with vitamin K deficiency potentiates the vitamin K deficiency, this effect is not clinically obvious with 400 IU/day or less.

Adult↗

PubMed1977

Thiamin metabolism in vitamin B6 or vitamin B12 deficient rats.

To clarify the effect of pyridoxine (vitamin B6) or vitamin B12 deficiency on thiamine metabolism, the following two experiments were carried out. In experiment 1, rats were separated into two groups. The first group was fed a complete diet and the second group was fed a vitamin B6 and B12 deficient diet for 25 days. The groups were pair fed. In experiment 2 rats were separated into four groups and fed for 25 days. Group 1 was fed a complete diet; group 2, a vitamin B6 deficient diet; group 3, a vitamin B12 deficient diet; group 4, a thiamin deficient diet. Diet intake was restricted to 10 g/day. Fecal thiamin content increased in B6-B12 (vitamin B6 and B12), B6 (vitamin B6), and B12 (vitamin B12) deficient rats as compared to controls. Thiamin levels in blood, sciatic nerve, liver, heart and kidney decreased in B6-B12, B6, and B12 deficient rats.

Animals↗

PubMed2003

Plasma folate, vitamin B6, vitamin B12, homocysteine, and risk of breast cancer.

BACKGROUND: In several epidemiologic investigations, folate intake has appeared to reduce the elevated risk of breast cancer associated with moderate alcohol consumption. However, data relating plasma folate levels to breast cancer risk are sparse. We investigated the association between plasma folate and other vitamins with breast cancer in a prospective, nested case-control study. METHODS: Blood samples were obtained during 1989 and 1990 from 32 826 women in the Nurses' Health Study who were followed through 1996 for the development of breast cancer. We identified 712 breast cancer case patients and selected 712 individually matched control subjects. Dietary information was obtained using food frequency questionnaires given in 1980, 1984, 1986, and 1990. Logistic regression was used to estimate the relative risks (RRs) of breast cancer (after adjustment for potential risk factors), and a generalized linear model was used to calculate the Pearson correlation coefficients between plasma estimates of folate, vitamin B(6), vitamin B(12), and homocysteine, and intakes of folate, vitamin B(6), and vitamin B(12). All statistical tests were two-sided. RESULTS: The multivariable RR comparing women in the highest quintile of plasma folate with those in the lowest was 0.73 (95% confidence interval [CI] = 0.50 to 1.07; P(trend) =.06). The inverse association between plasma folate and breast cancer risk was highly statistically significant among women consuming at least 15 g/day (i.e., approximately 1 drink/day) of alcohol (multivariable RR = 0.11, 95% CI = 0.02 to 0.59 for highest versus lowest quintile) in contrast with that of women consuming less than 15 g/day (multivariable RR = 0.72, 95% CI = 0.49 to 1.05). The multivariable RR comparing women in the highest quintile of plasma vitamin B(6) levels with those in the lowest quintile was 0.70 (95% CI = 0.48 to 1.02; P(trend) =.09). Plasma vitamin B(12) levels were inversely associated with breast cancer risk among premenopausal women (multivariable RR = 0.36, 95% CI = 0.15 to 0.86 for highest versus lowest quintile) but not among postmenopausal women. Plasma homocysteine was not associated with breast cancer risk. CONCLUSIONS: Higher plasma levels of folate and possibly vitamin B(6) may reduce the risk of developing breast cancer. Achieving adequate circulating levels of folate may be particularly important for women at higher risk of developing breast cancer because of higher alcohol consumption.

Adult↗

PubMed1990

The origin of the synchronization of the seminiferous epithelium in vitamin A-deficient rats after vitamin A replacement.

In seminiferous tubules of vitamin A-deficient rats, the remaining spermatogonia were A spermatogonia. These cells were topographically arranged as single and paired cells and clones of 4, 8, or more cells. The bromodeoxy-uridine-labeling index and the mitotic index of these cells were found to be 9% and 1%, respectively, indicating that these cells were slowly proliferating. Administration of vitamin A (retinol-acetate) resulted in a reinitiation of spermatogenesis in such a way that the epithelium became stage-synchronized. The rate of development of the spermatogenic cells between 7 and 21 days after vitamin A replacement was found to be similar to that in normal rats. At 24-30 h after administration of vitamin A, a 4- to 6-fold increase in the labeling index was found. In contrast, after 2 days, the labeling index was low, while the mitotic index was elevated (10%). A high labeling index was found again after 3 days. Assuming that during the first 7 days after vitamin A replacement the rate of development of the spermatogenic cells also was normal, it could be deduced that the spermatogonia labeled 24-30 h after vitamin A administration were A1 spermatogonia. These cells would then divide into A2 spermatogonia after about 2 days, which in turn would traverse their S phase after about 3 days. Hence, spermatogenesis in vitamin A-deficient rats would be arrested shortly before the S phase of the A1 spermatogonia. After administration of vitamin A, the spermatogonia synchronously start the series of six divisions leading to the formation of spermatocytes and, ultimately, they develop into mature spermatids.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Recovery after dietary vitamin E supplementation of impaired endothelial function in vitamin E-deficient rats.

1. Thoracic aortae, isolated from rats supplemented with dietary vitamin E after vitamin E deficiency, were analysed for changes in vascular reactivity. 2. Following 4 or 12 months of dietary vitamin E deficiency, endothelium-dependent vasodilator responses to acetylcholine were significantly impaired. However, when animals were fed after the first 4 months of vitamin E deprivation with a vitamin E-supplemented diet for 8 months, endothelium-mediated responses were completely restored. 3. In contrast, the endothelium-independent vasodilator or vasoconstrictor responses to sodium nitroprusside and noradrenaline, respectively were not altered either by vitamin E deficiency or supplementation. 4. These data indicate that vitamin E supplementation reversed the impairment of endothelial cell function which occurs during vitamin E deficiency.

Acetylcholine↗

PubMed1995

Effect of vitamin D repletion on testicular function in vitamin D-deficient rats.

Freshly weaned 30-day-old male Wistar rats were fed a vitamin D-deficient diet adequate in calcium and phosphorus for 3 months. On the 120th day of age three different doses of vitamin D were injected intramuscularly into three groups of rats and maintained for another month with water and a normal diet ad libitum. One group was continued with a vitamin D-deficient diet up to the 150th day. One group of animals was killed by decapitation on the 120th day and testicular functions like sperm count in testis and epididymis, testicular glutamyl transpeptidase activity and Leydig cell count as well as body weight were noted. On the 150th day animals of all groups were killed and testicular function was studied. Body weight and testicular function decreased significantly on the 120th and 150th day of age in vitamin D-deficient rats as compared to age-matched normal control rats. Injection of lower doses of vitamin D on the 120th day of age improved testicular function after 1 month whereas administration of a high dose of vitamin D caused a deterioration of the testicular function. The result suggests that retardation of spermatogenesis due to disturbances in Sertoli and Leydig cell function in vitamin D deficiency is reversible and can be corrected by supplementing an optimal dose of vitamin D.

Aging↗

PubMed1986

Postnatal distribution of vitamin A in liver, lung, heart and brain of the rat in relation to maternal vitamin A status.

The effect of low, medium and adequate vitamin A (6, 40 and 100 micrograms/day/kg body weight) supplementation to the dams was studied on the accumulation of vitamin A in various tissues of the rat during postnatal growth. The restricted supply of vitamin A to the mother resulted in an impaired growth of pups and their organs. The maternal hepatic stores of vitamin A were related to their vitamin A intake, being lowest in the low group and highest in the adequate group during their fetal development. The plasma vitamin A levels of dams were comparable in three groups at birth and on 10th day of postnatal age. The vitamin A contents of fetal hepatic and extra-hepatic tissues (lung, heart and brain) were increased with the age of pups and this increase was observed to be dependent on the supply of vitamin A to the mother.

Animals↗

PubMed1986

Vitamin D3 improves impaired glucose tolerance and insulin secretion in the vitamin D-deficient rat in vivo.

It has previously been shown in this laboratory that vitamin D3 is essential for normal insulin secretion from the perfused rat pancreas. In this present study, the influence of vitamin D status on insulin secretion in vivo was investigated. Intravenous glucose tolerance tests were performed on conscious vitamin D-deficient rats (-D), vitamin D-replete rats fed ad libitum (+D AL), and vitamin D-replete rats pair fed to the D-deficient animals (+D PF). Vitamin D deficiency, easily recognizable by low daily dietary intake and depressed plasma calcium levels, was found to impair plasma glucose clearance as characterized by an elevated KG value (representing a function of the area beneath the tolerance curve). KG values for the +D AL, +D PF, and -D groups were 504 +/- 15, 480 +/- 46, and 641 +/- 28, respectively. The increase in KG corresponded to a significant reduction in glucose-mediated insulin secretion as compared to the +D animals. This difference appeared not to be related to the increase caloric intake associated with vitamin D repletion, since +D rats which had been pair fed to the -D animals also exhibited restored plasma insulin levels in response to glucose. Plasma phosphorus concentrations were comparable in all three groups, and thus this parameter is also unlikely to be a contributory factor in the observed phenomenon. Additional experiments were conducted to evaluate the involvement of hypocalcemia in the observed impaired glucose tolerance. Normalization of plasma calcium levels (from 4.8 mg/100 ml to 9.6/100 ml) of the -D rats, by dietary calcium and phosphorus manipulation, failed to improve glucose clearance (KG for -D normocalcemic rats = 639 +/- 61) or insulin secretion. These results support the concept that vitamin D plays a physiological role in insulin secretion, acting, at least in part, independently of nutritional factors and the prevailing plasma calcium and phosphorus concentrations.

Animals↗

PubMed1988

The effect of vitamin D supplementation on vitamin D status and parathyroid function in elderly subjects.

Vitamin D deficiency is common in the elderly and may lead to secondary hyperparathyroidism, cortical bone loss, and hip fractures. The effect of vitamin D supplementation for 1 yr was studied in 72 people living in a nursing home and 70 people living in an aged people's home. The subjects were randomized into 3 groups: control, and 400 or 800 IU vitamin D3/day. The initial vitamin D status of each subject was classified as deficient or borderline [serum 25-hydroxyvitamin D (25OHD) less than 30 nmol/L] in 79% and adequate (serum 25OHD greater than or equal to 30 nmol/L) in 21%. Serum 25OHD concentrations increased about 3-fold in both groups receiving vitamin D supplementation. Serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations increased slightly but significantly, and the increase was inversely related to the initial serum 25OHD concentration. Serum intact PTH-(1-84) concentrations decreased about 15% during supplementation in both nursing home and aged people's home residents, whereas serum osteocalcin significantly decreased in the nursing home residents only. We conclude that a vitamin D3 supplement of 400 IU/day adequately improves vitamin D status in elderly people and increases 1,25-(OH)2D concentrations in those with vitamin D deficiency. Supplementation decreases parathyroid function and may depress bone turnover to some degree.

Aged↗

PubMed2006

Dietary folate, vitamin B12, and vitamin B6 and the risk of Parkinson disease.

BACKGROUND: Increased homocysteine levels might accelerate dopaminergic cell death in Parkinson disease (PD), through neurotoxic effects. Higher dietary intakes of folate, vitamin B12, and vitamin B6 (cofactors in homocysteine metabolism) might decrease the risk of PD through decreasing plasma homocysteine. Moreover, vitamin B6 might influence the risk of PD through antioxidant effects unrelated to homocysteine metabolism and through its role in dopamine synthesis. METHODS: In the Rotterdam Study, a prospective, population-based cohort study of people aged 55 years and older, the authors evaluated the association between dietary intake of folate, vitamin B12, and vitamin B6 and the risk of incident PD among 5,289 participants who were free of dementia and parkinsonism and underwent complete dietary assessment at baseline. PD was assessed through repeated in-person examination and continuous monitoring by computer linkage to medical records. Data were analyzed using Cox proportional hazards regression analysis. RESULTS: After a mean follow-up of 9.7 years, the authors identified 72 participants with incident PD. Higher dietary intake of vitamin B6 was associated with a significantly decreased risk of PD (hazard ratio per SD, 0.69 [95% CI 0.50 to 0.96]; for highest vs lowest tertile, 0.46 [0.22 to 0.96]). Stratified analyses showed that this association was restricted to smokers. No association was observed for dietary folate and vitamin B(12). CONCLUSIONS: Dietary vitamin B6 may decrease the risk of Parkinson disease, probably through mechanisms unrelated to homocysteine metabolism.

Administration, Oral↗