Vitamin H

The Basics On Vitamin H

What is Vitamin H?

A nutrient in the vitamin B complex that the body needs in small amounts to function and stay healthy.

What are other names for Vitamin H?

1H-THIENO[3,4-D]IMIDAZOLE-4-PENTANOIC ACID, HEXAHYDRO-2-OXO-, (3AS,4S,6AR)-, 1H-THIENO[3,4-D]IMIDAZOLE-4-PENTANOIC ACID, HEXAHYDRO-2-OXO-, [3AS-(3AA ,4B,6AA)]-, 1HTHIENO[3,4D]IMIDAZOLE4PENTANOIC ACID, HEXAHYDRO2OXO, [3AS(3AÃ ,4 ,6AÃ )], BIOTIN, COENZYME R, HEXAHYDRO-2-OXO- [3AS-(3AA ,4B,6AA)]- 1H-THIENO[3,4-D]IMIDAZOLE-4-PENTANOIC ACID, VITAMIN B7, VITAMIN H, [3AS-(3AA ,4B,6AA )]-HEXAHYDRO-2-OXO-1H-THIENO[3,4-D]IMIDAZOLE-4-PENTANOIC ACID, and [3AS-(3AA ,4B,6AA)]- 1H-THIENO[3,4-D]IMIDAZOLE-4-PENTANOIC ACID, HEXAHYDRO-2-OXO-

What is Vitamin H used for?

Vitamin H helps some enzymes break down substances in the body for energy and helps tissues develop. It is found in yeast, whole milk, egg yolks, and organ meats.

How Vitamin H is classified

Vitamins

Recommendations for using Vitamin H during pregnancy and breastfeeding

Limited data suggests no known risk

 

Vitamin H During Pregnancy

What we know about using Vitamin H while pregnant or breastfeeding

Limited information available.

Three groups of six female Holtzman rats, after having a normal estrus for three cycles, were dosed SC with 50 mglkg Biotin in 0.2 ml ofO.l N NaOH in morning and evening injections during the diestrus stage (Paul, Duttagupta, and Agarwal 1973a). The animals were killed 7, 14, or 21 days after dosing. A control group of six rats was given SC an equal volume of 0.1 N NaOH during the diestrus stage and killed after 7 days. The estrus cycle was studied daily, and the leukocyte concentration of vaginal smears was determined. The ovaries were examined microscopically and the hepatic and uterine glycogen concentrations were estimated. The Biotin-treated animals had irregular estrus cycles, and the number of vaginal leukocytes progressively increased until day 14, and then declined sharply. Biotin did not significantly alter ovarian, uterine, or liver weights, and body weight gain was normal. At microscopic examination of the ovaries, it was observed that the process of formation of the corpora lutea was enhanced, but several of the corpora lutea were atrophic. Hepatic glycogen, concentration and total, was significantly reduced after 14 days and returned to control amounts after 21 days. Uterine glycogen, concentration and total, was slightly reduced at 21 days after Biotin treatment. Groups of 12 female Holtzman rats were dosed with 50 mglkg Biotin dissolved in 0.5 ml of 0.1 N NaOH in two SC injections (Paul, Duttagupta, and Agarwall973b ). The rats were then mated with untreated males 7, 14, or 21 days after dosing. An untreated group of 12 rats was the negative-control group. Six rats of each group were killed on day 14 of gestation, and the remaining six were killed on day 21 of gestation. A group of six rats was treated with Biotin and mated, and the animals in this group were given 1 f.1,g 17 ,B-estradiol in 0.1 ml olive oil on days 6 to 21 of gestation. Another group of six rats was dosed SC with 100 mg/kg Biotin in 1 ml of 0.1 N NaOH in four injections for 2 days. The animals of these two groups were killed on day 21 of gestation. Of the animals killed on day 14 of gestation, six, four, and three mated 7, 14, and 21 days after dosing, respectively, had fetuses. Of the animals killed on day 21 of gestation, two, three, and one mated 7, 14, and 21 days after dosing, respectively, had fetuses. All negative-control animals had fetuses at both 14 and 21 days of gestation, and all of the animals given 17 ,B-estradiol had fetuses. None of the animals dosed with 100 mglkg Biotin mated in the 2 months following dosing. The fetal and placental weights of the existing neonates of animals dosed with 50 mglkg Biotin were decreased as compared to negative control values. The fetal and placental weights of neonates of animals given 17 .B -estradiol were comparable to those of the negative controls. SPF outbred rats (lbm:ROROt) were dosed SC with 5 or 50 mglkg d-Biotin in 0.1 N NaOH, pH 12, given in two doses 5 hours apart on the day of vaginal estrus (Mittelholzer 1976). One control group of eight animals was given SC 0.1 N NaOH, and an untreated control group of seven animals was not dosed. Groups of eight animals were mated 7, 14, and 21 days after dosing and killed and examined on day 21 of gestation. Significant differences were not observed in the number of implantations per gravid animal, the number of resorption sites, fetal weight, placental weight, ovary weight, or in the number of animals with irregular cycles or without evidence of mating between treated animals and animals of the control groups. The only difference observed was in the number of gravid animals. For the animals mated 7 days after dosing, 6/7, 8/8, and 7/8 animals of the 5-mg/k.g, 50-mg/k.g, or untreated-control groups, respectively, mated and 88%,71%, and 67%, respectively, of the animals that mated had fetuses on day 21 of gestation. Of the animals mated 14 or 21 days after dosing, all of the animals of each group mated, and 63%, 88%, and 100% of the animals in the 5-mg/k.g, 50-mg/k.g, or untreated-control groups, respectively, had fetuses on day 21 of gestation. Lesions were not observed in the ovaries at microscopic examination. Groups of Holtzman rats were mated and the gravid females were dosed SC with 100 mg D(+)-Biotin in 0.2 ml of 0.1 N NaOH/kg body weight on days 0 and 1 of gestation (Paul and Duttagupta 1975). Nine animals were dosed with Biotin only, seven were given Biotin and 0.1 f.1,g 17 ,B-estradiol in 0.05 ml olive oil SC on days 5 to 20 of gestation, and seven were given Biotin and 4 mg progesterone in 0.2 ml olive oil SC on days 5 to 20 of gestation. Nine gravid animals were untreated and used as a negative-control group. Three groups of six nongravid animals were dosed in the same manner as the gravid animals and used as nonpregnant treated controls. The animals were killed and examined on day 21 of gestation. Complete resorption of the fetuses occurred in eight of the nine rats dosed with Biotin only; dosing with estrogen or progesterone prevented the resorptions. Fetal and placental weights from animals dosed with Biotin and estrogen or progesterone were decreased as compared to controls, but the decrease was not statistically significant. Biotin caused a decrease in body weights of gravid and nongravid animals; body weights of gravid animals given Biotin and progesterone were similar to gravid untreated control, whereas body weights of gravid animals given Biotin and estrogen were increased. The uterine weights of Distributed for comment only — do not cite or quote BIOTIN 9 gravid animals given Biotin and estrogen were similar to that of gravid untreated controls, whereas the uterine weights of animals dosed with Biotin and progesterone were statistically significantly decreased. The hepatic glycogen concentration of the gravid animals of all treatment groups and of the nongravid animals given Biotin only was similar to that of gravid controls; a decrease in the hepatic glycogen concentration was observed for nongravid animals dosed with Biotin and estrogen or progesterone. A statistically significant decrease in uterine glycogen concentration was observed in the animals dosed with Biotin that had resorptions. The hepatic RNA concentration was statistically significantly reduced in gravid animals dosed with Biotin, but the uterine concentrations were not affected. Hepatic RNA concentrations of gravid animals dosed with Biotin and estrogen were similar to those of untreated gravid controls, whereas uterine RNA concentrations of animals of this group were greater than control values. A statistically significant increase in uterine DNA concentrations occurred in rats that were dosed with Biotin and had resorptions; uterine DNA concentrations of gravid animals dosed with Biotin and estrogen or progesterone were similar to control values. Hepatic and uterine protein concentrations were statistically significantly decreased in gravid animals dosed with Biotin; uterine protein concentrations of gravid animals dosed with Biotin and estrogen were similar to those of gravid controls. Glucose-6-phosphate dehydrogenase (G-6-PD) activity in the ovaries, adrenal glands, liver, and uterus of gravid animals dosed with Biotin were statistically significantly decreased as compared to gravid untreated controls; dosing with estrogen or progesterone in addition to Biotin significantly increased the enzymic activity as compared to animals given Biotin only, but the values were still lower than those of controls. In a similar study, groups of Holtzman rats were mated, and gravid females were dosed with 100 mg D(+)-Biotin in 0.2 ml of 0.1 N NaOH/kg body weight on days 13 and 14 of gestation (Paul and Duttagupta 1976). Eleven animals were dosed with Biotin only, seven were given Biotin and 0.1 {tg 17 ,8-estradiol in 0.05 ml olive oil SC until day 20 of gestation, and seven were given Biotin and 4 mg progesterone in 0.2 ml olive oil SC until day 20 of gestation. Nine gravid animals were untreated and used as a negative-control group. The animals were killed and examined on day 21 of gestation. Resorptions occurred in 2 of the 11 animals dosed with Biotin only. The maternal body weights and the fetal, uterine, and placental weights of the remaining nine animals of this group were statistically significantly decreased as compared to controls. The maternal body weights and the fetal, uterine, and placental weights of the animals dosed with Biotin and estrogen and the maternal body weights and uterine weights of the animals dosed with Biotin and progesterone were similar to control values. Hepatic and ovarian weights were similar for animals of the test and control groups. Dosing with Biotin or Biotin and progesterone resulted in a statistically significant decrease in uterine and placental glycogen concentrations; this decrease was not observed upon dosing with Biotin and estrogen. Hepatic glycogen and blood glucose concentrations were similar for animals of the treated and control groups. Biotin and Biotin plus progesterone caused a statistically significant decrease in the amount of hepatic protein. Hepatic RNA concentrations were statistically significantly increased by Biotin and estrogen. Ovarian, uterine, and hepatic, but not adrenal gland or placental, G-6-PD activity was statistically significantly decreased in animals dosed with Biotin; in animals dosed with Biotin and estrogen, adrenal gland G-6-PD activity was statistically significantly reduced. ICR mice were dosed with Biotin orally or SC to determine the reproductive and developmental effects of Biotin (Watanabe 1996). Groups of gravid mice were fed 0 or 1000 mg/kg Biotin (0.1%) in commercial feed throughout gestation, dosed SC with 0 or 150 mg/kg Biotin in olive oil, or dosed SC with 0 or 50 mg/kg Biotin in 0.1 N NaOH, pH 11; the animals of the SC groups were dosed with 0.5 ml in three abdominal regions on days 0, 6, and 12 of gestation. An untreated control group was fed commercial diet. The animals were killed and examined on day 17 of gestation. The Biotin concentration of maternal and fetal organs was determined microbiologically, and the biotinidase activity of mice in the dietary group was measured on day 17 of gestation. All animals were observed daily for signs of toxicity and any deaths were recorded. No signs of toxicity, behavioral changes, and mortality were observed. The number of resorbed or dead fetuses was slightly increased in the group dosed with Biotin in olive oil as compared to the group dosed with Biotin in NaOH; however, in none of the test groups was the increase statistically significant when compared to the untreated control group. Maternal body weight gain of all groups was statistically significantly decreased as compared to the untreated controls, but this difference was not attributed to Biotin. Fetal parameters were similar for all test groups, and a significant difference in external malformations was not observed between the Biotin-treated and untreated control groups. No microscopic differences in the maternal liver, placenta, or ovaries were observed. In the treated groups, Biotin accumulation was observed in maternal and fetal organs. A statistically significant increase in biotinidase activity was observed in the maternal serum and the placenta of rats fed Biotin as compared to controls, but no changes were observed in serum estradiol-E2 content between these groups. The researcher concluded that Biotin “did not disturb normal reproductive functions or embryonic development” in mice.

General safety info about Vitamin H from CIR

No report found.

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