Vitamin C

[ecstatichamster]

I wonder why Dr. Peat has been so negative about vitamin C. Or at least never positive.

 

[yerrag]

I wonder why Dr. Peat has been so negative about vitamin C. Or at least never positive.

His main beef is the presence of high levels of lead. But Ray has been negative more on account of high contaminant levels not just on vitamin C, but on many other substances that otherwise have beneficial effects.

 

[ecstatichamster]

His main beef is the presence of high levels of lead. But Ray has been negative more on account of high contaminant levels not just on vitamin C, but on many other substances that otherwise have beneficial effects.

yes. He probably has a point. "Sooner or later" supplements cause harm. And he's right about that.

I will have to see if he has ever said anything good about ascorbic acid.

 

[Amazoniac]

- Biological Significance of Ascorbic Acid (Vitamin C) in Human Health – A Review
- Biological Significance of Ascorbic Acid (Vitamin C) in Human Health – A Classic Review (??)

"The body uses it in two hours and then usually out of the blood within three to four hours."

"The synergistic combination of vitamin C and vitamin E may be further enhanced by the addition of vitamin A."

"A classical antioxidant combination is formed when vitamin C is added with vitamin E, beta-carotene and selenium." "It has helped to alleviate pancreatitis, or an inflammation of the pancreas, in one study."

"(Reactive Oxygen Species) ROS-induced enhancement in lipid per oxidation plays an important role in the mechanism of gastric damage induced by (aspirin) ASA, vitamin C attenuates the deleterious effect of ASA on ulcer healing due to its antioxidizing activity by mechanism involving preservation of gastric microcirculation and attenuation of lipid per oxidation and cytokine release and coupling of NO to aspirin fails to delay the ulcer healing suggesting that NO might compensate for prostaglandin deficiency induced by nonsteroidal anti-inflammatory drugs (NSAID) (Brzozowski et al., 2001)."

"A Californian study has concluded that people who consume more than 750 mg/d of vitamin C reduce their risk of dying prematurely by 60% (Enstrom, 1992)."

"Vitamin C fights off widespread environmental pollutants including CO, hydrocarbons, pesticides and heavy metals by stimulating enzymes in the liver that detoxify the body. In several studies, vitamin C has reduced chromosome abnormalities in workers exposed to pollutants such as coal tar, styrene, methyl methacrylate and halogenated ethers. Vitamin C also protects us by preventing the development of nitrosamines, the cancer causing chemicals that stem from the nitrates contained in many foods (Gaby and Singh, 1991)."

"Recent studies have shown that vitamin C concentration in the blood from rheumatoid arthritis patients are extremely low and that vitamin C may protect against further damage to inflamed joints (Lunec, 1985; Halliwell, 1987)." "Vitamin C may provide podiatrists with a supplemental or alternative treatment for patients with rheumatoid arthritis (Davis, 1990). Another study found that the rapid depletion of vitamin C at the site of an inflammation such as a rheumatoid joint-may facilitate proteolytic damage (Helliwell, 1987)."

"As supplementing with vitamin C has been found to significantly lower the risk of cataracts and glaucoma (Hankinson, 1992), some very recent works has shown that open angle glaucoma can be reversed by supplementing with large doses of vitamin C (Boyd, 1995)."

"Bioflavonoids, taken with vitamin C (1200 mg each) has been shown to help relieve hot flashes associated with menopause (Smith, 1964)."

"[..]vitamin C may contribute to immune defense in an even more fundamental way: skin and the epithelial lining of the intestines, both of which contain collagen, serve as first line of defense against foreign invaders (Gaby and Singh, 1991)."

"It also stimulates the production of PGE1, a prostaglandin, which assists lymphocytes, the defender cells in our immune system."

"Vitamin C helps the immune system to fight viruses (Anderson and Lukey, 1987). It acts as an antiviral agent (Gerber et al., 1975), elevating body's interferon level."

"In laboratories, Vitamin C has been found to inhibit HIV replication (Harakeh, 1990). With its antioxidant and immunity-enhancing abilities, vitamin C is an excellent supplement for HIV patients, as it may help with disease resistance and overall well being (Cathcart, 1984)."

"Vitamin C, taken at levels of 2 grams daily, may help the body fight against infection via hepatitis-contaminated blood (Morishige and Murata, 1978)."

"In one large study, 260 patients with viral hepatitis A took 300 mg of vitamin C a day for several weeks. The researchers, who studied immune indicators, such as serum immunoglobulin and neutrophil phagocytosis, concluded that vitamin C 'exerts a remarkable immunomodulating action' (Vasiliev et al., 1989)."

"Four weeks daily high ascorbic acid treatment in H. Pylori infected patients with chronic gastritis resulted in apparent H. Pylori eradication in 30% patients, which was associated with increased gastric concentration of ascorbic acid."

"The current RDA of 60 mg/d is clearly far too low and the proposed new RDA of 200 mg/d while perhaps adequate for healthy, young males, would seem to be quite inadequate for older people and certainly too low for sick people. As a matter of fact, a scientific advisory panel to the U.S. Government-sponsored Alliance for Aging Research recently recommended that all healthy adults increase their vitamin C intake to 250-1000 mg/d (Voelker et al., 1994)."

"A daily intake of 250-1000 mg/d may be adequate for preventive purposes, but far larger quantities are required in halting or reversing cancer and heart diseases."

"Deficiency of vitamin C can cause anemia, scurvy, infections, bleeding gums, muscle degeneration, poor wound healing, atherosclerotic plaques and capillary hemorrhaging. Neurotic disturbances consisting of hypochondriasis, hysteria and depression followed by decreased psychomotor performances have been reported in ascorbic acid deficiency (Kinsman and Hood, 1971). Vitamin C deficiency is often associated with gingivitis."​

So, is the urine acidity at 5.5 or less going to solve the urinary tract infection? If so, how long should the urine acidity have to stay at 5.5 or less? I suppose that for a limited duration, the body can tolerate such low urine pH. But then the body will have to go back to having its acid-base balance restored, otherwise being in an acidic state for a long period will cause excessive urination, loss of electrolytes and b1, to name a few nutrients lost, and it will weaken the immune system.

Some of the daily doses used aren't far from what people who supplement here get (I know you neutralize yours). The acidification is to help this drug work.

"Holland and West[two] described the use of ascorbic acid in combination with methenamine mandelate in children with recurrent urinary infection. These authors indicate that ascorbic acid (approximately 1.5 to 6.0 Gm. daily) given at the same time as methenamine mandelate ("in three to four divided doses") keeps the urine pH below 5.6."​

But here are their results:

"The 8 patients in Group I received ascorbic acid in 4 equally divided doses before each meal and at bedtime. The patients in Group II received the same total daily dosage, but it was administered every 4 hours."

Spoiler: Table I

How Measuring My Urine pH Got Me to Love Working Out Again | Chris Masteryohn

"'Normal' urine pH is 5.5-8.0. Optimal urine pH is probably 6.4-6.8 during most of the day."​

I wonder why Dr. Peat has been so negative about vitamin C. Or at least never positive.

I think the main reason is because he experienced some adverse effects from it and started to rationalize about it (apparently Gerson's stance against sodium is similar). But Unfortunately this likely limits other therapeutic approaches that won't work unless you have plenty of vit C available, one of them is getting extra iodine.

What's his opinion on vit C from powdered fruits?

 

[Amazoniac]

Is all of the ascorbate absorbed regardless of the pairing mineral? Because if some escapes initial digestion intact, it might depend on the complex..
http://www.george-eby-research.com/html/stability_constants.html

 

[Amazoniac]

Too much focus on one factor: iron.

The body needs ceruloplasmin to oxidize ferrous iron (iron II) to ferric iron (iron III), which is also less accessible to infectious organisms because iron III can be more readily sequestered by the ferritin protein. Ceruloplasmin is part of the ferroxidase complex in the body that accomplishes this.

Ceruloplasmin relies on bioavailable copper and whole food vitamin C (not ascorbic acid) to be formed. Whole food C has tyrosinase at its core, which is comprised of bioavailable copper. Magnesium is also a key factor in displacing unbound iron from tissues.

Without adequate ceruloplasmin, whole food C and magnesium, iron remains in ferrous form, remains unbound, and causes oxidative damage to the tissues. Most people in modern society are lacking in bioavailable copper and magnesium. Taking a copper supplement won't work, it'll just increase toxic copper in the body, no different than if you regularly drink water from copper pipes. Organic copper is found in things like sesame seeds, shellfish, bovine liver, etc.

If you flood a person's body with unbound iron and they are lacking in these important co-factors, then they will develop iron related diseases. It's why some people can get iron IVs and be just fine while others feel sick for days. The African studies are a reflection of this. People are poor and malnourished, so of course iron is going to feed infections. The people have no co-factors to buffer the unbound iron so that pathogenic organisms can't access it. Cancers work the same way. When the body develops cancer, it starts pumping out ferritin to sequester the iron from the cancer; but the ferritin can't bind the iron without ceruloplasmin.

You're making these claims again. It's not a C-complex, it's vit C, so it has to be ascorbic acid. I'm not playing the expert here, it's just that I only came across those statements when visiting websites that sell powdered fruits rich in C. Is it possible that you're currently working for this industry?

I'm confused by the tyrosinase thing and its usefulness. It's supposed to be present in foods that brown when they is cut, a reaction that involves the quinones that Alberto commented here.

- Polyphenol oxidase - Wikipedia

"PPO causes the rapid polymerization of o-quinones to produce black, brown or red pigments (polyphenols) that cause fruit browning. The amino acid tyrosine contains a single phenolic ring that may be oxidised by the action of PPOs to form o-quinone. Hence, PPOs may also be referred to as tyrosinases.[2]

Common foods producing the enzyme include mushrooms (Agaricus bisporus), apples (Malus domestica) and lettuce (Lactuca sativa)."​

- Fruits: Enzymatic Browning
- No more brown apples?


Camu-camu composition according to the following publication:
- Characterization of the Fruit Pulp of Camu-Camu (Myrciaria dubia) of Seven Different Genotypes and Their Rankings Using Statistical Methods PCA and HCA

Vitamin C: 2 g/g (or 1-6 g/g reported elsewhere)
Cupre: 3.5 mcg/g at most​

You've mentioned taking 1 g of vit C somewhere on the foro from powdered camu-camu. How is that even impacting your copper levels?


Arguing that flavonoids have a synergistic effect is another story, but the effects from ascorbic acid don't depend on them.

- Flavonoids
- USDA Database for the Flavonoid Content of Selected Foods


Apparently vit C changes copper's behavior in the body by making it available to the cell by reducing it to a state that's dissociable from ceruloplasmin (transfered by glutathiod to the antioxidant enzyme superoxide dismutase for example), which is why on greater intakes of vit C ceruloplasmin level can be decreased.

When copper intake is low, detrimental effects become evident. To not compromise copper on high intakes of vit C, you have to increase it as well. And it makes no sense to supplement copper if you can get plenty from diet.

 

[Orius]

You're making these claims again. It's not a C-complex, it's vit C, so it has to be ascorbic acid. I'm not playing the expert here, it's just that I only came across those statements when visiting websites that sell powdered fruits rich in C. Is it possible that you're currently working for this industry?

I'm confused by the tyrosinase thing and its usefulness. It's supposed to be present in foods that brown when they is cut, a reaction that involves the quinones that Alberto commented here.

- Polyphenol oxidase - Wikipedia

"PPO causes the rapid polymerization of o-quinones to produce black, brown or red pigments (polyphenols) that cause fruit browning. The amino acid tyrosine contains a single phenolic ring that may be oxidised by the action of PPOs to form o-quinone. Hence, PPOs may also be referred to as tyrosinases.[2]

Common foods producing the enzyme include mushrooms (Agaricus bisporus), apples (Malus domestica) and lettuce (Lactuca sativa)."​

- Fruits: Enzymatic Browning
- No more brown apples?


Camu-camu composition according to the following publication:
- Characterization of the Fruit Pulp of Camu-Camu (Myrciaria dubia) of Seven Different Genotypes and Their Rankings Using Statistical Methods PCA and HCA

Vitamin C: 2 g/g (or 1-6 g/g reported elsewhere)
Cupre: 3.5 mcg/g at most​

You've mentioned taking 1 g of vit C somewhere on the foro from powdered camu-camu. How is that even impacting your copper levels?


Arguing that flavonoids have a synergistic effect is another story, but the effects from ascorbic acid don't depend on them.

- Flavonoids
- USDA Database for the Flavonoid Content of Selected Foods


Apparently vit C changes copper's behavior in the body by making it available to the cell by reducing it to a state that's dissociable from ceruloplasmin (transfered by glutathiod to the antioxidant enzyme superoxide dismutase for example), which is why on greater intakes of vit C ceruloplasmin level can be decreased.

When copper intake is low, detrimental effects become evident. To not compromise copper on high intakes of vit C, you have to increase it as well. And it makes no sense to supplement copper if you can get plenty from diet.

No I don't work for an industry. I also said nothing about C complex, just whole food C. C complex supplements are a scam. You can add all the flavonoids you want to a product but if the base ingredient is ascorbate, you'll never have whole C. Ascorbic acid is not complete C because it lacks the tyrosinase core. This is important because although the body is incapable of manufacturing C, it can complete its missing function by using ceruloplasmin to complement the absence of tyrosinase at the core of ascorbate. This in turn depletes ceruloplasmin, which hinders feroxidase function.

It's not that whole food C provides copper, it's that it prevents bioavailable copper depletion. If people take several grams of ascorbate daily, it will eventually have deleterious effects on ceruloplasmin for this reason. This may be why Ray noted that ascorbic acid harmed him.

Tyrosinase is used by the adrenal gland as well. It's not just involved in melanin production. Whole food C as part of electrolyte formulas does wonders for adrenal fatigue.

Whole vitamin C also contains factor J, factor P, factor K, ascorbinogen and rutin. Ascorbic acid is just a fraction of the whole vitamin and doesn't have the same active properties. The body will draw on its own resources to make up these missing components. It can in some cases but not in others.

I encourage people to try whole food C vitamins derived from food to experience the difference. Don't buy C complex formulas, they're a scam and are still fractionated. Things like acerola cherry and camu have loads of whole food C.

 

[yerrag]

Ascorbic acid is just a fraction of the whole vitamin and doesn't have the same active properties.

Do you have references to back this? I'm interested in knowing more about this.

 

[Amazoniac]

No I don't work for an industry. I also said nothing about C complex, just whole food C. C complex supplements are a scam. You can add all the flavonoids you want to a product but if the base ingredient is ascorbate, you'll never have whole C. Ascorbic acid is not complete C because it lacks the tyrosinase core. This is important because although the body is incapable of manufacturing C, it can complete its missing function by using ceruloplasmin to complement the absence of tyrosinase at the core of ascorbate. This in turn depletes ceruloplasmin, which hinders feroxidase function.

It's not that whole food C provides copper, it's that it prevents bioavailable copper depletion. If people take several grams of ascorbate daily, it will eventually have deleterious effects on ceruloplasmin for this reason. This may be why Ray noted that ascorbic acid harmed him.

Tyrosinase is used by the adrenal gland as well. It's not just involved in melanin production. Whole food C as part of electrolyte formulas does wonders for adrenal fatigue.

Whole vitamin C also contains factor J, factor P, factor K, ascorbinogen and rutin. Ascorbic acid is just a fraction of the whole vitamin and doesn't have the same active properties. The body will draw on its own resources to make up these missing components. It can in some cases but not in others.

I encourage people to try whole food C vitamins derived from food to experience the difference. Don't buy C complex formulas, they're a scam and are still fractionated. Things like acerola cherry and camu have loads of whole food C.

That's unfortunate, they pay well.. I heard.


But now I'm more confused than before. The questioning was that there is no whole C, the rest are varied consaieutaoittsants of foods.

It seems that those are obsolete terms for discovered compounds:
- Vitamin - Wikipedia


Factor P are the flavonoids, rutin is one of them so it makes no sense to isolate it.

- The antioxidant effects of the flavonoids rutin and quercetin inhibit oxaliplatin-induced chronic painful peripheral neuropathy

"The flavonoids rutin and quercetin are polyphenolics compounds found in vegetables, fruits, herbs, leaves, seeds [13,14], red wine, tea, coffee, beer, and several medicinal plants. Rutin is a bioflavonoid and antioxidant. It is water-soluble and converted to quercetin once it enters the blood stream [15]. Several studies have found that these flavonoids have antiinflammatory [16-18], analgesic [19], and antioxidant [20] effects."
​

- Quercetin, but Not Its Glycosidated Conjugate Rutin, Inhibits Azoxymethane-Induced Colorectal Carcinogenesis in F344 Rats

"One of the major flavonoid representatives in the human diet is quercetin, which in its natural form is glycosylated and can be found in fruits and vegetables, including blueberries, onions, curly kale, broccoli, and leek (5). Once ingested, conjugated quercetin can be released by intracellular and membrane-bound β-glycosidases of small intestinal cells (6). In the colon, on the other hand, quercetin glycosidic bonds can be hydrolyzed by local β-glycosidases produced by bacteria, leading to colonic release and absorption of quercetin (7). This is also the case with rutin (quercetin-3-O-β-rutinoside), the major quercetin glycoside found in tea."
​

Factor J might be catechol..

- Catechol - Wikipedia

"Small amounts of catechol occur naturally in fruits and vegetables, along with the enzyme polyphenol oxidase (also known as catecholase, or catechol oxidase). Upon mixing the enzyme with the substrate and exposure to oxygen (as when a potato or apple is cut and left out), the colorless catechol oxidizes to reddish-brown melanoid pigments, derivatives of benzoquinone. The enzyme is inactivated by adding an acid, such as the citric acid contained in lemon juice. Excluding oxygen also prevents the browning reaction. However, the activity of the enzyme increases in cooler temperatures. Benzoquinone is said to be antimicrobial, a property that slows the spoilage of damaged fruits and other plant parts."
​

- Catechol oxidase - Wikipedia

"Polyphenol oxidases are a family of di-copper metalloenzymes that include tyrosinase and catechol oxidase.[4] In plants, both enzymes can catalyze the oxidation of ortho-diphenols substrates into their corresponding ortho-quinones. The key difference between the two related enzymes is that tyrosinase can catalyze the hydroxylation of monophenols to diphenols (monophenolase activity) as well as the oxidation of the o-diphenol to the o-quinone (diphenolase activity) whereas catechol oxidase only possesses diphenolase activity.[5]"
​

Ascorbinogens..

- Evaluation of Brassica spp. genotypes for minerals and other biomolecules in edible leaves

"In addition to ascorbic acid and dehydroascorbic acid, Brassica vegetables include ascorbinogens, which are formed as a result of the reaction between ascorbic acid and degradation products of indole-3-ylmethylglucosinolates produced in the myrosinase catalysed degradation (Buskov et al 2000, Hrncirik et al 2001)."
​

- Vitamin Losses in Storage and Preparation of Food

[..]the ascorbic acid in prepared cabbage is present in the bound form, ascorbinogen, a form which is absorbed very poorly by man."​

- Flavonoids | Linus Pauling Institute (link from previous post)

"Flavonoids are effective scavengers of free radicals in the test tube (in vitro) (24, 25). However, even with very high flavonoid intakes, plasma and intracellular flavonoid concentrations in humans are likely to be 100 to 1,000 times lower than concentrations of other antioxidants, such as ascorbate (vitamin C), uric acid, and glutathione. Moreover, most circulating flavonoids are actually flavonoid metabolites, some of which have lower antioxidant activity than the parent flavonoid (5). For these reasons, the relative contribution of dietary flavonoids to plasma and tissue antioxidant function in vivo is likely to be very small or negligible (26-28)."

"Metal ions, such as iron and copper, can catalyze the production of free radicals. The ability of flavonoids to chelate (bind) metal ions appears to contribute to their antioxidant activity in vitro (29, 30). In living organisms, most iron and copper are bound to proteins, limiting their participation in reactions that produce free radicals. Although the metal-chelating activities of flavonoids may be beneficial in pathological conditions of iron or copper excess, it is not known whether flavonoids or their metabolites function as effective metal chelators in vivo (26)."
​

Regarding tyrosinase part, I read it multiple times but still doesn't make sense to me. Where can I find details about what you described?

The enzyme can be inhibited through multiple ways, vit C is one of the candidates:

- Estimation of Inhibitory Effect against Tyrosinase Activity through Homology Modeling and Molecular Docking
- Natural, semisynthetic and synthetic tyrosinase inhibitors

When ingested, it might be degraded before adsorption.


- Synthetic or Food-Derived Vitamin C—Is They Equally Bioavailable?


The problem in this story is that these people are grouping a lot of plant compounds and implying that there is a C-complex. It's a skin to claiming that vitamin E derived from soy is incomplete or not whole because the flavonoids aren't present, perhaps worse with vit C because at least vitamin E itself is indeed a complex.

 

[InChristAlone]

Here is a good article on the issue: The Nature of Vitamin C

"A 15-year study of 85,000 nurses at Harvard found that a daily vitamin C pill as ascorbic acid reduces heart disease almost 30%. Interestingly, dietary intake of vitamin C seemed to have little effect on coronary heart disease risk. But if women used vitamin C supplements, their risk was reduced by 27 percent. According to the numbers in the Harvard study, a 360 mg vitamin C pill daily would save more than 300,000 lives per year. (Osganian 2003)"

"The biochemist Sherry Lewin writes in his book Vitamin C: Its Biology and Medical Potential (1976) about the exact biochemical nature of vitamin C. Lewin, perhaps the greatest authority on vitamin C other than Pauling never mentions even the possibility of a vitamin C-complex."

"Vitamin C as ascorbic acid is unique among the vitamins. Ascorbic acid is produced by most animals in large amounts. Rather than a complicated coenzyme, ascorbic acid is a rather simple sugar-like molecule and the animals synthesize it using a 4-step process. Few species have survived after losing the ability to synthesize ascorbate.

This has created a valid argument as to whether vitamin C is really a "vitamin" (the term vitamin implies a trace factor), or whether humans require this substance in much higher amounts."

 

[Orius]

I've said my piece :)

You have to decide for yourselves now. Cheers.

 

[Amazoniac]

- Altered Ascorbic Acid Status in the Mucosa from Inflammatory Bowel Disease Patients

"The activities of catalase, superoxide dismutase and glutathione peroxidase [in human colonic mucosa] have been reported to be only 4, 8, and 45% of that found in the liver.[6] Specific activities of these enzymes within the subfractionated mucosa suggest that the colonic epithelium is relatively well protected compared to the lamina propria. The colonic mucosal content of reduced glutathione (GSH), a co-substrate for GSH-peroxidase which catabolises H2O2 and can interact with ROS directly, is decreased by 27% in inflamed mucosa from IBD patients.[7] Such a decrease in GSH is suggestive of increased oxidative stress, but it is insufficient to establish the linkage definitively. Studies on plasma vitamin status in patients with IBD have found that plasma concentrations of vitamins A, C, E and b-carotene are decreased in IBD patients with 40-50% of patients at risk of developing hypovitaminois. Indeed, one report documents a CD patient with scurvy.[10] Among the chemical antioxidants, vitamin C or ascorbic acid is regarded as one of the most important in the prevention of lipid peroxidation.[11,12] Ascorbic acid acts as a strong reducing agent capable of reducing oxygen, nitrogen and sulphur-centred radicals.[13] In addition to scavenging radicals directly, ascorbic acid is a key reductant which acts in concert with other chain-breaking antioxidants such as vitamin E, ubiquinol-10, b-carotene, uric acid, thiols and bilirubin in the formulation of the overall antioxidant defence capacity.[14]"

"In this investigation, the mucosal concentrations of ascorbic acid and its redox status have been determined in paired biopsies from both inflamed and non-inflamed sites from IBD patients. When compared to the non-inflamed mucosa of the same patient, the content of reduced and total ascorbic acid was markedly decreased in the inflamed mucosa. The magnitude of the loss of ascorbic acid is such that it may seriously impair the antioxidant defences of the inflamed mucosa and place oxidative pressure on other antioxidant compounds."

"Here we present the first analysis of the redox status of ascorbic acid - the prime chain-breaking antioxidant - in mucosal biopsies from IBD patients." "There were two main observations arising from this investigation."

"The first was that the redox status of ascorbate in apparently normal mucosa was unusually low (about 30%) whereas in other tissues and in blood the redox ratio is typically >80-95%. The cause of the low redox status of ascorbate from apparently normal mucosa may be due to [usual] oxidative stress derived from faecal material containing multiple forms of metal ion catalysts, potential carcinogens and oxidising agents.[3,26,27] Indeed, ascorbic acid has been proposed to play an important role in the protection of the mucosa from ROS.[28] Compounding this, the mucosal ascorbate redox status would also be influenced by dietary ascorbate intake. It is not known how much ascorbate reaches the colonic lumen or its lumenal redox status,[29] however, given the faecal content of potentially oxidising agents, it is likely that a substantial proportion is present as dehydroascorbic acid (DHAA).

"The mechanisms of ascorbate transport which operate in the human colonic mucosa remain to be explored in detail, however, the high proportion of total ascorbate present as DHAA may well be due to the combined effects of luminal oxidant stress and uptake of DHAA at a rate which exceeds either the capacity of the DHAR or the supply of essential reducing equivalents."

"The second striking observation of these studies was the decrease in the absolute concentrations of both reduced and total ascorbic acid in the inflamed mucosa compared to that detected in paired specimens of non-inflamed mucosa from the same patient. The decrease in ascorbate content may be a direct result of overwhelming oxidative stress in the form of activated inflammatory cells resulting in depletion of the total ascorbate pool. Reduced ascorbic acid reduces the tocopherol radical at the lipid/aqueous interface, the formed ascorbyl radical decomposes to dehydroascorbic acid, which under normal homeostasis, is recycled or reduced to ascorbic acid either directly by GSH or by a GSH-dependent DHAR.[20] DHAR activity has been reported in rat colon[30] but there is no report in human colonic mucosa."

"In the present study, 9/15 IBD patients had decreased DHAR activity in the inflamed mucosa suggesting that recycling of dehydroascorbic acid may be hindered. Moreover, a constant supply of reducing equivalents in the form of NADPH would also be required to maintain GSH in its reduced form via glutathione reductase. Few details are available on the status of reducing equivalents in the mucosa, although the inflamed epithelial cell is known to be metabolically impaired by the oxidative inhibition of GAPDH[25] and the decrease in the inflamed mucosa GSH content.[7] The oxidation of GAPDH and the decrease in mucosal GSH levels may result from the decomposition of H2O2 by GSH peroxidase or insufficient NADPH to reduce the GSSG catalysed by GSH reductase. The outcome of either mechanism would be a decrease in the reduced ascorbic acid pool and an accumulation of dehydroascorbic acid, which if not reduced efficiently, hydrolyses to 2,3-DKG. The inability to account for the loss of total ascorbate by the formation of 2,3-DKG is probably due to the high reactivity of 2,3-DKG with biomolecules[31] and may play a role in the increased risk of colorectal cancer in UC patients."

"A proportion of the decrease in total ascorbic acid and in ascorbate recycling in the inflamed mucosa may result from inhibition of mucosal uptake of ascorbate by the inflamed mucosa mediated by inflammatory cell-derived oxidative stress on transport mechanisms."

"While the mechanism of oxidation-mediated inhibition of ascorbate transport was not investigated here, ascorbate accumulation in guinea pig ciliary body/iris preparations is dependent upon on glucose metabolism and is sensitive to inhibition by iodoacetate.[34] In IBD, inhibition of glycolysis mediated by oxidation of GAPDH[25] would restrict the flux of reducing equivalents required for cellular transport/reduction processes and potentially adversely affect ascorbate uptake by the inflamed mucosa.[28] Indeed, the plasma concentrations of ascorbic acid, vitamin E and b-carotene in IBD patients have been reported to be significantly lower than those in controls and despite dietary multivitamin (including ascorbic acid) supplementation, ascorbic acid concentrations remained unchanged.[8,9]"

"The potential for ascorbic acid to participate in pro-oxidant reactions in the presence of metal ions[35] represents a further mechanism for the decreased ascorbic acid content in IBD mucosa. The lumen of the colon, particularly the inflamed colon in patients with bloody diarrhoea, and aberrant ascorbate metabolism, may be exposed to potentially catalytic metal ions in multiple forms.[3] A prime candidate would be haem proteins, particularly degraded haemoglobin. In these circumstances, the antioxidant capacity of ascorbic acid may then become pro-oxidant thereby promoting the formation of ·OH, O2·-, H2O2 and ferryl iron species.[3] In chemical systems, these pro-oxidant reactions of ascorbic acid inactivate glucose-6-phosphate dehydrogenase (G6PDH),[36] the key enzyme in the hexose monophosphate shunt and one critical for the generation of NADPH."

"[In summary, this] paper reports that the antioxidant defence capacity associated with ascorbic acid is compromised in the inflamed mucosa of IBD patients. The cause of this deficiency remains unknown and specific mucosal ascorbate transport studies are required to address this. Never-the-less, the decreases in ascorbic acid and in DHAR reported here may seriously undermine the capacity of the inflamed mucosa to protect itself against sustained oxidative stress during recurrent disease."​

 

[Dave Clark]

They say this is one of the highest debated vitamins. When I am on the fence about a substance, I often try to find the positive uses for both sides of the argument. With vitamin C, right now I use whole food C for my maintenance doses (daily), and if I have a need for high gram doses for say constipation or a histamine reaction that I want to quell, I use a C ascorbate powder. I think both have their place, just like high dose IV C has miraculous benefits for someone fighting an extreme health issue. Here is what I use daily: Unripe Green Acerola Cherry Powder- Organic Freeze Dried Unripe Acerola
About a gram of natural whole food C per teaspoon. I also blend that with rose hips, camu, and amla, which I get from Z Natural.
I think both forms of vitamin C have their place, and don't need to be so hotly debated.

 

[yerrag]

They say this is one of the highest debated vitamins. When I am on the fence about a substance, I often try to find the positive uses for both sides of the argument. With vitamin C, right now I use whole food C for my maintenance doses (daily), and if I have a need for high gram doses for say constipation or a histamine reaction that I want to quell, I use a C ascorbate powder. I think both have their place, just like high dose IV C has miraculous benefits for someone fighting an extreme health issue. Here is what I use daily: Unripe Green Acerola Cherry Powder- Organic Freeze Dried Unripe Acerola
About a gram of natural whole food C per teaspoon. I also blend that with rose hips, camu, and amla, which I get from Z Natural.
I think both forms of vitamin C have their place, and don't need to be so hotly debated.

That's a fair way of putting it, and it puts into context the condition/situation of the person. You can see that no one's ever saying that vitamin C found in whole foods is harmful, but you have natural purists airing their opinions regarding synthetic C being unhelpful, and even harmful. Yet, when you ask for more validation to their stance, they get irritated and end the conversation.

It's not that I'm just gung-ho on everything that's ascorbic acid. I've shared my concerns about taking large quantities of it making my body more acidic, which has made me urinate much more and disturbed my sleep patterns. But I also have turned to using bicarbonates to counter its effect, and it's been helpful. Nothing is cut and dried, and the process of experimenting on oneself is necessary, so that one can derive the benefits of a substance without the attendant downsides to using it. And then there's the practicality of having to take large amounts of whole foods to satisfy the need for large amount of vitamin C, as determined by the C-Flush test. Of course, one can simply rationalize the need for large amounts of vitamin C intake, reasoning that nature does not allow for practical intakes of such large quantities. But such reasoning is rather circular. Another caution of large intakes of synthetic C is the contamination with lead. Sourcing synthetic C well is just as important. Still, use of large amounts of synthetic C is predicated on its ability to manage a condition, not necessarily to correct it, and subsequently its use can be stopped or reduced. But if one has to depend on synthetic C like one depends on prescription drugs, it has to be an option of last resort. One has to be able to determine the cause of one's condition, so that the dependency of synthetic C is alleviated. In the case of people where the ability of the body to function normally is compromised, as in the case of elderly people, the use of synthetic C can be helpful, and the purism associated with having to source from whole foods should not keep one from using synthetic C. Perfectionism shouldn't keep one from benefiting from the imperfect that may help.

 

[Whichway?]

The argument about C being a complex and taking just ascorbic acid (vitamin C) on its own without any of the other compounds found with it in fruits and vegetables, causing deficiencies just hasn’t been demonstrated as far as I am aware. Vitamin C is listed as practically non-toxic, and has been used in IV in doses by doctors like Frederick Klenner, Linus Pauling and Robert Cathcart in doses as high as 200 grams per day. You would expect that if the vitamin was working as a complex, or its high dose so disrupted ceuruloplasmin levels, that taking such large doses by IV would quickly bring on such an imbalance, but it hasn’t.

Here’s a link to toxnet with lots of abstracts about safety of C. TOXNET

If people have information about whole C please add it to the thread so we can all take a look.

 

[Dave Clark]

I think Yerrag and Wichway have good points. My perception is that possibly any downsides to taking synthetic vitamin C might not show up until long term chronic use. However, more studies should be done to see if any assertions on either side is correct. Robbins says synthetic C stops ceuruloplasmin production, etc., but are there any studies showing this? I am comfortable using the whole food C as maintenance, and synthetic C for acute conditions short term. Somehow I get the feeling it may be more about the amount taken than the type. I used to take up to 10 grams/day, and now it makes me wonder if that amount did cause a dysregulation with some of my minerals, etc. Now, I have backed down to only a few per day.
Of course. this is just speculation on my part, I keeping reading and learning on this forum and other places in hopes more studies will come about.

 

[Amazoniac]

Contaminants

As commented before, Raj's concern must extend to various industrial acids, not just ascorbic; including amino acids as well, such as glycine (aminoacetic/ethanoic acid).

The risk can't be their amount because other foods contain way more crap.

Great Lakes' gelatin for example: noordinary in her pioneer work made way to a field of investigation on the total amount of metal impurities, which is up to 600 mcg per serving; but more than half is copper, so there can be a good deal of it per serving: 0.35 mg. Followed by up to 60 mcg of iron and fluoride. She discovered that their breakened-down collagen can have up to 600 mcg. This is brutal.

But the reason to be mentioning this is because it might have up to 18 mcg of lead per serving. It's quite high given that a French group in 2000 investigated the average intake from adults and found out it was 18 mcg per day.

As Such would say: laugh not to cry.

And there are people who combine them to do the innocent gummy bear. Ascorbic acid doesn't enhance the intake of lead, but it must be the reaction with impurities that is concerning.


Polyphenol Oxidases

Here's what Raj thinks:
- Ray Peat Email Exchanges - Ray Peat Forum Wiki

"Plant enzymes aren't much help after they are eaten."​

- Isolation and purification of tyrosinase from different plant sources

"Tyrosinases (monophenol, o-diphenol: oxygen oxidoreductase, EC 1.14.18.1) belong to a larger group of proteins named type-3 copper proteins, which include the catechol oxidases from plants and the oxygen-carrier haemocyanins from mollusks and arthropods (Halaouli et al., 2006). Matoba (Matoba et al., 2006) determined the crystal structure of tyrosinase, isolated from Streptomyces castaneoglobisporus at a 1.4 Å resolution. Tyrosinase is a key enzyme in the biosynthesis of melanin (primary pigment in melanocytes) involved in determining the color of skin, eyes and hair in mammals (Kim et al., 2005). Studies of tyrosinases were motivated by the need to understand and prevent the enzymatic browning that occurs in the presence of air when mushrooms, fruits or vegetables are cut or bruised. This phenomenon is related to the tyrosinase activity and causes severe economic losses in the food industry. Recently, the focus has moved to the biotechnological and environmental applications of tyrosinases, and macrofungal tyrosinases have commonly been chosen for these studies. The most important application of the tyrosinases is related to the biosynthesis of L-DOPA, detection and quantification of phenolic compounds in water samples, removal of phenolic compounds from wastewaters and production of cross-linked proteins (Otavio de Faria et al., 2007). Therefore, finding inexpensive sources of tyrosinase for immobilization on solid matrices is very important."

"Tyrosinases have been isolated from: potatoes (Yang and Wu, 2006), edible fungi (Yuan et al., 2005), filamentous fungi (Haghbeen et al., 2004), rotting mushrooms (Selinheimo et al., 2007), apples (Carvalho da Silva et al., 2013), bananas (Galeazzi et al.,1981), avocados (Vieira et al.,2013), Sicilian tomatoes (Brisolari et al., 2014), eggplants (Duartea et al., 2002), and quince (Spagna et al., 2005), and even from green coconut water (Pérez-Gilabert et al., 2000), (Todaro et al., 2011)."

"Such enzymes have also been isolated from dog rose fruit, papaya, pear, potato leaf, tobacco, lobster, mouse and Homo sapiens. (Sambasiva et al., 2013)."

"pH optimum of industrial isolated and purified tyrosinase was determined at pH= 5.8 to 8.5 values. The temperature optimum was determined in the range of 30°C to 50°C."

"Tyrosinase from potato (Solanum tuberosum), banana (Musa acuminata) and edible mushrooms (Agaricus bisporus) was laboratory isolated by two methods. Either 50 mM K-phosphate buffer, pH=7.0 or 50 mM Tris-HCl buffer, pH=5.8 were used. In both methods, 100 g of the sources of tyrosinase has been blended with 120 ml of the respective buffer, and the resulting solution was filtered through a Buchner funnel."
​

When you eat those powdered fruits concentrated in vit C, you need very little of them to get plenty of C, so ingesting a few grams is already enough. Isolating the enzyme in labs, they probably select notable sources of it.

They had on average 160 mg of tyrosinase/100 g of food, but Orius for example only needs to supplement a few grams of his powdered camu camu.​

The skin represents about 15% of the weight of the body, the basal layer above the dermis (dermis being 90% of the skin) is where you find the melanin-producing cells (melanocytes). You'll find the density of those cells to be around 1200/mm² of skin, and varying depending on the region. I was getting distracted with this, but you can search for how much tyrosinase you is able to find in these specialized cells and then multiply by the surface area. And then compare it based on you much you ingest with your supplement, and you'll probably realize that it's insignificant.

- Skin melanocytes: biology and development
- Understanding the Melanocyte Distribution in Human Epidermis: An Agent-Based Computational Model Approach
- Degradation of Tyrosinase by Melanosomal pH Change and a New Mechanism of Whitening with Propylparaben​

Either way, it's likely that the polyphenol oxidases (tyrosinase and catechol oxidase) don't resist digestion. Here are more clues:

- Effect of pH and temperature on peroxidase and polyphenoloxidase activities of litchi pericarp

"Pre-incubation of the enzyme extract for 45 min at pH 2.5 or 9.5 [40ºC] completely inactivated the enzymes, with the highest degree of efficiency at pH 2.5."​

The 'interdigestive' pH of the stomach is around 1.7. A light fruit meal won't elevate it too much and it will quickly reacidify, especially in the presence of acids.

If the enzymes are inactived, they can only be useful by the compounds that they provide after digestion.

- Microbial Tyrosinases: Promising Enzymes for Pharmaceutical, Food Bioprocessing, and Environmental Industry

"Tyrosinases and catechol oxidases are collectively termed polyphenol oxidases due to their similar activity with catechol oxidase."

"[..]all tyrosinases have a common binuclear type III copper centre (T3Cu), of two copper atoms, each coordinated by three histidine residues, within their active site."​

With copper, Orius already writted the following..

"It's not that whole food C provides copper, it's that it prevents bioavailable copper depletion."​

How? This is what's puzzling.
Even more confusing is the fact that authors repeat the meme in their books without even checking what those terms mean. Ascorbinogen for example is formed in Brassicas and people use it to promote acerolas powders claiming it's part of the C-complex, (as quoted above) it appears when ascorbic reacts with degradation products and it's barely absorbable.


Cupre

When people claim that vit C from whole foods doesn't cause issues, it might be because their ratio of vit C to copper is relatively low when you consider both requirements. But this no longer applies to fruits with massive vit C content because to get a significant amout of copper you would have to ascorbalize yourself first (as implied above). So I suspect it has nothing to do with being synthetic or not.

What seems to be happening in the case of copper is not a loss, but a redistribution. Without enough ascorbic acid, copper might remain stuck in an unwanted state. With too much, it can stimulate its use in certain functions while compromising others if you don't supply more.

- Effect of Varying Ascorbic Acid Intakes on Copper Absorption and Ceruloplasmin Levels of Young Men

"Our finding that high AA intakes reduced ceruloplasmin oxidase activity while copper absorption and total serum copper were unchanged suggests a specific reducing effect of AA on the redox center, that is, Cu(II), of ceruloplasmin, rather than a copper deficiency effect per se."

"An alternative explanation for the reduced ceruloplasmin enzyme activity accompanying high AA in take is that AA promotes dissociation of copper from the ceruloplasmin metalloenzyme."

"High AA concentrations have been shown to favor the dissociation of copper ions from ceruloplasmin in vitro (26) and Frieden (27) has speculated that reduction of ceruloplasmin copper is a first step in making copper ions available to in tracellular ligands."

"In young men under our particular experimental conditions, a supplemental AA intake of 600 mg/d for 3 wk lowered ceruloplasmin oxidase activity but did not antagonize copper absorption or body copper status as a whole."​

- Ascorbate Enhances Copper Transport from Ceruloplasmin into Human K562 Cells

"Scorbutic guinea pigs accumulate copper in the liver and have higher ceruloplasmin oxidase activity and copper levels in serum (4, 11)."

"If ascorbate affects copper metabolism by influencing the movement of copper, then it follows that ascorbate could play a role in ceruloplasmin's delivery of copper to extrahepatic tissues."

"[..]it is likely that L-ascorbate serves as a nonspecific source of electrons for the reduction of Cp copper."

"Ascorbate (both the D and L-isomers) is known to reduce Cu(II) to Cu(I) which is a more favorable form for dissociation from ceruloplasmin (18). The reduction of Cu(II) to Cu(I) in ceruloplasmin has been proposed as a necessary step in promoting the availability of Cp copper for intracellular ligands (19)."

"The oxidation and reduction of copper in Cp occurs in a cyclic, reversible manner during substrate interaction. In normal catalysis, the copper atoms in Cp are known to cycle between oxidized and reduced states. Substrate turnover is not accompanied by the loss of copper from the protein as would have to occur in transport. This suggests that a third component, perhaps a factor in the cells or the membrane, is necessary for the actual transfer of copper. When ceruloplasmin was incubated with physiological levels of ascorbate with out cells in vitro, copper remained affixed to the structure of the protein. In the presence of cells, the copper was dissociated from the protein and transferred to the cytosol."

"Ascorbate not only affected the amount of copper transferred, but appeared to redirect the distribution of copper within the cytosol."

"Previous studies in this laboratory (unpublished data) and by others (21) have obtained evidence that copper is removed from Cp at the cell surface and transferred as free copper to the cytosol. A membrane carrier system that recognizes ionic copper has been characterized in lymphoid cells (22). The present study suggests that ascorbate may react with Cp extracellularly to reduce copper and with the dissociation factor in or on the cells render the copper in Cp available to such a carrier."

"Overall, more copper would be taken up by the cells in a time of need. The absence of ascorbate would impair copper delivery. This hypothesis, if valid, could explain several observations regarding ascorbate effects on copper homeostasis, specifically, why scurvy and copper deficiency seem to share common clinical signs. One could predict that without ascorbate (or reducing equivalent) in the surrounding environment, less copper would be as accessible to cells. Scorbutic guinea pigs have higher serum Cp oxidase activity and copper (4, 11). Increased levels in the serum could be a reflection of the inability to remove copper from Cp for up take into peripheral cells."

"Thus, ascorbate may be beneficial in promoting copper uptake by extrahepatic cells under certain conditions. Decreased levels of ceruloplasmin oxidase activity, an important experimental and clinical determinant of copper status, may not always reflect poor copper nutriture. One should be aware, based on the present study, that low oxidase could also be caused by high dietary ascorbate and the loss of copper from the protein through enhanced tissue uptake."​

- A role for ascorbic acid in copper transport (same author, published after the wards)

"Traditionally, ascorbate has been known to antagonize the intestinal absorption of copper in numerous animal species, including rabbits (1), rats (2), and fowl (3). Antagonistic effects are clearly seen in animals suffering from copper deficiency. When added to a deficient diet, 0. 1-1% ascorbic acid shortens survival times, hastens the onset, and increases the severity of deficiency symptoms (4-6). More recently, ascorbate has been shown to lower the ceruloplasmin oxidase activity in male human volunteers fed copper-deficient diets (7[↑])."

"[..]ascorbate administered with or 75 min before copper inhibited the copper-induced activation. Early (-75 min) treatment produced the strongest inhibition. When the vitamin was given after copper (+75 min) ie, in a postabsorption period, the activation response exceeded that of CuSO4 alone. Indeed, ascorbate was strongly stimulatory. Ceruloplasmin activity, also suppressed by the deficiency, responded upward and rapidly to the copper and it too was modulated by ascorbate; almost twice the activity as copper alone when ascorbate followed copper."

Was in chicks and injected (normal amounts), still worth considering if the copper intake has been low and vit C high.​

"Ceruloplasmin is known to undergo a series of well-characterized reactions in response to reducing agents and metal ion chelators. Ascorbate levels > 5 umol/L in a slightly acidic pH medium reduces the Cu(II) in ceruloplasmin as evidenced by the loss of blue color (16, 17). The reduced protein is more labile to exchange copper with chelators (18). Other reducing agents, sulfhydryl compounds especially, force the dissociation of copper atoms from ceruloplasmin (19, 20). These observations compel one to consider reduction a fundamental mechanism for rendering copper atoms available for exchange with cells."

"Evidence has been obtained that cuprous Cu(I) copper is the form absorbed by the cells from ceruloplasmin (22)."

"[..]an impairment due to a deficiency in the vitamin could give rise to symptoms of copper deficiency if the vitamin is indispensible to copper utilization."

"Bone and connective tissue defects, anemia, and subcutaneous hemorhaging are seen in both deficiencies."

"Ascorbate appears to play a dual role in copper transport: as an antagonist of intestinal transport and as a postabsorption stimulator of tissue copper utilization. Ascorbate may also influence the intracellular binding of copper to enzymes. The latter property may or may not have physiological significance but toxicological factors cannot be excluded. Failure to bind to enzymes could leave copper as a free metal and available for catalyzing Fenton-type reactions associated with free radicals and reduced oxygen species (33). All of the effects reported in these studies were observed at physiological levels of the vitamin. If ascorbate as a cofactor facilitates the removal of copper from ceruloplasmin, this would open a new vista of functions for the vitamin. More important is the realization that a vitamin C deficiency may impair copper metabolism to the extent that transport and regulated uptake of copper by cells would be compromised. In the long history of scurvy, little attention has been paid to the possibility that a copper deficiency either compounded or potentiated the symptoms."​

 

[sunraiser]

Influence of ascorbic acid supplementation on copper status in young adult men

"High dietary levels of ascorbic acid are antagonistic to the metabolism and function of the trace element copper in chicks (1, 2), rabbits (3, 4), rats (5), guinea pigs (6, 7), and monkeys (8). Some aspects of the chick and rabbit studies involved an exaggeration of severe dietary copper deficiency by ascorbic acid supplementation as evidenced by defects in aortic elastin and bone. There is, however, ample evidence that ascorbic acid supplementation is antagonistic to copper even when dietary copper levels are adequate. Significant reductions in growth, Hb, and hematocrit have been reported in both chicks (1) and guinea pigs (6, 7) fed diets adequate in copper and supplemented with ascorbic acid. In guinea pigs ascorbic acid supplementation also resulted in significant reductions in serum copper concentration, serum ceruloplasmin, and liver copper. Serum copper and serum ceruloplasmin were also reduced in ascorbic acid supplemented monkeys consuming a diet marginal in copper (8)."

"The results of this study show that copper status of adult men can be negatively influenced by ascorbic acid supplementation as evidenced by serum copper and serum centloplasmin determinations. Furthermore the decline in these parameters was reversed 20 days after the supplement was withdrawn."

"Although adverse health effects of reduced copper status in men as a result of ascorbic acid supplementation cannot be defined by the present study, it does provide knowledge that the potential for adverse effects exists. In the present study it was possible to demonstrate reduced copper status of men supplemented with ascorbic acid typical of intakes easily obtained from a variety of commercially available preparations [3x 500 mg/d]. The potential for an ascorbic acid antagonism of copper in man would therefore appear to be greatest for persons with a long history of elevated ascorbic acid supplementation coupled with a marginal intake of dietary copper."​

.

I have a vaguely related anecdote that might be interesting.

In general, I crave between probably 20mg and 150mg vitamin c each day (maybe little to none some days) via small kiwis and satsumas plus trace amounts from tomato and other veg.

When I take a copper supplement (4-6mg) my vitamin C cravings skyrocket to between 200mg and 600mg - I literally can't stop jamming down kiwis.

I notice a similar style pattern with kelp iodine tablets in that I immediately crave large amounts of goitrogenic veg like kale, an iodine antagonist.

It could be that the type of supplemental copper creates a much higher anti oxidant need via vit C, or it could be interaction via copper moving retinol stores from the liver and requesting more vit C for ceruloplasmin creation.

I have also read that while vitamin C antagonises copper in the intestinal tract, it's also used to push copper into the cell. I can't find the source, though (maybe unreliable).

Anyway, the antagonistic effect is plausible in my experience and it makes sense in that copper and vitamin c work together in several areas of our function. The problem with studies is they're all short term in the scheme of things and they don't show the problems that might develop in 10 years time or the undercurrent a certain approach is creating.

I often notice really acute impacts on food cravings after supplemental vits/minerals and I'm inclined by this to let my body find its own equilibrium for the most part. I find it interesting that I have never in my life craved 1g vitamin C in a day, though I'm sure some others have - we're all in different states and are different physiological beings (especially men and women).

This next bit is absolutely vague and completely theoretical but I wonder if so many people here do well on higher vit C doses directly BECAUSE it antagonises copper.

Not that copper is bad, but because it transports (perhaps activates) retinol from the liver, which could further antagonise vitamin D.

Many have eaten pretty inhuman levels of vitamin A via liver or supplementation and I think that can push a person beyond normal vit D depletion and maybe create a bodily environment that's lacking ability to uptake alkalising minerals like calcium and magnesium, (for extended periods) leaving it open to various pathogens and also an overburdened liver. Perhaps higher dose vit D via continuous sunshine is needed as a rectification tool? I know it has been a huge help to me in the past (accutane casualty!). Either the burden of balancing retinol or the burden of infection might create a higher vit D need.

That would mean getting copper to craving outside of liver would be key, then as much sunshine starting in spring to build tolerance as possible. Supplemental vit D is a much more challenging balancing act entirely!

Or perhaps vit C is helping for reasons I don't understand - my view may be completely useless to another with different physiology. Please don't take my absurd theory in the last part with too much weight, either.

 

[Amazoniac]

Camu-camu composition according to the following publication:
- Characterization of the Fruit Pulp of Camu-Camu (Myrciaria dubia) of Seven Different Genotypes and Their Rankings Using Statistical Methods PCA and HCA

Vitamin C: 2 g/g (or 1-6 g/g reported elsewhere)
Cupre: 3.5 mcg/g at most​

You've mentioned taking 1 g of vit C somewhere on the foro from powdered camu-camu. How is that even impacting your copper levels?

: nonono

There's more C than the total weight. The bizarre thing is that there were 2 typos in the document and the broscientist here repeated it. It's in every 100 g of the fruit.
0.2 (or much less) mg of copper for every gram of vit C.

 

[Amazoniac]

Protection of ascorbic acid from copper(II)-catalyzed oxidative degradation in the presence of flavonoids: quercetin, catechin and morin