A proposed treatment protocol.

As NMDA receptor dysfunction is the leading model of schizophrenia, I would like to propose the following experimental treatment protocol for NMDA based disorders:

Glycine chelated magnesium (2[NH2CH2COO]1- · Mg2+) 1,000 mg daily.

Glycine → L-Serine via serine hydroxymethyltransferase.

L-Serine → D-Serine via serine racemase.

Both glycine and serine are NMDA antagonists.

Magnesium regulates the NMDA ion channel through voltage-dependent activation.

N-methy Glycine (sarcosine) 2,160 mg daily.

NMDA antagonist, and also acts as a reuptake inhibitor.

N-acetyl Cysteine (NAC) 1,800 mg daily.

NAC → Glutathione.

Glutathione regulates the NMDA redox site.

Vitamin D3 5,000 I.U. daily.

Calcitriol is a major glutathione catalyst.

I've been on this combination for two full weeks and I'm actually feeling good for a change, the dosages listed are what I'm currently taking. For Vitamin D3, I took a loading dose 16 days ago to get my serum concentration up, I estimate my 25(OH)D level is around 50 - 60 ng/mL. Also I'm taking aspirin 325 mg daily, which among other things this is also active on NMDA. Furthermore, lamotrigine 150 mg daily, which is also active on NMDA. Additionally for completeness, Omega-3 1000 mg and iodine 200 mcg daily.

My source for sarcosine was biosciencenutra.com (which is a subsidiary of cerebralhealth.com), it came as a powder, so I had to pill it myself. Sigma-Aldrich also carries sarcosine powder; sarcosine is sweet tasting, you could quite literally use it as a sugar substitute. During my search for sarcosine, I found a supplier that packaged sarcosine with NAC, profrontal.com, however I did not buy from them because I already had NAC. I purchased NAC at my local GNC, it's available in 600 mg capsules. I purchased the chelated magnesium at my local Walgreens, the brand is Doctor's Best, High Absorption 100% Chelated Magnesium, sourced by Albion Laboratories, Inc. The vitamin D3 I'm taking is a liquid softgel produced by NatureMade, I picked it up at Walmart.

Good luck. I hope it helps you.

nbritton,

What symptoms would you say that your regimen seems to be helping with the most? Are there any symptoms of yours that don't seem to be improving with this regimen? If so, which ones?

I hope that you'll continue to benefit from the experimental treatment protocol that you've proposed. Perhaps what you've posted here will also be of some benefit to somebody else.

Before I end this, I came up with another question: Are you currently utilizing any treatment methods other than the supplements that you listed?

All the best,
shadow

At this time, I’m also suggesting a model that calcitriol deficiency, specifically a deficiency in the active metabolite of vitamin D3, is a contributing factor in schizophrenia. In rat studies, calcitriol was found to have a significant impact on glutathione production. Upon administration of calcitriol, glutathione levels in rat astrocyte primary cultures increased on average 42%, furthermore levels stayed elevated for over 96 hours after administration. Increased glutathione levels reduce reactive oxygen species. This is important, as the NMDA receptor is co-regulated by reduction-oxidation reactions via the redox modulatory site. Reductants have been show to dramatically enhance NMDA channel activity, but oxidants either reverse the effects of reductants or depress native responses.

The smoking gun linking all of this together are two studies that documented low serum vitamin D3 concentrations in patients with schizophrenia. While they state a correlation could not be established with their models, I’m of the opinion that had they measured glutathione and calcitriol they could have established a correlation. A number of things can go wrong in the production of calcitriol from cholecalciferol, it’s a two step process involving the conversion of cholecalciferol to calcifediol in the liver, and then calcifediol to calcitriol in the kidney. Defects in the organs can interfere in this process, and outside forces, such as alcohol consumption, can also interfere. Many supplements contain vitamin D2, but since calcitriol can only be produced from vitamin D3, a deficiency in vitamin D3 will inhibit calcitriol production, even when overall vitamin D intake is high. One reason for this is most foods fortified with vitamin D don’t actually contain vitamin D3, typically they’re fortified with vitamin D1 and D2. Additionally, once the solar azimuth angle drops below a certain point in autumn, our atmosphere filters out most of the UVB ultraviolet light, once this threshold is passed someone could sit in the sun all day long and not get enough UVB to produce sufficient vitamin D3. Sunscreen also filters out UVB, and the bottom line is many individuals are exposed to less direct sunlight then their ancestors. The cumulative effect of these things can lead to a situation were vitamin D intake is high, but calcitriol is deficient.

When doctors test vitamin D status, they actually check calcifediol levels. They’ve found that calcitriol is not a reliable indicator of vitamin D status, which is no surprise given all the reasons I just stated in the previous paragraph. I think this is the reason why studies have not correlated vitamin D status, specifically calcifediol, with mental health symptom severity. Again, I postulate that calcitriol status will correlate with glutathione status, and this will correlate with symptom severity. Actually, I believe this correlation has already been established in studies with NAC. I recall one study where NAC was evaluated in patients with trichotillomania; treatment with NAC alone led to complete remission of trichotillomania within 6 weeks. NAC has been used for decades in emergency care settings to treat tylenol (acetaminophen) overdose, it acts as a precursor for glutathione, and glutathione is what actually stops the reactive metabolite of acetaminophen, NAPQI, from causing oxidative damage to the liver, which if not prevented will cause liver failure.

I think my proposed model accurately explains why schizophrenia is more prevalent in people with black skin. Schizophrenia has also been linked to winter births, and calcitriol is significantly reduced in breast milk during winter months. Women that nurse through the winter would be susceptible to low calcitriol levels, but black mothers would be the most susceptible. Prolactin, the principal hormone that stimulates the production of milk has been show to increase calcitriol levels. It’s likely an infant is dependent on calcitriol that is supplied in the mothers milk. I postulate that this lack of calcitriol, and particularly glutathione, during fetal development and breastfeeding irrevocably damages normal brain development, presumably through reactive oxidation.

Calcitriol's catalytic effect may also partially explain the pathophysiology of seasonal affective disorder, as NMDA receptor dysfunction has also been implicated in mood disorders. I postulate that most individuals accumulate enough vitamin D3 from UVB radiation in the summer months to keep their calcitriol and glutathione levels within the optimal range through the winter. However, in those that don’t get enough, oxidative stress could become problematic at the NMDA redox site, depressing NMDA receptor function. I think research will show that low glutathione is one of several states that can induce NMDA receptor dysfunction, and I propose that sub-optimal calcitriol levels could be one of the root causes for this.

It shouldn't be assumed that the observed normal laboratory range for vitamin D is also the optimal range. Our sun, location, and skin is the rate limiting factor in vitamin D synthesis. As a result, this is a natural selection force on the population as a whole, and in evolutionary terms, many with statistically normal levels may not actually have enough to thrive; the consensus is that optimized levels are between 50 - 70 ng/mL, but these levels are not often seen in individuals. I think the reason a direct correlation may have been missed, or is otherwise not obvious, is the half-life of vitamin D3 is about 21 days, and it takes an additional 10 days for the body to process vitamin D3 into calcitriol; this means it takes nearly 5 months to reach peak serum concentrations when taking oral D3 supplements. Moreover, taking 2,500 I.U. daily may not be enough to reach the optimal goal of 50+ ng/mL, sometimes upwards of 10,000 I.U. daily might be need in overweight individuals.

A loading dose of 10,000 I.U. daily for 21 days should bring levels up to a steady state serum concentration that is roughly equivalent to 5,000 I.U. daily. Likewise a 5,000 I.U. loading dosing for 21 days would bring levels up to the steady state equivalent of 2,500 I.U. daily. This 2:1 ratio is true for any given dose at day 21, due to it's half-life of 21 days.

At the very least I think those who find NAC beneficial would likely also benefit from D3 supplementation, simply for the fact that calcitriol acts as a catalyst in the conversion of NAC to glutathione. For this reason, those who overdose on tylenol might benefit from the co-administration of calcitriol. This should be relatively easy to study in a clinical setting, by comparing patient outcomes of NAC versus NAC + calcitriol in acute care acetaminophen overdose cases. Calcitriol is available commercially in injectable form.

As acetaminophen depletes glutathione, it stands to reason that this would contribute to low glutathione levels, thus it’s probably wise that individuals with mental health disorders should not use it; aspirin has been show to have positive effects on mental health.

Furthermore, vitamin D supplementation can be started immediately without a physician's prescription, and is readily available in every market. I know of many government employees who must report psychiatric visits and medications to their employers, vitamin D supplementation would not have this requirement. Presuming calcitriol, glutathione, and NDMA are linked as I proposed, someone who responds to this would be a good candidate for traditional NDMA treatment protocols. In my opinion it's certainly worth exploring as a possible treatment avenue, as I can't think of anyone who wants to take a medication, but many would at least be willing to take a vitamin.

If this model pans out, pregnant women should begin vitamin D3 supplementation once they find out they’re pregnant, as it takes upwards of five months to reach steady state serum concentrations. I propose a daily dose of 2,000 I.U., with a 21 day 4,000 I.U. loading dose. This should raise 25(OH)D levels by 20 ng/mL in most women, which in deficient females would raise levels to the normal range, and in non deficient females would raise levels to the optimal range. Serum levels above 80 ng/mL appear to be counter productive, so higher doses are not necessarily better. Levels below 1,000 I.U. I think are insufficient. Looking at the dose-response analysis curves, adults taking 1,000 I.U. daily were not able to increase their serum concentrations during the winter. The response curve was logarithmic, and 1,000 I.U. wasn’t enough to appreciably raise levels. Ideally an obstetrician would monitor calcitriol and calcifediol levels, but I suspect many who are vulnerable may not have access to comprehensive prenatal care. 4000 I.U. has been determined by the government as the upper limit that can safely be taken by all pregnant and lactating women, regardless of current vitamin D status.

In summary, the model is simply that calcitriol is a principal glutathione catalyst or modulator, in addition to its role as a hormone and steroid, and that glutathione influences NMDA receptor function. It may also be a catalyst for cystine, it could possible involve glutamate too, or cystine's anti-inflammatory or modulating cytokine synthesis. This is simply a hypothesis, I don’t think enough information is currently available to make any definitive conclusions. However, it seems like common sense and pursuant to occam's razor, it’s one of the simplest explanations I have come across that that can account for a wide range of mental health disorders. I think the brain is sensitive to oxidative stress, and glutathione is a major antioxidant in the body. Inflammation has been implicated in various disorders, and this could be an autoimmune response to excessive reactive oxidation. The fact that simple reactive oxidations can induce liver failure, as is the case with acetaminophen toxicity, strongly supports this theory that glutathione is a critical component in normal brain function.

Hopefully someone will expand on this and put it to the test. One method to study this in the laboratory is to take four groups of rats: one control group, one calcitriol group, one NAC group, and one calcitriol + NAC group. After sufficient time you would homogenize brain matter and then measure calcitriol, cystine, glutamate, glutathione, and glycine concentrations directly.

Previously, I said sarcosine could be used as a sugar substitute. I tried this today, by sprinkling my normal morning dose into my coffee. I could not tell a difference with one gram of sarcosine I added in, so I added three grams, and I still could not tell a difference. It readily dissolves in solution and has the same general properties as granulated sugar; it’s crystalline like sugar, and also has a melting point similar to sugar.

One kilogram can be purchased from biosciencenutra.com for $195. Thus the cost per gram is 19.5 cents, and the standard daily dose is less than 40 cents a day. Two hundred dollars seems like a lot, but realize a one kilogram supply will last for over a year when taking two grams daily; it comes out to less than $10 a month.

So it appears that mixing sarcosine into food, especially coffee, is a viable method for delivery. Two grams of sarcosine equates to roughly 3/4 of a teaspoon. Furthermore, when purchased in bulk it is very cheap. Sprinkled onto food, this could be a viable solution for non compliant individuals; for instance, it could be mixed into a child’s cereal or even table sugar.

I'm impressed with all your research. I hope it helps you. Personally, however, I wouldn't recommend putting substances of any kind into another person's food without their permission and awareness. Especially if the person is paranoid since one of the common fears of paranoid people is that their food is being poisoned, contaminated, or tampered with. If you do the thing they're afraid people are doing then you're just proving them right and feeding that fear. And you won't have a leg to stand on later if you want to tell them their fear is groundless.

Hello again,

I was just reading about a new research study that concluded autophagy dsyfunction is a major factor in schizophrenia. The term autophagy could be described as cellular garbage collection, basically autophagy is how the body removes "junk" that is within our cells.

Here is the link to the study: Molecular Psychiatry - Autophagy has a key role in the pathophysiology of schizophrenia

Anyways, it turns out that glutathione is involved in the autophagy process. Here are a few studies I found on pubmed:

Reactive Oxygen Species Regulation of Autophagy in Skeletal Muscles.
Rahman M, Mofarrahi M, Kristof AS, Nkengfac B, Harel S, Hussain S Dr.
Antioxid Redox Signal. 2013 Nov 1.
PMID: 24180497

Glutathione participates in the modulation of starvation-induced autophagy in carcinoma cells.
Desideri E, Filomeni G, Ciriolo MR.
Autophagy. 2012 Dec;8(12):1769-81. doi: 10.4161/auto.22037. Epub 2012 Sep 10.
PMID: 22964495

N-Acetyl Cysteine Protects against Methamphetamine-Induced Dopaminergic Neurodegeneration via Modulation of Redox Status and Autophagy in Dopaminergic Cells.
Chandramani Shivalingappa P, Jin H, Anantharam V, Kanthasamy A, Kanthasamy A.
Parkinsons Dis. 2012;2012:424285. doi: 10.1155/2012/424285. Epub 2012 Sep 27.
PMID: 23056996

Lysosomal thiol reductase negatively regulates autophagy by altering glutathione synthesis and oxidation.
Chiang HS, Maric M.
Free Radic Biol Med. 2011 Aug 1;51(3):688-99. doi: 10.1016/j.freeradbiomed.2011.05.015. Epub 2011 May 23.
PMID: 21640818

DJ-1 regulation of mitochondrial function and autophagy through oxidative stress.
McCoy MK, Cookson MR.
Autophagy. 2011 May;7(5):531-2. Epub 2011 May 1.
PMID: 21317550

Role of autophagy in protection afforded by hypoxic preconditioning against MPP+-induced neurotoxicity in SH-SY5Y cells.
Tzeng YW, Lee LY, Chao PL, Lee HC, Wu RT, Lin AM.
Free Radic Biol Med. 2010 Sep 1;49(5):839-46. doi: 10.1016/j.freeradbiomed.2010.06.004. Epub 2010 Jun 9.
PMID: 20541008

Parkin deficiency increases the resistance of midbrain neurons and glia to mild proteasome inhibition: the role of autophagy and glutathione homeostasis.
Casarejos MJ, Solano RM, Rodriguez-Navarro JA, Gómez A, Perucho J, Castaño JG, García de Yébenes J, Mena MA.
J Neurochem. 2009 Sep;110(5):1523-37. doi: 10.1111/j.1471-4159.2009.06248.x. Epub 2009 Jun 22.
PMID: 19549073

Intracellular glutathione regulates sesquiterpene lactone-induced conversion of autophagy to apoptosis in human leukemia HL60 cells.
Itoh T, Ohguchi K, Nozawa Y, Akao Y.
Anticancer Res. 2009 Apr;29(4):1449-57.
PMID: 19414401

My cursory conclusion is that glutathione and antioxidants in general, and possibly even anti-inflammatory agents, protect proteins from degradation; so if blocked or inhibited autophagy is one of the problems in schizophrenia, then it makes sense why preventing reactive species (i.g. free radicals) from damaging cellular components would improve the symptoms of schizophrenia. That is to say, antioxidants reduce the total amount of garbage that needs to be cleared out through the autophagy process. If my conclusions are correct, adjunctive treatment with antioxidants (i.g. NAC, Alpha-lipoic acid, et. al.) should prove to be highly effective in the management of schizophrenia. More research and clinical trials are needed.

For those who are considering taking Vitamin D3 + NAC. Based on additional research, I would recommend that daily NAC intake should not exceed 1800 mg. Furthermore, I would suggest adding on lipoic acid (also known as alpha-lipoic acid). LA helps by recycling oxidized glutathione ("GSSG") back into it's reduced state ("GSH"). My educated guess is that with the combination of D3 and LA, 1200 mg of NAC daily should be sufficient to optimize glutathione. LA can be purchased locally at GNC and Wallgreens, other sources are available online. LA is chiral and has two enantiomers, the R- enantiomer is the only one that's naturally produced by the body, so ideally the best form of LA to purchase would be an R-LA salt (R-sodium lipoate), such as this; R-lithium lipoate would be the perfect source for mental health needs. Furthermore, LA functions as a heavy metal chelating agent, methyl-mercury in particular has a very high affinity with the two thiol groups in lipoic acid. LA appears to have some efficacy in preventing acne as well.

This appears to be a good overview of how glutathione interacts with other antioxidants: http://www.aim4health.com/antioxidant4.htm

What I meant to say is that racemic lipoic acid has a bioavailability of only about 30%, as the S- enantiomer is biologically inactive. R-lipoic acid has a greater bioavailability, and a stabilized R- enantiomer salt is the best type of lipoic acid to take*; lithium R-lipoate is ideally suited for use in psychiatric applications, as it provides a small amount of elemental lithium, roughly 3.3% elemental lithium by weight.

*Lipotic acid is unique in that it readily polymerizes into a long chain of thiol groups. Even room temperature water, due to it's pH, can polymerize it. In the gut, lipotic acid rapidly conjugates into a varied assortment of poly lipoate salts that have a half life of roughly three hours. It's also noteworthy that lipotic acid is soluble in lipids, alcohol, and water; most antioxidants are not lipid-soluable.

Due to it's bioavailability and half-life, when taking racemic alpha-lipoic acid, I'd suggest 300 mg three times daily as a starting point. I'm thinking that if you mixed ALA and NAC together, into a single capsule, it would prevent ALA from forming long polymer chains, and this would aid absorption.

Yes it appears so, I mixed one 600 mg capsule of ALA with one 600 mg capsule of NAC. There was a marked increase in initial gastrointestinal distress, which indicates to me that more of it was reacting and being absorbed. Also it feels like there is fluid in my lungs, which is perfectly normal given that NAC is also a mucolytic agent, however what was different about this time was it came on much faster and stronger than unusual... i.e. the thiols are cleaving the disulfide bonds in my lung mucus. ALA has two thiol groups, moreover ALA can reduce oxidized glutathione (GSSG) back into reduced glutathione (GSH), by extension this probably applies to NAC as well. I'm coughing at this point due to want feels like fluid in my lungs, this was only 600 mg of ALA mixed with 600 mg of NAC.

Disulfide bond cleavage is a reductive reaction, which means my lung mucus is being deoxidized. So at least I know it works, i'm giving the combo two thumbs up due to it's synergistic action... this means you can take less.

I was rummaging around pubmed and found a double blind randomized placebo controlled trial that showed Vitamin C improved symptoms in schizophrenia; it increased BPRS scores.

Vitamin C is another antioxidant just like the other ones I've been talking about in this thread. It appears this antioxidant thing may actually pan out as a viable treatment method for schizophrenia.

Here is the study link: Supplementation of vitamin C with atypical antipsychotics reduces oxidative stress and improves the outcome of schizophrenia - Springer

More rummaging around in pubmed, surprise surprise...

Int J Psychiatry Clin Pract. 2013 Feb;17(1):30-4. doi: 10.3109/13651501.2012.667111. Epub 2012 Apr 26.
Vitamin D, parathyroid hormone, serum calcium and phosphorus in patients with schizophrenia and major depression.
Jamilian H, Bagherzadeh K, Nazeri Z, Hassanijirdehi M.

Abstract:

OBJECTIVE:
Vitamin D deficiency has been associated with an increased risk of depression and schizophrenia. The aim was to compare serum levels of vitamin D, calcium, phosphorus and parathyroid hormone in schizophrenics, depressed patients and healthy subjects in an Iranian population.

METHODS:
In a cross-sectional study, 100 patients with schizophrenia and 100 with major depression were enrolled. A questionnaire was filled by using medical records of patients. After that a serum sample was taken and levels of vitamin D, calcium, phosphorus and parathyroid hormone were assessed and then compared between the three groups.

RESULTS:
Post-hoc analysis of Tukey showed that vitamin D level in healthy participants was significantly higher than depressed patients and schizophrenics while there was no significant difference between vitamin D level in depressed and schizophrenic patients.

CONCLUSION:
The findings suggest that vitamin D affects the brain independent of hormonal pathways which regulate serum level of calcium. Non-significant difference in the serum level of vitamin D between the schizophrenics and the depressed patients suggests that the independent effect of vitamin D in brain is a general effect and is not specialized to a specific region or pathway in the brain; however, differences between psychiatric and non-psychiatric patients might be resulted from differences in psychosocial backgrounds.

Found this on research gate, I originally missed it during my search on pubmed since the title doesn't contain the keyword schizophrenia:

Vitamin D and psychosis: Mini meta-analysis:

Martino Belvederi Murri, Matteo Respino, Mattia Masotti, Marco Innamorati, Valeria Mondelli, Carmine Pariante, Mario Amore
Department of Neurosciences Division of Psychiatry, University of Parma, Parma, Italy; King's College London, Institute of Psychiatry, Department of Psychological Medicine, London, UK.
Schizophrenia Research (Impact Factor: 4.59). 07/2013; DOI:10.1016/j.schres.2013.07.017

Abstract:

Individuals with psychotic disorders are more likely to have vitamin D (VD) deficiency, while evidence suggests VD could have pathophysiological roles. We summarized meta-analytically the available evidence on VD levels in psychotic disorders in comparison with healthy controls and other psychiatric illnesses. We found seven studies, all reporting insufficient VD levels in patients with psychosis. Schizophrenia had a medium effect size for lower VD than healthy controls, and a trend for lower levels than other psychoses. There were non-significant differences between schizophrenia and major depression. No study has investigated the potential psychotropic effects of VD supplementation in patients with psychosis.

The full paper can be downloaded here: http://www.researchgate.net/publicat...93efde0b27.pdf

I must take back what I said before about mixing NAC with LA. I was speaking with lead researcher for Geronova Research, and he clued me in that NAC can inhibit Nrf2 activation of lipoic acid. For optimal effect, NAC and LA should be taken at different times of the day.

This is what he stated:

"We had a product on the market for yrs composed of NaRLA and NAC (R+NAC). NAC doesn’t stop the polymer formation, it actually contributes to it which is one of the reasons we stopped making it. The contents of the caps became sticky, then solid over time. The reason we launched the product initially was because of the supposed synergism. It appears that unless NAC is taken at a different time, so it can act as a “pro-GSH” compound (providing the amino acids) it negates the Nrf2 activation of RLA by scavenging the oxidative signal induced by RLA."

Swanson vitamins sells NAC for $6.99 for a bottle of 600 mg x 100 capsules, this is a really good deal! I had a $10 off + free shipping coupon code for orders over $60, so I purchased 9 bottles (900 capsules) for a grand total of $52.91. The unit cost per pill comes out to about $0.059 and assuming a daily dose of 1,200 mg, the monthly cost comes out to $3.59. The coupon code I used was "WINTER", I found it simply by googling for swanson coupon codes. They also regularly have a 10% + free shipping deal for first time customers. For $43 bucks a year, NAC is absolutely worth adding to your treatment regimen.

Here is the link for NAC at Swanson's site: https://www.swansonvitamins.com/swan...00-mg-100-caps

Two more sources:
Sarcosine - Chem-Impex International
Sarcosine by Smart Powders

The cheapest source by far is Chem-Impex International located in Illinois, they offer it as cheap as $0.061 a gram if you buy in bulk, but one downside is they appear to only sell to businesses. If you're looking to try sarcosine for the first time I would suggest Smart Powders.

How has this regimen affected your symptoms since you started this in Dec? Do you also take prescription meds now or previously?

Just a general remark , vitamin d like glycine , is generally metabolised in the body , the smaller amounts are generally lost in the gut , taking large amounts of vitamin d , is thought by many studies to be unsafe , just like taking large amounts of glycine can impact kidney function. In terms of deficiency of vitamin d , this more than likely has little to do with pathology and more to do with a sedentary life style. Correlation and causation is a term rolled out by the sceptic community but is very apt when assessing schizophrenia. We have many in the anti psychiatry movement tell us that recovery rates are far greater in developing societies , yet ignore the fact that scientific endeavour is frowned upon because of inherent cultural mysticism. But it also swings the other way where there is opposing research that are promoted as legitimate.

So D is being pushed for colon cancer right now at higher than the rda values....one of the GI docs is taking 2000 units so that's probably fine if you're not getting other sources but I don't know about higher than that....apparently most cases of toxicity are 10,000 and up...

I ran out of magnesium glycinate and sarcosine, money is really tight for me and I haven't been able to afford to renew them. They seemed to help, I took them both in the morning, and afternoon, and they appeared to make me more functional. My house was spotless during the time I was taking them, this was a major accomplishment for me. I was doing great! I don't know for sure if I can attribute that success to these compounds though because I was trying multiple compounds at the same time, I took a shotgun approach. Now I'm in the process of trying them one by one to determine what was actually helping. My best guess is sarcosine was very helpful. It's important to note these are all adjuncts to lutuda, at the time I was taking them I was taking 40 mg of lutuda.

Vitamin D3, NAC, and zinc made the cut. Astaxanthin, Coenzyme q10, Vitamin C, and Vitamin E did not make the cut; I've come to the conclusion that taking exogenous antioxidants is bad because they disrupt the natural internal Nrf2-Keap1-ARE signaling pathway, this is bad because they may down-regulate the supply of endogenous antioxidants. The new approach I'm taking is to optimize my endogenous antioxidants, perticularly glutathione. Vitamin D3 and zinc are both glutathione modulator/catalysts, and NAC is a glutathione precursor. I think they have also helped significantly, here is everything I'm currently taking...

Have you been taking sarcosine again? If so, have you found any differences/withdrawal symptoms if you stopped taking it temporarily?