The Wolff–Chaikoff effect is a reduction in thyroid hormone levels caused by ingestion of a large amount of iodide. I think an effect similar to the Wolf-Chaikoff effect can upset thyroid hormone homeostasis where a Wolf-Chaikoff-like effect occurs when there are irregular supplies of iodide due to the sodium-dependent multivitamin transporter (SMVT) being dysregulated. The SMVT transports biotin, pantothenic acid, lipoateandiodide. See the page on Bipolar Depression on how the SMVT could be dysregulated.
Though the SMVT transports iodide what is usually thought of as the iodide transporter is the sodium/iodide symporter(NIS). NIS is strongly expressed in the stomach and on the thyroid gland. With the SMVT dysregulated in terms of absorbing iodide NIS has to be used exclusively. What is occurring with the Wolf-Chaikoff-like effect is that, with irregular supplies of iodide due to dysregulation of the SMVT, NIS on the thyroid gland is dysregulated leading to an upset of thyroid hormone homeostasis around normal levels of thyroid hormones with major depressive disorder resulting.
Iodide from potassium iodide and Se-methylselenocysteine are supplemented to treat major depressive disorder. Iodide from potassium iodide is a better source of iodide for the NIS than iodide in kelp. When supplementing with iodide from potassium iodide there could be a depression for a couple of days due to the Wolff–Chaikoff effect. Do not take nuclear catastrophe levels of iodide. No more than 1,500 micrograms of iodide from potassium iodide should be taken a day. No more than 200 micrograms of selenium from Se-methylselenocysteine should be taken a day. Selenium has important functions in the thyroid gland. Thyroid hormone levels must be checked.
Iodide from potassium iodide and Se-methylselenocysteine are not going to fix everything as the SMVT is still dysregulated. And besides individuals with major depressive orders can be in mixed states.
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.
The Geneis a popular introductory book on the gene. This is not a criticism as each new generation has to be introduced to a subject and this an acceptable popular introductory book.. With the field not at all crowded The Gene is a welcome popular introductory book on the gene.
The major criticism I have is that Mukherjee slights epigenetics in terms of behavior, is much too sanguine about genetic engineering to cure what are held to be polygenetic illnesses and is much too sanguine about genetic engineering to instill beneficial polygenetic traits. Geneticists apparently repeatedly assured Mukherjee that geneticists will one day be able treat polygenetic illnesses and moreover will be able to instill beneficial polygenetic traits most likely via some sort of embryo selection. Mukherjee took the geneticists at their word. Genetic determinism is almost a religion among geneticists as determinism is almost a religion in academia.
Medical horrors are apparently inadvertently being planned for the wealthy. Now the wealthy depressed are taking ketamine which can cause a schizophrenia-like psychosis. 10 years from now the wealthy could be selecting embryos on the basis of very abstruse calculations where if something goes wrong the advising geneticist will say ‘the odds slightly favored a favorable outcome. Look at these calculations. You must understand probabilities.’
The first step in the synthesis of thyroid hormones is catalyzed by thyroid peroxidasewhich requires hydrogen peroxide. Hydrogen peroxide used by thyroid peroxidase is produced by dual oxidase 1 and dual oxidase 2. Hydrogen peroxide is both required for thyroid hormone synthesis but also can be toxic to the thyroid gland. Selenium is required both for thyroid hormone synthesis and protection of the thyroid from hydrogen peroxide needed to synthesize thyroid hormones. .
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 verysketchy practice.
The appeal now of becoming part cyborgis 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 can treat psychosis. 200 micrograms of Se-methylselenocysteine taken once a day can treat disorganization. 1,500 micrograms of iodide from potassium iodide taken once a day can treat depression. Iodide from potassium iodide should be taken at bedtime away from chelating agents like curcumin. Do not take more iodide. The Wolff–Chaikoff effect could be a difficult with iodide from potassium iodide. 300 milligrams of thiamineis taken 4 times a day can decrease fatigue. Iron interacts with a whole lot 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 interact with iron in the gut. The last cup of coffee or cup of tea of the day should be drunk at least 6 or 7 hours before carbonyl iron is taken. Why does thiamine work? Not due to addressing thiamine deficiencies. The advantage of very high dosages of thiamine is that the effect would largely be confined to the the intestines. High dosages of thiamine could increase intestinal alkaline phosphatase activity and increase phosphate absorption from the intestines but would not have much of an effect on systematic alkaline phosphatase levels.
Curcumin increases intestinal alkaline phosphataselevels and could be very helpful. The very poor absorbability of curcumin is a feature rather than a bug. The goal is to only increase intestinal alkaline phosphatase levels not systematic alkaline phosphatase levels. Tests for intestinal alkaline phosphatase are available now. Liver alkaline phosphatase levels are measured routinely but liver alkaline phosphatase is not the relevant alkaline phosphatase. A curcumin supplement should not contain anything, for example, piperine, that will increase absorption. Curcumin should not be taken when iron is taken as curcumin could affect iron absorption. Curcumin is apparently a terrible place to start drug development from. So what. Curcumin increases levels of intestinal alkaline phosphatase and has very low toxicity. Curcumin is very poorly absorbed.
No other supplements would be taken.
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.
Everyone who is treated for depression has had their thyroid hormone levels checked. A search of PubMed using ‘thyroid major depressive disorder’ turns up 999 articles. Thyroid hormones have not proven efficacious in treating major depressive disorder. Yet I hold that major depressive disorder is due to thyroid dysregulation. The extra iodide from potassium iodide could be a kludge. Iron and selenium metabolism could be askew upsetting fine control of thyroid hormone synthesis and thyroid hormone homeostasis while leaving absolute thyroid hormone levels normal. Iodine from kelp is not nearly as effective.
Why would intestinal alkaline phosphatase levels be decreased? That is unclear. Curcumin and very high dosages of thiamine would have to be considered a pure kludge play. I have talked a lot on this website about a seemingly intractable osteomalacia. I now think my osteomalacia is at least partly due to decreased levels of intestinal alkaline phosphatase. By freeing phosphate so phosphate can be transported intestinal alkaline phosphataseis involved in phosphate absorption.
No other supplements should be taken.
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 cited on this website points to iron-sulfur cluster formation and selenoprotein metabolism being dysregulated in various neurological illnesses. Dysregulation of thyroid hormones can certainly result in depressive illnesses.
Supposedly individuals with schizophrenia have low IQ’s. However, low IQ’s of individuals with schizophrenia could be a reflection of a treatable disorganization. Doing well on IQ tests is very difficult when disorganized. Supplementation with Se-methylselenocysteine treats disorganization and cognitive symptoms in schizophrenia. With supplementation with Se-methylselenocysteine IQ’s of individuals with schizophrenia could be increased. Supplementation with more than 200 micrograms of selenium a day should be avoided.
With the transsulfuration pathway dysregulated homocysteine levels can be increased and L-selenomethioinine, the food form of selenium, not metabolized. L-seleomethionine is metabolized by cystathionine gamma-lyase (CTH) which is an an enzyme in the transsulfuration pathway. Supplementation with Se-methylselenocysteine could be particularly effective in raising IQ’s in individuals with schizophrenia who have high homocysteine levels which would indicate that .L-selenomethioinine is not being metabolized adversely affected selenoprotein levels,.
Why would Se-methylselenocysteine be effective in treating disorganization? Selenoproteins are very frequently antioxidant proteins. With lots of free radicals bouncing around thoughts bounce around which presents as disorganization and as cognitive symptoms. Se-methylselenocysteine can stop lots of free radicals from bouncing around stopping thoughts from bouncing around treating disorganization and cognitive symptoms and perhaps raising IQ’s in individuals with schizophrenia.
Iodide from potassium iodide can alleviate major depression. Higher amounts of iodide are needed than RDA amounts.
1500 micrograms of iodide from potassium iodide would be taken once a day with 200 micrograms of Se-methylselenocysteine taken once a day. Seleniumis also required for synthesis of thyroid hormones. No other supplements would be taken.
The effect is almost immediate so one would know in three days at most whether this works. If at the end of three days depression has not ameliorated the iodide and Se-methylselenocysteine would be stopped. If this works one would obtain regular thyroid function tests. Abnormal thyroid hormone levels must be avoided. Iodide could be involved in thyroid hormone homeostasis. Thyroid hormone homeostasis could be as important to mood as absolute levels of thyroid hormones.
In treating major depressive disorder iodide from potassium iodide works much better than iodide from kelp. There are two transporters for iodide, SLCA5 and SLC5A6. The sodium-dependent multivitamin transporter (SLC5A6, SMVT) transports iodide. The SMVT could be dysregulated. See the page on Bipolar Depression as to how the SMVT could be dysregulated. SLC5A5is highly expressed in the stomach though not in the rest of the gut Iodide from potassium iodide is much more bioavailable in the stomach, where iodide via SLC5A5, can be absorbed, than iodine from kelp.
1500 micrograms of iodide from potassium iodide taken once a day safe? That is not clear. Japanese iodine intake from seaweed is estimated to be between 1 mg and 3 mg a day. 1500 micrograms of iodide from potassium iodide taken once a day has to be lots safer than ketamine which is now being used to treat treatment resistant depression. Dosages of iodine from kelp may not be equivalent to dosages of iodide from potassium iodide. Thyroid tests are required when taking iodide from potassium iodide. Hashimoto’s thyroiditis is thought to be aggravated by high levels of iodide while seleniumis thought to be protective. Here is a paper on the consequences of excess iodine.
Decades ago when measuring thyroid function protein-bound-iodide levels were measured With the arrival of thyroid hormone level assays protein-bound iodide tests fell into disuse. Had protein-bound iodide tests not fallen into disuse there is some chance that treatment resistant major depression would not be so treatment resistant now. Not all old tech is appropriately abandoned. Electric cars were invented prior to gasoline engine cars.
The thyroid could, after all, be at the root of major depressive disorder. The operative word in the title is ‘quick’. If at the end of three days depression has not lifted then the iodide from potassium iodide would be stopped.
MCT oil which is combination of caprylic acid and capric acid works much better in terms of improving mood than MCT oil which is only caprylic acid. Caprylic is octanoic acid. Capric acid is decanoic acid. Decanoic acid but not octanoic acid provides better seizure control than valproic acid..
The effect of capric acid may not be all be via increased ketones.. Capric acid inhibitsglutamate AMPA receptors.
Dysregulation of glutamatergic neurotransmissionhas 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 cycleproduces 2-oxouglutarate. .L-glutamatecan 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 NMDAglutamate 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-serinewas 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.
Why are studies where twin babies are separated at birth needed 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. Apparently these 108 genetic lociare 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 exists as a costly trade-off, in the evolution of Homo sapiens, as 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 can, of course, matter too. The case for the genetic basis of schizophrenia is, I think, unfounded. Differences in genetic makeups can not explain various persistences in culture. . However cultures are persistent.
Employing the method of Sherlock Holmes slightly modified, ‘When you have eliminated all that is unfounded then whatever remains, must be the truth.’ Heritability of schizophrenia is due to transgenerational epigenetic inheritance. Various persistences in human cultures are also due transgenerational epigenetic inheritance. Scientists in terms of transgenerational epigenetic inheritance in humans now hold that ‘transgenerational epigenetic inheritance of humans does not exist because we have not found it’ which is not a scientific way of proceeding.