Vitamin C

Amazoniac

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- Ray Peat Email Advice Depository Discussion/Comment Thread
Microbial Reactions for the Synthesis of Vitamin C (l-Ascorbic Acid)

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Amazoniac

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Hi @Amazoniac, do you take supplemental vitamin C? If so, which one do you take, and how much?
I don't, but my needs are higher than average. A whale ago I purchased two supplements (by Northeast Pharmaceutical Group and DSM) to compare with foods. I commented this with one of our gurus. Both had decent lab analysis (which makes us question their validity), however the first was nasty (darker appearance and strange effects), I would rather get by with low dietary intakes than use it; the other was alright but behaved differently than foods. It's better if you can afford the food-based options, not a lot will be required if you distribute it wisely throughout the day. In case you have to opt for synthetic, it's worth trying to add it to some juice (such as orange) in hopes that the protective plant nutrients help to prevent adverse interactions with ascorbic acid. I suspect that large amounts of juice won't be good because minimizing the time it takes to digest must contribute to the prevention. These are speculations.
 
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Logan-

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(which makes us question their validity)
Why, could you elaborate?
the other was alright but behaved differently than foods.
How do you know the effects you ascribe to foods aren’t caused by things other than ascorbic acid in them? What made you question supplement’s effects, what were your expectations?

Another question: do you think vitamin C supplements shouldn’t be taken after a meal, because they can interact with the metals in the food, and also increase the absorption of iron? When is the best time to take it?
 

InChristAlone

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Just chiming in to say I take 4 g ascorbic acid with baking soda in the morning before my banana. I think there are interactions with food that is probably best to avoid.
 

boris

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Posted this in another thread. Thought this would be of interest here:

I think Peats problem with Vitamin C in combination with iron isn't necesseraily only about absorption anymore. Vitamin C can turn iron and copper into a reduced form, which is dangerous. Dr. Ray Peat, Ph.D - Vitamin D, Thyroid, Evolving Consciously and Much More -August 20, 2019 - One Radio Network after 21:40

Interesting too. Vitamin C is not an antioxidant it is an oxidant, but in a positive sense. It plays a role in the protein folding in the cells.
 

Amazoniac

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Why, could you elaborate?
There was a marked difference in effect from two products with a similar analysis, it's not a guarantee.
How do you know the effects you ascribe to foods aren’t caused by things other than ascorbic acid in them? What made you question supplement’s effects, what were your expectations?
On the best case scenario, there is factors in them that allow you to metabolize it better, so they can't be ignored because obtaining it isolated would be an inferior option. It's probable that the benefits still outweigh the potential issues.
I wasn't expecting anything, it was out of curiosity.
Another question: do you think vitamin C supplements shouldn’t be taken after a meal, because they can interact with the metals in the food, and also increase the absorption of iron? When is the best time to take it?
I would add it to taste in moderate amounts of juice when you is about to drink it, away from meals. Taste, because it will guide on the optimal dose; moderate amounts of juice, due to the reasons mentioned above; for immediate consumption and away from meals, to prevent degradation and adverse interactions.
 
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Jennifer

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Just chiming in to say I take 4 g ascorbic acid with baking soda in the morning before my banana. I think there are interactions with food that is probably best to avoid.
Hi Janelle! :) When your anxiety attacks were at their worst, did you have shortness of breath and if so, did you notice vitamin C helped to resolve it?
 

InChristAlone

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Hi Janelle! :) When your anxiety attacks were at their worst, did you have shortness of breath and if so, did you notice vitamin C helped to resolve it?
Yes shortness of breath was one of the most scary symptoms, well I'd say it was more air hunger where you feel like you can't get a good breath but that's basically hyperventilation, so at my worst I had to breathe in a bag to prevent panic. I think vitamin C has been one of the best things I've used. Can't say for sure it stopped the anxiety attacks themselves, but it definitely helps anxiety.
 

Jing

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Has anyone had iv drip of vitamin c I would love to know what that is like to have but it's so expensive, just looked online place in London 350 pounds for one treatment 37.5grams .
 

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Has anyone had iv drip of vitamin c I would love to know what that is like to have but it's so expensive, just looked online place in London 350 pounds for one treatment 37.5grams .
Great for infections and cancer. Haven't had to deal with either of those so have not tested.
 

Jennifer

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Yes shortness of breath was one of the most scary symptoms, well I'd say it was more air hunger where you feel like you can't get a good breath but that's basically hyperventilation, so at my worst I had to breathe in a bag to prevent panic. I think vitamin C has been one of the best things I've used. Can't say for sure it stopped the anxiety attacks themselves, but it definitely helps anxiety.
Perfect! Thank you! Yes, I agree that it's one of the scariest symptoms. I found myself unable to breath one night at the end of September and was in and out of the hospital most of October due to passing out daily. I finally got my doctor to prescribe me NDT after tests came back positive for Hashi's, and the syncope episodes stopped within a day of starting my first dose but I'm still fighting for air periodically throughout the day so I'll try loading up on vitamin C. Thanks again! :)
 

InChristAlone

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Perfect! Thank you! Yes, I agree that it's one of the scariest symptoms. I found myself unable to breath one night at the end of September and was in and out of the hospital most of October due to passing out daily. I finally got my doctor to prescribe me NDT after tests came back positive for Hashi's, and the syncope episodes stopped within a day of starting my first dose but I'm still fighting for air periodically throughout the day so I'll try loading up on vitamin C. Thanks again! :)
I'm sorry to hear that :( Air hunger is definitely a symptom of thyroid disease so I can't say that vitamin C cures thyroid disease especially if your diet is already high in it, but I found it to be really great at lowering inflammation levels which I thought might be an issue with my anxiety. Plus it's an electron donor so it provides energy that your body might be struggling with producing. Plus with a high carotenoid or retinol diet you need more of the other supporting nutrients.
 

Jennifer

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I'm sorry to hear that :( Air hunger is definitely a symptom of thyroid disease so I can't say that vitamin C cures thyroid disease especially if your diet is already high in it, but I found it to be really great at lowering inflammation levels which I thought might be an issue with my anxiety. Plus it's an electron donor so it provides energy that your body might be struggling with producing. Plus with a high carotenoid or retinol diet you need more of the other supporting nutrients.
Thanks, Janelle. I appreciate that. :) I was hoping that it would help the adrenals since they have an affinity for C and the syncope episodes always start off as adrenaline attacks but you're right, I already get a lot of it from my diet alone. I suppose it will just take more time on thyroid and filling nutritional deficiencies for the air hunger to fully resolve. I thought because of my size and history of hypoglycemia that 6oz of meat a day was plenty but tests showed I'm deficient in phosphate so I've been making sure to have a lot more and it has definitely been helping.
 

InChristAlone

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Thanks, Janelle. I appreciate that. :) I was hoping that it would help the adrenals since they have an affinity for C and the syncope episodes always start off as adrenaline attacks but you're right, I already get a lot of it from my diet alone. I suppose it will just take more time on thyroid and filling nutritional deficiencies for the air hunger to fully resolve. I thought because of my size and history of hypoglycemia that 6oz of meat a day was plenty but tests showed I'm deficient in phosphate so I've been making sure to have a lot more and it has definitely been helping.
Yes it definitely helps adrenals too. That's great meat has been helping you! It is very grounding for a lot of people.
 

Amazoniac

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It's rare to find publications acknowledging this:

- Vitamin C and Neutrophil Function: Findings from Randomized Controlled Trials

"Meta-analyses have indicated that vitamin C intakes of at least 200 mg/day can decrease the risk of acquiring respiratory infections [56, 57], however, gram doses of vitamin C are required once an infection has taken hold, due to increased requirements for the vitamin [10, 58]."​
 

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Amazoniac

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- Neuropsychiatric scurvy

"Scurvy is an ancient disease that persists, and surprises. Early descriptions can be traced back 3500 years to the Egyptians. Herodotus is often credited with the first formal description of scurvy. He emphasized the hemorrhagic features of the disorder.[1] James Lind’s landmark treatise among sailors did much to define the modern clinical image of scurvy as an acute, hemorrhagic, and potentially fulminant nutritional deficiency.[2] This view of scurvy, accurate in what it included, has been replicated and persists to this day.[3,4,5] Yet hidden within these descriptions, both early and late, are symptoms that do not derive from disturbances of collagen metabolism, but rather from the central nervous system (CNS) effects of vitamin C deficiency, such as extrapyramidal symptoms (EPS). This review summarizes what is known about the CNS effects and clinical presentation of hypovitaminosis C."

"World Health Organization recognizes an early or “latent” form of scurvy characterized in part by “lassitude, weakness and irritability.”[6] Apathy, irritability, and psychomotor retardation have been recognized for centuries as heralding the onset of scurvy."

"James Lind reported that scurvy began with the development of changes in mood and behavior.[2] Shapter echoed these findings a century later when he reported that “feelings of weakness, of listlessness,” “a disinclination to exertion,” and a “nervous” state heralded the onset of scurvy.[5]"

"In a study of 38 patients with confirmed scurvy, Fouron and Chicoine found that all of the patients were irritable, and that many more had psychomotor retardation than had hemorrhagic findings.[3] In an elegant study, Hodges and colleagues monitored the fall in plasma vitamin C levels, and the emergence of symptoms, in five healthy adult men maintained on a diet free of vitamin C. They observed a fall in plasma vitamin C levels over 30 days. Hemorrhagic findings, beginning with petechiae, emerged at this time.[7] In a companion article, Kinsman and colleagues carefully assessed “personality changes” and psychomotor performance in the same subjects. They found that “personality changes” developed among the five subjects maintained on a diet devoid of vitamin C for 84 to 97 days. They observed that four scales of the Minnesota Multiphasic Personality Inventory (MMPI) rose markedly after day 23 of depletion, and continued to rise until vitamin C was repleted. These scales measured Hypochondriasis, Hysteria, Depression and Social Introversion. Each subject tended to become “a depressed and withdrawn individual who is concerned about his physical state.” These scales rose before the emergence of hemorrhagic findings, and before there was any decline in psychomotor performance.[8] Recently, disturbances of basal motor nuclei (BMN) function, as a result of vitamin C deficiency, have been described as a late stage of scurvy."

"Logroscino and colleagues found that a diet rich in non-heme iron is associated with an increased risk of developing Parkinson’s disease, and that this risk is further increased if the diet is poor in vitamin C.[14]"

"In rodents, central nervous system deficiency of vitamin C clearly disrupts BMN activity. This has long been recognized and repeatedly shown.[18,19] In adult rats acutely depleted of striatal vitamin C, psychomotor activity rapidly slows. Novelty-seeking and social interactions are similarly reduced.[20]"

"Somewhat simply, deficiency of vitamin C impedes the ability of the cerebrocortex to activate the BMN effectively. This results in difficulty translating thoughts into willed activities. The patient presents with apathy, irritability, anxiety, and at times frank disturbances of extrapyramidal motor function."

"In scurvy, carnitine levels are reduced. Deficiency of carnitine may provoke some of the earliest symptoms of scurvy, well before the appearance of defects in collagen synthesis.[31,32]" "L-acetylcarnitine stimulates dopamine release from the rat substantia nigra.[34] L-acetylcarnitine also contributes acetyl groups to the synthesis in rodents of glutamate and GABA.[35] And, L-acetylcarnitine stimulates neuronal uptake of choline, as well as the synthesis and release of acetylcholine, in rodents.[36,37] Deficiencies of carnitine may affect all of these brain processes."

"While a reduction in carnitine synthesis is itself important, vitamin C deficiency may also reduce the kidney’s ability to reabsorb carnitine. In scorbutic guinea pigs, renal excretion of carnitine increases fourfold.[38] If carnitine is available in the diet, these challenges to carnitine availability may be limited. But for those patients with poor oral intake, carnitine deficiency may contribute to the symptoms of neuropsychiatric scurvy."

"The brain accounts for only 2% of human body weight, yet consumes 20% of the body’s oxygen supply.[45] The brain’s avidity for oxygen is matched by its normally high concentrations of vitamin C. These high concentrations of vitamin C help to protect cells against oxyradical damage in the presence of catalytic metals. This fact is thought important in the genesis of Parkinson’s disease, a model disorder of oxyradical toxicity.[46] Indeed, oxyradical toxicity mediated through copper and vitamin C is thought to play a role in the genesis of Parkinson’s disease, as well as Wilson’s disease.[47,48] But oxyradical toxicity is not unique to these disorders.[44] This leaves the question of why there might be Parkinsonism in scurvy. There may be an additional factor that helps explain this risk: the iron content of the substantia nigra."

"It happens that the substantia nigra is unusually rich in iron.[49] The more concentrated the iron, the more likely there is to be ascorbate-related oxyradical toxicity when vitamin C levels fall. This makes the substantia nigra a target for early decompensation in scurvy."

"The brain and adrenal medulla have the highest concentrations of vitamin C in the body. Because the brain avidly retains vitamin C, and is the last organ or tissue depleted of vitamin C, it may be that a protracted period of vitamin C depletion, consumption and elimination is required to reduce brain vitamin C levels.[51] However, once the brain is substantially depleted of vitamin C, it may compete ineffectively with other organs for this vitamin. This would be due to:
  1. the limited ability of SVCT2 to move vitamin C into its target tissues, compared to the SVCT1 and GLUT transporters;
  2. the normally high concentration of, and demand for, vitamin C within the brain: the relatively thin straw of the SVCT2 is thus obligated to fill the biggest glass; and,
  3. the ability of other tissues to divert vitamin C towards themselves under states of acute need, as for examples leukocytes may do to combat infection.[53]"
"The management of neuropsychiatric scurvy involves first its recognition, followed by adequate treatment and follow-up care. The clinician should be emboldened to consider the possibility of hypovitaminosis C, in part because this condition is not rare. Perhaps the most difficult barrier for the clinician to scale is the idea—indeed the misconception--that scurvy occurs only where there is nutritional catastrophe, such as war or famine may impose."

"At the author’s institution, it is common to request serum levels of vitamin C and of zinc when scurvy is suspected. Because there may be a delay in receiving the results of these laboratory studies, treatment is typically initiated before the results of these studies are available. Treatment begins with 200 milligrams of vitamin C, and 5 milligrams of zinc [same author quoted here and linked below], given intravenously daily. Intravenous replacement continues until the patient is judged to be able to meet his needs orally."

"There are several reasons why neuropsychiatric scurvy should not be treated initially with oral replacement. The first is that the bioavailability of oral vitamin C is limited by the gut." "After surgery, or during critical illness, consumption of vitamin C may increase several-fold. In such cases, it may be appropriate to provide several grams of vitamin C by vein each day.[60] Finally, the author has observed a case of refeeding-induced acute hemorrhagic scurvy. In this case, oral vitamin C replacement led to resolution of central nervous system symptoms of scurvy, but with the abrupt onset of diffuse hemorrhages. The bleeding resolved quickly once intravenous vitamin C was begun.[9↖]"

"Moving from the problem of non-specific findings, the clinician may find little solace in vitamin C blood levels. While a low level is strongly suggestive of deficiency, a normal level, and in particular a low-normal level, of a water-soluble vitamin does not ensure adequate tissue levels.[62] Furthermore, the serum vitamin C level is typically assayed at an outside laboratory, which means the clinician must usually wait for days to obtain a result."

- The Neuropsychiatry of Scurvy

"The crucial role of Vit C in neuronal maturation and functions, neurotransmitter action as well as responses to oxidative stress is well supported by the evidences presented in this review (Figure 2)."

"Vit C is a nutrient of greatest importance for proper functioning of nervous system and its main role in the brain is its participation in the antioxidant defense. Apart from this role, it is involved in numerous non-oxidant processes like biosynthesis of collagen, carnitine, tyrosine and peptide hormones as well as of myelin. It plays the crucial role in neurotransmission and neuronal maturation and functions [7]. For instance, its ability to alleviate seizure severity as well as reduction of seizure-induced damage have been proved [8,9]. On the other hand, disruption of vitamin C transport has been shown to contribute to brain damage in premature infants [10]. Furthermore, Vit C treatment has been reported to ameliorate neuropathological alterations as well as memory impairments and the neurodegenerative changes in rats exposed to neurotoxic substances like aluminum or colchicine [11,12]."

"The brain is an organ particularly exposed to oxidative stress and free radicals’ activity, which is associated with high levels of unsaturated fatty acids and high cell metabolism rate [16]. Ascorbic acid, being an antioxidant, acts directly by scavenging reactive oxygen and nitrogen species produced during normal cell metabolism [30,31]. In vivo studies demonstrated that the ascorbate had the ability to inactivate superoxide radicals—the major byproduct of fast metabolism of mitochondrial neurons [32]. Moreover, the ascorbate is a key factor in the recycling of other antioxidants, e.g., alpha-tocopherol (Vitamin E). Diokine-tocopherol, found in all biological membranes, is involved in preventing lipid peroxidation by removing peroxyl radicals. During this process a-tocopherol is oxidized to the a-tocopheroxyl radical, which can result in a very harmful effect. The ascorbate could reduce the tocopheroxyl radical back to tocopherol and then its oxidized form is recycled by enzymatic systems with using NADH or NADPH [33]. Regarding these facts, vitamin C is considered to be an important neuroprotective agent."

"One non-antioxidant function of vitamin C is its participation in CNS signal transduction through neurotransmitters [16]. Vit C is suggested to influence this process via modulating of binding of neurotransmitters to receptors as well as regulating their release [34,35,36,37]. In addition, ascorbic acid acts as a co-factor in the synthesis of neurotransmitters, particularly of catecholamines—dopamine and norepinephrine [26,38]. Seitz et al. [39] suggested that the modulating effect of the ascorbate could be divided into short- and long-term ones. The short-term effect refers to ascorbate role as a substrate for dopamine-b-hydroxylase. Vit C supplies electrons for this enzyme catalyzing the formation of norepinephrine from dopamine. Moreover, it may exert neuroprotective influence against ROS and quinones generated by dopamine metabolism [16]. On the other hand, the long-term effect could be connected with increased expression of the tyrosine hydroxylase gene, probably via a mechanism that entails the increase of intracellular cAMP [39]. It has been stated that the function of ascorbic acid as a neuromodulator of neural transmission may be also associated with amino acidic residues reduction [40] or scavenging of ROS generated in response to neurotransmitter receptor activation [34,41]. Moreover, some have studies showed that ascorbic acid modulates the activity of some receptors such as glutamate as well as y-aminobutyric acid (GABA) ones [22,40,42,43,44]. Vit C has been shown to prevent excitotoxic damage caused by excessive extracellular glutamate leading to hyperpolarization of the N-methyl-d-aspartate (NMDA) receptor and therefore to neuronal damage [45]. Vit C inhibits the binding of glutamate to the NMDA receptor, thus demonstrating a direct effect in preventing excessive nerve stimulation exerted by the glutamate [26]. The effect of ascorbic acid on GABA receptors can be explained by a decrease in the energy barrier for GABA activation induced by this agent. Ascorbic acid could bind to or modify one or more sites capable of allosterically modulating single-channel properties. In addition, it is possible that ascorbic acid acts through supporting the conversion from the last GABA-bound closed state to the open state. Alternatively, ascorbic acid could induce the transition of channels towards additional open states in which the receptor adopts lower energy conformations with higher open probabilities [40,44]."

"There have also been reports concerning the effect of Vit C on cognitive processes such as learning, memory and locomotion, although the exact mechanism of this impact is still being investigated [26]. However, animal studies have shown a clear association between the ascorbate and the cholinergic and dopaminergic systems, they also suggested that the ascorbate can act as a dopamine receptor antagonist. This was also confirmed by Tolbert et al. [46], who showed that the ascorbate inhibits the binding of specific dopamine D1 and D2 receptor agonists."

"Another non-antioxidant function of Vit C includes modulation of neuronal metabolism by changing the preference for lactate over glucose as an energy substrate to sustain synaptic activity. During ascorbic acid metabolic switch, this vitamin is released from glial cells and is taken up by neurons where it restraints glucose transport and its utilization. This allows lactate uptake and its usage as the primary energy source in neurons [47]. It was observed that intracellular ascorbic acid inhibited neuronal glucose usage via a mechanism involving GLUT3 [48]." [¿]

"Vit C is involved in collagen synthesis, which also occurs in the brain [26]. There is no doubt that collagen is needed for blood vessels and neural sheath formation. It is well recognized that vitamin C takes part in the final step of the formation of mature triple helix collagen. In this stage, ascorbic acid acts as an electron donor in the hydroxylation of procollagen propyl and lysyl residues [16]. The role of Vit C in collagen synthesis in the brain was confirmed by Sotiriou et al. [49]. According to these authors in mice deficient in SVCT2 ascorbate transporter, the concentration of ascorbate in the brain was below detection level. The animals died due to capillary hemorrhage in the penetrating vessels of the brain. Ascorbate-dependent collagen synthesis is also linked to the formation of the myelin sheath that surrounds many nerve fibers [26]. In vitro studies showed that ascorbate, added to a mixed culture of rat Schwann cells and dorsal root ganglion neurons, promoted myelin formation and differentiation of Schwann cells during formation of the basal lamina of the myelin sheath [7,29]."

"In the literature data, there are only a few studies considering association between MS and Vit C. However, the existing ones showed that MS patients displayed significantly lower Vit C level as compared to healthy individuals [135,136,138]. Besler et al. [138], in turn, observed an inverse correlation between the serum levels of Vit C and lipid peroxidation in MS patients. The authors concluded that decreased Vit C level, observed in MS patients during relapse of the disease, might be dependent on the elevated oxidative burden as reflected by increased lipid peroxidation. Hejazi et al. [139], in turn, found no significant difference between daily intake of Vit C (recorded from a 24-h dietary recall questionnaire for 3 days) in MS patients (n = 37) in comparison with healthy subjects. The intake of Vit C in both groups was below dietary reference intake (DRI), however in control group it was near the DRI value."

"The available literature data indicate that Vit C deficiency is very common in patients with depressive disorders." "Basing on several animal studies [153,155,164,165,166], there is preliminary evidence that Vit C exerts an antidepressant-like effect via:
  1. modulation of monoaminergic systems [167] (e.g., Vit C was shown to activate the serotonin 1A (5-HT1A) receptor, this activation is a mechanism of action of many antidepressant, anxiolytic and antipsychotic drugs);
  2. modulation of GABAergic systems (via activation of GABAA receptors and a possible inhibition of GABAB receptors) [155];
  3. inhibition of N-methyl-d-aspartate (NMDA) receptors and l-arginine-nitric oxide (NO)-cyclic guanosine 3,5-monophosphate (cGMP) pathway—the blockade of NMDA receptor is associated with reduced levels of NO and cGMP, whereas reduction of NO levels within the hippocampus was shown to induce antidepressant-like effects [119];
  4. blocking potassium (K+) channels—Vit C administration was shown to produce an antidepressant-like effect in the tail suspension test via K+ channel inhibition [119]; as K+ channels were reported to belong to the physiological targets of NO and cGMP in the brain, their inhibition plays a significant role in the treatment of depression;
  5. activation of phosphatidylinositol-3-kinase (PI3K) and inhibition of glycogen synthase kinase 3 beta (GSK-3ß) activity [112,119];
  6. induction of heme oxygenase 1 expression—it is a candidate depression biomarker which may be a link factor between inflammation, oxidative stress and the biological as well functional changes in brain activity in depression; its decreased expression is associated with depressive symptoms [166,168];
  7. since depression is well known to be associated with altered anti- and prooxidant profiles, Vit C may play antidepressant function also by its antioxidant properties [118,119]."

Refer to this article for more information on the topic.


- Nonalimental Scurvy With Relapse Symptoms After Stopping Oral Vitamin C Supplementation

- The Roles and Mechanisms of Actions of Vitamin C in Bone: New Developments
 

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