from 2 hours up to 4 days, this is too much of a variance.
Would anyone know how long water soluble vitamins last within the body before they are excreted?
Thank you in advance, reps for your help
The water-soluble vitamins, excluding vitamin C, popularly are termed the B-complex vitamins. There are eight of them, namely; B1 (thiamine), B2 (riboflavin), B6 (pyridoxine), niacin (nicotinic acid), B12, folic acid, pantothenic acid, and biotin. The water-soluble vitamins, inactive in their so-called free states, must be activated to their coenzyme forms. B-complex vitamins and vitamin C are water-soluble vitamins that are not stored in the body and must be replaced each day, preferably through a high-quality liquid multivitamin..
The water-soluble vitamins are absorbed in our intestine, pass directly to the blood, and are carried to the tissues in which they will be utilized. Vitamin B12 requires a substance known as ?intrinsic factor for absorption".
Water-soluble vitamins usually are excreted in the urine on a daily basis. Thiamine (B1), riboflavin (B2), pyridoxine (B6), ascorbic acid (C), pantothenic acid, and biotin appear in urine as free vitamins Tissue storage capacity of water soluble vitamins is limited and, as the tissues become saturated, the rate of excretion increases sharply. This keeps us from overdosing but this is also why we need to take these vitamins daily. Unlike the other water-soluble vitamins, however, vitamin B12 is excreted solely in the feces. Some folic acid and biotin is also normally excreted in this way. Although fecal excretion of water-soluble vitamins (other than vitamin B12, folic acid, and biotin) occurs, their source probably is the intestinal bacteria, which synthesize the vitamins, rather than vitamins that we have eaten and used.
Water-soluble vitamins consist of the B vitamins and vitamin C. With exception of vitamin B6 and B12, they are readily excreted in urine without appreciable storage, so frequent consumption becomes necessary.
The Metabolism of Small Doses of Vitamin B-6 in Men
The metabolism of small doses of pyridoxine (PN) and of equimolar doses of PN, pyridoxal (PL) and pyridoxamine (PM) was studied in five men. Fasting subjects were given 0, 0.5, 1, 2, 4 and 10 mg pyridoxine HCl and 19.45 ?moles of PN, PM and PL; one dose was administered a week. Plasma total vitamin B-6 (B-6) and pyridoxal phosphate (PLP), and urinary B-6 and 4-pyridoxic acid (4PA) were determined in timed blood and urine samples collected after each dose. The PN doses had a significant (P < 0.01) overall effect on all of these measurements; the relationship between PN level and the subjects' responses was linear (P < 0.01). Plasma B-6 peaked at 0.5 or 1 hour after the PN doses; PLP at 0.5, 1 or 3 hours, depending on size of dose. Plasma B-6 but not PLP approached fasting levels 3 to 5 hours after the 0.5- to 4-mg PN doses; both plasma B-6 and PLP were still elevated 24 hours after 10 mg PN. In general, the rate of urinary B-6 and 4PA excretion was maximal the first 3 hours after the doses. With increasing PN doses, the percent of the dose recovered as urinary B-6 and 4PA decreased from 9 to 7% and 63 to 35%, respectively. Immediately following PL, plasma B-6 and urinary 4PA rose steeply indicating the rapid plasma clearance and oxidation of this B-6 vitamer. Responses to PM were generally slower than for PN or PL, suggesting that PM is absorbed more slowly or metabolized differently, or both, than PL or PN. A dose of at least 1 mg of B-6 is necessary to obtain measurable changes in vitamin B-6 metabolism.
Vitamin C Pharmacokinetics: Implications for Oral and Intravenous Use
Background: Vitamin C at high concentrations is toxic to cancer cells in vitro. Early clinical studies of vitamin C in patients with terminal cancer suggested clinical benefit, but 2 double-blind, placebo-controlled trials showed none. However, these studies used different routes of administration.
Objective: To determine whether plasma vitamin C concentrations vary substantially with the route of administration.
Design: Dose concentration studies and pharmacokinetic modeling.
Setting: Academic medical center.
Participants: 17 healthy hospitalized volunteers.
Measurements: Vitamin C plasma and urine concentrations were measured after administration of oral and intravenous doses at a dose range of 0.015 to 1.25 g, and plasma concentrations were calculated for a dose range of 1 to 100 g.
Results: Peak plasma vitamin C concentrations were higher after administration of intravenous doses than after administration of oral doses (P < 0.001), and the difference increased according to dose. Vitamin C at a dose of 1.25 g administered orally produced mean (?sd) peak plasma concentrations of 134.8 ? 20.6 ?mol/L compared with 885 ? 201.2 ?mol/L for intravenous administration. For the maximum tolerated oral dose of 3 g every 4 hours, pharmacokinetic modeling predicted peak plasma vitamin C concentrations of 220 ?mol/L and 13 400 ?mol/L for a 50-g intravenous dose. Peak predicted urine concentrations of vitamin C from intravenous administration were 140-fold higher than those from maximum oral doses.
Limitations: Patient data are not available to confirm pharmacokinetic modeling at high doses and in patients with cancer.
Conclusions: Oral vitamin C produces plasma concentrations that are tightly controlled. Only intravenous administration of vitamin C produces high plasma and urine concentrations that might have antitumor activity. Because efficacy of vitamin C treatment cannot be judged from clinical trials that use only oral dosing, the role of vitamin C in cancer treatment should be reevaluated.