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Vitamin C (Ascorbic Acid)

Nutrient Names: Vitamin C, ascorbic acid.
Synonyms: Antiscorbutic vitamin, ascorbate, ascorbic acid, ascorbyl palmitate, calcium ascorbate, cevitamic acid, chromium ascorbate, dehydroascorbic acid (DHA), isoascorbic acid, magnesium ascorbate, manganese ascorbate, molybdenum ascorbate, potassium ascorbate, sodium ascorbate, zinc ascorbate; Ester-C.
Related Substances: Acerola, rose hips.

Summary Table
nutrient description

Chemistry and Forms

The generic term vitamin C is used to describe the various compounds that exhibit the biological activity of ascorbic acid. Albert Szent-Györgyi first isolated ascorbic acid in 1928 from porcine adrenal glands. Originally called “hexuronic acid,” ascorbic acid (Latin a , “not”; scorbutus, “scurvy”) became the official nomenclature in 1933 after the correct structural formula was determined and it was successfully synthesized.

In nature, vitamin C appears in both its reduced form (L-ascorbic acid) and its oxidized form (L-dehydroascorbic acid), which interconvert in a reversible equilibrium.L-Ascorbic acid is the most active form, but both possess antiscorbutic activity. Vitamin C is water soluble and easily oxidized in solution and with heat.

Physiology and Function

Unlike many species that are able to synthesize vitamin C, humans require intake as a nutrient. Vitamin C is readily absorbed, predominantly in the distal portion of the small intestine (jejunum) and to a lesser degree in the mouth, stomach and proximal small intestine, through active transport mechanisms as well as passive diffusion. The pharmacokinetic profile of vitamin C is significant for decreased nonlinear absorption and increased nonlinear elimination with increasing oral doses. Intake of 400 mg per day (or 75 mg/dL) is required to saturate serum. Thus, although 70% to 90% of the dietary intake is absorbed, absorption falls to 50% with a dose of 1.5 grams (g). Once maximum serum level (>1.4 mg/dL) has been attained, intake of greater than 400 mg/day results in increased tissue levels of vitamin C. It is transported in the free form with higher concentrations in leukocytes and platelets than red blood cells (RBCs) and plasma. RBCs reach saturation with 60 mg/day. Once in circulation, vitamin C is readily taken up and concentrated in a wide range of body tissues, with the adrenal glands containing the highest concentration, and other glandular tissues (e.g., pituitary, thymus, corpus luteum) also holding relatively higher concentrations. Whole-body stores are typically about 1.5 g. Vitamin C crosses the placenta and is excreted in breast milk. It is primarily eliminated through urine, but only a small proportion is excreted unchanged (unless plasma concentration >1.4 mg/dL).

Vitamin C plays a central role in the biosynthesis and function of many key physiological substances. Given its high concentration in the adrenals (50 times that of serum), it is not surprising that vitamin C is required for the synthesis of adrenaline/epinephrine, noradrenaline/norepinephrine, cortisol, and histamine, all of which are involved in stress response. Moreover, adrenocorticotropic hormone (ACTH) stimulation induces significant loss of ascorbic acid from the adrenal cortex as part of glucocorticoid mobilization. Vitamin C is necessary for the synthesis of carnitine and thus essential to metabolism of fat as an energy source. It is also essential in the metabolism of folic acid, histamine, phenylalanine, tryptophan, and tyrosine and the optimal activity of several enzymes, specifically enabling the conversion of folacin to tetrahydrofolic acid, dopamine to epinephrine, and tryptophan to 5-hydroxytryptophan and eventually 5-hydroxytryptamine (serotonin). Vitamin C also enhances the bioavailability of iron, as well as aiding the reduction of ferric iron to ferrous iron and limiting the degradation of ferritin to hemosiderin.

Vitamin C is a powerful protective agent within the antioxidant, detoxification, and immune systems. Its activity as an antioxidant par excellence is well established and widely recognized. As a water-soluble substance with universal access to cells throughout the body, vitamin C acts as a powerful reducing agent in its own right, neutralizing free radicals by donating hydrogen atoms from its two hydroxyl (OH) positions. Furthermore, it functions synergistically with other antioxidants, particularly glutathione, the other major hydrophilic antioxidant, and vitamin E, a major lipophilic antioxidant, which it can regenerate. Moreover, unlike other antioxidants that exhibit the potential of converting to pro-oxidant activity under conditions of high oxidative stress (or during in vitro experiments involving free metal ions), evidence from well-designed and physiologically relevant research is lacking to substantiate suggestions that oral vitamin C intake promotes oxidative damage in humans under physiological conditions. 1 Vitamin C protects cholesterol from oxidative damage by free radicals, lowers elevated low-density lipoprotein (LDL) cholesterol, and increases high-density lipoprotein (HDL) cholesterol. It decreases total cholesterol by facilitating the formation of bile, aiding cholesterol degradation/metabolism, and participating in its conversion to bile acids for excretion. It also decreases levels of lipoprotein(a) or Lp(a), which forms atherosclerotic plaques and helps dissolve such plaques, by reacting with insoluble calcium-phospholipid-cholesterol plaque to form soluble sodium-phospholipid-cholesterol and calcium ascorbate; it may also reverse dysfunction of endothelial cells lining the blood vessels.

Vitamin C is essential for the optimal activity of many important detoxification systems, particularly the hepatic cytochrome P450 (CYP450) mixed-function oxidase system and other enzymes responsible for metabolizing toxic substances, including heavy metals (e.g., mercury, lead, arsenic, cadmium, nickel) and many pharmaceuticals. Vitamin C inhibits hyaluronidase (the enzyme that degrades hyaluronic acid, a high-molecular-weight compound that functions as an intercellular matrix) and prevents formation of nitrosamines, carcinogenic compounds formed from dietary nitrate/nitrite compounds in the digestive tract. The numerous and profound roles of vitamin C in facilitating and regulating immune function include increasing levels of macrophage activity, lymphocyte production (neutrophils, lymphocytes, natural killer cells), and antibodies (IgA, IgG, IgM). It also elevates interferon production, modulates prostaglandin synthesis, and exerts antihistamine effects.

The activity of vitamin C is fundamental to the structural integrity, strength, and elasticity of the human body through its central role in the synthesis of collagen and elastin. These organic materials are essential to the formation, activity, and maintenance of skin, tendons, cartilage, muscles, intercellular connective tissue matrix, blood vessels, bone matrix, and tooth dentin. Specifically, the hydroxylysine cross-links in collagen require the activity of prolylhydroxylase and lysyl hydroxylase, enzymes that hydroxylate lysine and proline, and for which ascorbic acid acts as a reducing agent and coenzyme. Overall, collagen comprises 25% to 30% of total body protein, making it the most abundant protein in the body. Thus, vitamin C and its allied nutrients inherently play an important role in the healing and rebuilding of damaged tissues, such as strains, sprains, burns, scars, and fractures.

nutrient in clinical practice

Known or Potential Therapeutic Uses

Vitamin C surpasses almost every other nutrient in the range of claims made for its use in promoting health and treating disease and in the popularity of its use as a supplement. Nevertheless, after more than half a century of controversy, evidence from controlled clinical trials and epidemiological studies remains limited and often speculative. Many groups within the general population, such as children, the elderly, and smokers, exhibit significant risk of vitamin C deficiency due to inadequate and inconsistent intake of vitamin C–rich foods and depletion due to medications and stressors. Nevertheless, observational studies largely indicate that populations with a higher dietary intake of vitamin C exhibit a lower incidence of cataracts, macular degeneration, cardiovascular disease, osteoarthritis, and some cancers.

Assertions of vitamin C's efficacy in the prevention of the common cold and cancer, in particular, have been focal points in a contentious and often unsubstantiated war of words, citations, and incongruous sets of assumptions, methods, and goals among divergent schools of medicine. For example, evidence for the protective effects of vitamin C against cancer is mixed, depending on study design, size and duration, nutrient source, dose, mode of administration, and the form of cancer involved, with cancers of the mouth, throat and vocal chords, lungs, esophagus, stomach, colon-rectum, and breast demonstrating inverse correlations, broadly or in select populations, in at least some studies. The application of “megadose” vitamin C as part of nutritional therapies in cancer care is even more controversial, and substantive dialogue between advocates and critics has rarely produced meaningful data or mutually satisfactory research. Review of numerous studies indicates beneficial effects of regular vitamin C, at moderate to high doses, in modestly reducing the duration of the common cold and respiratory infections and possibly the severity of symptoms. Research findings are more mixed regarding reductions in the frequency of infection. The weight of evidence in research within conventional medicine suggests a lack of benefit from long-term daily supplementation in preventing colds, except in individuals with low dietary intake, marathon athletes, or other populations with unusual circumstances.

Nevertheless, issues such as dosing strategies and delivery techniques, possible differences in physiological potency of supplemental forms from different sources, and concomitant nutrient synergies continue to separate the divergent therapeutic approaches. For example, in conventional discourse (and most human trials) a daily dose of 200 mg orally is often termed as “megadose vitamin C,” and 2000 mg is considered a tolerable daily upper limit. However, among physicians specializing in nutritional therapeutics, such descriptors would be reserved for doses starting at 4 g (4000 mg) daily, and therapeutic intervention can involve intravenous (IV) administration. Consequently, the parties in this long-standing debate too often operate from such divergent views of clinical application, research methodology, and outcomes interpretation, so fundamental questions often go unanswered, the most meaningful issues remain go unresolved, and opportunities for effective collaboration can be lost.

Although findings from well-designed and adequately powered clinical trials have rarely attained the dramatic level of benefit asserted by pioneers and proponents, clinicians experienced in nutritional therapeutics have regularly been able to offer substantive critiques of conventional research methodology and suggest limited relevance of many trials to actual clinical application. As with nutritional research to this point in many areas, mixed findings may result more from variations in intervention (forms used, dose levels, methods of administration), trial characteristics (duration, patient populations, methods of assessing outcomes), and other variables than from the actual effects of the “vitamin C.” Here the issues of dietary versus “supplemental” sources, as well as the multitude of supplemental forms, constitute fundamental factors in parsing evidence and extrapolating research findings. Overall, the use of oral doses may be appropriate for maintaining or restoring tissue levels, whereas IV administration of pharmacological doses is significantly more effective at obtaining greatly elevated plasma levels for short periods. Likewise, the benefits of multiple interdependent and synergistic nutrients in food sources and many prescribing strategies using nutrients as cotherapies render distinguishing the effects of any single component virtually impossible and contrasts sharply with the more decontextualized, single-agent investigational methodology modeled on studies designed for pharmacological interventions and pathological conditions. Meaningful and enduring conclusions and an operative consensus within the broader medical community will require development of an expansive set of in-depth research from controlled clinical trials integrating insights from the full range of therapeutic perspectives.

Historical/Ethnomedicine Precedent

The discovery of scurvy prevention through citrus intake among British sailors resulted from what is generally considered the first example of a controlled experiment comparing results in two populations administered different diets. It implicitly revealed a connection between the diets of disparate cultures and their respective ecological settings and traditional diets and the impact of their deficits on human health and disease.

Possible Uses

Acute anterior uveitis, aging or sun-damaged skin, alcohol withdrawal, allergies, anti-inflammatory, asthma, atherosclerosis, autism, bedsores, bronchitis, bruising (easy, excessive), cancer (risk reduction), cancer treatment, candidiasis, capillary fragility, cataract, cervical dysplasia, chronic obstructive pulmonary disease (COPD), common cold, Crohn's disease, dermatitis, diabetes mellitus, dysbiosis, eczema, fatigue, gallbladder disease, gallstone prevention, gastritis, gingivitis, glaucoma, gout, hay fever, heart disease prevention, heavy metal detoxification, hepatitis, Helicobacter pylori infection, herpes simplex infection, herpes zoster infection, human immunodeficiency virus and acquired immunodeficiency syndrome (HIV/AIDS) support, hives, hypercholesterolemia, hypertension, hypertriglyceridemia, hypoglycemia, immune function enhancement, influenza, insomnia, intervertebral disc inflammation, iron deficiency anemia, low back pain, macular degeneration, male infertility (sperm agglutination, low sperm count), menopausal symptoms, menorrhagia, mitral valve prolapse, multiple sclerosis, muscle soreness recovery (postexercise), nausea of pregnancy, nitrate tolerance, oral premalignant lesions (risk reduction), osteoarthritis, otitis media (recurrent), Parkinson's disease, peptic ulcers, periodontal disease, peripheral vascular disease, photosensitivity, platelet adhesiveness, postherpetic neuralgia, preeclampsia (prevention), premature placental rupture, reflex sympathetic dystrophy (RSD) prevention, retinopathy, rheumatoid arthritis, schizophrenia, scurvy, sinusitis, skin ulcers, sports injuries, stress, sunburn (prevention), tardive dyskinesia, urinary tract infection, vascular dementia prevention, viral or bacterial infections, vitiligo, wound healing.

Deficiency Symptoms

Scurvy is the fundamental and defining picture of severe vitamin C deficiency and its description as the first identified nutritional deficiency disease constituted a landmark development in nutritional medicine. Frank scurvy is rare in the United States (U.S.) and Europe, but subclinical deficiencies are common. Symptoms of advanced vitamin C deficiency derive primarily from defective collagen synthesis and degenerative changes in capillaries, bone, and connective tissue, and include listlessness, fatigue, weakness, fever, shortness of breath, anorexia, erupted teeth with bleeding gums, ecchymoses, hemorrhage, anemia, edema, hypotension, convulsions, personality changes, hypertrophy of the cornea, icterus, perifollicular hyperkeratotic papules, dry skin, muscle cramps, aching bones, joints, and muscles, and secondary infections. Scurvy, uncorrected, is eventually fatal. Children can experience abnormal development of bones, teeth, and blood vessels and disturbances of growth. Capillary fragility, bleeding gums, easy bruising, poor wound healing, diminished antioxidant protection, increased susceptibility to infection, and fatigue are among the indicators of possible subclinical vitamin C deficiency.

Smokers are foremost among groups at risk of vitamin C deficiency, but the elderly, institutionalized persons, hospital patients, and diabetics are also highly susceptible. The Third National Health and Nutrition Examination Survey also identified those who did not use supplements and non-Hispanic black males as having elevated risks of vitamin C deficiency and depletion in the U.S. 2 Other groups characterized by specific metabolic stresses may need greater levels of vitamin C intake for proper physical activity and protective functions, including individuals with high alcohol intake, those with increased oxidative stress (e.g., exposure to chemicals, heavy metals, radiation), those in life phases of rapid growth (pregnancy, lactation, childhood, adolescence), and individuals with chronic illnesses (e.g., rheumatoid arthritis, diabetes, hyperthyroidism, chronic kidney failure). As discussed later, numerous medications can deplete vitamin C or interfere with its normal activities. Increased risk of developing cataracts and heart disease can result from degenerative processes associated with chronic vitamin C deficiency.

Other than humans and other primates (specifically gorillas, chimpanzees, and monkeys), guinea pigs and a rare species of bat are the only mammals that lack the ability to synthesize ascorbic acid from glucose.

Dietary Sources

Public education is necessary to correct the widely held misconception, founded more in marketing and advertising than in nutritional science, that fruits, especially citrus, are exceptionally rich sources of vitamin C. In fact, vegetables are richer dietary sources. Vitamin C can be lost through oxidation during storage and cooking, and boiling can cause leaching of the nutrient into the water (unless recovered by use, such as in gravy or soup).

Almost all fresh vegetables and fruits are potential sources of vitamin C. Foods particularly rich in vitamin C include broccoli, cauliflower, red bell peppers, red chili peppers, black currants, Brussels sprouts, cantaloupe, kale, parsley, turnip greens, collard, rose hips, citrus fruits, strawberries, apples, persimmons, papaya, guava, acerola cherries, potatoes, cabbage, tomatoes, and green bell peppers.

Nutrient Preparations Available

Vitamin C is present in most multivitamin preparations. Intravenous ascorbate solutions (sodium ascorbate, or ascorbic acid buffered to a pH >5.5) are only administered by drip; IV push is contraindicated because of venous irritation. Osmalality of IV ascorbate solutions up to 1200 mOsm/L are well tolerated if the patient can take adequate fluids by mouth.

Scientific evidence is lacking to demonstrate superior bioavailability of any single form of orally administered vitamin C (L-ascorbic acid) compared with any other form. Although vitamin C from naturally occurring sources is favored by advocates of vitamin C therapy, naturally derived and synthesized forms ofL-ascorbic acid are chemically identical, and limited human research has thus far demonstrated no significant differences in their respective biological activities or bioavailability, using standard assay methods and parameters of physiological effect. When formulated as a mineral salt, ascorbic acid is buffered (i.e., less acidic) and thus theoretically less irritating than simple ascorbic acid to the gastrointestinal (GI) tract. A wide range of mineral ascorbates are available, with sodium ascorbate (131 mg sodium per 1000 mg ascorbic acid) and calcium ascorbate (114 mg calcium per 1000 mg ascorbic acid) being the most common. The addition of small amounts of dehydroascorbate (oxidized ascorbic acid), calcium threonate, and trace levels of xylonate and lyxonate, all metabolites of vitamin C, to a base of calcium ascorbate, marketed as Ester-C, is purported to provide for enhanced bioavailability, but supportive evidence is lacking, although Ester-C does appear to be “much better tolerated” than “regular ascorbic acid,” as indicated by “fewer epigastric adverse effects.” 3 Similarly, although bioflavonoids and vitamin C often occur together in many fruits and vegetables, claims that combining them in supplements provides superior activity have yet to be substantiated. Vitamin C is normally water soluble, but a fat-soluble form, known as ascorbyl palmitate, has been synthesized for use in topical applications by esterifying vitamin C to palmitic acid, a saturated fatty acid; an oral form would be unlikely to escape breakdown through hydrolyzation before being absorbed in the digestive tract. Erythorbic acid is an isomer of ascorbic acid but may lack the primary antiscorbutic activity of ascorbic acid; it is used in the U.S. as a food additive, but not as a nutritional supplement.

Based on the finding that some tumors accumulate high levels of vitamin C, concern has been raised that vitamin C might make cancer treatment less effective. 4 However, there is virtually no evidence from clinical trials that vitamin C interferes with any type of cancer therapy. In contrast, multiple animal and clinical studies suggest that vitamin C may enhance cancer therapy, possibly by acting as a pro-oxidant when accumulated in large intracellular stores by tumors, then exposed to chemotherapy or radiation. 5-7,7a(See Chemotherapy for further discussion.)

The tissue levels of ascorbic acid concentration obtained through IV administration are significantly greater than those associated with oral intake. Intravenous administration of vitamin C at 18 g/day can produce plasma concentrations 25 times those resulting from oral administration of the same dose. Recent pharmacokinetics models indicates that with oral administration, even large frequent doses of vitamin C, will increase plasma concentrations only modestly, from 70 mmol/L to a maximum of 220 mmol/L, whereas IV administration increases concentrations as high as 14,000 mmol/L. Plasma concentrations of 1000 to 5000 mmol/L are selectively cytotoxic to tumor cells in vitro, and emerging evidence indicates that vitamin C at concentrations achieved only by IV administration may function as a prodrug for hydrogen peroxide (H2O2) delivery to tumor tissues. 8-15Such observations may account for the inconsistent findings and divergent conclusions in studies using oral versus IV modes of delivery. Rigidly imposing a preconceived model of the beneficial or adverse effects of pro-oxidant effects of nutrients is not likely to lead to clinically useful conclusions.

Dosage Forms Available

Capsules, liposomal spray, powders, tablets, chewable tablets, effervescent tablets.

Source Materials for Nutrient Preparation

Commercial vitamin C is synthesized from glucose by two primary methods. The Reichstein process, developed in the 1930s, applies a single prefermentation, followed by a purely chemical route. The two-step fermentation process, introduced in China in the 1960s, replaces the later chemical stages with further fermentation. The yield from either process is approximately 60% ascorbic acid from the glucose feed, usually derived from corn.

Sago palm–derived ascorbic acid has been developed for individuals with putative corn sensitivity.

Camu camu (Myrciaria dubia), a bioflavanoid-rich berry from the Amazon rain forest, is an innovative source of vitamin C emerging in the marketplace

Dosage Range

Adult

Dietary: Vitamin C intake of 10 mg per day can prevent scurvy. The U.S. recommended dietary allowance (RDA) for vitamin C, or the daily dose required to prevent deficiency disease, is 90 mg/day for men and 75 mg/day for women; it was recently revised upward from 60 mg daily and had been 45 mg until 1974. The new, higher RDA takes into account for the first time the vitamin's role as an antioxidant as well as protection from deficiency. A special RDA has been established for adult smokers: 125 mg/day for men and 110 mg/day for women; Ames 16 has recommended that smokers need to consume two to three times more vitamin C than nonsmokers. The mean dietary intakes of vitamin C for adults in the United Kingdom (U.K.) and Germany were 87 and 76 mg daily and 75 and 72 mg daily for adult men and women, respectively. 17,18Among elderly men and women in the U.K., vitamin C intakes of 72 and 68 mg daily, respectively, have been reported. 19 The National Health and Nutrition Examination Survey found that the median consumption of vitamin C from foods during the years 1988 to 1991 was 73 and 84 mg daily for men and women in the U.S., respectively. 20 All these studies have demonstrated a wide variation in vitamin C intake, with 25% to 30% of the U.S. population consuming less than 2.5 servings of fruit and vegetables daily. Dietary intake levels in other areas, such as Latin America, Africa, and Asia, are typically lower. Based on a review of the scientific literature, the Linus Pauling Institute recommends “that the RDA for vitamin C should be 120 mg/day for optimum risk reduction of heart disease, stroke, and cancer in healthy individuals. Special populations, such as older adults and individuals with disease, may require substantially larger amounts of vitamin C to achieve optimum body levels and derive therapeutic benefits.” 21 Consuming at least five servings of fruits and vegetables daily may provide about 200 mg of vitamin C. 22

Supplemental/Maintenance:

  • 60 to 1000 mg/day.
  • Optimal daily intake: 0.5 to 3 g/day, depending on the individual.

Some research suggests that blood levels reach saturation at an oral intake of approximately 200 mg daily in healthy individuals, and assuming tissues are saturated, any intake above that amount may be excreted. However, the Linus Pauling Institute recommends a vitamin C intake of at least 400 mg daily; this amount has been found to fully saturate plasma and circulating cells with vitamin C in young, healthy nonsmokers. 12,22Individual variability can alter the metabolic effects of supplemental vitamin C, including nutrigenomic response variability, body weight, depletion status, and degree of tissue saturation based on recent patterns of intake.

Pharmacological/Therapeutic:

  • 300 to 1000 mg/day typical for adults treated for scurvy.
  • 500 mg/day to 20 g/day reported in scientific literature.
  • Up to 70 g/day used therapeutically and in research settings.

Dosing to bowel tolerance is typically applied clinically as a practical (as well as variable and evolving) parameter in therapeutic administration of vitamin C. The laxation effects of large oral doses of vitamin C are likely because of the osmotic effects of unabsorbed ascorbate. The common clinical observation that the bowel tolerance of vitamin C increases substantially during acute viral illnesses suggests that more ascorbate is absorbed from the GI tract during such episodes.

Toxic: Although toxicity is rare, the tolerable upper intake level (UL) established by the Food and Nutrition Board (FNB) of the Institute of Medicine for vitamin C in adults was set at 2000 mg. Notably, this advisory body established the “no adverse effect level” (NOAEL) for vitamin C arbitrarily out of necessity because they were mandated to do so, even though their review of the scientific literature failed to find any “solid data” to support a toxic dose for vitamin C. 23 As stated by Johnston 24 in 1999: “The available data indicate that very high intakes of vitamin C (2 to 4 grams per day) are well tolerated biologically in healthy mammalian systems. Currently, strong scientific evidence to define and defend a UL for vitamin C is not available.” Thus, this level is based on the potential for discomfort from possible diarrhea and GI disturbances (i.e., temporary and easily reversible responses) rather than actual toxicity in most individuals and is derived from uncontrolled case reports. 23

Pediatric (<18 years)

Dietary:

  • Neonates to 6 months: 40 mg/day (AI, adequate intake)
  • 6 to 12 months: 50 mg/day (AI)
  • 1 to 3 years: 15 mg/day (RDA)
  • 4 to 8 years: 25 mg/day (RDA)
  • 9 to 13 years: 45 mg/day (RDA)
  • Adolescents, 14 to 18 years: 65 mg for females; 75 mg for males (RDA)

Supplemental/Maintenance: Usually not recommended for children under 12 years of age.

Pharmacological/Therapeutic: The treatment of scurvy in children typically requires 100 to 300 mg per day orally in divided doses for 2 weeks. Otherwise, vitamin C is generally not administered in pharmacological doses to infants or children.

Toxic: UL levels (oral):

  • 0 to 12 months: none established
  • 1 to 3 years old: 400 mg/day
  • 4 to 8 years old: 650 mg/day
  • 9 to 13 years old: 1200 mg/day
  • Adolescents, 14 to 18 years old, including pregnant or breast-feeding females: 1800 mg/day

Toxicity is rare.

Laboratory Values

Physicians usually do not test vitamin C status, except for rare occasions of suspected scurvy. Most methods of laboratory assessment are generally considered neither sensitive nor precise in determining functional deficiency or systemic depletion. Further, high intake of vitamin C can interfere with some of the more frequently used laboratory tests.

Assessment of deficiency or depletion status.

Leukocyte ascorbate:

  • Normal range: not established.
  • Levels less than 114 mmol/108 cells (buffy coat) indicate deficiency.
Leukocyte concentrations may provide a good index of tissue stores of vitamin C.

Plasma ascorbate:

  • Normal range: not established.
  • Levels less than 2.6 mg/L (15 µmol/L) may indicate deficiency, but consistency in standards is lacking.

Plasma levels indicate metabolic turnover status of vitamin C. However, “extreme individual variability” has been documented with an identical vitamin C repletion dose in different individuals producing different plasma ascorbate levels based on body weight, prior depletion, and prior repletion. 25

Urinary ascorbate:

  • Normal range: not established.
  • Excretion of less than 10 mg/day indicates severe deficiency.

Urinary ascorbate is generally considered an insensitive index of status except in severe deficiency.

Ascorbate loading test: An oral dose of 0.5 to 2.0 g ascorbic acid is administered over 4 days, and then urinary ascorbate is measured; excretion of less than 60% of dose indicates depletion of tissue ascorbate.

Lingual ascorbic acid test (LAAT): In this physician-administered test, a drop (from 25-gauge needle) of blue dye (2,6-dichloroindophenol sodium salt solution) is put on the tip of the tongue. Vitamin C status is indicated by the time required for the dye to disappear. Less than 20 seconds indicates normal levels; 20 to 25 seconds, marginal levels; and longer than 25 seconds, depletion of vitamin C levels. This is a functional test of the oxidation-reduction (redox) status of saliva and tissue, which is influenced by ascorbate status, but not specific for it.

As a strong reducing agent, ascorbic acid (>1 g daily) can interfere with some diagnostic tests, particularly those based on redox reactions. Evidence for some of these effects is mixed.

False-negative results on stool occult blood (guaiac assay) have been attributed to “high-dose” vitamin C intake within preceding 48 to 72 hours. False-negative results on urine acetaminophen tests have also been reported.

Vitamin C intake may produce false increases in levels in these serum tests: bilirubin, carbamazepine, creatinine, aspartate transaminase (AST; glutamic-oxaloacetic transaminase [SGOT]), uric acid.

Vitamin C intake may produce false decreases in levels in these serum tests: lactate dehydrogenase (LDH), theophylline.

Inaccurate readings on urinary glucose tests have been observed, with false negatives using glucose oxidase and false positives using cupric sulfate as the reagent test. Vitamin C–induced interference with blood glucose tests has been reported in the scientific literature but disputed.

Several unqualified case reports from the 1970s suggested that high-dose vitamin C could lower prothrombin time (PT) and cause increased clotting. Vigilance is appropriate whenever employing anticoagulant therapy, but evidence is too weak and inconsistent to represent this potential effect as highly probable or predictable, as discussed later.

safety profile

Overview

Vitamin C is safe across a broad range of intakes for most adults, according to a review and editorial by a team of eminent nutritional researchers. 26 Scientific evidence is lacking to demonstrate that even very large amounts of vitamin C are toxic or exert adverse health effects. Regular intake of dose levels well above the RDAs has been common in large numbers of individuals for decades. Adverse effects have been lacking in individuals, including Linus Pauling, who have consumed 10 g or more daily for extended periods. Systemic toxicity is improbable in healthy individuals because the primary effects of excess intake are mainly caused by large amounts of unabsorbed ascorbic acid in the intestine and, as such, typically do not alter circulating levels, are easily excreted, and respond rapidly to a decrease in intake. Thus, the Linus Pauling Institute, Oregon State University, concluded “that there is currently no consistent and compelling data for serious adverse effects of vitamin C in humans, and a UL can therefore not be established.” 21

Nutrient Adverse Effects

General Adverse Effects

Gastrointestinal (GI) discomfort, abdominal bloating, flatulence, dysuria, increased urinary frequency, skin rashes, loose stools, and diarrhea, resulting from the osmotic effects of unabsorbed vitamin C in the intestine, constitute the primary adverse effects in most individuals. Although providing the basis for the UL in the U.S., these responses are all dose related, resolve rapidly with decreased intake, and present no serious risk. Tolerance typically develops over time with gradual increase in dose. Diarrhea usually occurs with doses of 6 to 10 g daily but has been reported to afflict some individuals after only a single 1-g dose. Lowering the dosage to the highest level that does not provoke diarrhea (i.e., to “bowel tolerance”) is a common method of determining maximal dosage for therapeutic effect.

Adverse Effects Among Specific Populations

Because of the importance of excretion as a regulatory process, individuals with compromised renal function may experience impaired elimination, excess accumulation, and increased lithogenicity.

Individuals with inadequate levels of glucose-6-phosphate dehydrogenase (G6PD) are at increased risk of a potentially severe adverse reaction, including possible hemolysis, after intake of certain oxidizing substances, such as high doses of vitamin C, orally or intravenously, suggesting that ascorbate might function as a pro-oxidant under certain conditions. 27 Genetic or G6PD enzyme activity testing is appropriate, particularly when IV ascorbic acid administration is contemplated.

In the general (U.S.) population, researchers have found “no association between serum ascorbic acid level and prevalence of kidney stones in women or men.” 28 Nevertheless, certain individuals may theoretically exhibit increased risk of calcium oxalate stones with high-dose vitamin C intake becasue of potentially increased oxalate levels. 29 Vitamin C (ascorbic acid) is metabolized to dehydroascorbic acid, which in turn is metabolized to oxalic acid. In general, individuals who consume large amounts of vitamin C have shown either no change or a decreased risk of kidney stone formation in large-scale observational studies. 28,30,31However, one of every 400 individuals possesses a defect in oxalate metabolism, resulting in idiopathic hypercalciuria, that could put them at increased risk of stone formation due to elevated urinary oxalic acid levels when administered high dose vitamin C (4-10 g orally). In a trial investigating the effect of calcium citrate supplementation on urinary calcium oxalate saturation in female stone-formers, Levine et al. 32 and associates found that “calcium citrate supplementation did not increase the lithogenicity.” However, 2 years later in a study of vitamin C pharmacokinetics in healthy volunteers, these researchers reported that some individuals can experience an elevation in urinary oxalate levels after consuming 1000 mg of vitamin C per day, even in the absence of a history of kidney stones. 11 Auer et al. 33 expressed concern in reporting a small trial in which they observed sharp increases in excretion of urinary oxalate and sudden onset of hematuria due to formation of kidney stones in a single male subject who had consumed “large doses of ascorbic acid” for 8 days. Notably, in the paper describing the trial as a whole, these same authors “concluded that ingestion of large doses of ascorbic acid does not affect the principal risk factors associated with calcium oxalate kidney stone formation.” 34

In an interesting line of research, several small trials and a decade of clinical experience have consistently demonstrated the efficacy of lemonade in improving urinary citrate levels and reducing the occurrence of hypocitraturic calcium nephrolithiasis, in a manner similar to that of potassium citrate. 35-37

Oxalate formation is saturable, and most of the population is unlikely to experience this complication. Hoffer 38,39and other senior vitamin C researchers consider this kidney stone risk as exaggerated and inadequately demonstrated, possibly an artifact resulting from failure to acidify urine samples during collection. Some physicians experienced in nutritional therapies suggest that this risk may be mitigated by vitamin C's tendency to bind calcium, causing it to be excreted in urine, and rendering it unavailable for forming calcium oxalate stones. Likewise, Ester-C may be less likely than other forms of vitamin C to cause this rise in oxalate. Research is lacking to validate either of these propositions conclusively. Vitamin B6decreases oxalate production and may mitigate this risk. 31 Thiamine can also inhibit oxalate formation, as can correction of magnesium deficiency. 40 Nevertheless, health care professionals treating individuals at risk are advised to exercise extra caution in administering doses greater than 300 mg/day on a regular basis and to consider measuring urinary oxalate levels before and after beginning ascorbate supplementation.

Pregnancy and Nursing

Vitamin C is not known to cause mutations or birth defects in healthy individuals. 23 However, in one randomized, placebo-controlled trial involving 722 pregnant women at risk for preeclampsia, researchers observed a slightly elevated incidence of small-for-gestational-age neonates among women administered vitamin C (1000 mg) and vitamin E (RRR alpha-tocopherol, 400 IU) versus placebo. 41 A larger trial would be necessary to determine if this is a statistically significant and etiological effect, or if these events occurred by chance.

Infants and Children

The risk of “rebound scurvy” has been reiterated in innumerable secondary sources for decades, even though substantive scientific evidence is lacking. Theoretically, rebound scurvy could potentially occur in infants if the mother takes megadoses of vitamin C during gestation. This assertion is largely based on one poorly controlled study done by Cochrane in 1965 involving two infants whose mothers who had consumed 400 mg of supplemental vitamin C during pregnancy. The vitamin C was discontinued abruptly after the births. These infants were receiving formula, and it was presumed that the formula had adequate levels of vitamin C. However, there was no analysis of the vitamin C content in the formula, nor was any attention given to the storage, preparation, or administration of the formula. 42 Thus, considering the number of women who have taken vitamin C during pregnancy, this small study occurring more than 30 years ago, and no similar cases documented, the risk is likely to be extremely low, if existent at all. The FNB Panel on Dietary Antioxidants and Related Compounds concluded that vitamin C does not cause “rebound scurvy” in healthy individuals. 23

Contraindications

  • Cystinuria.
  • Glucose-6-phosphate dehydrogenase (G6PD) deficiency.
  • Individuals with a history of hemosiderosis, hemochromatosis, or other forms of iron overload.
  • Individuals with a history of recurrent nephrolithiasis, especially oxalate stone-formers, should avoid daily doses of 1000 mg or more outside the context of close supervision by an appropriately trained and experienced health care professional.
  • Megadoses (>4 g/day) in individuals with a history of renal failure outside the context of supervision by an appropriately trained and experienced health care professional, particularly on initiation of intake or significant change in dose.
  • Pregnant women should avoid daily doses above 500 mg without close medical supervision.

Use of doses greater than 1000 mg/day is generally contraindicated during forms of chemotherapy and radiation in which free-radical formation is an intentional part of the therapeutic mechanism. As discussed later, vitamin C and other antioxidants should be administered only in the context of direct supervision and close monitoring because of their potential inhibition of oxidation.

Precautions and Warnings

  • Patients with renal impairment or on chronic hemodialysis. Doses of vitamin C should not exceed 100 to 200 mg daily in individuals with renal failure.
  • Caution and close supervision are appropriate in administering vitamin C to individuals diagnosed with sickle cell anemia, sideroblastic anemia, or thalassemia.
  • Patients preparing for major surgery, particularly those at increased risk of hemorrhage, should not exceed 400 mg daily in the week before the procedure except under the supervision of an experienced health care professional. 43
  • Individuals with sensitivities to corn may react to commercially available forms of vitamin C because most are derived from corn. Ascorbates derived from sago palm have been produced for extremely corn-sensitive individuals.
  • Long-term intake of high doses of vitamin C may induce copper deficiency.

interactions review

Strategic Considerations

Whether in cardiovascular health, immune function, oncology, or preventing the common cold, vitamin C, or perhaps more accurately “the view of vitamin C,” may constitute the most contentious and misunderstood topic, and thus probably the greatest single test of scientific discovery and clinical pragmatism, in integrative therapeutics and patient self-care. For decades, vitamin C has been the subject of intense controversy in medicine, the virtual bogeyman of medicine's Cold War era, and with its central physiological roles and its pervasive therapeutic potential, it presents a central opportunity for transdisciplinary collaboration and the emerging model of integrative therapeutics. Leading scientists and experienced clinicians, and throngs of self-administering patients, have voiced strong support for the preventive and therapeutic value of ascorbic acid ever since it was taken up by Linus Pauling and the clinicians proposing “orthomolecular medicine.” On the side of the status quo, researchers and the institutions of conventional medicine have consistently voiced skepticism, disinterest, and often disdain for the exuberance of what they have seen as overamplified extrapolations of questionable anecdote. Nevertheless, the paradigm and treatment protocols of the pioneers and their successors have rarely been studied or applied intact by the conventional researchers who have investigated vitamin C. Richards, 44 Segerstråle, 45 and others have described a systematic pattern of bias against vitamin C therapeutics, particularly in contrast to conventional agents such as 5-fluorouracil and interferon. Hemilä 46 has suggested that “Pauling's conclusions were dismissed because of the fundamental divergence with the traditional notion that the only purpose of vitamin C is to prevent scurvy and not because of experimental findings.” He also cited the work of Goodwin and Tangum 47 as providing “several examples to support the conclusion that there has been systematic bias against the concept that vitamins might be beneficial in levels higher than the minimum required to avoid classic deficiency diseases.” 46

In the absence of a theoretically clear and clinically operative model of integrative medicine, a strident attitude and lack of respect on both sides have contributed to the absence of a substantive scientific debate, to the detriment of both scientific knowledge and patients. Fortunately, scientific knowledge of vitamin C has grown progressively, as has a deeper appreciation of nutritional therapies in general. Moreover, new “discoveries” have become possible with the greater openness in scientific research to incorporating the therapeutic models of natural medicine, and thus more accurately resembling its clinical practice. These changes within the broader world of medical practice, education, and research have opened the doorway for a more systematic and comprehensive study of vitamin C, its essential role in human health, possibilities for therapeutic application, and the operative considerations for beneficial and adverse interactions within a clinical context encompassing conventional pharmacology. Considering the widespread use of vitamin C by all sectors of the patient population, self-administered or prescribed by nonconventional health care professionals, the sparsity of substantive clinical research data is striking and the basis for any sweeping generalizations about benefits, dangers, or interactions woefully inadequate.

It is useful to divide the clinical investigation of vitamin C into its physiological (coenzyme and antioxidant) functions (up to intakes of 400 mg/day, at which point tissue levels become saturated) and its pharmacological dosage range (multigram doses orally, up to 100 g intravenously). Evidence suggests that high-dose, particularly parenteral, ascorbic acid functions as a redox potential–modulating agent rather than a vitamin or antioxidant. Confusion between these two distinct roles of ascorbic acid may be the source of conflicting data in this field.

Under certain conditions, ascorbic acid, whether from natural or synthetic sources, can interact with numerous pharmacological agents, beneficially, adversely, or bimodally, depending on clinical management. In particular, through its antioxidant activity and influence on drug-metabolizing enzymes, vitamin C may amplify or mitigate adverse effects (sometimes intended effects) of numerous pharmacological agents or, in some cases, potentially impair the desired therapeutic activity of such agents. Here the issue of ascorbic acid coadministration with chemotherapy or statin drugs has been the most contentious. In both regards, theoretical concerns about the antioxidant or pro-oxidant effects of vitamin C in conjunction with conventional therapies have been based all too often on questionable assumptions and limited research. Many conclusions have been made absent substantive evidence from large, lengthy, and well-designed trials focusing on the specific proposed interactions involving vitamin C. Health care professionals of all schools of thought and therapeutic approaches share these concerns, but those experienced in their application in clinical settings regularly point out that most cited research is preliminary and of only limited similarity to actual clinical practice. The paramount need is for well-designed and adequately powered trials that will critically assess the therapeutic use of vitamin C in these clinical contexts; determine the frequency, character, and clinical significance of any substantive interactions; and offer guidelines for shaping the clinical adaptations necessary for ensuring safety and optimizing outcomes. Moreover, in such investigations, particular attention must focus the form, dosage, and mode of vitamin C administration, concomitant conditions and treatments, and individual pharmacogenomic, lifestyle, and personal history factors characterizing the subject population, so as to discern specific influential variables and customize therapeutic responses accordingly.

Distinguishing use of vitamin C as nutritional supplement and patient self-care practice from high-dose ascorbic acid administration, orally or intravenously, by trained and experienced health care professionals applying coherent multidisciplinary strategies constitutes a critical first step to any meaningful scientific dialogue and productive research agenda. For example, approaches such as alternating administration but avoiding simultaneous intake, as practiced in many integrative oncology clinics, and purposeful selection of IV or oral administration represent significant clarifications that could benefit research design. Thus, in most observed interactions, doses less than 1 g/day are generally much less likely to precipitate adverse interactions, particularly given adequate separation of intake when indicated. High versus low dosage levels and IV versus oral administration almost always need to be considered as distinct from each other.

Likewise, few conclusive judgments can be made (or even hypothesized) as to the efficacy or risks of vitamin C within oncological treatment programs until further research is conducted into the contentious but largely unexplored issue of whether vitamin C always acts as an antioxidant or whether and when it may shift to pro-oxidant activity, as well as the corollary questions as to under what certain conditions this might occur and how that might affect interactions, effects, and outcomes. Further, the question of whether vitamin C can and should be investigated as an isolated nutrient or as a component of a broader nutrient-based interventions needs to be recognized, addressed, and sorted, especially with regard to such key issues as the preventive and therapeutic use of antioxidants and the respective emphasis on dietary versus supplement versus pharmacological forms. The important concepts embodied in the work of Bruce Ames and his collaborators regarding the importance of nutrients to genetic stability and exemplified by the extended SU.VI.MAX study in France provide useful models for the further development of research methodology that can deliver clinically relevant findings.

A wide range of drugs and drug classes can cause adverse effects or induce harmful reactions by interfering with the normal physiological activities of vitamin C and depleting functional levels in diverse tissues. As with most patterns of nutrient depletion or physiological impairment, patient susceptibility to clinically significant adverse effects from drug-induced vitamin C depletion depends largely on the nutritional status, concomitant medical conditions, and drug intake and other patient-specific factors, as well as the dosage level and treatment duration of the medication(s) involved. In some situations, coadministration of vitamin C, usually with synergistic nutrients, may only be appropriate for individuals with compromised nutritional status resulting from diet, disease, genetics, or medications, and then primarily in relation to intensive or prolonged drug regimens. In other situations, where concomitant ascorbic acid presents no significant risk of adverse effects or interactions, routine prophylactic administration may be judicious.

nutrient-drug interactions
Acetaminophen
Acetylsalicylic Acid (Aspirin) and Salsalate
Antihypertensive Medications (Generally)
Chemotherapy and Radiotherapy
Cimetidine and Related Histamine (H 2 ) Antagonists
Corticosteroids, Oral and Topical, Including Prednisone
Cyclosporine
Desferoxamine and Related Chelating Agents
Desferoxamine (Desferrioxamine mesilate, desferoxamine mesylate; Desferal). Similar properties but evidence lacking for extrapolation: Deferasirox (Exjade); EDTA, ethylenediaminetetraacetic acid.
Bimodal or Variable Interaction, with Professional Management
Beneficial or Supportive Interaction, with Professional Management

Probability: 2. Probable
Evidence Base: SYMBOL AMPERSANDthinsp; Preliminary

Effect and Mechanism of Action

In general, vitamin C can slightly to moderately increase absorption of nonheme iron; it also modulates iron transport and storage in the body. Iron overload may theoretically result from coadministration of iron and vitamin C in patients genetically (hemochromotosis) or medically (frequent RBC transfusions) predisposed to it. Conversely, high iron levels or iron administration can reduce blood levels of ascorbic acid, a water-soluble antioxidant as well as a reducing agent, through oxidation. Administration of vitamin C can enhance the activity of deferoxamine in excreting iron, even at low levels such as 200 mg daily, but with dose-dependent enhancement particularly in the 750 to 2000 mg dose range. 163

Ascorbic acid is reported to enhance the toxic effects of deferoxamine, but no mechanism of action has been confirmed. Ascorbate has been proposed to induce cytotoxicity from iron-catalyzed oxidation, even in iron-deficient medium, but these in vitro findings of a pro-oxidant action of ascorbate in the context of free metal ions do not correlate with generally accepted observations under physiological conditions in humans. 164-166 Complications involving left ventricular dysfunction are reported to be of particular concern, and its occurrence is purported to be rapid in onset and severe.

Research

Hussain et al. 163 investigated the effect of dose, time, and ascorbate on iron excretion after subcutaneous desferrioxamine in a series of experiments involving 13 patients with beta-thalassemia major and one with congenital sideroblastic anemia, all of whom were receiving regular blood transfusions. After establishing that midlevel doses (1500 or 2000 mg) of desferrioxamine were more effective than lower doses (750 mg), with higher doses (4000 mg) showing a variable response, these researchers found that concomitant ascorbic acid therapy was invariably associated with increased iron excretion after subcutaneous desferrioxamine (D.F.). “In twelve studies at different dose levels of D.F., ascorbate therapy was associated with increased iron excretion ranging from 24 to 245%.” They concluded that “in most patients with transfusional iron overload subcutaneous D.F over a 12 h period, at a dose ranging from 2 to 4 g daily with ascorbic-acid saturation, is at present the most satisfactory method of removing excess iron.”

Coadministration of ascorbic acid is reported to enhance the toxic effects of desferoxamine, but evidence from large human trials is lacking to confirm any deleterious effect of vitamin C on iron status in patients with iron overload being treated with desferrioxamine. However, published reports have described a few incidents of clinically important, transient deterioration of left ventricular function in patients receiving 500 mg/day of ascorbic acid concurrent with iron chelation therapy. Henry et al. 167 have documented echocardiographic abnormalities in the majority of patients with transfusion-dependent anemia and secondary myocardial iron deposition. Nevertheless, the authors reported that they subsequently “observed a reduction in ejection fraction in several of the patients at National Institutes of Health following the addition of ascorbic acid to a program of iron chelation with intramuscular desferrioxamine.” Also, “discontinuation of the ascorbic acid has been followed by a return to normal left ventricular function in all but one patient.” 167

Nutritional Therapeutics, Clinical Concerns, and Adaptations

The coadministration of vitamin C with parenteral agents, especially desferoxamine, may enhance therapeutic efficacy by increasing iron excretion, but rarely may also increase risks of left ventricular dysfunction or other significant adverse effects.

Many clinicians experienced in iron chelation therapy of iron overload states administer 500 mg of vitamin C an hour before beginning each desferal infusion to mobilize iron from storage sites and render it more available for chelation and subsequent excretion. Clinicians should monitor for cardiac decompensation, particularly in patients with preexisting cardiac disease. Administration of vitamin C after desferal injection may increase toxicity.

The limited state of the evidence and the mixed outcomes suggest the need for continued research through well-designed clinical trials. Particularly because deferasirox is orally active and a more potent iron chelator than parenteral desferoxamine, clinical studies of potential interactions, both positive and negative, between deferasirox and ascorbate should be performed.

Disulfiram
Erythropoiesis-Stimulating Agents
Furosemide and Related Loop Diuretics
HMG-CoA Reductase Inhibitors (Statins)
Indinavir and Related Protease Inhibitors
Lansoprazole-Amoxicillin-Metronidazole (LAM) Triple-Therapy Regimen
Levodopa, Carbidopa, and Related Antiparkinsonian Medications
Methotrexate
Nitroglycerin and Related Nitrates
Oral Contraceptives: Monophasic, Biphasic, and Triphasic Estrogen Preparations (Synthetic Estrogen and Progesterone Analogs)
Propranolol and Related Beta-1-Adrenoceptor Antagonists (Beta-Adrenergic Blocking Agents)
Tetracycline Antibiotics
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Aluminum Hydroxide and Related Aluminum-Containing Antacids
Amphetamines, Mixed
Ampicillin, Related Beta-Lactam and Other Antibiotics
Anticonvulsant Medications, Including Phenytoin and Valproic Acid
Clozapine and Related Atypical Antipsychotics
Epinephrine
Fenofibrate
Haloperidol and Other Neuroleptic Agents
Heparin, Unfractionated; Low-Molecular-Weight Heparin
Indomethacin and Related Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Isoniazid and Related Antitubercular Agents
Mexiletine
Phenothiazines
Probenecid
Selective Serotonin Reuptake Inhibitor (SSRI) Antidepressants
Tacrine
Warfarin and Related Oral Vitamin K Antagonist Anticoagulants
nutrient-nutrient interactions
Alpha-Lipoic Acid
Bioflavonoids
Copper
Folic Acid
Glutathione (GSH)
Grape Seed Extract
Iron
Lutein
Selenium
Taurine
Vitamin B 6
Vitamin B 12
Vitamin E
Vitamin K
herb-nutrient interaction
Reishi Mushroom (Ganoderma lucidum)
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