Mental illnesses – gut-brain illnesses

The gut is a staging area, The vagus nerve sends signals to liver and the brain that prep the liver and the brain for soon to be there nutrients. Without the prepping via the gut other parts of the body cannot use nutrients that are delivered. Supplements and/or drinks that are formulated to bypass the gut and/or decrease use of nutrients by the gut upset homeostasis and utilization of key nutrients throughout the body and/or starve the gut of nutrients..

Individuals until very recently in history were tied to the nutrients found in immediate environments in which such individuals lived. Individuals were constrained by environments. Supplement formulations that bypass the gut or drinks that affect absorption of nutrients can apparently but only apparently free individuals from environmental constraints. Soft drinks are sold on the basis of soft drinks imparting a bounce to individuals. Chelated minerals can give a bounce. That bounce is paid for with deleterious effects on long term health and with deterioration in immediate functioning.

Paternal age as a risk factor for schizophrenia points to epigenetics as being involved in inheritance of schizophrenia

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Paternal age is a risk factor for schizophrenia. There is no evidence of harmful genetic loci in schizophrenia except for some very rare high impact alleles.

Besides there being no evidence of deleterious genetic loci in schizophrenia except for some very rare high impact alleles.there is not enough time in spermatogenesis to accumulate a lot of mutations. For humans, the entire process of spermatogenesis is variously estimated as taking 74 days[8][9] (according to tritium-labelled biopsies) and approximately 120 days[10] (according to DNA clock measurements).

DNA methylation and histone methylation occurs in spermatogenesis. Dysregulation of epigenetic mechanisms could have occurred over time in aged dads resulting is dysregulation of spermatogenesis. This does not answer the question of how methyl marks are not stripped from embryos, however, the circumstantial evidence points to epigenetic dysregulations rather than genetic mutations as being the factor in paternal age which increases the risk for schizophrenia in offspring.

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.

Why would there be a gut-brain axis?

The gut has the highest exposure to the environment of any organ. The gut-brain axis could assist with appropriate environmental regulation of behavior. Prior to 5000 years ago the environments given individuals lived in were basically stable though those such environment varied across the Earth. What individuals placed into their mouths was an accurate reflection of the environments they lived in whereby the gut-brain axis assisted individuals adapting to environments lived in.

What individuals place into their mouths today has very little connection to the locality such individuals are living in. Now individuals place into their mouths junk food, sodas, chemicals, supplements, coffee and tea from very distant places. A main site of actions of junk food, sodas, chemicals, supplements, coffee and tea would be the gut whereby the brain would be affected.

Williams James held that emotions were cognitive readings of bodily states which is going too far. However, basal states of individuals could be very closely tied to the basal states of the environment where the environment can partly but strongly act on individuals via the gut-brain axis. Junk food, sodas, chemicals, supplements, coffee and tea could be affecting the brain quite directly.

An appropriate diet would demand that there be no attempt to escape the gut. As an example supplements formulated for better absorption would not be supplemented. Pharmacokinetics considerations used with pharmaceuticals could be very misleading when used with nutrients and foods generally. Processing of nutrients in the gut could be a key part of nutrients being nutrients. The adverse affects of refined sugars would be an example of ingested substances not being nutrients via a bypassing of carbohydrate processing in the gut.

The sodium-dependent multivitamin transporter (SMVT) is a key regulator of mood

The sodium-dependent multivitamin transporter transports pantothenic acid, biotin, lipoate and iodide. The sodium iodide symporter (NIS) is the key iodide transporter on the thyroid, however, the SMVT apparently has a key role in gut absorption of iodide. Pantothenic acids lifts mood, biotin sustains energy levels and iodide can alleviate sadness. Pantothenic acid, biotin and iodide can have countervailing effects on each other. Perhaps the evolutionary goal is euthymic states combined with some environmental control, however, in terms of delivering euthymic states the SMVT is a complete fail is all too many instances.

Genes in the gut for the SMVT are in all probability hypermethylated. Environmental factors could lead to the hypemethylation of genes for the SMVT in the gastrointestinal tract..Hypermethylation of genes in the gut is the first place to look for genes that are hypermethylated due to environmental factors as the gut has the greatest exposure to environmental factors.

Biotin is synthesized by gut microorganisms. Changes is gut microorganisms could lead to decreases in biotin synthesis adversely affecting energy levels. Pantothenic acid is also synthesized by gut microorganisms. Changes is gut microorganisms could lead to decreases in pantothenic acid synthesis by gut microorganisms. Addressing dysregulation of the SMVT is not a simple, straightforward operation.

Serine palmitoyltransferase and neuropathy

Serine palmitoyltransferase is the first enzyme in the sphingolipid metabolism pathway . Serine palmitoyltransferase, is a key enzyme of sphingolipid metabolism. Mutations in serine palmitoyltransferase, result in neuropathy.

Serine palmitoyltransferase requires palmitoyl-CoA and PLP (active vitamin B6). The upshot of this is that dysregulation of pantothenic acid transport, coenzyme A synthesis and/or dysregulation of vitamin B6 levels could result in dysregulation of serine palmitoyltransferase leading to neuropathy.

Given pantothenic acid and coenzyme A deficiencies supplemental vitamin B6 could worsen neuropathy via dysregulation of sphingolipid metabolism. Sphingosine-1-phosphate lyase 1 is vitamin B6-dependent enzyme in the sphingolipid metabolism pathway whose up-regulation via vitamin B6 supplementation could result in difficulties given a shortfall in substrates due to dysregulation of serine palmitoyltransferase.

Vitamin B6 associated neuropathy attributed to high dosages of vitamin B6 could stem from dysregulation of pantothenic acid transport and coenzyme A synthesis. Vitamin B6 in the context of pantothenic acid and coenzyme A deficiencies could worsen neuropathy.

Given individuals have unexplained neuropathies which appear to worsen with vitamin B6 supplementation, supplementation with pantothenic acid could be of assistance. Biotin would have to be supplemented, too, however, biotin should never be supplemented at the same time as pantothenic acid except in RDA dosages of biotin. Biotinylation of histones at the SMVT locus can reduce transcription of the SMVT which transports biotin and pantothenic acid. Biotin in more that RDA amounts should only be supplemented once a day. Sublingual formulations of biotin are avoided. Supplementation with biotin around 4-5 PM appears optimal. Pantothenic acid would be taken three times a day away from biotin. Cautiously re-introducing vitamin B6 could be tried. No more than 50 mg of vitamin B6 taken two times a day would be supplemented.

A serious difficulty with supplementing only with pantothenic acid and biotin is that pantothenic acid and biotin would competitively inhibit transport of iodide by the SMVT. If one supplements with pantothenic acid and biotin one would almost have to also supplement with iodide from kelp, L-tyrosine and Se-methylselenocysteine.

How could individuals be apparently euthyroid but still have thyroid difficulties?

Deiodinases are selenoproteins. Deiodinases both activate and inactivate thyroid hormones. T3 is the active thyroid hormone. Deficiencies in selenium could lead to decreased activation of T3 by deiodinase I but also decreased inactivation of T3 by deiodinase III whereby individuals would appear to be euthyroid though thyroid hormone homeostasis would be upset. Dysregulation of CTH (cystathionine gamma-lyase), which metabolizes L-seleonomethionine the food form of selenium so selenium can be used to synthesize selenoproteins, could result in dysregulation of DIO1 and DIOIII.

The internet is jam full of terrible advice on supplements. Why take the advice given on this blog?

The internet hoards all terrible advice on supplements with the hoard ever growing.

First of all, a lot the recommendations on this blog sensibly should not be followed. I am stumbling around more than a bit. Any advice on the Web on supplements to be followed must pass an absolutely extraordinary set of tests. .

The suggestions must be safe. Tests must be readily available to check for safety. The suggested supplements must work very quickly.. I am talking on the order of a week. The effects of the supplements must be very dramatic. What is more supplements must target very specific symptoms of mental illness. That is very important. The suggested supplements must not be oversold. Given the suggested supplements are taken individuals could still feel far below par.

Carbonyl iron for psychosis passes this extraordinary set of tests. Iron from carbonyl iron is taken at bedtime. Taking the carbonyl iron in taking the iron away from antioxidants, for example, coffee and tea, which can interfere with absorption of iron.

Iodide from kelp and L-tyrosine for sadness pass this extraordinary set of tests. Iodide from kelp and L-tyrosine would not treat all states associated with depression only sadness. Kelp and L-tyrosine have to be taken three or four times a day. Thyroid tests must be obtained. The goal is most definitely not high thyroid hormone levels. Iodide from potassium iodide apparently reacts with too many substances. The effect of iodide from potassium iodide is not dependable. Approximately 1000 micrograms of iodide from kelp have to be taken each dosage.

Se-methylselenocystiene for anosognosia and disorganization passes this extraordinary set of tests. Se-methylselenocystiene also assists with thyroid hormone homeostasis.

Very high dosages of thiamine could be helpful. 300 mg of thiamine taken 3 times a day could be needed.. Lower dosages of thiamine would be tried first.. Supplemental vitamin B6 can also be helpful. No more than 50 mg of vitamin B6 is taken twice a day.

Ill individuals would still require a neuroleptic. Low dosages of risperidone could be the neuroleptic of choice due to the high 5-HT2A to dopamine D2 binding ratio of low dosages of risperidone. Risperidone could be taken once a day at bedtime. The risperidone would not be for psychosis but rather would treat an intensely spaced out feeling.

I take other supplements but I am stumbling around more than a bit. If the supplements work get MD’s to do research. A couple of decades of research is required to follow up on the recommendations. Mothers and fathers of formerly very, very ill children could be extraordinarily helpful is advocating for research for their now insightful but still ill children.

If the advice on supplements on this blog is not followed then I would advise individuals not to take any advice on supplements given on the Web, not to take any supplements except perhaps a Centrum, eat balanced meals, exercise and reduce stressors in life. Avoid sodas, all citric acid based drinks and limit coffee and tea to a couple of cups a day. . Carbonated water that is only carbonated water, with no added natural flavors, is safe to drink. Adding natural flavors to carbonated water would make the carbonated water unhealthy.The Goldilocks rule should be followed in terms of psychiatric medications .Not too much medicine and not too little medicine is the right amount of psychiatric medicine to take.

Rule of thumb for advancing research on mental illness

Never directly research monoamine neurotransmitters. By 2021 levels of monoamine neurotransmitters can be regulated every which way and the results in terms of the treatment of mental illnesses are far from spectacular. Dopamine antagonists are neuroleptics. Dopamine antagonists work to the extent that dopamine antagonists work due to dopamine antagonists being neuroleptics.

Serotonin re-uptake inhibitors are in all probability also neuroleptics, but milder neuroleptics than dopamine antagonists with a much better side-effect profile. Serotonin re-uptake inhibitors can inhibit dopaminergic neurotransmission. At the end of the day monoamine neurotransmitters.could once again become important in research but this is early morning..

Drug companies could research dopamine antagonists that target specific brain regions in terms of reducing the side-effect profile of dopamine antagonists. Atypical antipsychotics preferentially enhance dopamine release in the prefrontal cortex as opposed to the limbic system which makes atypical antipsychotics milder neuroleptics than first generation antipsychotics. Risperidone at low dosages has a particularly favorable profile in terms of high serotonin 5-HT2A inverse agonism and low dopamine D2 antagonism.

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.