Vitamin D deficiency and associated factors in adolescent girls in Beijing

BACKGROUND: Several locally published reports indicate a high prevalence of vitamin D deficiency among adolescents in China, but no systematic population-based survey has been conducted. OBJECTIVE: The objective was to determine the prevalence of vitamin D deficiency and to study associated factors in adolescent girls in Beijing. DESIGN: A cross-sectional study was conducted in a random sample of 1248 Beijing girls aged 12-14 y. Nutrient intakes, ultraviolet light exposure, anthropometric characteristics, physical activity, signs and symptoms of rickets, and plasma concentrations of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and calcium were measured and X-rays of the hand and wrist were taken. RESULTS: The prevalence of clinical vitamin D and calcium deficiency (plasma 25-hydroxyvitamin D <12.5 nmol/L, plasma calcium <2.25 mmol/L, and muscle spasm at least once per week) was 9.4% in winter. The prevalence of subclinical vitamin D deficiency (25-hydroxyvitamin D <12.5 nmol/L) was 45.2% in winter and 6.7% in summer (P < 0.0005). Logistic regression analysis showed that subclinical and clinical vitamin D deficiency in winter were associated with low plasma 25-hydroxyvitamin D concentrations (<12.5 nmol/L) in summer, low calcium intake ( x +/- SD: 280 +/- 48 compared with 440 +/- 61 mg/d), and low plasma calcium concentrations (<2.25 mmol/L) in winter. The odds ratios for these associations were 3.1, 1.5, and 1.5, respectively. CONCLUSIONS: Subclinical vitamin D deficiency was widespread among Beijing adolescent girls in winter. Low plasma 25-hydroxyvitamin D concentrations in summer, low calcium intake, and low plasma calcium concentrations in winter were the main risk factors for vitamin D deficiency in winter.     

Vitamin D status and its association with parathyroid hormone concentrations in women of child-bearing age living in Jakarta and Kuala Lumpur

OBJECTIVE: To describe the vitamin D status of women living in two Asian cities,--Jakarta (6 degrees S) and Kuala-Lumpur (2 degrees N), to examine the association between plasma 25-hydroxyvitamin D and parathyroid hormone (PTH) concentrations, and to determine a threshold for plasma 25-hydroxyvitamin D above which there is no further suppression of PTH. Also, to determine whether dietary calcium intake influences the relationship between PTH and 25-hydroxyvitamin D. DESIGN: Cross-sectional. SETTING: Jakarta, Indonesia and Kuala Lumpur, Malaysia. PARTICIPANTS: A convenience sample of 504 non-pregnant women 18-40 years. MAIN MEASURES: Plasma 25-hydroxyvitamin D and PTH. RESULTS: The mean 25-hydroxyvitamin D concentration was 48 nmol/l. Less than 1% of women had a 25-hydroxyvitamin D concentration indicative of vitamin D deficiency (<17.5 nmol/l); whereas, over 60% of women had a 25-hydroxyvitamin D concentration indicative of insufficiency (<50 nmol/l). We estimate that 52 nmol/l was the threshold concentration for plasma 25-hydroxyvitamin D above which no further suppression of PTH occurred. Below and above this concentration the slopes of the regression lines were -0.18 (different from 0; P=0.003) and -0.01 (P=0.775), respectively. The relation between vitamin D status and parathyroid hormone concentration did not differ between women with low, medium or high calcium intakes (P=0.611); however, even in the highest tertile of calcium intake, mean calcium intake was only 657 mg/d. CONCLUSION: On the basis of maximal suppression of PTH we estimate an optimal 25-hydroxyvitamin D concentration of approximately 50 nmol/l. Many women had a 25-hydroxyvitamin D below this concentration and may benefit from improved vitamin D status.     

Plasma 25-hydroxyvitamin D in growing kittens is related to dietary intake of cholecalciferol

Vitamin D synthesis by growing kittens exposed to ultraviolet light is ineffective. Concentration of 25-hydroxyvitamin D (25-OHD) in plasma (the most useful index of vitamin D status) was measured in six groups each of seven kittens given a purified diet (12 g calcium and 8 g phosphorus/kg, calculated metabolizable energy = 20 kJ/g) that contained either 0.0, 3.125, 6.25, 12.5, 18.75 or 25 microg of cholecalciferol/kg diet. All kittens received these diets from 9 to 22 wk of age, and the two groups given the 0.0 and 3.125 microg cholecalciferol/kg treatments continued to receive the diets until they were 34 wk old. Total and ionizable calcium and phosphorus in plasma were not affected by treatments. No adverse clinical changes were observed or found on radiographic examination of the kittens at 22 or 34 wk of age. Plasma concentration of 25-OHD was linearly related (r2 = 0.99, P < 0.001) to dietary intake of cholecalciferol. Plasma concentration of 25-OHD in kittens given the diet without added vitamin D was significantly less at 22 wk than at 9 wk, whereas kittens receiving the diet containing 3.125 microg cholecalciferol/kg had significantly higher 25-OHD concentrations at 22 and 34 wk than at 9 wk of age. Kittens given the 6.25 microg cholecalciferol/kg diet had plasma 25-OHD concentrations at 22 wk > 50 nmol/L which is considered replete for humans. An allowance of 6. 25 microg (250 IU) of cholecalciferol/kg diet is suggested to provide a margin of safety.     

Vitamin D-fortified milk achieves the targeted serum 25-hydroxyvitamin D concentration without affecting that of parathyroid hormone in New Zealand toddlers

For young children, the level of vitamin D required to ensure that most achieve targeted serum 25-hydroxyvitamin D [25(OH)D] ≥50 nmol/L has not been studied. We aimed to investigate the effect of vitamin D-fortified milk on serum 25(OH)D and parathyroid hormone (PTH) concentrations and to examine the dose-response relationship between vitamin D intake from study milks and serum 25(OH)D concentrations in healthy toddlers aged 12-20 mo living in Dunedin, New Zealand (latitude 46°S). Data from a 20-wk, partially blinded, randomized trial that investigated the effect of providing red meat or fortified toddler milk on the iron, zinc, iodine, and vitamin D status in young New Zealand children (n = 181; mean age 17 mo) were used. Adherence to the intervention was assessed by 7-d weighed diaries at wk 2, 7, 11, 15, and 19. Serum 25(OH)D concentration was measured at baseline and wk 20. Mean vitamin D intake provided by fortified milk was 3.7 μg/d (range, 0-10.4 μg/d). After 20 wk, serum 25(OH)D concentrations but not PTH were significantly different in the milk groups. The prevalence of having a serum 25(OH)D <50 nmol/L remained relatively unchanged at 43% in the meat group, whereas it significantly decreased to between 11 and 15% in those consuming fortified study milk. In New Zealand, vitamin D intake in young children is minimal. Our findings indicate that habitual consumption of vitamin D-fortified milk providing a mean intake of nearly 4 μg/d was effective in achieving adequate year-round serum 25(OH)D for most children.     

Associations of diet, supplement use, and ultraviolet B radiation exposure with vitamin D status in Swedish women during winter

BACKGROUND: Vitamin D is produced endogenously after sun exposure but can also be obtained from natural food sources, food fortification, and dietary supplements. OBJECTIVE: We aimed to determine the vitamin D status of women (61-86 y old) living in central Sweden (latitude 60 degrees ) during winter and its relation with vitamin D intake and exposure to ultraviolet B radiation. DESIGN: In a cross-sectional study, we assessed the vitamin D status (serum 25-hydroxyvitamin D [25(OH)D]) of 116 women by using an enzyme immunoassay. The women completed questionnaires covering food habits, use of dietary supplements, and sun-related behavior. RESULTS: In a multiple linear regression model, the main determinants of serum 25(OH)D concentrations (x +/- SD: 69 +/- 23 mmol/L) were dietary vitamin D (6.0 +/- 1.8 mug/d), travel to a sunny location during winter within the previous 6 mo (26%), and the use of dietary supplements (16%). There was no association between serum 25(OH)D status during the winter and age, time spent outdoors, the use of sunscreen, or skin type. Serum 25(OH)D concentrations increased by 25.5 nmol/L with 2-3 servings (130 g/wk) fatty fish/wk, by 6.2 nmol/L with the daily intake of 300 g vitamin D-fortified reduced-fat dairy products, by 11.0 nmol/L with regular use of vitamin D supplements, and by 14.5 nmol/L with a sun vacation during winter. Among nonsupplement users without a wintertime sun vacation, 2-3 servings fatty fish/wk increased serum vitamin D concentrations by 45%. CONCLUSION: Fatty fish, vitamin D-fortified reduced-fat dairy products, regular supplement use, and taking a sun vacation are important predictors for serum concentrations of 25(OH)D during winter at a latitude of 60 degrees .     

Copper deficiency does not lead to taurine deficiency in rats

Copper deficiency has been reported to cause a decrease in urinary taurine excretion in rats. We determined whether Cu deficiency would decrease taurine status and the hepatic activities of cysteine dioxygenase (CDO) and/or cysteine sulfinic acid decarboxylase (CSAD) in rats. Ten weanling male rats were assigned to either a Cu-adequate (+Cu) or Cu-deficient (-Cu) group. All rats consumed a Cu-deficient purified diet and water ad-libitum for 16 wk. The water for the (+Cu) group contained 20 mg Cu/L as CuSO(4). At wk 16, the groups differed (P < 0.05) in the following variables (means +/- SEM, -Cu vs. +Cu): body weight (BW), 375 +/- 19 vs. 418 +/- 2.9 g; food intake, 16.2 +/- 0.7 vs. 18.5 +/- 0.4 g/d; hematocrit, 0.294 +/- 0.027 vs. 0.436 +/- 0.027; hemoglobin, 95.2 +/- 9 vs 134 +/- 10 g/L; liver Cu, 8.7 +/- 2.0 vs. 65.9 +/- 2.5 nmol/g; plasma Cu, 0.38 +/- 0.09 vs. 13.4 +/- 0.61 micromol/L; plasma ceruloplasmin activity, 1.75 +/- 1.0 vs. 67.9 +/- 8.4 IU; relative heart weight, 0.56 +/- 0.04 vs. 0.35 +/- 0.02% BW; relative liver weight, 4.06 +/- 0.23 vs. 3.37 +/- 0.06% BW; and liver CSAD activity, 18.8 +/- 1.37 vs. 13.5 +/- 1.11 nmol x min(-1) x mg protein(-1). The groups did not differ at wk 16 in: plasma taurine, 249 +/- 14 vs. 298 +/- 63 micromol/L; whole blood taurine, 386 +/- 32 vs. 390 +/- 25 micromol/L; urinary taurine excretion, 82.5 +/- 15 vs. 52.0 +/- 8.3 micromol/d; liver taurine, 2.6 +/- 0.7 vs. 2.8 +/- 0.4 micromol/g; liver total glutathione, 6.9 +/- 0.48 vs. 6.3 +/- 0.40 micromol/g; liver cyst(e)ine, 96 +/- 7.1 vs. 99 +/- 5.3 nmol/g and liver CDO activity, 2.19 +/- 0.33 vs. 2.74 +/- 0.21 nmol x min(-1) x mg protein(-1). These findings support the conclusion that Cu deficiency does not affect body taurine status.     

Hypervitaminosis A and calcium-regulating hormones in the rat

The effect of vitamin A on calcium-regulating hormones was studied in rats. A single oral dose of 30 mg retinol equivalents (RE) given to adult rats caused no change to serum biologically active parathyroid hormone (bioactive-PTH) concentrations. Bioactive-PTH secretion from rat thyroparathyroid gland complexes was not significantly altered after in vitro incubation with 1.18 X 10(-6) M retinol. Chronically intoxicated rats given 15 mg RE 3 times a week for 6 wk, showed higher osteoclast numbers and lower osteoid than controls. Serum bioactive-PTH was not detectable and serum 25-hydroxyvitamin D (25-OHD) (25.2 +/- 12.5 nmol/L) was significantly (P less than 0.03) lower than controls (43.3 +/- 3.1). In acutely intoxicated rats (60 mg RE/d for 2 d), serum bioactive-PTH levels were significantly lower (0.02 +/- 0.05 ng/ml, P less than 0.03) than in control animals (0.14 +/- 0.08). Lower doses of vitamin A, 7.5 mg RE 3 times a week for 3 wk, suppressed serum bioactive-PTH to undetectable levels but had no significant effect on serum 25-OHD. Serum calcium and 25-OHD levels were significantly lower in vitamin D-intoxicated rats given 7.5 mg RE 3 times a week (ca. 3.16 +/- 0.19 mmol/L; 25-OHD 599.7 +/- 110.6 nmol/L) than vitamin D-intoxicated controls (3.42 +/- 0.17; 789.3 +/- 17.7). These results suggest that hypervitaminosis A can alter the metabolism of calcium-regulating hormones.     

Gamma-tocopherol enhances sodium excretion as a natriuretic hormone precursor

Endogenous natriuretic factors are believed to be responsible for extracellular fluid homeostasis in mammals. A new endogenous natriuretic factor, Loma Linda University-alpha (LLU-alpha) has recently been proven to be a 2,7,8-trimethyl-2-(2'-carboxyethyl)-6-hydroxychroman (gamma-CEHC), which is a metabolite of gamma-tocopherol (gamma-Toc). The purpose of this study was to investigate whether gamma-Toc could accelerate sodium excretion into rat urine as a natriuretic hormone precursor. Male SD strain rats were divided into two groups; one was a control diet group, while the other was a high NaCl group (50 g/kg diet). Next, the two groups were each subdivided into two groups consisting of a placebo group and a gamma-Toc group. After the oral administration of one experimental dose of 20 mg gamma-Toc or placebo, rat urine was collected at 6 h intervals for 24 h, and then the urine volume, sodium and potassium and gamma-CEHC content were determined. gamma-Toc increased in the urine volume of the high-NaCl intake group. The sodium excretion in the high-NaCl group given gamma-Toc was 8.29+/-2.20 g, while in the control group given gamma-Toc it was 6.24+/-1.49 g from 12-18 h. In contrast, the potassium excretion in the rat urine did not change in any of the groups. Our findings suggested that gamma-Toc accelerates the degree of sodium excretion in rats with a high sodium intake.     

Response of vitamin B-6 content of muscle to changes in vitamin B-6 intake in men

Previous reports indicated that in growing rats the vitamin B-6 pool in muscle was relatively stable during deficiency but increased in response to increased vitamin B-6 intake. To determine whether human muscle would show a similar response 10 college-aged males received a low vitamin B-6 diet (1.76 mumol/d) for 6 wk followed by 6 wk on a self-selected diet supplemented with 0.98 mmol pyridoxine HCl/d. During depletion, excretion of pyridoxic acid rapidly adjusted to approximate the intake. Plasma pyridoxal phosphate concentrations at the end of the baseline, depletion, and supplementation periods were 81 +/- 51, 9 +/- 3, and 455 +/- 129 nmol/L, respectively, whereas muscle concentrations were 21 +/- 9, 20 +/- 4, and 25 +/- 7 nmol/g, respectively and total vitamin B-6 in muscle was 28 +/- 10, 27 +/- 4, and 35 +/- 10 nmol/g, respectively. These data provide further confirmation that the vitamin B-6 pools in skeletal muscle are resistant to depletion. They also demonstrate that in humans with constant body weight, vitamin B-6 supplementation is not associated with marked increases in vitamin B-6 in muscle.     

Nutritional interventions related to bone turnover in European space missions and simulation models

Low energy intake, low calcium intake, low plasma 25-hydroxy-vitamin D or low calcitriol levels, and high salt intake might support the development of space osteoporosis. Therefore, my colleagues and I monitored the daily energy and calcium intakes in eight astronauts during their respective space missions (Spacelab D2, Euromir 94, Euromir 95). In most of these astronauts, energy intake was reduced by more than 20% compared with their calculated energy expenditure. In all three missions, the average daily calcium intake of the eight astronauts was 25% lower than the German recommended daily allowances of 900 mg/d for healthy people without osteoporosis risk. In some astronauts, the calcium intake was extremely low at 53 and 74 mg/d. Sodium intake in these astronauts varied from 39 mEq/d to a very high intake of 462 mEq/d. As a consequence of these results, we examined in the 21-d Mir 97 mission a preventative dietary approach of high calcium intake of at least 1000 mg/d with vitamin D supplementation (650 IU/d of Ergocalciferol) and constant sodium intake (180 mEq/d). Total serum calcium concentration and urinary calcium excretion significantly increased during this mission. Synthesis of 25-OH-cholecalciferol synthesis was markedly reduced because of inadequate ultraviolet light, whereas total 25-OH-Vitamin D levels were unchanged. However, parathyroid hormone and calcitriol levels decreased significantly. Sodium excretion decreased significantly, resulting in positive sodium balances. Based on these results, dietary calcium and vitamin D do not stabilize bone turnover because markers of bone formation were reduced and markers of bone resorption were increased. We concluded that, in contrast to terrestrial conditions, adequate or even high calcium and vitamin D intakes during microgravity do not efficiently counteract the development of space osteoporosis. Conversely, vitamin K (Konakion) seemed to counteract microgravity-induced reduction of bone formation markers. In the 179-d Euromir 95 mission, investigators administered 10 mg of vitamin K from inflight day 86 to day 136 in one astronaut. During and after supplementation, bone formation markers increased significantly during this part of the mission. Therefore, vitamin K seems to play a significant role in bone turnover during space flight.     

Calcium absorption and kinetics are similar in 7- and 8-year-old Mexican-American and Caucasian girls despite hormonal differences

To assess the possibility of ethnic differences in mineral metabolism in prepubertal children, we compared measures of calcium metabolism in 7- and 8-y-old Mexican-American (MA) and non-Hispanic Caucasian (CAU) girls (n = 38) living in southeastern Texas. We found similar fractional calcium absorption, urinary calcium excretion, calcium kinetic values and total-body bone mineral content in the MA and CAU girls. In contrast, parathyroid hormone (PTH) concentrations were greater in MA girls (4.01 +/- 0.47 vs. 1. 96 +/- 0.50 pmol/L, P = 0.005) than in CAU girls. Serum 25-hydroxyvitamin D concentrations were lower in MA girls (68.9 +/- 7.7 vs. 109.4 +/- 8.4 nmol/L, P = 0.001) than in CAU girls, but 1, 25-dihydroxyvitamin D concentrations did not differ between groups. Seasonal variability was seen for 25-hydroxyvitamin D concentrations in girls of both ethnic groups, but values in all of the girls were >30 nmol/L (12 ng/mL). We conclude the following: 1) greater PTH levels in MA girls than CAU girls are present without evidence of vitamin D deficiency; and 2) differences in 25-hydroxyvitamin D and PTH concentrations between MA and CAU girls do not have a large effect on calcium absorption, excretion or bone calcium kinetics. These data do not provide evidence for adjusting dietary recommendations for mineral or vitamin D intake by MA girls.     

Comparative effects of vitamin K and vitamin D supplementation on calcium balance in young rats fed normal or low calcium diets

We examined the effect of vitamin K and vitamin D supplementation on calcium balance in young rats fed a normal or low calcium diet. Eighty female Sprague-Dawley rats, 6 wk of age, were randomized by the stratified weight method into eight groups with 10 rats in each group: 0.5% (normal) or 0.1% (low) calcium diet, 0.5% or 0.1% calcium diet+vitamin K (vitamin K2, menatetrenone, 30 mg/100 g, food intake), 0.5% or 0.1% calcium diet+vitamin D (25 microg/100 g, food intake), and 0.5% or 0.1% calcium diet+vitamin K+vitamin D. The duration of the study was 10 wk. Vitamin K supplementation promoted the reduction in urinary calcium excretion and retarded the abnormal elevation of serum PTH level in rats fed a low calcium diet, and stimulated intestinal calcium absorption in rats fed a normal calcium diet. Vitamin D supplementation stimulated intestinal calcium absorption with prevention of the abnormal elevation of serum PTH levels and prevented hypocalcemia in rats fed a low calcium diet, and stimulated intestinal calcium absorption in rats fed a normal calcium diet. The stimulation of intestinal calcium absorption was associated with increased serum 1,25-dihydroxyvitamin D levels. An additive effect of vitamin K and vitamin D on intestinal calcium absorption was found only in rats fed a normal calcium diet. This study shows the differential effects of vitamin K and vitamin D supplementation on calcium balance in young rats fed a normal or low calcium diet.     

Soymilk intake is associated with plasma and liver lipid profiles in rats fed a high-cholesterol diet

OBJECTIVE: This study investigated the effects of soymilk on lipid metabolism in Sprague-Dawley rats fed a cholesterol-enriched (0.3%) diet. METHODS: Thirty male Sprague-Dawley rats weighing 230.0 +/- 9.8 g were randomly assigned to one of three groups: control, S1 (containing 15% soymilk powder in the diet), and S2 (22.5%). After 8 wk, lipid profiles of the plasma, liver, and feces were determined. RESULTS: Body weight gain, daily food intake, and feeding efficiency showed no differences across groups (P > 0.05). The experimental groups had significantly lower plasma levels of cholesterol, triacylglycerol, and low-density lipoprotein cholesterol than the control group (P < 0.05) at weeks 4 and 8. However, total fecal excretion of neutral steroid did not significantly differ across groups (P > 0.05). CONCLUSION: Soymilk affects the metabolism of plasma cholesterol in Sprague-Dawley rats.     

Influence of dietary chloride on fluoride bioavailability in the rat

A factorial experiment was conducted with weanling rats fed a purified diet to determine the influence of dietary chloride (0.02, 0.10 and 0.50%) as sodium chloride on fluoride bioavailability (2 or 10 ppm as sodium fluoride). After 6 wk, rats fed the lowest chloride-containing diets had significant reductions of plasma chloride, urinary chloride excretion and growth rate compared to other chloride groups. Depressed growth occurred in rats fed chloride-deficient diets despite the fact that food intake was similar for all treatments. Fluoride retention was greatest in chloride-deficient rats, which was reflected in enhanced skeletal uptake of fluoride. Fluoride absorption was not inhibited by high chloride intake. We therefore conclude that emphasis on the effect of chloride on fluoride bioavailability should be directed towards an enhancement of fluoride retention by low salt (sodium chloride) diets rather than in terms of a possible negative effect of a high salt diet on fluoride absorption.     

Human metabolism of mammalian lignan precursors in raw and processed flaxseed

BACKGROUND: The mammalian lignans enterolactone and enterodiol are produced in the colon by the action of bacteria on the plant precursor secoisolariciresinol diglycoside, which is found in high concentrations in flaxseed. OBJECTIVE: Two experiments were conducted to determine 1) whether there is a dose response in urinary lignan excretion with increasing flaxseed intake, 2) whether flaxseed processing affects lignan excretion, 3) peak plasma lignan concentrations, and 4) plasma lignan concentrations after chronic supplementation. DESIGN: Nine healthy young women supplemented their diets with 5, 15, or 25 g raw or 25 g processed (muffin or bread) flaxseed for 7 d during the follicular phase of their menstrual cycles. Twenty-four-hour urine samples were collected at baseline and on the final day of supplementation. As an adjunct to the 25-g-flaxseed arm, subjects consumed the supplement for an additional day and blood and urine samples were collected at specific intervals. All blood and urine samples were analyzed for enterolactone and enterodiol by gas chromatography-mass spectroscopy. RESULTS: A dose-dependent urinary lignan response to raw flaxseed was observed (r = 0.72, P < 0.001). The processing of flaxseed as a muffin or bread did not affect the quantity of lignan excretion. Plasma lignan concentrations were greater (P < or = 0.05) than baseline by 9 h after flaxseed ingestion (29.35+/-3.69 and 51.75+/-7.49 nmol/L, respectively). The total plasma area under the curve was higher on the eighth than on the first day (1840.15+/-343.02 and 1027.15+/-95.71 nmol x h/L, respectively). CONCLUSION: Mammalian lignan production from flaxseed precursors is dependent on time and dose but not on processing.     

Ineffective vitamin D synthesis in cats is reversed by an inhibitor of 7-dehydrocholestrol-delta7-reductase

Changes in plasma 25-hydroxyvitamin D (25-OHD) were used as an index of vitamin D status of cats. Plasma 25-OHD concentration of kittens given a purified vitamin D-free diet and exposed to direct summer sun for 15 h/wk declined at a similar rate as kittens given the same diet kept indoors. Similarly, plasma 25-OHD of kittens exposed to ultraviolet (UV) lamps declined at a similar rate as kittens not exposed, and these kittens developed clinical signs of vitamin D deficiency. Eight weaned kittens were given the vitamin D-free purified diet until their plasma concentrations of 25-OHD were < 5 nmol/L. They then had the hair on their backs clipped at weekly intervals and were paired on the basis of skin color and exposed to UV light for 2 h/d. One member of each pair was given an inhibitor of 7-dehydrocholesterol (5, 7-cholestradien-3beta-ol)-delta7-reductase (EC 1.3.1.21) in the diet. Cats receiving the inhibitor had a progressive increase in 25-OHD concentration of plasma with time to 91 +/- 22 nmol/L (mean +/- SEM), whereas cats not receiving the inhibitor had plasma 25-OHD concentrations that were not detectable (P < 0.001). Biopsy samples of skin from cats receiving the inhibitor had more than five times the concentration of 7-dehydrocholesterol (P < 0.001) than the skin of control cats. Low concentration of 7-dehydrocholesterol (presumably due to high activity of the reductase) in the skin of cats is the major impediment to effective vitamin D synthesis. Analysis of wild caught potential prey of cats indicated that these animals could supply adequate vitamin D to meet the requirement of growing kittens.     

Daily supplementation with 25 μg cholecalciferol does not increase calcium absorption or skeletal retention in adolescent girls with low serum 25-hydroxyvitamin D

In healthy adolescents, cross-sectional studies show either no or negative relationships between serum 25-hydroxyvitamin D [25(OH)D] and calcium (Ca) absorption. Using a 2-period metabolic balance study, the effect of vitamin D supplementation on Ca absorption and retention in adolescent girls was investigated. Eleven girls aged 12-14 y with a mean entry serum 25(OH)D of 35.1 nmol/L consumed a controlled intake (providing 5 μg vitamin D and 1117 mg Ca/d) for two 3-wk metabolic balance periods separated by a 1-wk washout period. Sunlight exposure was minimized by sunscreen with a sun protection factor ≥ 15. After the first metabolic balance period, participants received 25 μg/d cholecalciferol supplementation for 4 wk. Fractional Ca absorption was measured in each metabolic balance period using a stable Ca isotope method. All urine and fecal samples were collected and analyzed to measure net Ca absorption and Ca retention. Paired t tests and correlations were used to analyze the data. Daily supplementation with 25 μg vitamin D resulted in a mean increase in serum 25(OH)D of 13.3 nmol/L (P < 0.01) but a decrease in fractional Ca absorption of 8.3% (P < 0.05) and no significant change in fasting serum 1,25-dihydroxyvitamin D, parathyroid hormone, net Ca absorption, or Ca skeletal retention. In pubertal girls with vitamin D status considered insufficient in adults, vitamin D supplementation of 25 μg/d for 4 wk did not improve fractional Ca absorption, net Ca absorption, or Ca retention.     

Hypovitaminosis D prevalence and determinants among African American and white women of reproductive age: third National Health and Nutrition Examination Survey, 1988-1994

BACKGROUND: Recent reports of rickets among African American children drew attention to the vitamin D status of these infants and their mothers. African American women are at higher risk of vitamin D deficiency than are white women, but few studies have examined determinants of hypovitaminosis D in this population. OBJECTIVE: We examined the prevalence and determinants of hypovitaminosis D among African American and white women of reproductive age. DESIGN: We examined 1546 African American women and 1426 white women aged 15-49 y who were not pregnant and who participated in the third National Health and Nutrition Examination Survey (1988-1994). Hypovitaminosis D was defined as a serum 25-hydroxyvitamin D concentration < or =37.5 nmol/L. Multiple logistic regression was used to examine the independent association of dietary, demographic, and behavioral determinants of hypovitaminosis D. RESULTS: The prevalence of hypovitaminosis D was 42.4 +/- 3.1% ( +/- SE) among African Americans and 4.2 +/- 0.7% among whites. Among African Americans, hypovitaminosis D was independently associated with consumption of milk or breakfast cereal <3 times/wk, no use of vitamin D supplements, season, urban residence, low body mass index, and no use of oral contraceptives. Even among 243 African Americans who consumed the adequate intake of vitamin D from supplements (200 IU/d), 28.2 +/- 2.7% had hypovitaminosis D. CONCLUSIONS: The high prevalence of hypovitaminosis D among African American women warrants further examination of vitamin D recommendations for these women. The determinants of hypovitaminosis D among women should be considered when these women are advised on dietary intake and supplement use.     

Response to vitamin D supplementation during Antarctic winter is related to BMI, and supplementation can mitigate Epstein-Barr Virus Reactivation

Maintaining vitamin D status without sunlight exposure is difficult without supplementation. This study was designed to better understand interrelationships between periodic vitamin D supplementation and immune function in Antarctic workers. The effect of 2 oral dosing regimens of vitamin D supplementation on vitamin D status and markers of immune function was evaluated in people in Antarctica with no UV light exposure for 6 mo. Participants were given a 2000-IU (50 μg) daily (n = 15) or 10,000-IU (250 μg) weekly (n = 14) vitamin D supplement for 6 mo during a winter in Antarctica. Biological samples were collected at baseline and at 3 and 6 mo. Vitamin D intake, markers of vitamin D and bone metabolism, and latent virus reactivation were determined. After 6 mo, the serum 25-hydroxyvitamin D concentration (mean ± SD) increased from 56 ± 17 to 79 ± 16 nmol/L and from 52 ± 10 to 69 ± 9 nmol/L in the 2000-IU/d and 10,000-IU/wk groups, respectively (main effect over time, P < 0.001). Participants with a greater BMI (participant BMI range = 19–43 g/m2) had a smaller increase in 25-hydroxyvitamin D after 6-mo supplementation (P < 0.05). Participants with high serum cortisol and higher serum 25-hydroxyvitamin D were less likely to shed Epstein-Barr virus in saliva (P < 0.05). The doses given raised vitamin D status in participants not exposed to sunlight for 6 mo, and the efficacy was influenced by baseline vitamin D status and BMI. The data also provide evidence that vitamin D, interacting with stress, can reduce risk of latent virus reactivation during the winter in Antarctica.     

Contribution of dietary protein and inorganic sulfur to urinary sulfate: toward a biomarker of inorganic sulfur intake

BACKGROUND: Sulfiting agents are widely used as food additives. Limits are set on their use in foods because they may adversely affect health. Sulfiting agents are excreted in urine as sulfate, which is indistinguishable from sulfate derived from sulfur amino acids. OBJECTIVE: The objective was to assess the contribution of inorganic sulfur to urinary sulfate excretion and of dietary protein to urinary sulfate and nitrogen excretion with the aim of developing a urinary biomarker of inorganic sulfur intake. DESIGN: Nine healthy men were fed a sequence of 3 diets for 15 d (n = 7), 5 diets for 10 d (n = 6), or both. The diets contained 51-212 g protein/d (0.43-1.71 g S/d) and 0.17-0.27 g inorganic S/d; p-aminobenzoic acid-validated 24-h urine samples (n = 47) were analyzed for sulfate and nitrogen. RESULTS: Dietary inorganic sulfur was efficiently excreted as sulfate in urine. Urinary sulfate derived from protein correlated strongly (r(2) = 0.86) with urinary nitrogen. Urinary recovery of protein sulfur and nitrogen decreased from 84% at average protein intakes (72 g/d) to 70% at high protein intakes (212 g/d). The nitrogen:sulfur ratio (in g) of the protein in the study diets was 18.9, which was maintained in urine (18.4 +/- 0.1) after dietary inorganic sulfur intake was subtracted from urinary sulfate. Therefore, inorganic sulfur intake (g/d) = urinary sulfur (g/d) - 0.054 x urinary nitrogen (g/d). For typical UK intakes of inorganic sulfur (0.25 g/d), this biomarker should produce mean (+/- SD) values of 0.24 +/- 0.10 g S/d. CONCLUSION: Twenty-four-hour urinary nitrogen and sulfate values can be used to predict inorganic sulfur intake.