The thyroid gland, a Wolff–Chaikoff-like effect, and major depressive disorder

Thyroid Gland

The Wolff–Chaikoff effect[1] 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, lipoate and iodide. 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.

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.

The Gene: An Intimate History by Siddhartha Mukherjee

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The Gene is 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.’

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 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 thiamine is 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 phosphatase levels 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.

Cons

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 phosphatase is involved in phosphate absorption.

No other supplements should be taken.

Pros

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.

Decanoic acid in MCT oil

Decanoic acid (capric acid)

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 inhibits glutamate AMPA receptors.

Caprylic acid could still be very important to the action of MCT oil. Capryilc acid is octanoic arid which is required for the synthesis of lipoic acid. Lipoic acid is a co-factor for the 2-oxoglutarate dehydrogenase complex. .and the pyruvate dehydrogenase complex.

Plus MCT oil which is combination of caprylic acid and capric acid is energizing via metabolism of MCT’s.

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.

Taurine chloramine inhibits prostaglandin E2

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Prostaglandin E2 (PGE2) is highly inflammatory. Inflammation is associated with major depressive disorder. Taurine chloramine inhibits PGE2.

Taurine chloramine inhibits prostaglandin E2 production in activated RAW 264.7 cells by post-transcriptional effects on inducible cyclooxygenase expression.

Quinn MR, Park E, Schuller-Levis G.

Abstract

Taurine chloramine (Tau-Cl) was recently demonstrated to inhibit production of nitric oxide and tumor necrosis factor-alpha (TNF-alpha) by activated macrophages. Since increased production of prostaglandin E2 (PGE2), a reaction catalyzed by induction of cyclooxygenase-2 (COX-2), is also associated with the inflammatory response, we determined the effects of Tau-Cl on PGE2 production and on expression of COX-2 protein and COX-2 mRNA in activated RAW 264.7 cells, a murine macrophage-like cell line. Tau-Cl inhibited production of PGE2 in a concentration dependent manner with an IC50 of 0.4 mM. The decrease in PGE2 production was largely accounted for by decreased expression of COX-2 protein. Although the kinetics of COX-2 mRNA expression was altered in Tau-Cl treated cells, mRNA expression appeared to be quantitatively unimpaired. These results suggest that Tau-Cl affects the post-transcriptional regulation of COX-2 expression and support the idea that Tau-Cl may function as an inhibitory modulator of the inflammatory response.

See also –

Selective inhibition of cyclooxygenase 2-generated prostaglandin E2 synthesis in rheumatoid arthritis synoviocytes by taurine chloramine.

Kontny E, Rudnicka W, Kowalczewski J, Marcinkiewicz J, Maslinski W.

Objective: To investigate the effects of taurine chloramine (Tau-Cl), a chlorinated derivative of the amino acid taurine, on the expression of cyclooxygenase (COX) isoenzymes and prostaglandin E(2) (PGE(2)) synthesis in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS).

Methods: FLS, isolated from the synovial tissue of RA patients, were treated in vitro with either interleukin-1beta (IL-1beta; 1 ng/ml) alone or together with 200-500 microM Tau-Cl. The expression of COX isoenzymes was evaluated at both the protein (Western blotting) and the messenger RNA (mRNA) (reverse transcriptase-polymerase chain reaction) levels. The concentration of PGE(2) was measured by competitive acetylcholinesterase enzyme immunoassay.

Results: Resting FLS expressed mRNA encoding both COX-1 and COX-2, but only COX-1 was present at the protein level. These cells produced negligible amounts of PGE(2). Upon stimulation with IL-1beta, elevation of COX-2, but not COX-1, mRNA and protein preceded the enhancement of PGE(2) synthesis. In the presence of 300-400 microM Tau-Cl, significant inhibition of IL-1beta-triggered COX-2 mRNA and protein, and a related decrease in PGE(2) production, was observed. In contrast, no significant changes in COX-1 mRNA and protein levels were noted.

Conclusion: Tau-Cl inhibits IL-1beta-triggered elevation of COX-2 and generation of PGE(2) by RA FLS. These results expand the spectrum of known antiinflammatory activities of this compound.

Whey protein and athletics

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More than half of high school athletes take protein supplements and percentages could increase in college and in professional sports. The NFL website strongly suggests that protein supplements can be helpful. Whey protein supplements that are quickly absorbed can have very adverse effects. Whey protein isolates are very quickly absorbed and can have very adverse effects. Most whey protein supplements contain at least some whey protein isolates. Whey protein isolate would contain only whey protein isolates but supplements labeled as whey protein usually are partly whey protein isolates.

Head injuries may not be the only problems of athletes are facing in terms of cognitive abilities. Whey protein isolates can negatively affect cognitive abilities. Any supplement formulated for quick absorption can have negative effects with whey protein isolate being one such supplement.

Casein is a much safer protein supplement but I am not recommending that athletes switch to casein from whey protein as taking supplements is full of pitfalls. The calcium phosphate in casein, for example, could decrease absorption of iron. Athletes who hold they need more protein should eat more high protein meals.

Why do individuals have differences in gut microbiota?

Gut microbiota are dependent on the environment of the gut for nutrients. If metabolic processes are dysregulated in the gut this will affect nutrients available in the gut. Some species of microbiota could be favored by various gut metabolic dysregulations while other microbiota could be disfavored. Certain microbiotic ecosystems could have direct effects, for example, causing diarrhea while other microbiotic ecoystems could only be markers for iron dysregulation in the gut which can have systematic effects.

Iron in the gut is a nutrient in the gut that affects the microbiotic ecosystem of the gut. Gut microbiota and iron are held to be crucial actors in health where many species (see Table) of gut microbiota are affected by iron supplementation.

Differences in gut microbiota could largely be a marker for iron dysregulation in the gut. Lots of substances in the diet bind with iron which could be affecting gut microbiota. Probiotics can affect iron metabolism in the gut. Lactobacillus plantarum 299v can increase iron absorption. A meta-analysis indicates that Lactobacillus plantarum 299v increases iron absorption. Lactobacillus plantarum 299v does not require iron which could make iron more available in the gut besides assisting with the absorption of iron via more iron being available to be absorbed. Bifidobacteria,. another beneficial microorganism in the gut, requires iron.

In sum gut microbiota is dysregulated in so many illnesses as iron metabolism in the gut is dysregulated in so many illnesses.

The difficulties the US is facing should be due to profound aporias

A great nation brought to it’s knees by supplements, coffee, tea and sodas? There should be profound reasons for the US going very far astray. Shouldn’t the Western tradition stemming from Socrates and Plato be fundamentally flawed? Didn’t it all go wrong with the Enlightenment? Isn’t the problem unbridled materialism? Isn’t the problem too much Christianity or too little Christianity?

Perhaps not. Coffee and tea have been very widely drunk for the last 500 years. Widespread coffee and tea drinking starts with the coming of the modern age. Coffee and tea interact with iron. And even where there are normal blood levels of iron coffee and tea could affect iron metabolism in the gut. Sodas contain polyphenols which can affect iron levels. When minerals are supplemented very frequently chelated minerals are supplemented. When multivitamin multimineral supplements are taken usually the minerals are chelated. Prenatal formulas very frequently contain chelated minerals. And there is no proof that chelated minerals are equivalent in the gut to non-chelated minerals which are the mineral formulations that have been studied in human clinical trials..

Could lead poisoning have been a factor in the fall of ancient Rome? I would say yes. Besides water from aqueducts wine in ancient Rome also contained high levels of lead.