Vitamin C

[Amazoniac]

- l-dehydroascorbic acid can substitute l-ascorbic acid as dietary vitamin C source in guinea pigs
- NAD/NADH Ratio - The One Metabolic Cause To Rule Them All

Any opinions?

 

[Mito]

- l-dehydroascorbic acid can substitute l-ascorbic acid as dietary vitamin C source in guinea pigs
- NAD/NADH Ratio - The One Metabolic Cause To Rule Them All

Any opinions?

Ray Peat right again?

 

[tara]

. This stuff has me feeling worried everytime I take my vitamin C and that's not cool because I have had one of the worst colds and yet I hear in my head "no one needs mega doses" despite everything I have read to the contrary when you are battling infectious disease.

I don't know what makes sense long term with vit C supplementation in general for everyone, but it sure makes sense to me if you take big doses when you are fighting a cold, especially since you've had such good experience with vit C. I really like your posts, and hope you'll keep posting.

I'm not denying the positive side, I'm wondering if there's a price to it.

This seems to me like a useful part of a general discussion about vit C.

 

[Whichway?]

- l-dehydroascorbic acid can substitute l-ascorbic acid as dietary vitamin C source in guinea pigs
- NAD/NADH Ratio - The One Metabolic Cause To Rule Them All

Any opinions?

That first link suggests that oxidized vitamin C is still effective, as it can be recycled. A lot of vitamin C on the market is partially oxidized, so your body has to work to convert it back to ascorbic acid so that it can accept electrons again and function as an antioxidant.

That second link has so many studies listed I don’t know where to begin. Too much!

 

[Amazoniac]

Tolerance and Effects of High Doses of Ascorbic Acid

"Urine becomes less acid during gastric hydrochloric acid secretion and more acid when pancreatic juice is excreted. This diurnal variation in urinary pH has been recognized for many years, whilst diurnal variation of urinary redox potential has been poorly investigated. Changes in urinary pH are of great interest with respect to urological diseases as well as to changes in solubility of metabolites and drugs occurring in human urine."

"Ascorbic acid has often been proposed as a urinary acidifying agent, and dangerous effects due to over-acidification of urine by high doses of ascorbic acic have been claimed, especially due to alterations in the dissolubility characteristics of strongly acid urine. This is particularly important when drugs with low pKa values are taken, in addition."

"In general the pH of human urine should be kept in the acidic range. Alkaline urine always suggests a urinary tract infection and favours it. Oral ascorbic acid intake normalizes pathological urinary pH [46] and may be used for the prevention of recurrent urinary tract infection [37]."

"Following a daily intake of 10 g ascorbic acid for 10 days, a mild metabolic acidosis and moderate urinary acidification was reported [54]."

"All our data (Table XIII) show that even with very high daily dosage of ascorbic acid normally achievable acidic urinary pH is not exceeded."

"The ability of high doses of ascorbic acid to stabilize urinary pH in the acidic range is favourable and only in exceptional cases unfavourable, for example, when it is therapeutically desirable to obtain alkaline urine. In this connection, the question of the contribution of ascorbic acid intake to oxalic acid formation would appear to be of greater significance. Part of the ingested ascorbic acid is transformed in the body into oxalic acid and eliminated in the urine."

"Investigations using labelled ascorbic acid have shown that, with ascorbic acid intake in the RDA range, roughly 44% is metabolized to oxalate which is then eliminated in the urine [29]. The total amount of oxalate normally eliminated by this route is around 30 mg (range 13 to 49 mg) daily. Approximately 40% results from the breakdown of ascorbic acid, while the rest comes from dietary sources or from general cell metabolism; chiefly from glycine via glyoxylic acid."

"On the basis of the contribution of ascorbic acid to the urinary oxalate pool, several experiments have been carried out in animal and man [8, 17, 42, 56, 62, 65, 71]. Results of the studies in man are summarized in Table XIV."

"The data available suggest that in general ascorbic acid intakes up to about 5 g per day will not significantly influence urinary oxalate excretion. Higher daily intakes may give rise to an increase in urinary oxalate. But it has to be taken into account that part of the excreted ascorbic acid may also be decomposed into oxalic acid in the final urine. Besides that, in very rare cases individuals may show an accelerated turnover to oxalic acid. But how this relates oxaluria to urolithiasis is unclear, since oxaluria may often occur in relation to high oxalate and low calcium intake by chance."

"In general, the formation of renal calculi is thought to follow simple physicochemical rules: when the solubility product of the components is exceeded, renal calculi are formed. The solubility product of the components of renal calculi is very low; thus in many studies only oxalic acid excretion in urine is checked in relation to ascorbic acid intake. But an influence on oxalate excretion does not mean automatically an influence on the formation of calcium oxalate calculi within the urinary tract. Urinary calculi can form in urine with a normal calcium content. An important factor in calculus formation seems to be the formation of an abnormal activated mucoprotein. This abnormal mucoprotein derives from a mucoprotein of molecular weight 7 x 10^6 Daltons which is considered to be the principal product of the secretory activity of the urinary epithelium. This uromucoid is found in the urine of both normal subjects and patients with calculus disease, whereas the abnormal one is found only in calculus formers. This abnormal anti-infective mucoprotein is thought to initiate calcinosis. It forms calculi in the urine of normal patients as well as in that of patients already suffering from renal calculi. The abnormal mucoprotein binds all calcium and oxalate available, forming calculi, whereas the normal uromucoid solubilizes calcium and oxalate even in hypersaturated solutions. It is suggested that the abnormal mucoproteins, brought about, e.g. by bacterial infection, chelate calcium from solution to form relatively insoluble micelles of colloidal calcium mucoprotein units. This is the initial step in calcigerous stone formation and is followed by crystallization within the meshes of the mucoprotein micelle [12]. Endogenous oxalic acid production cannot be blocked entirely, and even on zero intake of oxalate or ascorbic acid renal calculi already formed will continue to grow. Prophylaxis against infection seems therefore to be a major point in the prophylaxis against renal calculi."

"For prophylaxis of renal calculi, ascorbic acid has even been recommended [36]. Judging from experience gained from cancer patients with a daily intake of far higher doses of ascorbic acid (15 g) for several months or even years, ascorbic acid may not play a major role in urolithiasis, even in these extreme doses, since no complaints have been reported."

 

[Amazoniac]

Ascorbic Acid and Urinary pH

"In a recent letter to the editor, the issue was again raised of whether or not ascorbic acid lowers urinary pH.[1] There are reports that ascorbate does[2-6] and reports that it does not[7-9] change urine acidity. These contradictory results arise from a difference in (1) selection of patients and (2) semantics. The studies that evaluated subjects with urinary tract infection showed a decrease in the pH of voided urine; studies using subjects without infection showed no change. The inhibition of bacterial urease[10-13] is undoubtedly the cause of change, when it occurs. The ascorbic acid effect is more accurately described as preventing the alkalinization of urine rather than producing an acid urine. This occurs by preventing or decreasing ammonia production by bacterial urease. This is illustrated by an experiment in which urea, urease, and ascorbic acid were put into 0.1M phosphate buffer. In the presence of ascorbic acid, the rise in pH was markedly inhibited as was the ammonia formation (Table)."

"The ascorbate effect on the pH of voided urine depends on (1) the number and multiplication of urease-producing bacteria, (2) the concentration of urea, (3) the concentration of ascorbic acid, and (4) the incubation time of the urine in the bladder and collecting system. The ascorbic acid concentration can be increased by increasing the dose. The metabolic acid load excreted by the kidney and the pH of the urine are related to the catabolism of sulfur-containing amino acids[14] and the intake of a metabolizable cation with a fixed anion (eg, ammonium chloride). This acid load is decreased by the intake of metabolizable anion with a fixed cation (eg, potassium citrate). The pH of the urine formed by the kidney depends on the availability of buffer material with a suitable pKa (eg, phosphate) and the activity of ammonium production."

"The ascorbic acid effect on urease is also affected by the presence of cysteine, which cancels the ascorbate effect, and copper, which enhances it.[16] Another area where the production of ammonia by urease activity produces dysfunction is in hepatic encephalopathy. Ascorbic acid might also be useful in this disorder."

 

[Amazoniac]

Changes in serum ceruloplasmin levels with commonly used methods of contraception

"Certain side effects of oral contraceptives have been attributed to chronic increase in serum ceruloplasmin. The oestrogen component is mainly responsible for the increased level of serum ceruloplasmin while progesterone causes a less drastic rise (5)."

"[..]ceruloplasmin [] oxidizes compounds like ascorbic acid, epinephrine, melatonin, serotonin and other amines. Under physiological conditions this oxidation is minimized by common metabolite citrate (6). Any condition leading to rise in serum ceruloplasmin can lead to increased oxidation of the above mentioned substrates. Reduced levels of vitamin C have been detected in the plasma, leukocytes and platelets and urine of women taking oral contraceptives with a mean reduction of 30 to 40% (1,5,7)."

"According to Stich et al the cupric ion catalysed oxidation of ascorbate can induce mutation and DNA damage (5). This could possibly be the mechanism by which long term use of oral contraceptives can give rise to carcinogenic effects and cervical dysplasia. Several studies indicate that women receiving oral contraceptives are in induced hypovitaminotic C condition due to raised serum ceruloplasmin and require supplementary vitamin C (1,5,7)."​

[1] Vitamins and oral contraceptive use

"Reports concerning the interaction between steroidal contraceptives (the combined pill) and vitamins indicate that in users the mean serum-vitamin-A level is raised and the mean serum-vitamin-B2 (riboflavine), vitamin-B6 (pyridoxine), vitamin-C, folic-acid, and vitamin-B12 levels are reduced. Other vitamins have been insufficiently studied for comment. Biochemical evidence of co-enzyme deficiency has been reported for vitamin B2, vitamin B6, and folic acid. Clinical effects due to vitamin deficiency have been described for vitamin B6—namely, depression and impaired glucose tolerance. Folic-acid deficiency with megaloblastic anæmia has been reported in only 21 cases."​

[5] Vitamin C Requirements and Oral Contraceptives

[7] Copper in Mammalian Reproduction

"The fact that copper is the most powerful catalyst for the autooxidation of ascorbic acid has implications in reproductive physiology, some examples of which we have already discussed (see Sections 111, A and VII, A). The cupric ion-catalyzed autooxidation of ascorbic acid generates free radicals (see Staudinger et al., 1964; also Section 11, B, 8), and this combination can induce mutations and damage DNA (Stich et al., 1976). This has a practical implication in terms of vitamin C deficiency for women taking oral contraceptives. Increased ceruloplasmin associated with exogenous estrogens is accompanied by reduced plasma levels of ascorbic acid (see Section 111, A). A woman taking oral contraceptives must take about 500 mg vitamin C per day, i.e., 10 times the normal recommended daily level, to compensate for the increased loss (see Wynn, 1975 [1]; Rivers and Devine, 1975)."

"Vitamin C also has effects on copper metabolism. In copper-deficient animals, additional vitamin C makes the deficiency more severe. On the other hand, in copper toxicity, the vitamin has a protective effect (Spivey Fox, 1975; see also Hunt et af., 1970). Both vitamin C and copper are required for collagen synthesis, but for different stages. Vitamin C is required for hydroxylation of peptidyl proline, and is also known to be required for hydroxylation of peptidyl lysine in collagen fiber formation (Barnes, 1975). Lysyl oxidase, required for the crosslinking of the collagen fibers, is a copper enzyme (see Sections V, A-C)."​

 

[Amazoniac]

Estradiol decreases taurine level by reducing cysteine sulfinic acid decarboxylase via the estrogen receptor-α in female mice liver
↳ Estradiol-Induced Effects on Glutathione Metabolism in Rat Hepatocytes

"Estrogens undergo metabolic transformations in the liver involving various enzymes and subcellular compartments. A major pathway is the formation of catechol estrogens catalyzed by microsomal cytochrome-P450 oxidases. Catechol estrogens and the subsequently formed o-quinones can be further metabolized to semiquinones and other reactive species (1-3). These estrogen derivatives are able to consume hepatic GSH and appear to be involved in the development of liver injury occurring after estrogen treatments (4-8)."

"Estradiol (0.1-1.5 mM) produced a dose-dependent depletion of cellular reduced glutathione (GSH), whereas it did not alter the glutathione disulfide (GSSG) excretion into the medium."​

Don't know about the relevance of this for people, but it's interesting nevertheless. It's worth checking out.

 

[Amazoniac]

- The physiological role of dehydroascorbic acid

"Ingesting either AA or DHA raises the serum AA concentration to similar extents in normal human subjects [3,4]. Thus DHA can serve as a dietary source of vitamin C for humans, although it is a poor source for some animals (e.g. Osteogenic Disorder Shionogi rat [5]). Evidently cellular mechanisms of transport and metabolism convert DHA to AA. These mechanisms are important because the human diet normally contains DHA as well as AA [6]. Indeed, the commercial and domestic processing of foods oxidizes AA to DHA. There exists a widely held understanding that dietary AA and DHA possess roughly equivalent bioavailability in humans. It is because both molecules are commonly thought to be bioavailable that the vitamin C content of foods is usually reported as total vitamin C, i.e. the sum of AA and DHA contents."

"The gastrointestinal tract is the principal site of absorption for AA and DHA. In addition to the amounts ingested, DHA is produced when AA reacts with oxidants in the lumen of the gastrointestinal tract [7]. For instance, oxidation of AA by quercetin metabolites [2] may contribute to the decrease in AA bioavailability caused by quercetin administration in rats [8]. DHA itself is degraded to diketogulonic acid by bicarbonate at alkaline pH in vitro [9]. However, it is unlikely that DHA is exposed to these destabilizing conditions in vivo, because the alkaline secretions from the pancreas and duodenal glands mix with the strongly acidic gastric juice to form a slightly acidic fluid in the lumen of the small intestine."

"[..]glucose inhibits AA but not DHA uptake, which may increase the relative bioavailability of the oxidized form of vitamin C [10]."

"Human enterocytes contain DHA reductases that convert DHA to AA [11]. These enzymes keep the intracellular concentration of DHA low and thereby maintain a gradient favoring continued uptake of oxidized vitamin C across the enterocytes’ luminal membrane."

"Instead of allowing its immediate excretion from the body [after use], numerous cell types can clear DHA from the extracellular fluid. Among those that take up DHA and reduce it to AA are neutrophils, erythrocytes, smooth muscle cells, hepatocytes, astrocytes and osteoblasts [19-21,23-28]."

"The dismutation of a pair of ascorbyl radicals, which is catalyzed by NADH-dependent semidehydroascorbate reductase, produces one molecule of AA and one of DHA. DHA can be converted to AA by NADPH-dependent thioredoxin reductase or glutathione-dependent DHA reductase [31]. In contrast to an unsubstantiated opinion published recently [32], these reactions do not produce hydrogen peroxide or other reactive oxygen species while regenerating AA."

"Reductants derived from cell metabolism convert intracellular DHA to AA. The NADPH generated by the pentose phosphate pathway of glucose metabolism is an example. It is likely that redundant mechanisms involving NADPH, glutathione, and perhaps other thiols ensure DHA reduction [21]."

"Reduction of large amounts of DHA to AA by NADPH- and glutathione-dependent reactions may decrease the intracellular concentrations of NADPH and glutathione markedly [21,33,34]. DHA also inhibits the activities of purified hexokinase, glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate dehydrogenase, but this does not occur when sufficiently high concentrations of the enzymes’ specific substrates are present [34]. Moreover, DHA indirectly stimulates the pentose phosphate pathway to produce NADPH and subsequently increases intracellular glutathione concentration above basal levels [35]."

"After intracellular DHA becomes reduced to AA, the latter can function as a reductant. Each equivalent of AA in a cell can reduce several equivalents of oxidants if the DHA thereby produced can be recycled in the same cell, as has been demonstrated for human erythrocytes [37]. The AA derived from DHA also provides electrons to plasma membrane oxidoreductases and through them to extracellular oxidants [38]. Furthermore, DHA uptake into cells may be followed by AA efflux. For example, human erythrocytes [27] and HepG2 liver cells [28] take up DHA, reduce it intracellularly and subsequently release AA to the extracellular fluid. This process allows the reducing equivalents derived from cell metabolism to be carried into the extracellular fluid and made available to neighboring cells."

"An excess of glucose during uncontrolled diabetes may impair DHA uptake into cell types where DHA transport is mediated largely by facilitative glucose transporters (Fig. 1). Hormonal dysregulation may also contribute to local deficiencies in DHA recycling."

"Slowing of DHA uptake may lead to impaired regeneration of AA and weakening of antioxidant defences in diabetes, especially in the presence of hyperglycemia. For instance, the AA concentration is decreased and the DHA concentration is increased in the sciatic nerve of rats made diabetic by streptozotocin [40]. Furthermore, because intracellular AA is required for collagen synthesis by osteoblasts [29], deficient recycling of DHA to AA in this cell type may contribute to the developmentof osteopenia [20]."

"Under pathological conditions characterized by oxidative stress, AA is oxidized by reactive oxygen species at rates that overwhelm the ability of cells to regenerate the vitamin. For example, inflammation in skin during wound healing raises the extracellular concentration of DHA markedly [44]. Similarly, gastritis decreases the AA concentration and increases the DHA concentration in the gastric juice of human patients [45]."

"Redox cycling of vitamin C may also be abnormal during the inflammatory response to microbial infection, since the rate of AA oxidation is increased in the serum of septic patients [46]. Moreover, findings with an in vitro model indicate that septic conditions decrease recycling of DHA [25]. The model consists of applying bacterial endotoxin (lipopolysaccharide) and the inflammatory cytokine interferon-Q (IFNQ) to primary cultures of astrocytes. Lipopolysaccharide and IFNQ induce nitric oxide synthase isoform 2, increase intracellular levels of reactive oxygen species, and decrease the rate of intracellular AA accumulation from extracellular AA or DHA [25]. The oxidants produced during inflammatory reactions may directly alter the mechanisms by which cells recycle DHA. For instance, prior exposure of astrocytes to peroxyl radicals decreases their subsequent accumulation of intracellular AA from extracellular DHA [23]."

"DHA killing of susceptible cell types, such as neurons [36], may be explained by the stress caused by depletion of NADPH and glutathione. But other cell types, such as astrocytes and osteoblasts, recycle DHA abundantly without undergoing acute injury."​

 

[Amazoniac]

- The Vitamins: Fundamental Aspects in Nutrition and Health (978-0-12-802965-7)

--
@haidut, unrelated but it's on you to.. MAAGA.

 

[Amazoniac]

- The Vitamins: Fundamental Aspects in Nutrition and Health (978-0-12-802965-7)

- Vitamin C elevates red blood cell glutathione in healthy adults​

- Riboflavin | Instituting Linus Pauling

 

[haidut]

MAAGA.

Make what great again?

 

[Luk3]

Are there any reasons I shouldn't mix AA with calcium carbonate? I'm off dairy now, so want the extra calcium + buffer the acidity of the AA.

 

[Amazoniac]

- Vitamin C: should we supplement?

Spoiler: Table 1. Pleiotropic effects of vitamin C

Read from the article if you prefer a version that's not blurred.

Has anyone noticed an increased requirement for antidote C after (red/sun) light exposure?

 

[Amazoniac]

- Bimodal Effects of Megadose Vitamin C on Adrenal Steroid Production in Man

"[..]each subject received two 500 mg vitamin C tablets q 6 h until the end of the study (days 3 to 10)."

"All the subjects tolerated the vitamin C dose (4 g/day) well. Serum ascorbate levels were 2.5 times higher during vitamin C ingestion than in the control period (1.82 ± 0.18 vs. 4.42 ± 0.29 mg/dl, p < 0.001)."

"Although ingestion of vitamin C did not alter the normal pattern of diurnal variation of plasma cortisol levels, it significantly lowered mean plasma cortisol levels at 0400, 0800, 1600, and 2000 hours (p < 0.05). Moreover, a significant decrease in the overall 24-hour plasma cortisol curve during vitamin C ingestion compared to the control period was observed (p < 0.02). TABLE 1 [one] demonstrates that there was a reduction in the maximum daily cortisol levels during vitamin C ingestion (p < 0.05) with a reciprocal increase of concomitant DHEA levels in association with vitamin C ingestion (p < 0.001)."

"Our studies indicate that megadose vitamin C decreases the sensitivity but not the capacity of adrenal gland to respond to ACTH. The present findings are in support of our earlier work in vitro, in that vitamin C in beef adrenal inhibited 21-hydroxylase[4] and shifted the ACTH dose-response curve of corticosterone in rat adrenal to the right.[5] It is tempting to postulate that with vitamin C ingestion there may be a partial blockage of 21-hydroxylase so that more substrate becomes available for the androgenic pathway. This blockage is incomplete since a higher ACTH dose reverses the abnormal cortisol response to the low dose. Additional studies are required to determine the long-term effect of ascorbic acid ingestion on the hypothalamic-pituitary-adrenal axis in young adults and older age groups."​

 

[InChristAlone]

- Bimodal Effects of Megadose Vitamin C on Adrenal Steroid Production in Man

"[..]each subject received two 500 mg vitamin C tablets q 6 h until the end of the study (days 3 to 10)."

"All the subjects tolerated the vitamin C dose (4 g/day) well. Serum ascorbate levels were 2.5 times higher during vitamin C ingestion than in the control period (1.82 ± 0.18 vs. 4.42 ± 0.29 mg/dl, p < 0.001)."

"Although ingestion of vitamin C did not alter the normal pattern of diurnal variation of plasma cortisol levels, it significantly lowered mean plasma cortisol levels at 0400, 0800, 1600, and 2000 hours (p < 0.05). Moreover, a significant decrease in the overall 24-hour plasma cortisol curve during vitamin C ingestion compared to the control period was observed (p < 0.02). TABLE 1 [one] demonstrates that there was a reduction in the maximum daily cortisol levels during vitamin C ingestion (p < 0.05) with a reciprocal increase of concomitant DHEA levels in association with vitamin C ingestion (p < 0.001)."

View attachment 14584​

"Our studies indicate that megadose vitamin C decreases the sensitivity but not the capacity of adrenal gland to respond to ACTH. The present findings are in support of our earlier work in vim, in that vitamin C in beef adrenal inhibited 21-hydroxylase[4] and shifted the ACTH dose-response curve of corticosterone in rat adrenal to the right.[5] It is tempting to postulate that with vitamin C ingestion there may be a partial blockage of 21-hydroxylase so that more substrate becomes available for the androgenic pathway. This blockage is incomplete since a higher ACTH dose reverses the abnormal cortisol response to the low dose. Additional studies are required to determine the long-term effect of ascorbic acid ingestion on the hypothalamic-pituitary-adrenal axis in young adults and older age groups."​

Interesting. All I know is Vitamin C has helped my anxiety. I feel bad for all the people with bad anxiety who are too afraid to try higher doses.

 

[baccheion]

24-32 ounces (body temperature) water each morning on an empty stomach at least 1 hour before eating. Add 1g NaCl (~1/4 tsp Redmond salt) and 1g vitamin C for each 8 ounces. That's an adrenal cocktail. Could also add magnesium, potassium, and other minerals.

 

[Amazoniac]

Interesting. All I know is Vitamin C has helped my anxiety. I feel bad for all the people with bad anxiety who are too afraid to try higher doses.

- Becoming Stress Proof: The History Of Stress With Hans Selye

Ascorbic Acid Effects on Vitamin D Hormone Metabolism and Binding in Guinea Pigs

- Ascorbic acid deficiency in guinea pigs: contrasting effects of tissue ascorbic acid depletion and of associated inanition on status indices related to collagen and vitamin D

"Recently a study was reported (Sergeev et al. 1990 [⇈]) suggesting that vitamin D metabolism may also be sensitive to ascorbic acid deficiency in guinea pigs, and that the consequent alterations in hormonal control of calcium may be responsible for some of the bone defects seen in ascorbic-acid-deficient animals. However, this study did not include inanition controls, and did not report growth curves; thus it was unclear whether the reported effects were specific for ascorbic acid depletion, or secondary to inanition." "Other differences in their assay methodology included the use of renal cortex slices rather than isolated mitochondria, a higher concentration of 25-hydroxycholecalciferol substrate (4.3 uM) and a different method of separating the products of reaction, based on HPLC. Although observations from other studies (Turnbull & Omaye, 1980; Bjorkhem et al. 1987; Crivello, 1988) have indicated possible mechanisms whereby tissue ascorbic acid depletion may affect steroid hydroxylations in ways which might also affect vitamin D metabolite formation, the evidence that this actually occurs in vivo remains incomplete."

..

"Table 1 shows the final body weights and body-weight changes over the last 2 weeks of [our] study. Whereas the ad-lib.-fed control group (E) increased in its mean body weight from 257 to 656g during the entire 8-week period of the experiment, group A, which was moderately to severely deficient in ascorbic acid, increased only to 421 g by the end of the 8-week period, despite receiving 0.5 mg ascorbic acid/d for the last 5 weeks. Group B, which was weight-matched to A, needed to be given less food than was apparently consumed by group A (measurements of food intake may have been biased slightly by spillage). Group C, the mildly deficient group, which received 1 mg ascorbic acid/d throughout the study, maintained a growth weight which was very similar to that of the ad lib. control group E [getting about 60 mg antidote C/d] for most of the study."

Spoiler: Table 1

"The concentration of ascorbic acid in two tissues which typically concentrate the vitamin to a high level, namely adrenals and spleen, are shown in Table 1. Both of the ascorbic acid-restricted groups (A and C) exhibited reduced tissue ascorbic acid concentrations in comparison with the three control groups (B, D and E) which in turn did not differ greatly from each other, despite large differences in food intake and in growth rates between group B on one hand and groups D and E on the other. The striking difference in growth rate between groups A and C was accompanied by only a moderate difference in their tissue ascorbic acid levels. Group A had relatively enlarged adrenals and spleens in comparison with body weights (not shown), which is a well-established and characteristic feature of ascorbic acid deficiency."


"Table 3 shows the effects of ascorbic acid restriction and inanition on the two major vitamin D metabolites, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol, in plasma, and the apparent activity of kidney 25-hydroxycholecalciferol-1-hydroxylase in kidney mitochondrial preparations. For plasma 25-hydroxycholecalciferol there was a marginally significant (t test P < 0.05) difference between groups A and B; group E had intermediate values. Inanition may thus increase levels of this metabolite, whereas low ascorbic acid intakes may produce the opposite effect, but neither influence was very striking in the present study. In the case of 1,25-dihydroxycholecalciferol, inanition in groups B and D reduced the levels in comparison with group E, and when expressed on a log scale, groups B and D both differed from group E by Students’ t test (P < 0.05). However, there was no clear-cut effect of ascorbic acid deficiency, independent from that of inanition. The kidney 1-hydroxylase assay (Table 3) did not reveal a clear-cut effect of either ascorbic acid deficiency or inanition."

Spoiler: Table 3

--
- Effects of Feeding Methods (Water vs. Feed) of Vitamin C on Growth Performance and Carcass Characteristics in Broiler Chickens

 

[Amazoniac]

Haven't read yet:
- Vitamin C Activates Osteoblastogenesis and Inhibits Osteoclastogenesis via Wnt/β-Catenin/ATF4 Signaling Pathways

 

[Amazoniac]

- Vitamin C
⮤ [10] Scurvy and vitamin C deficiency in Crohn's disease.

"Several vitamin deficiencies have been described in association with Crohn's disease, including the B complex, B12, D and K. Other deficiencies may include iron, folic acid, calcium, magnesium, sodium, potassium or zinc (Avery Jones, Gummer and Lennard-Jones, 1968; Donaldson, 1973; Bockus, 1976)."

"It has been shown by Gerson and Fabry (1974) that vitamin C (ascorbic acid) concentrations in patients with Crohn's disease are decreased compared to normal controls. They postulated that fistula formation could be due to local ascorbate deficiency. Hughes and Williams (1978) have recently reported low concentrations of leucocyte ascorbic acid (LAA) in Crohn's disease."

"In view of [the reported case], it was decided to examine the next 9 out-patients with proved Crohn's disease for evidence of scurvy."

"No clinical evidence of scurvy was detected in any of the 9 patients examined. The Crohn's disease was clinically quiescent in all patients apart from patient 7, who had colicky abdominal pain requiring intermittent pentazocine." "Seven of 10 patients had low LAA levels. Of these, 4 had a low dietary intake by any criteria. Two of the patients had LAA levels below the safe antiscorbutic concentration of 85 nmol/10^8 WBC despite an adequate [¿] diet."

Spoiler: Table 1

"James Lind (1753) has probably recorded the best clinical description of scurvy. He stated that the first sign of cutaneous bleeding was often to be found in the lower thighs just above the knees. Large spontaneous bruises almost always appear first on the legs. This was the case in the present patient who also exhibited the early non-specific symptoms of scurvy, namely fatigue, malaise, lassitude and joint aching. Oral lesions occur almost exclusively in patients who have retained their own teeth (Van Itallie, 1977). As the patient was edentulous it is not surprising that she had no oral lesions and none of the gum changes often seen in this condition. It has been said that the LAA level falls to zero just before scurvy develops (Herman, Stibel and Greene, 1976) and in this, the present patient was not typical although the level of 25 nmol/10^8 WBC was far below the 'safe' antiscorbutic level of 85 nmol/10^8 WBC (Hughes and Williams, 1978)."

"Vitamin C deficiency can lead to malaise, anorexia weakness, lassitude, bone and joint aching and psychological changes. It causes poor collagen formation due to failure to convert proline to hydroxyproline and failure of synthesis of chondroitin sulphate, an important constituent of ground substance. Wounds therefore heal poorly. There is a failure to utilize iron and convert folic acid to folinic acid with the potential to develop folate deficiency and anaemia (Schrimshaw, 1975). Some of these features are seen in Crohn's disease and it is possible that deficiency of vitamin C may be a factor in their aetiology."

"However, it should be noted that vitamin C deficiency is not specific to Crohn's disease and is well recognized in conditions which damage the body, such as burns, fractures or surgical operations. These lead to rapid disappearance of the reduced vitamin (Davidson et al., 1975). Deficiency is also seen in a wide variety of chronic illnesses, especially sepsis, neoplastic disease, etc., and is thought to be due to increased utilization of the vitamin (Burns, 1975; Latner, 1975)."

"It is [then] possible that there is an increased demand for vitamin C in Crohn's disease rather than malabsorption."​

- The effect of high ascorbic acid supplementation on body iron stores
- Ascorbic acid supplementation: Its effects on body iron stores and white blood cells