My ideas about the etiology of schizophrenia are presented in Treatment-resistant schizophrenia: focus on the transsulfuration pathway which was published in Reviews in the Neurosciences. The treatment section of the paper is out of date.
Everything should be made as simple as possible, but not simpler. – Albert Einstein.
First of all do no harm. Most importantly do not take any supplement that could raise L-cysteine levels except taurine which could spare cysteine. Second of all avoid the too be avoided supplements. Third of all cut out coffee, sodas, tea including herbal teas. Two cups of coffee in the morning taken an hour before iron is supplemented seems the least harmful way to drink coffee though not recommended. Supplemented iron from iron carbonyl is an antipsychotic. Anemia panels must be obtained. Se-methylselenocysteine will address disorganization. Taurine is taken to assist with absorption of fatty acids, spare cysteine and regulate calcium and sodium metabolism. Calcium carbonate is supplmented to assist with calcium homeostasis. Vitamin D is supplemented as vitamin D works with calcium. Pantothenic acid and biotin are supplemented. The SMVT, which transports pantothenate and biotn, could be dysregulated. See the paper on bipolar disorder. Biotin-dependent enzymes have bicarbonate as a substrate. Sodium bicarbonate is supplemented. Acetlyl-CoA caboxylase is involved in fat metabolism. Lignan free flax seed oil is taken. Lignan free flax seed oil will supply omega-3 fatty acids which are lacking in the diet. The SMVT also transports iodine. Iodine is supplemented. That iron carbonyl, Se-methylselenocysteine, taurine, pantothenic acid,biotin, lignan free flax seed oil, iodine, vitamin D, and calcium can address psychosis, disorganization and negative symptoms in schizophrenia is highly noteworthy.
With a dysregulation of the transsulfuration pathway (homocysteine to L-cysteine) sufficient L-cysteine for iron-sulfur cluster formation is not synthesized. Sulfur for iron-sulfur cluster biogenesis is derived from L-cysteine. Supplemental iron increases levels of iron-sulfur proteins. Supplemental iron can partly compensate for dysregulation of the transsulfuration pathway in schizophrenia. Selenomethionine, the food form of selenium is metabolized by enzymes in the transsulfuration pathway. Metabolism off Se-methylselenocysteine by-passes the transsulfuration pathway whereby Se-methylselenocysteine can provide bioavailable selenium for individuals with schizophrenia. Taurine is synthesized from L-cysteine. With L-cysteine not synthesized appropriately taurine will not be synthesized at appropriate levels. Taurine is needed to form various bile acids. With low levels of taurine there will not be sufficient taurine conjugated bile acids. Fat absorption requires bile acids. With low levels of taurine due to low levels of L-cysteine fat absorption will be impaired. Supplemental taurine will compensate for low levels of taurine due to low levels of L-cysteine which are in turn due to dysregulation of the transsulfuration pathway. Taurine by sparing L-cysteine will also increase levels of L-cysteine. Taurine will assist in the absorption of fatty acids. The SMVT is dysregulated, likely due to dysregulated sodium homeostasis attendant on dysregulation of taurine. Dysregulation of the SMVT calls for supplementation with biotin, pantothenic acid, lignan free flax seed oil, iodine, sodium bicarbonate, and taurine. What happens in the gut is key to successful treatment. Aconitase 1 in the gut must be addressed by iron from iron carbonyl and taurine in the gut will improve fat absorption.
Iron from iron carbonyl and Se-methylselenocysteine can end treatment resistant schizophrenia. There would still be a humongous difficulty. Iron from iron carbonyl and Se-methylselenocysteine do not treat negative symptoms or depression. Other supplements are needed to address negative symptoms and depression. A lot of the difficulties I had could be avoided if the ‘to be avoided supplements’ are avoided. Individuals could take iron carbonyl and Se-methylselenocysteine alone for psychosis and disorganization but at that point individuals would almost be committed to the complete treatment as even when one is not hallucinating or disorganized one can feel absolutely wretched.
200 milligrams of iron from iron carbonyl is taken two times day. Iron from iron carbonyl is slowly absorbed from the gut which is a large plus. Iron carbonyl is a non-toxic form of iron. Iron carbonyl is taken with the other supplements. Anemia panels must be obtained to insure that iron levels are not high. 200 micrograms of selenium from Se-methylselenocysteine is taken once a day. Dosages of selenium should not exceed 200 micrograms a day. 1000 mg. of taurine is taken 3 times a day. Biotin is needed for synthesis of non-essential fatty acids. See the page on bipolar disorder on how biotin metabolism can be dysregulated. 5 milligrams of biotin is taken three times a day. Biotin must apparently be available in the gut so sublingual biotin is not taken. 650 milligrams of sodium bicarbonate is taken 4 times a day. Bicarbonate is needed for biotin dependent enzymes. Bicarbonate also is a pH buffer. 500 milligrams of pantothenic acid is taken once a day away from biotin. Pantothenic kinase is the rate limiting step in the synthesis of coenzyme A. 325 micrograms of iodine from kelp is taken three times a day away from pantothenic acid.. 1200 mg. of calcium from calcium carbonate is taken daily in two divided doses. 1000 mg of taurine is taken in four times a day. Taurine is involved in calcium homeostasis. 2000 IU’s of softgel vitamin D is taken once a day. One tablespoon of lignan free flax seed oil is taken twice a day when the iron carbonyl is taken. Flax seed oil supplies omega-3 fatty acids which are lacking in diets.
Iron from iron carbonyl must be taken with lignan free flax seed oil so as to delay the reduction of iron in the gastronintestinal tract as long as possible. Iron is needed in the gastrointestinal tract so lignan free flax seed oil which could prevent reduction of iron could delay absorption of iron and thereby be of assistance. Fatty acid suppplements with high levels of polypenols are worse than useless. Refined flax seed oil would be better but linseed oil which is for external use must be avoided as it is very likely unsafe to consume. Taurine can be taken with iron carbonyl and lignan free flax seed oil.
Blood pressure should be monitored. Individuals with low blood pressure must watch their blood pressure carefully as taurine especially when taken on an empty stomach can decrease blood pressure noticebly.
Iron must be iron from iron carbonyl as iron carbonyl stays in the gut for an extended time. Iron sulfate is avoided as iron sulfate is quickly absorbed. Iron bisglycinate is avoided as iron from iron bisglycinate may not be available in the gut. The difficulty with heme iron polypeptide is that the iron in heme iron polypeptide may not have much of an effect on iron metabolism in the gut. Supplementation with heme iron polypeptide is avoided at least for now.
Taurocholic acid, derived from taurine, is a bile acid which aids in fat absorption. Supplemental taurine upregulates cystathionine beta-synthase and cystathionine gamma-lyase which are the two enzymes in the transsulfuraiton pathway (Sun et al., 2016). Supplemental taurine reduces homocysteine levels (Ahn, 2009) likely due to the upregulation of the transsulfuration pathway by taurine. Taurine reduces cholesterol levels (Guo et al., 2017; Chen et al., 2012). Taurine also has an anti-obesity effect. Taurine deficiencies result in premature aging. Taurine is negatively associated with ischemic heart disease. Taurine ameliorates diabetes. The Observed Safe Level for supplementation with L-taurine is 3 grams a day (Shao and Hathcock, 2008). Supplemental taurine can by aiding fat absorption and calcium homeostasis positively affect brain function.
Deceased levels of biotin would lead to increased beta-oxidation as decreased levels of biotin would decrease levels of malonyl-CoA which inhibits beta-oxidation. Increased beta-oxidation sounds terrific. Rev up metabolism, increase energy, burn fats, loose weight, live life to the fullest. However increased beta-oxidation due to decreases is biotin transport would also lead to decreases in fatty acid elongation which requires malonyl-CoA, leading to serious difficulties. See the page on bipolar disorder as to why there could be difficulties in biotin transport.
The wrong fatty acid supplement is worse than no fatty acid supplment. Fatty acid supplemnents high in omega-9 or omega-6 fatty acids do not work.
Sodium bicarbonate contains sodium so intake of sodium bicarbonate has to be limited.
500 milligrams of pantothenic acid taken once a day away from biotin should can supply all the pantothenic acid one needs by passive diffusion.
With deficiencies in taurine fat absorption is impaired and vitamin D is not absorbed from the diet. Supplemental vitamin D is required. Vitamin D will help with calcium absorption and calcium regulation. Supplemental vitamin D is not helpful without supplemental taurine.
Treatments using supplements have an additional constraint. Treatments using supplements should be very safe. First of all avoiding the ‘to be avoided supplements’ is absolutely safe. Iron carbonyl is a non-toxic form of iron. Anemia panels can be easily obtained to monitor iron levels. The Tolerable Upper Limit for selenium is 400 mcg. per day. Only 200 micrograms of Se-methylselenocysteine is recommended. The Observed Safe Level for supplementation with L-taurine is 3 grams a day (Shao and Hathcock, 2008). Adverse reactions to pantothenic acid and biotin have not been observed. Eliminating drinks with polyphenols is extremely safe though somewhat of an upset. . A 100 mg caffeine capsule taken twice a day could be could be okay. Avoiding supplements on the ‘supplements too be avoided’ list is very safe. Calcium from calcium carbonate and vitamin D at the suggested dosages have been extensively studied Blood pressure must be monitored. Supplements can be taken with prescribed medications.
Very surprisingly iodine is helpful. Thyroid tests can be completely normal but still supplemental iodine is required. There is no need to take thyroid hormones. Supplemental iodine addresses an intense sadness. Iodine works quickly. The sodium-dependent multivitamin transporter (SMVT) transports iodide. Transports of iodide is apparently a very important function of the SMVT. There is another transporter of of iodide, the sodium/iodide cotransporter, (SLC5A5) which is largely expressed in the thyroid. The SMVT is expressed in the digestive tract. The SMVT is apparently not a spare in terms of the transport of iodine. Iodine homeostasis is very important in terms of thyroid function. Even with normal levels of thyroid hormones there can be thyroid associated depressions due to upset of iodide homeostasis.
The treatment could also be effective in Alzheimer’s disease. There are a lot of biological commonalities between schizophrenia and Alzheimer’s disease. See my papers Treatment-resistant schizophrenia: focus on the transsulfuration pathway and A disease-modifying treatment for Alzheimer’s disease: focus on the trans-sulfuration pathway. One might wonder whether taking iron from iron carbonyl for Alzheimer’s disease would be appropriate. A meta-analysis, however, indicates that serum iron levels are significantly lower in AD patients than in healthy controls. Another meta-analysis also indicates that serum iron is significantly lower in patients with Alzheimer’s disease than in healthy controls. Iron from iron carbonyl is regulating aconitase 1 in the gut, the citric acid cycle in the gut and iron metabolism in the gut. As iron levels are only regulated by absorption and excretion regulating iron levels in the gut can affect iron metabolism systematically.
Below are some comments on supplements that could also be helpful and also some comments on what supplements must be avoided.
‘Mammalian thioredoxin reductase is one selenoprotein that shows increased activity with Se supplementation in the nutritional to supranutritional range.’ With selenium there is an end of dosage effect after about six hours in all likihood due to decreased activity of thioredoxin reducatase. 100 micrograms of Se-methylselenocysteine two times a day would work better than 200 micrograms of Se-methylselenocysteine once a day. End of dosage effects could be why selenium has been a bust as a cancer preventive. That there is an end of dosage effect during the course of the day with selenium is suprising but very easy to test. Just take 200 micrograms of Se-methylselenocysteine and wait about 6 hours. However, taking 200 micrograms of Se-methylselenocysteine twice a day is problematical. Why go to all the bother with selenium? Selenium treats disorganization in schizophrenia. Billions of free radicals bouncing around in the brain generate bouncing around thoughts and disorganization.
L-carnitine is useless as supplement due to the fumarate or tartrate which carnitine is bound to. L-carnitine from carnitine fumarate is avoided as fumarate can inhibit enzymes that demethylate DNA and histones. Carnitine tartrate is avoided as tartaric acid can greatly increase iron absorption. A tartrate is a salt or ester of the organic compound tartaric acid, a dicarboxylic acid.
A ketogenic diet is not advisable as a ketogenic diet would increase beta-oxidation. Low carbohydrate diets could result in weight loss but the side-effects are too significant. None of us would have weight problems if ketogenic diets improved health. Individuals could live with the bland ketogenic diet. Ideas that should work but do not work are terrible ideas to put into practice. Ketogenic diets, unless used to treat epilepsy, are ill advised. There still could be a benefit to avoiding high glycemic foods as long as ketosis is avoided.
A difficulty with polyphenols is that polyphenols complex with iron making iron unavailable in the gut. Another difficulty with polyphenols is that polyphenols can increase beta-oxidation which can result in difficulties if there are problems in fat absorption and fatty acid metabolism.
Polyphenols in sodas, coffee and tea including herbal tea can adversely affect absorption of iron. Caffeine is apparently not the culprit. Polyphenols in polyphenol supplements could be highly available and should be particularly avoided. Flavonoids are polyphenols. Flavonoid supplements should be avoided. Getting off caffeine by switching to non-caffeinated sodas and herbal teas is disastrous move. Polyphenols rather than caffeine is the culprit.
Sodas, for example, Mountain Dew, as this advertisement shows are frequently associated with goofyness where the goofyneness could be due to polyphenols and/or citric acid in the sodas adversely affecting iron metabolism in the gut. Citric acid drinks really do befuddle thinking. Someone might say, ‘Individuals would have to consistently take substances that befuddle thinking. Is that even possible?’ I cite the horrendous narcotics problem throughout the world and rest my case. Making an only citric acid and water drink with four grams of citric acid is easy which could be drunk 4 times a day for five days no test the idea. Food grade citric acid can be purchased on Amazon. The idea that citric acid drinks can befuddle individuals is very easy to test, however, the effect of citric acid on iron is not entirely clear though I think the befuddlement is due to iron dysregulation. 4 grams of citrate is in a 600 milligram tablet of calcium citrate.
Calcium from calcium calcium citrate is avoided. The citrate in the calium citrate could bind to iron in the gastrointestinal tract making iron unavailable in the gastronistenital tract with very negative consequences. With deficiencies in taurine difficulties in calcium transport and homeostasis can arise. A point about calcium supplements is that the wrong calcium supplement is worse than no calcium supplement at all. Taurine regulates calcium transport.
Polyphenols increase beta-oxidation. This can be extremely problematical given there are difficulties in fat absorption and fatty acid synthesis. I have been emphasizing how polyphenols decrease iron absorption but increases in beta-oxidation due to polyphenols where those increases are unsupportable due to difficulties in fat absorption and fat metabolism could also lead to serious difficulties. Even after fat absorption and fatty acid synthesis are re-regulated polyphenol laden drinks would still be avoided due to effects on iron.
Clearly no general argument is being made that beta-oxidation is ‘bad’ and fatty acid synthesis is ‘good’. All depends on what illnesses individuals have and metabolic states that individuals are in.
A very significant difference between the socioeconomic classes may be that the higher socioeconomic classes very frequently drink bottled water rather than sodas while the lower socioeconomic classes very frequently drink sodas rather than bottled water.
Coffee drinking is very widespread. Here is a coffee advertisement from another planet.
Very surprisingly taking large dosages of vitamin C must be avoided. Vitamin C increases iron absorption at least intially but long term ascorbic acid can downregulate iron absorption by down-regulating iron independent and iron dependent Nramp2 (DMT1) and duodenal cytochrome B (Dcytb) expression. Vitamin C will also decrease copper absorption. Megadosages of vitamin C are definitely to be avoided. Vitamin C can be very surprising. Initially large dosages of vitamin C appear to have very positive effects but long terme those postive effects are lost. First impressions of megadosages of vitamin C are wrong impressions.
Linus Pauling, the greatest chemist of the 20th century, starts taking megadosages of vitamin C and his work deteriorates. That mental illnesses are orthomolecular in nature is the correct viewpoint, however, the devil is in the details.
Sulfur amino acids can be very toxic. L-cysteine taken as supplements can be very toxic. Very unfortunately, as the hypothesis posits a basic L-cysteine deficiency, strategies to directly increase L-cysteine levels directly can be disastrous. N-acetyl-l-cysteine and alpha lipoic acid are, for example,totally disastrous as supplements. Any supplement that increases L-cysteine by decreasing levels of cystine, as do n-acetyl-l-cysteine and lipoic acid, must be avoided. Pantethine is also avoided as pantethine could decrease cystine levels. N-acetyl-l-cysteine and alpha lipoic acid should not be OTC. Alpha lipoic acid should never be used and N-acetyl-l-cysteine should only be used for acetaminophen poisoning if then. Lipoic acid could also competively inhibit biotin and pantothenic acid transport by the SMVT as biotin, pantothenic acid and lipoic acid are all transported by the SMVT. L-methionine taken as a supplement could result in inappropriate DNA methylation. Cystine supplements must not be taken.
Absolutely the worst supplement strategy, that has some scientific support, is trying to increases L-cysteine levels via sulfur containing amino acids except via taurine which spares cysteine. This is likely due to the fact that cystine has to be available to enter cells via the cystine/glutamate antiporter. Supplemental cystine would very likely be reduced to cysteine in the context of other supplements taken. Anyone who has been on n-acetyl-l-cysteine or lipoic acid for awhile should have copper and manganese levels tested. I think somehow or other n-acety-l-cysteine and/or lipoic acid could increase gene hypermethylation dysregulating copper and manganese absorption.
Lipoic acid is also a total disaster. Lipoic acid will competitively inhibit biotin and pantothenic acid transport. Lipoic acid and pantethine also must not be supplemented as lipoic acid and pantethine will reduce cystine to L-cysteine but cystine must be available to enter cells via the cystine/glutamate antiporter. Import of L-cystine into cells and export of glutamate out of cells are both important. Cysteine is very toxic and is not supplemented. Cystine must not be supplemented either. Cystine can be quite toxic.
Supplemental glycine is avoided. Attempting to increase synthesis of L-cysteine by supplementing with amino acids can have negative effects. Serine is needed for homocysteine metabolism and serine can be synthesized from glycine but still glycine is not helpful. However, taurine, which can spare cysteine, is of assistance.
Ubiquinol is avoided. Ubiquinol is the reduced form of coenzyme Q10. Ubiquinol could increase succinate levels.
That there is oxidant stress is many illnesses is well established however thousands and thousands of oxidation reactions are needed. Increasing levels of free antioxidants, such as vitamin C, vitamin E and beta-carotene via supplementation is not of assistance.
That increasing re-methylation of homocysteine to L-methionine, via supplemental folic acid and vitamin B12 in more that RDA amounts, is counterproductive, is another surprising rule. Homocysteine must be available to be metabolized to cysteine via the transsulfuration pathway. Decreasing homocysteine levels via increasing activity of enzymes in the transsulfuration pathway, which taurine and perhaps glycine do, is the only helpful way to reduce homocysteine levels. Supplementation with taurine decreases homocysteine levels. Folic acid and vitamin B12 supplements do not prevent cognitive decline though the supplements can reduce homocysteine levels.
Benfotiamine and thiamine can help. I think the metabolism of megadoses of vitamin B2 and vitamin B6 can interfer with the metabolism of thiamine. Benfotiamine and thiamine will support activities of pyruvate dehydrogenase and 2-oxoglutarate dehydrogenase which are the E1 components of pyruvate dehydrogenase complex and 2-oxoglutarate dehydrogenase complex respectively. The E1 step in the pyruvate dehydrogenase complex is the rate-limiting step in the whole pyruvate dehydrogenase complex. To increase activities of the E2 components of the pyruvate dehydrogenase complex and 2-oxoglutarate dehydrogenase complex activities of the E1 components must first be increased. The E1 components have thiamine diphosphate as cofactors.
Oral thiamine must be taken when benfotiamine is taken. Apparetntly orally taken thiamine will inhibit the metabolism of phosphorylated thiamine derivatives prolonging the actions of thiamine diposphate which benfotiamine produces. Acid phosphatase is involved in both thiamine and and riboflavin metabolism. Acid phosphatase metabolizes thiamine monophosphate to thiamine but the reaction can go in either direction. The goal is to supply thiamine so thiamine monophosphate is not degraded due to end product inhibition. With thiamine monophosphate not degraded the reaction that metabolizes thiamine diphosphate will be impeded whereby the combination of benfotiamine and thiamine can treat neuropathy. Alkaline phosphatase is involved in both thiamine metabolism and vitamin B6 metabolism.
Fursultiamine, a thiamine derivative, in vitro inhibits hepicidin which regulates iron levels, is hard to get in the US, sold by very small compapanies who in all likelhood do not have extensive quality control programs and likely buy lowest cost ingredients and as stated there is a large question mark about the effect of fursultiamine on hepcidin so supplmenting with fursultiamine is avoided. Sulbutiamine, another thiamine derivative, has most of these disadvantages too so sulbutiamine is avoided. The advantages of benfotiamine is that benfotiamine is quite widely taken, is sold by large supplement corporations who could have quality control programs and works. Benfopure is made by a Japanese corporation. When taking benfotiamine oral thiamine must also be taken with the benotiamine. Benfotiamine that also contains lipoic acid should not be purchased. Benfotiamine and thiamine could be necessary supplements.
Supplementing with branched-chain amino acids could be of assistanece give biotin and pantothenic acid are also supplemented. Methylcrotonyl CoA carboxylase and propionyl-CoA carboxylase are two biotin-dependent enzymes in the branched-chain amino acid degradation pathway. Dysregulation of the sodium-dependent multivitamin transporter which transports biotin anh pantothenate could dysregulate the branched-chain amino acid degradation pathway leading to shortages of dowstream products in the branched-chain amino acid degradation pathway. Elevated circulating levels of branched-chain amino acids have been associated with insulin resistance, however, insulin resistance may not be a problem with supplemental branched-chain amino acids given biotin and pantothenic acid are also supplemented. Glucose levels and HbA1C levels would have to be tested for when supplmenting with branched-chain amino acids to check for glucose dysregulations.
An L-arginine/citrulline combination could be of assistance. L-arginine induces cystathionine gamma lyase an enzyme in the transsulfuration pathway. Hydrogen sulfide, which is produced by enzymes in the transsulfuration pathway, down regulates the arginine/nitric oxide synthase/nitric oxide pathway in rats. This could be due to arginine depletion.
Putting L-arginine/citrulline and branched-chain amino acids in this section rather than the treatment section at top is likely a misstep. Without arginine/citrulline one feels like one is running on empty. When taking arginine/citrulline one needs to take branched-chain amino acids.
A combination of EPA and DHA could be a useful supplement. EPA and DHA levels where EPA levels are greater than 60% are effective against depression. Some DHA is apparently needed. EPA levels should be about around 60% to 65% of the EPA and DHA combination. The International Society for Nutritional Psychiatry recommends for depression that a supplement with a total of 1-2 grams of EPA can be taken daily. EPA and DHA are not sufficient in terms of fatty acid supplementation.
A large part of the difficulty with coffee is that coffee can increase beta-oxidation. Once supplements are taken that support beta-oxidation, for example, flax seed oil , and taurine to assist with fat absorption modest amounts of coffee drunk away from iron could be okay.
Supplemental niacin or niacinamide and/or riboflavin in much more than RDA amounts are avoided as supplemental niacin or niacinamide and riboflavin could increase activity of the E3 components of the pyruvate dehydrogenase complex and and alpha-ketoglutarate dehydrogenase complex whose products can inhibit E1 components of the pyruvate dehydrogenase complex and and alpha-ketoglutarate dehydrogenase complex. Supplementing with niacin or niacinamide and/or riboflavin in much more than RDA amounts is a very large misstep.
Supplmenting vitamin B6 in much higher than RDA amounts is avoided.
All B-50 vitamin formulations are avoided. One Centrum a day could be okay.
Molybdenum from molybdenum bound to Krebs cycle intermediates will increase levels of xanthine oxidase. Xanthine oxidase, is a molybdenum containing protein. Xanthine oxidase is a powerful ferroxidase and could assist with iron transport. Molybdenum from molybdenum bound to Krebs cycle intermediates would be readily available in the gut which could be a strong advantage. Molybdenum chelated to glycine is avoided as xanthine oxidase levels must be increased in the gut. Molybdenum from molybdenum glycinate may not be readily available in the gut. Douglas Laboratories sells a 500 microgram molybdenum supplement where the molybdenum is complexed with Krebs cycle intermediates, which is not ideal, however, the Krebs cycle intermediates must be in such low amounts that the Krebs cycle intermediates would not present difficulties. Douglas Labs also sells a 250 microgram molybdenum supplement, which is an an amino acid chelate, that is not purchased. The 250 microgram supplement of Douglas Laboratories use to to be chelated to glycine. Whether this is still true or not is unclear. The advertising of Albion Minerals which states that glycine is very tightly bound to minerals in glycine chelates is absolutely accurate.
No minerals bound to glycine should should supplemented. Advertising of Albion Minerals is absolutely accurate. Glycine in minerals bound to glycine is tightly bound to minerals which makes the minerals unavailable in the gut, however, minerals to be of assistance must be available in the gut as well as be available systematically. Taking any glycinated minerals is a very large misstep.
At this time the treatment is complementary medicine rather than alternative medicine. Prescribed medications should not be stopped without consultation with MDs.
Supplements are a minefield. Do not start the treatment unless contraindicated supplements are at the same time avoided.
What not to supplement is as important as what to supplement. Supplementing with L-methionine or S-adenosyl-l-methionine are avoided. Supplementing with N-acetyl-l-cysteine, L-cysteine, cystine, r-lipoic acid and/or alpha lipoic acid supplements is avoided. N-acetyl-l-cysteine and alpha lipoic acid increase L-cysteine levels by decreasing cystine levels which is not of assistance. Supplementing with iron sulfate is avoided. Iron carbonyl will reside in the gut longer whereby aconitase 1 in the gut can be better regulated by iron carbonyl compared to iron sulfate. Iron carbonyl is also safer that iron sulfate. Pantetheine is not supplemented as pantetheine could decrease cystine levels. Sodium selenite, sodium selenate and any form of L-selenomethionine are not supplemented. Minerals bound to succinate should be avoided. Folic acid and vitamin B12 are not supplemented in much more than RDA amounts. To produce L-cysteine via homocysteine there must be homocysteine. Increasing re-methylation of homocysteine to L-methionine by taking more that RDA amounts of folic is counterproductive. Huge doses of B12 are not helpful. Supplementing with more than RDA amounts of niacin, niacinamide, riboflavin and/or vitamin B6 are avoided. B-50 formulations are avoided. Supplementation with iron sulfate and ferrous bisglycinate are avoided. No minerals bound to glycine should should supplemented. All minerals bound to citrate must be avoided unless amounts are minuscule. Calcium citrate is avoided. All minerals bound to succinate must be avoided unless amounts are minuscule. L-carnitine from L-carnitine fumarate and carnitine tartrate are avoided as fumarate could decrease activity of enzymes involved in demethylation of DNA and histones while tartrate could increase iron absorption. Any supplement with more than miniscule amounts of Krebs cycle intermediates should be avoided. Vitamin C supplements above RDA amounts are avoided. All citric acid based drinks are avoided. Carotenoid supplements, like beta-carotene and lycopene are avoided. Vitamin E is avoided. Apparently there are various needed oxidant reactions that vitamin E can adversely affect. Free antioxidants are only healthy is amounts found in food. Coffee, soft drinks, and tea tea including herbal teas are best completely avoided. A couple of cups of coffee in the morning an hour before supplements are taken is the least worse way to drink coffee though definitely not recommended.
Treatment failure is predicted unless the recommendations as to what not to supplement with are adhered to.
The treatment is clearly a lot but the treatment treats schizohrenia which is either the worst disease humans face or is in a tie for worst disease humans face. Iron carbonyl and Se-methylselenocysteine can treat psychosis and cognitive sypmtoms of schizophrenia and from the viewpoint of society that solves more than half the problem, however, from the viewpoint of the patient that solves about 20% of the problem. Individudals only on iron carbonyl and Se-methylselenocysteine could be in very vulnerable states. Possessing insight and feeling absolutely wretched is not a terrifc combination. Going on to try a more complete treatmemt would almost be a necessity.
Avoid the supplements on the to be avoided list. L-methionine, S-adenosyl-l-methionine, N-acetyl-l-cysteine, L-cysteine, cystine, r-lipoic acid and/or alpha lipoic acid supplements must be absolutely avoided. Do not take glycinated minerals. Get anemia panels, thyroid panels, metabolic panels and CBCs done regularly. These panels can be ordered online.