Vitamin C: What It Does, and How Much Actually Absorbs

Vitamin C is the required cofactor for at least eight human enzymes — the ones that build collagen, carnitine and norepinephrine, and the ones that erase methyl marks from DNA. Absorption is saturable and falls as the dose rises: roughly 87% of a 30 mg dose is taken up, about 63% of a 500 mg dose, and under half above a gram. Plasma stops rising past about 400 mg a day.

What Does Vitamin C Actually Do? The Enzyme List

Most articles say "antioxidant" and stop. That is the least specific thing vitamin C does, and it is not the reason you die without it.

Ascorbate is a one- and two-electron reductant, and its main job is keeping metal ions at enzyme active sites reduced. A large family called Fe(II)/2-oxoglutarate-dependent dioxygenases holds an iron atom in the ferrous state and uses it to split molecular oxygen. Every so often the catalytic cycle uncouples and leaves the iron as Fe(III), at which point the enzyme is dead in the water. Ascorbate reduces it back. It is not consumed on every turn; it is the reset button. A second, smaller group are copper monooxygenases, where ascorbate performs the same service for Cu(II) → Cu(I).

That is a parts list, not a list of vague benefits. The Linus Pauling Institute and the NIH Office of Dietary Supplements both frame vitamin C's core function this way. Notice how many of these enzymes need a metal as well as the vitamin: two need copper, six need iron. That interdependence is the subject of our guide to why nutrients rarely work alone.

Why Scurvy Starts With Fatigue, Not Bleeding

The bleeding gums are the famous part. They are not the first part.

The earliest reliable symptom of depletion is fatigue, and it precedes any hemorrhagic sign. The likely reason is carnitine. Both TMLD and BBH — the first and last enzymes of the carnitine pathway — are ascorbate-dependent dioxygenases, so a falling ascorbate pool constrains carnitine synthesis before it constrains anything visible. Carnitine is the shuttle that carries long-chain fatty acids into the mitochondrion. Without enough of it, a major fuel line into the machinery that actually makes your ATP narrows.

That is a mechanism, not a promise. In someone whose status is already adequate, there is no reason to expect more ascorbate to build more carnitine — the enzymes are already running. But it explains why the naval accounts describe listlessness first and bleeding weeks later, and it belongs on the list of things worth checking when working through the reasons people feel flat.

Frank scurvy appears after roughly a month of intake below 10 mg a day, corresponding to a body pool under about 300-350 mg. Perifollicular hemorrhage, corkscrew hairs, bleeding gums, poor wound healing, joint pain, eventually tooth loss: one story told in different tissues, all of it collagen assembled without enough hydroxyproline to hold its shape.

How Much Vitamin C Do You Need, and Who Is Actually Short?

The RDA is 90 mg a day for adult men and 75 mg for adult women, with 35 mg more for smokers, whose turnover is measurably higher. The upper limit is 2,000 mg a day, and it is worth knowing what that limit is built on: osmotic diarrhea and GI distress, not organ damage.

CDC analysis of NHANES puts mean US serum vitamin C at 51.2 µmol/L in 2017-2018, essentially unchanged from 54.0 µmol/L in 2003-2006. Frank deficiency, under 11.4 µmol/L, sat at 6.8%. Among smokers it runs about 15% — roughly triple the non-smoker rate — with a mean of 39.9 µmol/L. Women score higher than men, 56.0 versus 46.1 µmol/L, and adults over 60 have the highest levels of any age band.

Averages hide the distribution. Reider and colleagues, analysing NHANES 2005-2016 across 26,282 adults in Nutrients, found 46% of US adults below the Estimated Average Requirement for vitamin C from food alone, falling to 33% once supplements were counted. For context in the same dataset: vitamin D 95% below EAR from food, vitamin E 84%, magnesium 48% — but zinc only 15%, iron 5%, selenium under 1%. Some gaps are real and some are invented, which is the same distinction we draw in our guides to vitamin D and why magnesium comes first and which trace minerals are actually essential.

That is the practical case for a daily dose that is generous rather than minimal — not because more is better, but because intake is erratic and the people with the highest turnover are frequently the ones eating the least produce. It is the reasoning behind the 500 mg of vitamin C in Current, alongside 220 mg of magnesium and 70+ trace minerals: a floor you hit on the bad-diet days, not a ceiling you climb.

How Much Vitamin C Actually Absorbs?

This is the section the rest of the internet skips, and it is the one that changes how you buy vitamin C.

The definitive human dataset is still Levine and colleagues at the NIH, published as "Vitamin C pharmacokinetics in healthy volunteers: evidence for a recommended dietary allowance" in PNAS in 1996. Seven healthy young men were admitted as inpatients and depleted to scorbutic plasma levels, then repleted through a full dose ladder from 30 mg to 2,500 mg a day, with plasma, leukocyte and urine measurements at each steady state. A parallel study in healthy young women followed in PNAS in 2001. You cannot run that trial today, which is part of why it remains the reference.

Three findings, and they interlock.

One: fractional absorption falls as the dose rises. Uptake runs through the sodium-dependent vitamin C transporters — SVCT1 in the intestine and kidney, SVCT2 in most other tissues. These are saturable carriers, not open doors. Once SVCT1 is working flat out, extra ascorbate passes through, which is also why gram doses produce osmotic GI effects.

Figures from Padayatty and Levine's summary in CMAJ (2001;164:353). NIH ODS states the same shape: 70-90% absorption at intakes of 30-180 mg a day, dropping below 50% above 1 g.

Two: plasma saturates, and it saturates early. The curve is sigmoid. It rises steeply between 30 and 100 mg a day, then bends hard. By 200 mg plasma is about 75 µmol/L, roughly 95% of the achievable maximum. By 400 mg it is flat near 80 µmol/L. Ten times that intake buys about 5 µmol/L more. A single 1.25 g dose does produce a transient peak near 135 µmol/L, but it is gone within hours.

Three: there is a renal threshold, and it is low. In Levine's study, no vitamin C appeared in the urine of six of the seven volunteers until the 100 mg dose. Above roughly 100 mg a day — about 60 µmol/L in plasma — the kidney begins excreting ascorbate rather than reclaiming it through SVCT1.

Put those together and you have the oral bioavailability ceiling: saturable uptake at the gut, a plateau in plasma, an active dump at the kidney. Three independent mechanisms pointing the same way, which is why no oral dose and no delivery format has produced sustained plasma much above 80-100 µmol/L.

Two more numbers worth holding onto. Circulating neutrophils, monocytes and lymphocytes are fully saturated at about 100 mg a day, well before plasma is. And plasma is the least concentrated compartment in the body — adrenal and pituitary glands, brain, eye lens, liver, spleen and leukocytes all hold far more, with leukocytes reaching roughly 1 millimolar. The number your blood test reports is the low end of the range.

Why IV and Oral Vitamin C Are Pharmacologically Different Drugs

Every ceiling above — saturable SVCT1 uptake, the plasma plateau, the renal threshold — applies to swallowed vitamin C. Intravenous ascorbate bypasses the gut entirely, so the intestinal transporter is out of the picture and the only remaining brake is renal clearance. The result is a plasma concentration in a different range altogether: oral dosing tops out near 80-100 µmol/L, while infusion can reach the tens of millimoles per litre — several hundred times higher.

At those concentrations ascorbate stops behaving like a vitamin. It becomes a pro-drug for extracellular hydrogen peroxide generation, which is a pharmacological mechanism, not a nutritional one, and it is why high-dose IV ascorbate is studied as an investigational agent under medical supervision rather than sold in a canister. None of that research says anything about what a supplement does. Any page citing intravenous studies to sell an oral powder is either confused or hoping you are.

The rule: oral vitamin C is a nutrient at a saturating dose; intravenous vitamin C is a drug at a pharmacological dose. Levine's group made this argument explicitly in Annals of Internal Medicine in 2004, and the NIH ODS fact sheet maintains the same separation.

Where Does a 500 mg Dose Sit on the Curve?

Past every measured saturation point, with margin.

White blood cells max out at about 100 mg a day, so 500 mg is five times that. Plasma is at roughly 95% of maximum by 200 mg and fully plateaued by 400 mg. Single-dose bioavailability at 500 mg is 63%, so about 315 mg is absorbed and roughly 185 mg passes through unabsorbed — and of what is absorbed, most of the amount above the renal threshold leaves in the urine within hours.

So why not just take 200 mg? Three defensible reasons and one that is only a hypothesis. Doses get missed, and with a body pool of 1,500-2,000 mg turning over at about 3% a day, a generous intake keeps that pool topped up through the gaps. Smokers, people under sustained inflammatory load, and people with metabolic disease run measurably lower plasma at the same intake. Several trials using vitamin C for vascular and antioxidant endpoints have used 500 mg specifically. The fourth argument — that some tissue compartments may not saturate when plasma does — is plausible and has never been shown to produce a benefit. We are not going to pretend otherwise.

What 500 mg does not do is give you five times the effect of 100 mg. The pharmacokinetics rule that out, flatly.

Infection, Inflammation, and Why Turnover Changes the Question

Vitamin C status is not a fixed property of your diet. It is a balance between intake and consumption, and consumption is not constant.

Neutrophils and monocytes concentrate ascorbate against a steep gradient, reaching roughly 1 millimolar inside the cell — on the order of 10 to 100 times plasma, depending on where plasma is sitting. After a respiratory burst, intracellular concentrations rise further, toward 10 mM, as the cell takes up oxidised dehydroascorbate and reduces it back. That is an expensive habit, and it is why Carr and Maggini's review in Nutrients (2017) reports plasma vitamin C falling measurably during infection.

Their dosing conclusion is the one to remember, and it is the figure our guide to who actually benefits from antioxidants points here for: prophylactic adequacy — saturating plasma and immune cells before anything happens — takes 100-200 mg a day. Treating an established infection is a different question with far weaker evidence, and the literature attempting it uses gram doses specifically to offset inflammation-driven turnover. Those two claims get merged into one sentence in marketing copy. They should not be.

What ascorbate does inside those cells is better characterised than "supports immunity" suggests. In people with inadequate status, below about 50 µmol/L, supplementation increased neutrophil chemotaxis by roughly 20% and oxidative burst capacity by a similar margin. It also promotes neutrophil apoptosis and macrophage clearance of spent neutrophils — resolving an inflammatory response rather than prolonging it, the under-communicated half of the story. And collagen reappears here: epithelial and mucosal barriers are collagen structures, and a barrier is the first immune defence there is.

Sustained oxidative load does the same thing on a slower clock, which is why we treat smoke exposure and heavy training as separate topics. The population whose turnover is elevated is not the population the average RDA was calculated for.

Where Vitamin C Sits in the Antioxidant Network

Vitamin C is the primary water-soluble chain-breaking antioxidant in plasma, cytosol and extracellular fluid. It is the first plasma antioxidant consumed when oxidants arrive — measurably depleted before urate, tocopherol or bilirubin. That much is settled. The more useful fact is that it does not work alone. It is one node in a recycling chain:

• α-Tocopherol sits in the membrane and terminates lipid peroxidation chains. Doing so turns it into the α-tocopheroxyl radical — a spent antioxidant that is itself a radical.
• That radical's chromanol head projects into the membrane-water interface, where ascorbate can reach it and reduce it back to α-tocopherol. Without that step, one tocopherol molecule handles one radical and is finished. With it, a small pool handles many.
• Ascorbate becomes the ascorbyl radical, reduced back by NADH-cytochrome b5 reductase and thioredoxin reductase, or disproportionating to dehydroascorbate.
• Dehydroascorbate is reduced back to ascorbate by glutathione, via glutaredoxin.
• Oxidised glutathione is regenerated by glutathione reductase, which requires FAD from riboflavin and NADPH from the pentose phosphate pathway.

The vitamin C to vitamin E step is thoroughly established in vitro and in human erythrocytes, and Traber and Stevens's review in Free Radical Biology and Medicine (2011) summarises the in vivo human work — deuterated α-tocopherol kinetic studies in smokers, where vitamin C supplementation slowed the disappearance of plasma α-tocopherol. Vitamin C spares vitamin E in living people, not just in a test tube.

Follow the chain to its end and you land somewhere useful: every enzyme in it is built around a mineral or a B vitamin. Glutathione peroxidase needs selenium. Glutathione reductase needs riboflavin-derived FAD. Superoxide dismutase needs copper and zinc in the cytosol and manganese in the mitochondrion. Catalase needs heme iron. You cannot buy antioxidant capacity in a bottle; you build the machinery from a spread of trace elements and B vitamins in usable forms. Honestly noted: riboflavin is load-bearing in that chain and Current does not contain it — its six B vitamins are B1, B3, B5, B6, B9 and B12. Riboflavin comes from dairy, eggs, almonds and fortified grains.

One more honest note. The existence of this network is not an argument for megadosing any single node. It is closer to the opposite — flooding one input mostly raises disposal flux and can shift redox signalling in directions you did not intend, which is the story of why the large antioxidant trials failed.

Vitamin C, BH₄, and Nitric Oxide

Tetrahydrobiopterin, or BH₄, is the obligate cofactor for endothelial nitric oxide synthase, and also for phenylalanine, tyrosine and tryptophan hydroxylases. When BH₄ is oxidised, eNOS "uncouples" and produces superoxide instead of nitric oxide — a central mechanism in endothelial dysfunction, and a vicious cycle, because the peroxynitrite formed from superoxide plus nitric oxide oxidises more BH₄.

Vitamin C intersects this, but not the way most articles claim. The mechanism is probably not direct reduction of BH₂ back to BH₄. Reviews including Heller, d'Uscio and colleagues in Nitric Oxide (2014) conclude that ascorbate more likely stabilises BH₄ chemically by scavenging the trihydrobiopterin radical before it disproportionates, scavenges superoxide so nitric oxide is not consumed forming peroxynitrite, and may increase BH₄ binding affinity at the enzyme.

The defensible sentence: vitamin C helps protect tetrahydrobiopterin, a cofactor your blood vessels need in order to make nitric oxide. More specific than "vitamin C is an antioxidant," more accurate than "vitamin C regenerates BH₄." We take the full pathway apart in our guide to nitric oxide and circulation, including the dietary nitrate route that runs in parallel and does not depend on eNOS at all.

This is also where the 50 mg VitAlign complex in Current fits — a seven-food polyphenol blend studied in three peer-reviewed human trials at 50 mg a day: Nemzer 2017 in Free Radical Research, Nemzer 2021 in the Journal of Food Research (double-blind, placebo-controlled, randomised), and Fink 2025 in the International Journal of Molecular Sciences (randomised, double-blind, with vitamin C as the positive control). The supplier's approved language is that it increases a stable long-lasting form of NO and supports healthy endothelial and cardiovascular function. Keep the frame straight: that is evidence about an ingredient at a specified dose, several studies are manufacturer-affiliated, and sample sizes are modest. You can read the ingredient list in full on the Current product page.

Does Vitamin C Help You Absorb Iron?

Yes, and the honest version of that answer is smaller than the version you have read elsewhere.

The mechanism is solid. Non-heme iron — the form in plants, eggs and fortified foods — is absorbed by the DMT1 transporter, which accepts only ferrous Fe²⁺. Most dietary non-heme iron arrives as ferric Fe³⁺. Ascorbate reduces Fe³⁺ to Fe²⁺ and chelates it into a soluble complex that resists the inhibitors in food: phytate in grains and legumes, polyphenols and tannins in tea and coffee, and calcium. Siegenberg and colleagues in the American Journal of Clinical Nutrition (1991) showed ascorbate overcoming dose-dependent phytate and polyphenol inhibition directly.

Then comes the counter-evidence, which almost nobody quotes. Cook and Reddy, also in the AJCN (2001), used isotope-labelled iron in 12 subjects across three dietary periods with ascorbic acid intake varying from 51 to 247 mg a day. There was no significant difference in mean iron absorption among the three periods. Their conclusion, verbatim: "The facilitating effect of vitamin C on iron absorption from a complete diet is far less pronounced than that from single meals."

Why the gap? Single-meal studies are designed to maximise the effect — one simple, low-iron, high-inhibitor test meal after a fast. Across a whole mixed diet, with heme iron, meat factor, several meals a day and hepcidin regulating uptake at the enterocyte, the marginal contribution of extra ascorbate largely washes out. That is also the best explanation for why long-term supplementation trials have repeatedly shown negligible effects on iron status.

So the accurate claim is narrow and still useful: at a plant-based, phytate-heavy, iron-poor meal, a vitamin C source at the same sitting can meaningfully improve iron uptake. Across an omnivorous mixed diet, do not expect much. How minerals compete and cooperate at shared transporters is covered in the trace minerals guide and in our comparison of sea-derived versus synthetic mineral sources.

Vitamin C and the Common Cold: The Honest Numbers

We agree with Cochrane. Then we add the part the headline leaves out. Hemilä and Chalker's Cochrane review is the reference; doses in the included trials were generally 200 mg a day or more, most commonly 1 g.

Two things follow. "Vitamin C prevents colds" is not a defensible sentence in the general population, and taking it at the first sniffle has not shown consistent benefit. And that 0.48 under sustained physical and cold stress is one of the most striking context effects in nutrition — the same intervention does nothing in ordinary adults and halves incidence in soldiers on subarctic exercises. The variable is not the molecule. It is the state of the person taking it.

Where to Get Vitamin C From Food

Food first, and it is not hard. Vitamin C is water-soluble and heat-labile, so boiling leaches it into the water and long cooking degrades it.

Values from the NIH Office of Dietary Supplements. Two servings of most things on that list clears the RDA, which is why the 46%-below-EAR figure is a story about eating patterns rather than food quality — a different problem from the declining mineral density in the soil depletion data.

Cautions: Who Should Be Careful

Vitamin C at 500 mg a day is a very safe dose. That is not the same as saying no caution applies to anyone.

Kidney stones. Ascorbate is metabolised in part to oxalate. The best evidence is Ferraro and colleagues in the American Journal of Kidney Diseases (2016), pooling the Nurses' Health Studies I and II and the Health Professionals Follow-up Study — 197,271 participants, median follow-up over 11 years, 6,245 incident stones. Men taking 1,000 mg a day or more from supplements had a hazard ratio of 1.19 (95% CI 1.01-1.40). Women showed no association at any intake, and dietary vitamin C showed none in either sex. At 500 mg a day no cohort has demonstrated increased risk. With a history of calcium-oxalate stones or hyperoxaluria, keep supplemental vitamin C moderate and talk to your clinician.

Iron overload conditions. In hereditary hemochromatosis, thalassemia and transfusional iron overload, high-dose vitamin C could exacerbate iron loading, and there are case reports of arrhythmia in iron-overloaded patients. For the general population there is no evidence that supplemental vitamin C causes iron overload — healthy people downregulate uptake as stores rise.

GI effects. Osmotic diarrhea, cramping and nausea at gram doses. This is what the 2,000 mg upper limit is built on.

Lab interference. High-dose vitamin C can falsely elevate some glucometer readings and produce false negatives on fecal occult blood tests.

If you are comparing products on total formulation rather than one number, we have done that work: the electrolyte powder comparison puts the category side by side, Current versus LMNT covers the sodium-first approach and what it leaves out, and daily minerals versus sports hydration explains why the two categories solve different problems.

Where the Evidence Is Weak

• Tissue saturation above plasma saturation. The argument that adrenal, brain or lens compartments benefit from intakes above the plasma plateau is mechanistically plausible and has never been shown to produce a measurable benefit in humans. It is a hypothesis.
• The leukocyte concentration figure. Sources give 50-100× plasma, 10-30× plasma, and "at least 14-fold." They measure at different plasma states. The honest version is "roughly 1 millimolar inside the cell, on the order of 10 to 100 times plasma depending on status."
• The BH₄ mechanism. Protection versus regeneration is not settled. Claims that vitamin C "regenerates BH₄" outrun the data.
• The iron multiplier. The widely repeated "100 mg triples non-heme iron absorption" figure comes from single-meal protocols, we could not verify a specific multiplier against a primary source, and the whole-diet data contradict the framing. So we are not publishing a number.
• Specialty forms. Liposomal, buffered and Ester-C products are marketed on bioavailability claims that mostly lack head-to-head human pharmacokinetic support.
• Treating established infection. Gram-dose protocols are a live research question, not settled practice, and entirely separate from prophylactic adequacy at 100-200 mg a day.

Myths Worth Retiring

• "Vitamin C prevents colds." RR 0.97 across 29 comparisons and 11,306 people. It does not. Say the marathoner and soldier finding instead — that one is real and more interesting.
• "Take it at the first sign of a cold." Seven comparisons, 3,249 episodes, no consistent effect.
• "More vitamin C means more in your blood." Plasma plateaus at 200-400 mg a day, and bioavailability falls from 87% at 30 mg to 63% at 500 mg to under 50% at 1,250 mg.
• "It's all just expensive urine." Wrong in the other direction — that dismissal ignores 6.8% frank deficiency, 46% of adults below the EAR from food, and the real 8-14% duration effects.
• "Vitamin C causes kidney stones." Only supplemental intake at 1,000 mg a day or more, only in men, HR 1.19. Dietary vitamin C: no association. Women: no association.
• "Vitamin C is dangerous because of iron." Only in diagnosed iron-overload conditions.
• "Vitamin C triples iron absorption." In a single test meal, perhaps. Across a whole diet at 51-247 mg a day, Cook and Reddy found no significant difference.
• "Liposomal C is dramatically more bioavailable." Not established, and no format escapes the transporter ceiling.
• "Rebound scurvy" after stopping megadoses. No controlled human evidence.
• "Vitamin C boosts immunity." It is required for normal immune function, and deficiency impairs it. In replete people, more is not better — the cells are saturated at 100 mg a day.

Frequently Asked Questions

How much vitamin C should I take a day?

The RDA is 90 mg for adult men and 75 mg for adult women, plus 35 mg more for smokers. White blood cells saturate at about 100 mg a day and plasma plateaus between 200 and 400 mg. Intakes of 100-200 mg cover adequacy for most people; 500 mg sits past every measured saturation point and well under the 2,000 mg upper limit.

Can you take too much vitamin C?

The upper intake level is 2,000 mg a day for adults, set on osmotic diarrhea and GI distress rather than organ toxicity. In three large prospective cohorts, supplemental intakes of 1,000 mg a day or more were associated with a 19% higher relative risk of kidney stones in men, with no association in women and none for dietary vitamin C.

Does vitamin C prevent colds?

No. The Cochrane review pooled 29 comparisons in 11,306 people and found a risk ratio of 0.97 for cold incidence in the general community. Regular supplementation does modestly shorten colds, by about 8% in adults and 14% in children. The exception is people under extreme physical stress, such as marathon runners, skiers and soldiers on subarctic exercises, where incidence was roughly halved.

Is liposomal vitamin C better absorbed?

Not established. Comparative human data mostly show modest or no difference versus plain ascorbic acid at equivalent doses, and no delivery format changes the saturable transport ceiling or the renal threshold that dumps the excess. Treat bioavailability claims as unproven unless a head-to-head human pharmacokinetic study is cited.

What are the symptoms of vitamin C deficiency?

The earliest symptoms are fatigue and lethargy, which reflect impaired carnitine synthesis rather than bleeding. Frank scurvy follows roughly a month of intake below 10 mg a day and produces perifollicular hemorrhage, corkscrew hairs, bleeding gums, poor wound healing and joint pain, all downstream of under-hydroxylated collagen.

Should I take vitamin C in the morning or at night?

Timing barely matters for status, because the body pool at saturation is 1,500 to 2,000 mg and turns over at roughly 3% a day. What matters is splitting large doses, since fractional absorption falls as single-dose size rises, and taking it with a plant-based meal if the goal is iron absorption.

Does vitamin C help with iron absorption?

It reduces ferric iron to the ferrous form the DMT1 transporter accepts and chelates it against phytate and polyphenol inhibitors. The effect is large in single-meal test protocols and much smaller across a whole mixed diet: one isotope study found no significant difference in whole-diet iron absorption across a 51-247 mg per day range. It matters most at a plant-based, phytate-heavy meal.

What foods have the most vitamin C?

Half a cup of raw red bell pepper has about 95 mg, three quarters of a cup of orange juice about 93 mg, a medium orange 70 mg, a kiwifruit 64 mg, half a cup of cooked broccoli 51 mg and half a cup of sliced strawberries 49 mg. Vitamin C is water-soluble and heat-labile, so boiling leaches it and raw or lightly steamed produce retains more.

Vitamin C is one of the few nutrients where the honest story beats the marketing. It is not a shield against colds. It is the reset button on eight enzymes that build the physical structure of you, and it obeys a saturation curve that has been mapped in humans since 1996. Know where you sit on that curve, cover the gap, and stop paying for urine. Life's better mineralized.

Sources

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22. Fink B, et al. Randomised double-blind study of a polyphenol complex with vitamin C as positive control. International Journal of Molecular Sciences, 2025.

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. This article is for educational purposes and is not medical advice. Talk to your doctor before starting any supplement, especially if you are pregnant, nursing, have kidney disease, or take prescription medication.