Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VITAMIN D”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1984

Simultaneous measurement of 1.25-dihydroxy-vitamin D, 24.25-dihydroxy-vitamin D and 25-hydroxy-vitamin D from a single two milliliters serum specimen. Preliminary clinical application.

A simple method for extraction, purification and separation of the principal vitamin D metabolites from a single serum sample is described. The method involved extraction of serum with acetonitrile followed by a first purification employing C-18 Sep-pak cartridges eluted with methanol/water and acetonitrile. Final separation before assay was carried out by high pressure liquid chromatography. 1.25-dihydroxy-vitamin D was measured with radioimmunoassay using an antiserum (S11) with high selectivity for 1 alpha-OH function of the hormone at a final dilution of 1:100,000. 24.25-dihydroxy-vitamin D and 25-hydroxy-vitamin D were measured employing a competitive binding assay with normal rat serum at a final dilution of 1:10,000 as source of binding protein. The mean (+/- SD) serum 1.25-dihydroxy-vitamin D, 24.25-dihydroxy-vitamin D and 25-hydroxy-vitamin D concentrations for a group of healthy subjects were 50.4 +/- 17.3 pg/ml, 2.3 +/- 2.6 ng/ml and 20.8 +/- 12.3 ng/ml, respectively. 1.25-dihydroxy-vitamin D concentrations were low or undetectable in patients on dialysis or with mild renal failure. High 1.25-dihydroxy-vitamin D levels were found in 2 out of 17 patients with primary hyperparathyroidism. In 4 normal subjects treated for two weeks with large doses of 25-hydroxy-vitamin D, serum 25-hydroxy-vitamin D rose from 12.5 ng/ml to 119 ng/ml and from 0.89 ng/ml to 15 ng/ml, respectively; no changes in the 1.25-dihydroxy-vitamin D assay were found.

24,25-Dihydroxyvitamin D 3↗
PubMed1986

The metabolism and functions of vitamin D.

Vitamin D functions by stimulating intestinal calcium and phosphorus absorption, by stimulating bone calcium mobilization, and by increasing renal reabsorption of calcium in the distal tubule. These functions on bone and possibly kidney, but not intestine, require the parathyroid hormone. As a result of these functions, serum calcium and phosphorus concentrations are elevated to supersaturating levels required for the mineralization of bone to prevent rickets, osteomalacia, and hypocalcemic tetany. Recent experiments demonstrate that maintaining serum calcium and phosphorus levels in vitamin D-deficient rats in the normal range results in normal bone growth and mineralization. However, increased calcification results because bone resorption by osteoclasts is a vitamin D-dependent process. Thus, bone resorption, modeling and remodeling must be considered vitamin D-dependent processes. Vitamin D must be metabolized to 25-hydroxyvitamin D3 by the liver and subsequently by the kidney to 1,25-dihydroxyvitamin D3 before function. 1,25-Dihydroxyvitamin D3 is metabolized to a C-23 carboxylic acid (calcitroic acid) but the pathway is unknown. Although 25-hydroxyvitamin D3 is metabolized to 24R,25-dihydroxyvitamin D3, 25,26-dihydroxyvitamin D3 and 25-hydroxyvitamin D3-26,23-lactone, these pathways play no role in the function of vitamin D as shown by appropriate fluoro analogs of 25-hydroxyvitamin D3. 1,25-Dihydroxyvitamin D3 binds to a specific receptor in the intestinal nuclei to elicit a stimulation of calcium transport. 1,25-Dihydroxyvitamin D3 plus the receptor causes transcription of specific genes that code for calcium and phosphorus transport proteins. Only one protein, the calcium binding protein, has been identified as being vitamin D dependent. Two others have been described, but no clear description of the molecular mechanism of action of 1,25-dihydroxyvitamin D3 is yet available.

Animals↗
PubMed1981

[Calcium binding by rat small intestine epithelium microvilli at different contents of vitamin D].

Vitamin D does not essentially affect the association constants and the number of sites of Ca2+ binding by small intestine epithelium microvilli. Ca2+ binding to the lipids isolated from the microvilli is similar to Ca2+ binding by intact microvilli in some parameters, e. g. existence of two types of binding sites, values of association constants and number of sites. This is in agreement with the assumption on the possible role of phospholipids in the mechanism of Ca2+ binding by the microvilli. The deficiency of vitamin D does not affect Ca2+ binding by microvilli lipids. The data obtained suggest that the insufficiency of Ca2+ transport in the intestine under vitamin D deficiency probably affects Ca2+ transfer processes other than Ca2+ binding to the microvilli membrane.

25-Hydroxyvitamin D 2↗
PubMed2003

[Intestinal calcium absorption and vitamin D].

Vitamin D is required for efficient absorption of dietary Ca. Accumulated observations indicated that active form of vitamin D is involved in the three steps of intestinal Ca absorption:incorporation of Ca by epithelial cells through brush border membrane, intracellular Ca movement, and excretion of Ca into systemic circulation via basolateral membrane. It is also known that activated vitamin D takes part in growth and differentiation of intestinal epithelial cells.

English Abstract↗
PubMed2006

Effect of vitamin D supplementation on vitamin D status and bone turnover markers in young adults.

OBJECTIVE: To assess the vitamin D status of healthy young people living in Northern Ireland and the effect of vitamin D supplementation on vitamin D status and bone turnover. DESIGN: Double-blinded randomised controlled intervention study. SETTING: University of Ulster, Coleraine, Northern Ireland. SUBJECTS: In total, 30 apparently healthy students (15 male and 15 female subjects), aged 18-27 years, were recruited from the university, with 27 completing the intervention. INTERVENTIONS: Subjects were randomly assigned, to receive either 15 microg (600 IU) vitamin D(3) and 1,500 mg calcium/day (vitamin D group), or 1,500 mg calcium/day (control group) for 8 weeks between January and March. Vitamin D status, bone turnover markers, serum calcium and parathyroid hormone concentrations were measured at baseline and post intervention. RESULTS: At baseline, vitamin D status was low in both the vitamin D group (47.9 (s.d. 16.0)) and the control group (55.5 (s.d. 18.6) nmol/l 25(OH)D). Post intervention vitamin D status was significantly higher in the vitamin D-treated group (86.5 (s.d. 24.5)) compared to the control group (48.3 (s.d. 16.8) nmol/l) (P<0.0001). There was no significant effect of supplementation on bone turnover markers or PTH concentrations. CONCLUSIONS: This study suggests that young adults in Northern Ireland do not consume an adequate daily dietary intake of vitamin D to maintain plasma vitamin D concentrations in the wintertime. A daily supplement of 15 microg vitamin D(3) significantly increased vitamin D status in these individuals to levels of sufficiency. Achievement of an optimum vitamin D status among young adults may have future positive health implications.

Adolescent↗
PubMed2002

Vitamin D intake and vitamin D status of Australians.

The main source of vitamin D for Australians is exposure to sunlight. Thus, levels of serum 25-hydroxyvitamin D(3), the indicator of vitamin D status, vary according to the season and are lower at the end of winter. In Australia and New Zealand, the prevalence of vitamin D deficiency varies, but is acknowledged to be much higher than previously thought. One study found marginal deficiency in 23% of women, and another frank deficiency in 80% of dark-skinned and veiled women. The groups at greatest risk of vitamin D deficiency in Australia are dark-skinned and veiled women (particularly in pregnancy), their infants, and older persons living in residential care. Only a few foods (eg, fish with a high fat content) contain significant amounts of vitamin D. In Australia, margarine and some milk and milk products are currently fortified with vitamin D. The average estimated dietary intake of vitamin D for men is 2.6-3.0 g/day and for women is 2.0-2.2 g/day. The estimated dietary requirement of vitamin D is at least 5.0 g/day and may be higher for older people. Adequate intake of vitamin D is unlikely to be achieved through dietary means, particularly in the groups at greatest risk, although vitamin D-fortified foods may assist in maintaining vitamin D status in the general population. An appropriate health message for vitamin D needs to balance the need for sunshine against the risk of skin cancer.

Adult↗
PubMedDate not supplied

Maternal vitamin D deficiency and vitamin D supplementation in healthy infants.

The objective of this study was to evaluate the common effects of maternal vitamin D deficiency, various doses of vitamin D given to newborns and the effects of these on vitamin D status in early childhood. Seventy-eight pregnant women and 65 infants who were followed up in various health centers were included in the sudy. 25-hydroxyvitamin-D (25-OHvitD), calcium (Ca), phosphorus (P) and alkaline phosphatase levels were measured in blood samples drawn from pregnant women in the last trimester. Infants born to these mothers were given 400 or 800 IU of vitamin D subsequently at the start of the second week. 25-OHvitD, Ca, P and alkaline phosphatase levels of the 65 infants who were brought in for controls (May-September 2000) were measured and hand-wrist X-rays were evaluated. We analyzed the relationship between vitamin D status of the mothers and infants and socio-economic status; mothers' dressing habits (covered vs uncovered), educational level, and number of pregnancies; and sunlight exposure of the house. Covered as a dressing habit meant covering the hair and sometimes part of the face and wearing dresses that completely cover the arms and legs. In 40 infants who were breast-fed and received the recommended doses of vitamin D on a regular basis, the relationship between serum vitamin D levels and supplementation doses given was analyzed. Serum 25-OHvitD level of the mothers was 17.50 +/- 10.30 and 94.8% of the mothers had a 25-OHvitD level below 40 nmol/L (below 25 nmol/L in 79.5%). The risk factors associated with low maternal 25-OHvitD were low educational level (p = 0.042), insufficient intake of vitamin D within diet (p = 0.020) and "covered" dressing habits (p = 0.012). 25-OHvitD level of the infants was 83.70 +/- 53.70 nmol/L, and 24.6% of the infants had 25-OHvitD levels lower than 40 nmol/L. Risk factors for low 25-OHvitD levels in infants were a) not receiving recommended doses of vitamin D regularly (p = 0.002) and b) insufficient sunlight exposure of the house (p = 0.033). There was a pour but significant correlation between maternal vitamin D levels and infants' 25-OHvitD levels at four months (r = 0.365, p < 0.05). No significant correlation was found between 25-OHvitD levels and supplementation doses of vitamin D (19 infants were supplemented with 400 IU/day and 21 with 800 IU/day of vitamin D) (p = 0.873). Severe maternal vitamin D deficiency remains a commonly seen problem in Turkey. However, vitamin D deficiency can be prevented by supplementation of vitamin D to newborns (at least 400 IU). Supplementation of 800 IU vitamin D in the areas of maternal vitamin D deficiency has no greater benefits for the infants.

Adult↗
PubMed1986

Relationships among vitamin D, 25-hydroxyvitamin D, and vitamin D-binding protein concentrations in the plasma and milk of human subjects.

We measured plasma and milk concentrations of vitamin D2, vitamin D3, 25-hydroxyvitamin D2 (25OHD2), 25-hydroxyvitamin D3 (25OHD3), and vitamin D-binding protein (DBP) in a group of lactating women. All vitamin D compounds were quantitated using competitive protein binding assay, while DBP concentrations were determined by rocket electrophoresis. Vitamin D3 was the most abundant vitamin D compound in human milk, followed by vitamin D2, 25OHD3, and, finally, 25OHD2. The average vitamin D activity in milk was between 33-68 IU/liter, depending on the criterion of biological activity used. DBP concentrations in milk were approximately 3% of those in plasma. Significant relationships were found between plasma and milk levels for all vitamin D compounds. The milk to blood concentration ratio was greatest for vitamin D2, followed by vitamin D3, 25OHD2, and 25OHD3. (Thus, the parent compounds gained access into milk in a much more efficient fashion than their 25-hydroxy metabolites. It is postulated that this differential translocation is controlled by the DBP in the circulation.) There was no significant correlation between plasma and milk DBP concentrations, nor were milk DBP concentrations related to the vitamin D content of milk. This investigation supports the concept that the nutritional status of lactating mothers affects the vitamin D sterol potential of her milk which, in turn, would likely have an effect on the vitamin D status of her nursing infant.

25-Hydroxyvitamin D 2↗
PubMed1995

Serum levels of free 1,25-dihydroxyvitamin D in vitamin D toxicity.

OBJECTIVE: To determine the serum level of free 1,25-dihydroxyvitamin D [1,25-(OH)2D] in patients with vitamin D toxicity and to assess the in vitro effect of differing concentrations of vitamin D metabolites on the free serum levels of 1,25-(OH)2D. DESIGN: 1) A case study of patients hospitalized with vitamin D toxicity after accidentally ingesting a veterinary vitamin D concentrate and 2) an in vitro experiment in which vitamin D metabolites in various concentrations were added to normal serum and their effect was noted on percentage of free 1,25-(OH)2D. PATIENTS: 11 patients (age range, 8 to 69 years) were studied 10 to 40 days after hospitalization for hypercalcemia. MEASUREMENTS: Serum total 25-hydroxyvitamin D (25-OHD) and 1,25-(OH)2D levels were measured by radioreceptor assays. The percentage of free 1,25-(OH)2D was measured by centrifugal ultrafiltration isodialysis and was used to calculate actual free 1,25-(OH)2D levels. In the in vitro studies, vitamin D metabolites [25-OHD; 24,25-(OH)2D; 25,26-(OH)2D; and 25-OHD-26,23 lactone] were added to normal serum in concentrations expected to occur with vitamin D toxicity. The percentage of free 1,25-(OH)2D was measured by isodialysis. RESULTS: All patients presented with marked hypercalcemia (mean calcium level, 3.99 +/- 0.33 mmol/L). Serum 25-OHD levels ranged from 847 to 1652 nmol/L, and total 1,25-(OH)2D levels (mean, 106 +/- 86 pmol/L) were elevated in only three patients. The percentage of free 1,25-(OH)2D (mean, 1.023% +/- 0.366%) was elevated in all nine patients in whom it was measured. Actual free 1,25-(OH)2D levels (mean, 856 +/- 600 fmol/L) were elevated in six of the nine patients. Total 1,25-(OH)2D levels were correlated with 25-OHD levels (r = 0.66; P = 0.03), whereas total and free 1,25-(OH)2D levels were highly correlated (r = 0.957; P < 0.001). In the in vitro studies, the percentage of free 1,25-(OH)2D increased after 25-OHD or 24,25-(OH)2D was added. CONCLUSIONS: Although the patients had normal or near-normal total 1,25-(OH)2D values, most patients had elevated free 1,25-(OH)2D levels. These findings suggest that elevated free 1,25-(OH)2D levels might play a role in the pathogenesis of hypercalcemia in vitamin D toxicity.

Adolescent↗
PubMed1999

Vitamin D therapy of osteoporosis: plain vitamin D therapy versus active vitamin D analog (D-hormone) therapy.

Normal intestinal calcium (Ca) absorption is an essential feature of bone homeostasis. As with many other organ systems, intestinal Ca absorption declines with aging, and this is one pathological factor that has been identified as a cause of senile osteoporosis in the elderly. This abnormality leads to secondary hyperparathyroidism, which is characterized by high serum parathyroid hormone (PTH) and an increase in bone resorption. Secondary hyperparathyroidism due to poor intestinal Ca absorption has been implicated not only in senile osteoporosis but also in age-related bone loss. Accordingly, in population-based studies, there is a gradual increase in serum PTH from about 20 years of age onward, which constitutes a maximum increase at 80 years of age of 50% of the basal value seen at 30 years of age. The cause of the increase in PTH is thought to be partly due to impaired intestinal Ca absorption that is associated with aging, a cause that is not entirely clear but at least in some instances is related to some form of vitamin D deficiency. There are three types of vitamin D deficiency: (1) primary vitamin D deficiency, which is due to a deficiency of vitamin D, the parent compound; (2) a deficiency of 1,25(OH)(2)D(3) resulting from decreased renal production of 1,25(OH)(2)D(3); and (3) resistance to 1,25(OH)(2)D(3) action owing to decreased responsiveness to 1, 25(OH)(2)D(3) of target tissues. The cause for the resistance to 1, 25(OH)(2)D(3) could be related to the finding that the vitamin D receptor level in the intestine tends to decrease with age. All three types of deficiencies can occur with aging, and each has been implicated as a potential cause of intestinal Ca malabsorption, secondary hyperparathyroidism, and senile osteoporosis. There are two forms of vitamin D replacement therapies: plain vitamin D therapy and active vitamin D analog (or D-hormone) therapy. Primary vitamin D deficiency can be corrected by vitamin supplements of 1000 U a day of plain vitamin D whereas 1,25(OH)(2)D(3) deficiency/resistance requires active vitamin D analog therapy [1, 25(OH)(2)D(3) or 1alpha(OH)D(3)] to correct the high serum PTH and the Ca malabsorption. In addition, in the elderly, there are patients with decreased intestinal Ca absorption but with apparently normal vitamin D metabolism. Although the cause of poor intestinal Ca absorption in these patients is unclear, these patients, as well as all other patients with secondary hyperparathyroidism (not due to decreased renal function), show a decrease in serum PTH and an increase in Ca absorption in response to therapy with 1, 25(OH)(2)D(3) or 1alpha(OH)D(3). In short, it is clear that some form of vitamin D therapy, either plain vitamin D or 1,25(OH)(2)D(3) or 1alpha(OH)D(3), can be used to correct all types of age-dependent impairments in intestinal Ca absorption and secondary hyperparathyroidism during aging. However, from a clinical standpoint, it is important to recognize the type of vitamin D deficiency in patients with senile osteoporosis so that primary vitamin D deficiency can be appropriately treated with plain vitamin D therapy, whereas 1,25(OH)(2)D(3) deficiency/resistance will be properly treated with 1,25(OH)(2)D(3) or 1alpha(OH)D(3) therapy. With respect to postmenopausal osteoporosis, there is strong evidence that active vitamin D analogs (but not plain vitamin D) may have bone-sparing actions. However, these effects appear to be results of their pharmacologic actions on bone formation and resorption rather than through replenishing a deficiency.

Aging↗
PubMed2004

Overview of general physiologic features and functions of vitamin D.

Vitamin D3 is a prohormone produced in skin through ultraviolet irradiation of 7-dehydrocholesterol. It is biologically inert and must be metabolized to 25-hydroxyvitamin D3 in the liver and then to 1alpha,25-dihydroxyvitamin D3 in the kidney before function. The hormonal form of vitamin D3, ie, 1alpha,25-dihydroxyvitamin D3, acts through a nuclear receptor to carry out its many functions, including calcium absorption, phosphate absorption in the intestine, calcium mobilization in bone, and calcium reabsorption in the kidney. It also has several noncalcemic functions in the body. This overview provides a brief description of the physiologic, endocrinologic, and molecular biologic characteristics of vitamin D. It also provides information on new selective analogs of 1alpha,25-dihydroyvitamin D3 for therapy.

Bone and Bones↗
PubMed1989

Vitamin D requirements and vitamin D intoxication in infancy.

Without vitamin D supplementation, the majority of infants seems to be at risk of vitamin D-deficiency rickets. On the other hand, routine vitamin D supplementation of breast-fed infants is not recommended by all authors. In this paper we give an overview of vitamin D metabolism and vitamin D regulation in newborns, which may differ in a certain way from the regulation in adults. Based on this, minimal and optimal requirements for vitamin D in newborns and infants is determined. Furthermore, the paper aims at defining dosages and conditions that are at risk of vitamin D intoxication.

Humans↗
PubMed2001

Serum concentrations of vitamin D metabolites, vitamins A and E, and carotenoids in six canid and four ursid species at four zoos.

Nutritional status for six captive canid species (n=34) and four captive ursid species (n=18) were analyzed. The species analyzed included: African wild dog (Lycaon pictus), arctic fox (Alopex lagopus), gray wolf (Canis lupus), maned wolf (Chrysocyon brachyurus), Mexican wolf (Canis lupus baleiyi), red wolf (Canis rufus), brown bear (Ursus arctos), polar bear (Ursus maritimus), spectacled bear (Tremarctos ornatus), and sun bear (Ursus malayanus). Diet information was collected for these animals from each participating zoo (Brookfield Zoo, Fort Worth Zoo, Lincoln Park Zoological Gardens, and North Carolina Zoological Park). The nutritional composition of the diet for each species at each institution met probable dietary requirements. Blood samples were collected from each animal and analyzed for vitamin D metabolites 25(OH)D and 1,25(OH)(2)D, vitamin A (retinol, retinyl stearate, retinyl palmitate), vitamin E (alpha-tocopherol and gamma-tocopherol) and selected carotenoids. Family differences were found for 25(OH)D, retinol, retinyl stearate, retinyl palmitate and gamma-tocopherol. Species differences were found for all detectable measurements. Carotenoids were not detected in any species. The large number of animals contributing to these data, provides a substantial base for comparing the nutritional status of healthy animals and the differences among them.

Animals↗
PubMed2001

Vitamin D, calcium, and vitamin D receptor polymorphism in colorectal adenomas.

Experimental studies suggest that vitamin D and calcium protect against cancer by reducing proliferation and inducing differentiation. The effects of vitamin D and calcium may be mediated by the vitamin D receptor (VDR), which is encoded by the VDR gene. The present study investigated whether calcium intake and serum vitamin D, as an integrated measure of intake and endogenous production, were associated with risk of colorectal adenoma, known precursors of invasive colorectal cancer. In addition, the interrelation among vitamin D, calcium, and FokI polymorphism of the VDR gene was investigated. Persons (239) with histologically confirmed colorectal adenomas and 228 control individuals without colorectal adenomas confirmed by sigmoidoscopy were enrolled in this case control study conducted at the National Naval Medical Center, Bethesda, MD. We observed an inverse association of serum 25-OH vitamin D [25-(OH)D] with colorectal adenoma. With each 10 ng/ml increase of serum 25-(OH)D, the risk of colorectal adenoma decreased by 26% (odds ratio 0.74, 95% confidence interval 0.60-0.92). The results provided limited evidence for a weak association between calcium intake and colorectal adenoma (odds ratio 0.97, 95% confidence interval 0.93-1.01 per each 100-mg calcium intake). However, the inverse association of serum 25-(OH)D with colorectal adenoma is suggested to be stronger in subjects with calcium intake above the median (P for multiplicative interaction 0.13). The VDR FokI polymorphism was not significantly associated with colorectal adenoma and did not modify the effect of vitamin D or calcium. In conclusion, the study results suggested a protective effect for vitamin D on colorectal adenoma.

Adenoma↗
PubMed1954

The second international standard for vitamin D: crystalline vitamin D3.

This report was presented to the Subcommittee on Fat-Soluble Vitamins of the WHO Expert Committee on Biological Standardization in 1949 by the Vitamin D Sub-Committee of the Accessory Food Factors Committee of the Medical Research Council of Great Britain and formed the evidence on which the first-mentioned subcommittee based its recommendation of the adoption of crystalline vitamin D(3) as the International Standard for Vitamin D, replacing the solution of irradiated ergosterol which had been adopted as Standard in 1931.The Vitamin D Sub-Committee organized a collaborative assay in which 32 laboratories in seven countries participated. In addition to 29g of crystalline vitamin D(3) generously contributed by five firms, the following preparations were compared for vitamin D activity by biological tests on rats or chicks or both: the then current International Standard, a preparation of the purest calciferol obtainable, the British Standards Institution (BSI) Standard, the United States Pharmacopeia (USP) Reference Cod Liver Oil, and the Swedish provisional standard.Altogether 29 rat assays and 25 chick assays were carried out, and the results were subjected to standard methods of analysis. The BSI Standard and the pure calciferol were found less potent than the Old Standard (potency ratios: 0.916 and 0.933, respectively); and the New Standard may be slightly less potent (0.981), but it is more potent than the BSI Standard (1.071). The USP Reference Oil is less potent than the BSI Standard (0.949), the Old Standard (0.896), and the New Standard (0.886). The fiducial range is generally less than 10%, but even where it is greater, it is still satisfactory for a biological test.

Animals↗
PubMed1977

[Methods for determination of vitamins by means of high performance liquid chromatography (HPLC). I. Determination of vitamin D in vitamin concentrates, vitamin mixtures and mineral feedstuffs].

A method is described for the determination of vitamin D in vitamin-concentrates, -mixtures, and mineral feedstuffs. After saponification of the sample, vitamin D is extracted and purified on two columns. Vitamin D is separated by HPLC and determined photometrically.

Chromatography, High Pressure Liquid↗
PubMed1988

25-Hydroxyvitamin D and vitamin D in human milk: effects of supplementation and season.

Breast-milk 25-hydroxyvitamin D (25-[OH]D) and vitamin D were measured in mothers supplemented with 2000 or 1000 IU (50 or 25 micrograms) of vitamin D/d or with no supplementation. Fore- and hindmilk samples were collected at two stages of lactation (8 and 15 or 20 wk after delivery) and at different seasons. Season affected the levels of 25-(OH)D and vitamin D. The 25-(OH)D levels were higher in hind- than in foremilk. Supplementation had no effect on vitamin D levels. Milk 25-(OH)D levels of mothers receiving either 1000 or 2000 IU (25 or 50 micrograms) vitamin D/d were significantly higher than those of unsupplemented mothers in February and April. In theory, supplementation with 2000 IU (50 micrograms) vitamin D should have increased the calculated antirachitic activity of the milk in winter to the levels of unsupplemented mothers in September; however, responses varied widely among individuals.

Breast Feeding↗
PubMed1986

Serum concentrations of vitamin D metabolites in vitamin D supplemented pregnant women. A longitudinal study.

The serum concentrations of the vitamin D metabolites 25-OHD, 1,25-(OH)2D, 24,25-(OH)2D and 25,26-(OH)2D, and of vitamin D binding protein (DBP), were determined longitudinally in 22 vitamin D supplemented pregnant women, and in 17 age-matched non-pregnant women studied during the summer. The pregnant women had higher 25-OHD and 1,25-(OH)2D, similar 24,25-(OH)2D, and lower 25,26-(OH)2D concentrations than the non-pregnant group. The relative concentrations of 24,25-(OH)2D and 25,26-(OH)2D (expressed as the molar ratio of these metabolites to 25-OHD) were lower during pregnancy. The DBP levels were increased in pregnancy, but the calculated free fraction (i.e. not bound to DBP) of the hormonal form of vitamin D, 1,25-(OH)2D, was still persistently higher in the pregnant than in the non-pregnant women. The study suggests that a daily vitamin D supplement of 400 IU satisfies the vitamin D requirement of pregnant women living in a cool climate with limited sun exposure. The increased absolute and relative concentration of 1,25-(OH)2D and decreased relative levels of 24,25-(OH)2D and 25,26-(OH)2D further suggest that the increased intestinal calcium and phosphate absorption, which is known to occur during pregnancy, is at least partially mediated by the vitamin D endocrine system.

24,25-Dihydroxyvitamin D 3↗