Adrenochrome & Schizophrenia; and the AHA! award for Accurate Health research.

Also, glycine deficiency may result adding to risk of salicylate sensitivity.

Ehden shared a chapter from a book (on Telegram) that is about the chemistry of adrenochrome and the health of patients with schizophrenia.

Chapter III. Adrenochrome and Some of Its Derivatives, The Hallucinogens, by A. Hoffer and H. Osmond, 1967, Academic Press, (pdf in my Dropbox)

*The ‘chapter’ is 181 pages long. My notes follow.

The gist seems to be that people with schizophrenia are not clearing adrenalin/adrenochrome adequately and accumulation of adrenochrome causes hallucinations and disordered thinking. Alternate breakdown of adrenochrome causes a brown colored version of melanin to form (rather than black which forms from dopachrome) and people with schizophrenia tend to get brown hair earlier as children (rather than stay blonde or have black hair) and to not go white-haired as soon as an older adult.

Photo op, some of my hair, not much gray yet:

A little white streaking though (age 57 3/4) {*lighting from a different angle}:

Last night I woke up early again, got up and had some food I made last night but didn’t really eat at that time but have made somewhat regularly in the past - Nutritional Yeast ‘cheesy’ vegan noodles made with red lentil pasta. I started feeling really bad, racing heart, and wasn’t sure if it was the bright light at 2 am or sudden change of temperature (basement 62’F, upstairs 72’F). I was suddenly feeling super hot, got sweaty even like night sweats. Went back downstairs wondering if I needed to throw up but didn’t. Lay there in the cold, but sweaty wet forehead. Thought about this adrenochrome info, salicylate sensitivity, which spices I use in my cheesy vegan pasta, and essential oil info; and got back upstairs to use some of my recently purchased Ylang Ylang oil. It has sesquiterpenes which may help calm tachycardia. My heart felt like it was trying to get out of my chest. The rest of me was getting weaker and my limbs were starting to hurt, like crampy pain, but maybe oxygen lack?.

I used two drops of Ylang Ylang on my hands and wrists with a little coconut body lotion to dilute it - and huffed my wrists - inhaled deeply. It seemed to help. I went back downstairs. Got suddenly chilled after feeling so sweaty, laid back down and started piling the covers back on - continuing to inhale at my wrists occasionally. It continued to help calm the racing heart rate and I feel asleep again and woke up feeling okay.

My cheesy pasta seasonings: sage powder - 21.7 g salicylate per 3 grams - OH. Also nutritional yeast flakes are a source and I used some powdered leek which would be a source too - and a little rosemary powder, also salicylate rich. Sigh. BUT - I hadn’t made myself my glycine ‘cheerful juice’ yesterday. I have been doing better about having some every day and that was the first miss in a bit. I think if I do consistently better at taking glycine as a supplement, then I might be able to tolerate a little of my favorite spices - but maybe not all in the same ‘cheesy’ sauce.

I made myself some Cheerful Juice and I will cautiously try the cheesy pasta in a small amount before rinsing off the sauce and calling it a mistake to not repeat. *Or f that, rinse off the pasta and start over. I do have a it of a headache this morning. As a human genetic ‘knockout mouse’ my troubles can help clarify what treatment might help, or how much restriction might be needed. Taking the Mucinex seems to be a factor too. I had one at 2 am when I woke up the first time feeling okay.

Salicylism will usually present as a mimic” The Internet Book of Critical Care, (emcrit.org)

*Hyperthermia - body temperature elevated above normal.

Tachypnea - very rapid breathing rate compared to normal.

(emcrit.org/ibcc/salicylates)

Lymphedema update: My leg swelling has been better since stopping the nicotine mints and increasing movement and use of the bamboo compression socks. Avoiding much salt is still a need though.

~~

This passage explains why people with schizophrenia likely need the 3000 mg of niacin/nicotinic acid each day:

“Ehrensvard et al. (1960) and Heath and Leach (1962) found that schizophrenic serum oxidized 3-hydroxyanthranilic acid enzymatically more slowly than did normal serum. This suggests schizophrenic serum contains less of the enzyme which converts 3-hydroxyanthranilic acid into nicotinic acid. The result would be an increase in 3-hydroxyanthranilic acid, an increase in 3-hydroxykynurenine, an increase in ommochromes formation, and a deficiency of nicotinic acid.” (page 287,

Lack of glutathione or cysteine or glycine would be likely to increase adrenochrome accumulation too. And excess of it depletes glycine and glutathione. That helps explain my risk in part - genetically low in dimethylglycine, DMG.

It is too bad that the insider cult people keep preventing science breakthroughs to reach patients. Instead patients are forced into taking harmful drugs that do not help the condition. If you are being forced to take a drug that makes you feel really sick, wouldn’t you rather escape and live homeless - and not feel really physically sick? (just kind of crazy). Anyway, neither choice (crazy or drugged) is as good as taking high dose niacin and correcting other nutrient deficiencies and restoring normal cognition.

The Accurate Health Award - the AHA! award

The Adrenochrome notes continue after this. I am going to insert a summary section here - the Accurate Health Award - the AHA! award, as an alternative or parallel to the largely bad science Nobel Prize.

Hindsight being 20/23 these days - the work on adrenochrome and schizophrenia was suppressed. Schizophrenia patients are still not being treated based on these findings. Personally I am really fed up with the stupid insider cult and their stupid suppression of all helpful medical research while promoting kill protocols or disabling non-treatments.

The “Nobel Prizes” - hindsight being 20/23 - are a big farce or fraud. They are largely awarded to insider cult bad science like the bioweapon, turbocancer promoting, CoV mRNA injections, CRSPR gene tech, or given to people like Obama, the massive radioactive dirty drone bomber, who got a Nobel peace award.

I have created a new award system - parallel/alternative to the insider cult system of awarding bad science (Einstein was wrong about space being empty - his theory is just theoretical math with no basis in physical proof) and evil doers.

The new award will be given for Accurate Health findings - the AHA award. Mildred Seelig and Andrea Rosenoff will receive one for their work on magnesium and pharma substitutes, and A. Hoffer and H. Osmond will receive one for their work on schizophrenia, nicotinic acid and adrenochrome. Linus Pauling and Paul Marik will receive one for vitamin C discoveries. Chris Exley for aluminum and Alzheimer’s; Stephanie Seneff and Anthony Samsel for research on glyphosate and autism/other chronic conditions that have increased at epidemic rates; Judy Mikovits for contaminants in medical products that are causing cancer; Andrew Wakefield for making the correct connection between autism and gut dysbiosis, which can be affected/worsened by vaccine injury.

Wilhelm Reich (and his daughter who continued his biofield therapy work) for his work on aether/orgone and biofield healing. James DeMeo for continuing the work on aether and Reich’s Cloudbuster apparatus for regreening areas of drought. When things work, they work. Pretending they don’t work, is just pretense.

And Bong Han Kim for his discovery of the Primo Vascular System. It exists. Western medical system needs to be recognized as a backward, inaccurate industry that is harming people and distorting accurate research findings with disinformation.

I am sure there are many others who have been fighting the good fight against insider cult disinformation. That is a start though on who I think deserves recognition for important advances in health research.

~~

Adrenochrome and Schizophrenia notes continued - it really explains a lot.

Excess adrenochrome would then lead to reduced GABA which is calming and that would just add to the mental over-activity.

Retaining phosphorus, or losing too much - phosphate imbalance also seems involved in schizophrenia genetics - that might go hand in hand with fibromyalgia seeming to have odd phosphorus issues too.

Adrenochrome can reduce sensitivity to histamine and schizophrenia patients have ben found to have higher levels of histamine than average while not having as quick of a reddening reaction on the skin when scratched.

High pressure oxygen situations replicate the poor judgement or distorted thinking of schizophrenia.

Adrenochrome excess may cause schizophrenics to get colder in cold temperatures more than average. Adrenochrome excess may add to anti-thyroid problems. Schizophrenia patients seemed to tolerate larger and need larger than average doses of thyroid treatment (pre days of Synthroid - something like porcine thyroid extract was used). Or 200 micrograms of iodine helped patients with schizophrenia. Thyroid function and hormone levels were normal. The problem was found in peripheral use of thyroid hormone. Higher dosing seems to help bypass anti-thyroid effects caused by excess adrenochrome within the body tissues.

Adrenochrome is a topic I looked into at the request of someone, and I saw that there had been a bunch of research on it in the 50s and then not much. It caused ‘schizophrenia-like symptoms’ but might have anti-aging effects due to effects on mitochondrial health. The following passage shows adrenochrome is involved with uncoupling of mitochondrial ATP production similar to what high dose niacin can do with activation of the GP109a receptor.

“Rawson et al. (1957) stated that adrenochrome prevented metamorphosis of tadpoles. This is a property shared with other indoles and provides direct evidence that thyroid hormone and adrenochrome are antagonists.

It is curious that both thyroxine and adrenochrome are uncouplers of oxidative phosphorylation. J. Bain (1957) reported that a subeffective dose of thyroxin (5 X 10—5 M) and a subeffective dose of adrenochrome ( 2 X 10—5 M) added together produced 50% uncoupling of oxidative phosphorylation.” (page 303)

Interfering with tadpole metamorphosis suggests to me that excess adrenochrome negatively affects quantum energy flow and structuring of cell water - disrupting the holographic like formation of a new shape for the developing frog.

Fetal development is or involves ‘quantum biology,’ whatever that term means these days.

~~

Adrenochrome excess seems to protect against diabetes that is due to lack of insulin, by inhibiting breakdown of insulin by insulinase.

~~

Regarding disrupted phosphorus metabolism - it is the uncoupling of ATP production:

“There is a good deal of data which show that schizophrenic erythrocytes do not metabolize glucose in the same way as normal erythrocytes. Boszormenyi-Nagy and Gerty (1955) found that insulin pretreatment of normal erythrocytes inhibited the accumulation of adenosine triphosphate (ATP) by hemolysates incubated with pyruvate and hexose diphosphate. This inhibition of ATP buildup was not observed with schizophrenic erythrocytes. Since adrenochrome is a very powerful inhibitor of ATPase while adrenaline alone has no effect it is likely this differential effect of erythrocytes is due to an accumulation of oxidized adienaline derivatives. That is with normal erythrocytes insulin would increase utilization of ATP but with ATPase inhibited by adrenochrome this could not occur in schizophrenic cells. Orstrum and Skaug (1950) also found a decreased turnover of ATP in schizophrenics. Randall (1946) and Meyerhoff, and Randall (1948) found that adrenochrome inhibited hexokinase and phosphohexokinase. A concentration of 4 X 10 — 5 M inhibited these enzymes 50% . The degree of inhibition was inversely related to the amount of ATP present.

These earlier findings have some relevance to recent work on toxic protein fractions in schizophrenics. Frohman et al. (1960) found that schizophrenic red cells under basal conditions took up much more labeled 32 P than did normal subjects. There was an inability to utilize ATP.” (page 307)

Excess of a copper based enzyme may be involved in schizophrenia but it seems protective, like a counteracting effect rather than being the enzyme causing excess adrenochrome conversion:

“Ceruloplasmin, a copper protein enzyme, normally present in serum oxidizes catechol, adrenaline, serotonin, and other amines. Leach et al. (1956) believed it was the catalyst in the oxidation of adrenaline to adrenochrome. Akerfeldt (1957a,b) found that N,N-diethyl-p-phenylenediamine was a useful substrate for measuring ceruloplasmin levels. Akerfeldt reported that schizophrenic patients generally were higher in ceruloplasmin thus supporting the suggestion of Angel et al. (1957) that schizophrenic serum converted more adrenaline into adrenolutin.” (page 315)

“Melander (1957) found that ceruloplasmin absorbs adrenolutin.” (page 316)

The alleged anti-aging effect of adrenochrome may be a reduction in cell division - cells survive longer before dividing into two new cells.

“However, we would expect that schizophrenics would have less clear diurnal rhythm of mitosis if they really do have increased concentrations of adrenochrome. Increased quantities of adrenochrome-chalone would suppress mitosis and promote cell survival. Schizophrenics would be expected to have better cell survival rates and, indeed, many schizophrenics do appear to be remarkably youthful in appearance.” (page 317)

Potential treatments for patients with schizophrenia:

“Adrenaline Oxidase Inhibitors. Payza and Hoffer (1959) found only 4 inhibitors of this enzyme, sodium cyanide, ethylenediaminetetraacetate (EDTA) tris buffer and ascorbic acid. Sodium cyanide could not be tested as an hallucinogen. In nontoxic doses it has produced lucid episodes in some schizophrenic patients. EDTA has not been used clinically and its toxic properties are not known. We would expect it to be nontoxic and, in fact, therapeutic for schizophrenics as is penicillamine. Both are copper chelating agents and by removing copper would inhibit adrenaline oxidase. G. J. Martin et al. (1942) found that p-aminobenzoic acid inhibited oxidation of adrenaline to adrenochrome by tryosinase. We have not heard of any psychotic reactions following the use of heavy doses of PABA. In its absence convulsions may develop. PABA should be therapeutic for schizophrenia.

Inhibitors of tryosinase also include cysteine, thioureas, glycine, and histidine (Hirsch, 1959), and monohydroxybenzoic acid isomers (Yasunobu, 1959). Benzoic acid itself is a good inhibitor. These compounds may be valuable therapeutic chemicals for some schizophrenics, dPhenylalanine is another inhibitor and is believed responsible for the deficiency of melanization in phenylpyruvic oligophrenia.” (page 336)

The chapter includes detailed accounts by the researchers who tried the adrenochrome. The first hand experiences written after the trial and observers accounts are included. The biggest take home point is most of the people trying it did not recognize how changed their behavior was. Loss of good judgement, paranoia, irritability were all frequent symptoms along with changes in depth perception and other visual hallucinatory effects - no longer safe to drive was perceived by most but the researchers suggest not leaving people alone when using adrenochrome for research or therapy purposes. This was early days in the discoveries - a brand new chemical being isolated. Throughout the chapter the authors make it clear that there was controversy at the time - discovery of adrenochrome/adrenalin metabolism was being questioned/disbelieved.

Disclaimer: This information is being provided for educational purposes within the guidelines of Fair Use and is not intended to provide individual health care guidance.

Salicylate References

(Gajewska, et al., 2020) Gajewska D, Kęszycka PK, Sandzewicz M, Kozłowski P, Myszkowska-Ryciak J. Intake of Dietary Salicylates from Herbs and Spices among Adult Polish Omnivores and Vegans. Nutrients. 2020 Sep 6;12(9):2727. doi: 10.3390/nu12092727. PMID: 32900002; PMCID: PMC7551261. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7551261/

Cites these as food content databases:

Gajewska D., Kęszycka P., Harton A., Myszkowska-Ryciak J. Salicylates food sources in adults’ diets. Bromatol. Chem. Toksykol. 2014;XLVII:403–408. [Google Scholar]

32. Scotter M.J., Roberts D., Wilson L., Howard F., Davis J., Mansell N. Free salicylic acid and acetyl salicylic acid content of foods using gas chromatography–mass spectrometry. Food Chem. 2007;105:273–279. doi: 10.1016/j.foodchem.2007.03.007. [CrossRef] [Google Scholar]

33. Janssen P.L., Hollman P.C., Reichman E., Venema D.P., Van Staveren W.A., Katan M.B. Urinary salicylate excretion in subjects eating a variety of diets shows that amounts of bioavailable salicylates in foods are low. Am. J. Clin. Nutr. 1996;64:743–747. doi: 10.1093/ajcn/64.5.743. [PubMed] [CrossRef] [Google Scholar]

34. Paterson J.R., Baxter G., Lawrence J., Duthie G. Is there a role for dietary salicylates in health? Proc. Nutr. Soc. 2006;65:93–96. doi: 10.1079/PNS2005477. [PubMed] [CrossRef] [Google Scholar]

35. Venema D.P., Hollman P.C.H., Janssen K.P.L.T.M., Katan M.B. Determination of Acetylsalicylic Acid and Salicylic Acid in Foods, Using HPLC with Fluorescence Detection. J. Agric. Food Chem. 1996;44:1762–1767. doi: 10.1021/jf950458y. [CrossRef] [Google Scholar]

36. Swain A.R., Dutton S.P., Truswell A.S. Salicylates in foods. J. Am. Diet. Assoc. 1985;85:950–960. [PubMed] [Google Scholar]

37. Malakar S., Gibson P.R., Barrett J.S., Muir J.G. Naturally occurring dietary salicylates: A closer look at common Australian foods. J. Food Compos. Anal. 2017;57:31–39. doi: 10.1016/j.jfca.2016.12.008. [CrossRef] [Google Scholar]

38. Kęszycka P., Szkop M., Gajewska D. Overall Content of Salicylic Acid and Salicylates in Food Available on the European Market. J. Agric. Food Chem. 2017;65:11085–11091. doi: 10.1021/acs.jafc.7b04313. [PubMed] [CrossRef] [Google Scholar]

39. Szkop M., Szkop U., Kęszycka P., Gajewska D. A Simple and Robust Protocol for fast RP-HPLC Determination of Salicylates in Foods. Food Anal. Methods. 2016;10:618–625. doi: 10.1007/s12161-016-0621-4. [CrossRef] [Google Scholar]