The case for autism being biochemically similar to schizophrenia and Alzheimer’s disease


Aconitase activity was significantly decreased in cerebellums of individuals who had autism. Glutathione levels were decreased in individuals with autism. Glutathione peroxidase activity is decreased in individuals with autism. Homocysteine levels are increased in children with autism. Vitamin D levels are decreased in individuals with autism. Individuals with autism have reduced bone mineral density. Taurine levels are low in a subset of individuals with autism. There are low levels of biotin in patients with autism. Iron deficiency is very common in autism.

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 as to how similar biochemical abnormalities are also present in schizophrenia and Alzheimer’s disease. Other posts on this blog are also relevant to biochemical abnormalities found in schizophrenia.

Autism, schizophrenia and Alzheimer’s disease are epigenetic illnesses. Despite various biochemical commonalities between autism, schizophrenia and Alzheimer’s disease there are epigenenetic differences with these epigenetic differences channeling the illnesses in divergent directions. However, with autism, schizophrenia and Alzheimer’s disease being fundamentally similar treatments for autism, schizophrenia and Alzheimer’s disease could be very similar. As there are now no biological treatments for autism treatments currently used in autism and which are partially effective can not now be clearly hooked up to a treatment for schizophrenia.

Social skills interventions is individuals with autism aged 6-21 have shown limited and equivocal effectiveness. Biological treatments for autism are needed.

Opioids can result in euphoria so opioid antagonists would be perfect for individuals with schizophrenia


Samidorphan is an opioid antagonist. Samidorphan supposedly reduces weight gain that very frequently occurs with olanzapine. ALKERMES INC, a pharmaceutical corporation, concluded that individuals with schizophrenia could benefit from less than normal opioid agonism, which fits right in with the history of the treatment of schizophrenia. Some terrible treatment is somehow or other a boon to individuals with schizophrenia. Olanzapine/samidorphan, with olanzapine being the antipsychotic and samidorphan being the opioid antagonist, combines two pleasure killing drugs in one pill so, of course, olanzapine/samidorphan is a treatment advance for individuals with schizophrenia. Metabolic parameters did not vary between olanzapine and olanzapine/samidorphan and individuals on olanzapine/samidorphan still gain weight. Also a meta-analysis indicates that olanzapine/samidorphan is not effective in reducing weight gain due to olanzapine. LYBALVI, an olanzapine/samidorphan combination, was recently approved by the FDA for the treatment of schizophrenia and bipolar 1 disorder.

Mental illnesses – parts of a sole huge illness

Psychiatric genetics is basically a research program with no connection to treatment except for very rare high impact genetic loci.

An endophenotype refers to a characteristic that is not easily observed on the surface. Almost all mental illnesses are due to epigenetic dysregulations. The endophenotypes of psychiatric illnesses would be the sets of epigenetic marks that are associated with given mental illnesses. The variability in symptoms in given illnesses is due to variations on the basic sets of epigenetic marks associated with such illnesses.

Mental illnesses arise due to dysregulation of TET enzymes and JmnjC-domain containing .proteins with TET enzymes involved in DNA demethylation and JmnjC-domain containing proteins involved in histone demethylation. Histone acetylation which requires acetyl-coenzyme A also plays a part.

Though dysregulation of TET enzymes and JmnjC-domain proteins and dysregulation of acetyl-coenzyme A are fundamental to all mental illnesses various mental illnesses separate from each other as spatially closely associated pathways fall together. Use the pathways or lose the pathways. And as these are epigenetic dysregulations, pathways that are lost are spatially localized to various organs and/or regions of organs, for example, regions of the brain. Trying to distinguish mental illnesses by examining genes is pointless.

Trying to isolate endophenotypes so as to enhance treatments is not necessary. With basic epigenetic dysregulations addressed almost all mental illnesses. can be treated. A treatment that addresses dysregulation of TET enzymes and JmnjC-domain proteins and dysregulation of acetyl-coenzyme A could address all mental illnesses.

Cortical thickness and antipsychotics

Cortical thickness is negatively correlated with normalized antipsychotic dosage with first generation antipsychotics having an especially negative effect on cortical thickness. The negative effect of antipsychotics on cortical thickness provides additional grounds for using antipsychotics in the lowest feasible dosage. Individuals with schizophrenia not on antipsychotics have decreased cortical thinning compared to individuals with schizophrenia on antipsychotics.. Cortical thickness effect sizes were two to three times larger in individuals receiving antipsychotic medication relative to unmedicated individuals. See also Antipsychotic Effects on Cortical Morphology in Schizophrenia and Bipolar Disorders. Antipsychotics are flat out toxic to brains.

Schizophrenia, anosognosia and Se-methylselenocysteine

Lack of insight or lack of awareness of illness in schizophrenia is termed anosognosia with some 30% of individuals with schizophrenia having anosognosia. The cardinal feature of anosognosiais not elaborate delusions rather the cardinal feature of anosognosia is confusion and disorganization. Individuals with agonosgnosia are having terrible cognitive difficulties. Se-methylselenocysteine treats cognitive symptoms of schizophrenia. Supplemental Se-methylselenocysteine could be a treatment for anosognosia.

Patients might not be responsive to treatment for anosognosia with Se-methylselenocysteine given patients are intensely sad. With the SMVT dysregulated, which transports biotin, needed for synthesis of saturated fatty acids, fatty acids are not being synthesized. 15 grams of cococa butter must be supplemented three time a day.

Patients on Se-methylselenocysteine and cocoa butter could have ahedonia but there would be an awareness of illnesses. More organized delusions though with an awareness of illness could be a feature of the treatment. I hold more can be done to treat schizophrenia, however, Se-methylselenocysteine and cocoa butter would be a treatment for agonosgnosia…Individuals with schizophrenia could benefit greatly from 600 mg of iron from iron carbonyl taken away from other supplements, food and drinks except water.

An exclusive focus on absorption of minerals is at odds with the gut being a key to various illnesses

The gut has become a primary focus of a lot of research on various illnesses. The gut has become a focus in research on major depressive disorder, schizophrenia, bipolar disorder, obsessive compulsive disorder, autism, anxiety, Parkinson’s disease, Alzheimer’s disease, osteoporosis, amyotrophic lateral sclerosis etc.

Yet the key selling point of most mineral supplements is increased absorption with increased absorption demanding that the gut be bypassed. Moreover almost all clinical studies done on humans employ inorganic forms of minerals rather than chelated organic forms of minerals. ‘Zinc gluconate human‘ turned up 560 results in Pubmed whereas ‘zinc methionine human, turned up 11 results where there were two human trials with an equivocal result in one of the trials and a positive result on a narrow measure of reduced acne in the other.

Individuals taking organic chelated mineral supplements are venturing into unknown lands and I think dangerous lands. Chelated minerals are highly absorbed but that is a bug not a feature.

Biohack mental illness now!

l CRISPR DIY kit not required

A lot of biohacking does not appear to be safe. For example, trying to alter at home one’s genetic makeup via CRISPR seems beyond unsafe.

A lot of biohacking is undertaken to achieve increased longevity. Biohacking for increase longevity requires that one wait around for decades to see the results. One has to wait 30 or 40 years to see whether one selected a right mix of supplements and then in all probability if one lives to a healthy 100 years of age one would not know exactly which supplements were the key supplements. Knowledge as to what increases longevity would still be lacking. One could be interviewed with questions asked as to how longevity was achieved and a laundry list of supplements would then be detailed. Someone listening to the interview could say, ‘I will eat 3 strips of bacon every morning. The other guy eats three strips of bacon every morning and is an alert, healthy 102 year old.’

A lot of specialty nootropics taken for cognitive enhancement have unclear effects and have not been widely tested in clinical trials . Moreover most nootropics are likely manufactured in China which does not have a reputation for tight controls on drug manufacture. What is more there would be a huge mainstream market for nootropics given noontropics worked. Individuals with mental illnesses very frequently could use some cognitive enhancement but nootropics are not being prescribed. After decades of use and study use of nootropics appears to be a very sketchy practice.

The appeal now of becoming part cyborg is 98% aesthetic. Becoming part cyborg now does not result in cognitive enhancements or health enhancements.

Biohacking mental illness

I hold that a lot of mental illness can be biohacked now, this week. 600 milligrams of carbonyl iron taken once a day at bedtime away from other supplements, food and drinks except water can treat psychosis. Iron interacts with lots of substances, coffee and tea being two examples. The point of taking the carbonyl iron at bedtime is to take the iron away from substances that can interfere with iron metabolism in the gut. The last cup of coffee or cup of tea of the day is drunk at least 6 or 7 hours before carbonyl iron is taken. 200 micrograms of Se-methylselenocysteine taken once a day in the morning. can treat disorganization. Cocoa butter. taken three times a day away from iron is very helpful. Difficulties in the transport of biotin could lead to difficulties in the synthesis of saturated fatty acids, Difficulties in synthesis of saturated fatty acids could be addressed by supplementation with cocoa butter. MCT oil and olive oil do not work.


I hold that iron-sulfur proteins are dysregulated in schizophrenia and that 600 milligrams of carbonyl iron taken once a day at bedtime can address the psychosis of schizophrenia. There is no direct clinical evidence that iron-sulfur proteins are dysregulated in schizophrenia. Given iron-sulfur proteins were dysregulated in schizophrenia this would cause major difficulties where psychosis could be one such difficulty.

There is no clinical evidence Se-methylselenocysteine effectively treats cognitive symptoms of schizophrenia.


Dirt simple and very quick. Very safe for at least a week. If the treatment has not worked at the end of week the treatment would be stopped. If the treatment is effective then safety of the supplements can be studied further and necessary tests obtained.

A lot of research I have cited cited on the website and in papers points to iron-sulfur cluster formation and selenoprotein metabolism being dysregulated in various neurological illnesses. Dysregulation of the SMVT which has been repeatedly addressed in this blog could result in dysregulation of saturated fatty acid synthesis which could certainly result in depressive illnesses.

There could a difficulty in synthesis of saturated fatty acids due to biotin deficiencies which supplementation with cocoa butter.could address. Difficulties in the transport of biotin could lead to difficulties in the synthesis of saturated fatty acids.

Not dangerous for at least a week. Would not be taken longer than a week if not effective.

L-glutamate and schizophrenia

NMDA receptor

Dysregulation of glutamatergic neurotransmission has been widely postulated as being involved in the etiology of schizophrenia. In the etiology of schizophrenia I have been stressing the dysregulation tricarboxylic acid (TCA) cycle via dysregulation of aconitase and the 2-oxoglutarate dehydrogenase complex stemming from shortages of coenzyme A.

The TCA cycle produces 2-oxouglutarate. .L-glutamate can be synthesized from 2-oxoglutarate. With dysregulation of the TCA cycle there can be a disruption in the synthesis of L-glutamate which would adversely affect glutamatergic neurotransmission whereby symptoms of schizophrenia could develop. .

Increasing glutamatergic neurotransmission alone via glutamate receptor agonists, however, does not solve the problem. The TCA cycle is still dysregulated.

There is strong focus on NMDA glutamate receptors in research on schizophrenia. Dysregulation of the TCA cycle, however, would dysregulate glutamatergic neurotransmission generally and also dysregulate GABA neurotransmission as GABA is synthesized from L-glutamate . D-serine which is an NMDA receptor agonist has failed in phase II trials where d-serine was being tested for effectiveness against symptoms of schizophrenia though a deuterated (i.e patenable) form of D-serine could still be effective for hair loss.

I hold that only addressing NMDA receptors will always fail in terms of the treatment of schizophrenia. Dysregulation of glutamatergic neurotransmission plays a key role in the etiology of schizophrenia, however, to address dysregulations of glutamatergic neurotransmission in schizophrenia dysregulation of the TCA cycle must be first addressed.

Culture and ‘polygenetic’ illnesses unique to humans


Apes don’t get schizophrenia. Apes also don’t have culture which is not to to state that there is not some variability in how apes behave in different locales and not to state there is not some use of sticks and rocks to obtain food and most definitely not to state that apes should not be protected. Culture demands use of media.

Why are studies where twin babies are separated at birth required in heritability studies of schizophrenia? Geneticists can’t nail down the genes. Given twin babies separated at birth have similar incidences of schizophrenia then various environmental influences are supposedly ruled out. The take away point is that heritability studies in schizophrenia are not finding genes that confer heritability rather the evidence for environmental effects is ruled out by twin studies where babies are separated at birth so schizophrenia susceptibility must be largely genetic.. The case for the genetic basis of schizophrenia is entirely circumstantial.

Independent assortment occurs where alleles of two different genes get sorted into gametes independently of one another. In research on the genetics of schizophrenia 108 independent genetic loci have been found to be associated with schizophrenia . The 108 genetic loci are not being inherited together. So what does the genetic theory of schizophrenia amount to – ‘Bad stuff happens mysteriously. ‘.

There is a lot of speculation on why only humans can get schizophrenia..Some have argued that schizophrenia represents s a costly trade-off, in the evolution of Homo sapiens, with schizophrenia being a by-product of a yet unknown uniquely human quality. I would not say the quality is a yet unknown quality though I would strongly agree that the quality is uniquely human The quality is culture.

;Schizophrenia is epigenetic in origin. So are various persistences in culture. Education of course, matters too in terms of persistencen of culture . The case for the genetic basis of schizophrenia is unfounded. Differences in genetic makeups can not explain various persistences in culture. Various persistences in human cultures and heritability of schizophrenia are both to due to transgenerational epigenetic inheritance.