Why acamprosate? Why not taurine?

Acamprosate is used to assist with alcohol abstinence. Acamprosate is compound that is structurally very closely related to taurine. Would taurine be as effective for alcohol abstinence as acamprosate? Sometimes small changes in molecular structure can have large effects on the actions of drugs. Acamprosate could have advantages over taurine for alcohol dependence but then again maybe the advantage of acamprosate was that at one time acamprosate was patentable.

Acamprosate agonizes GABA A receptors and modulates NMDA receptors Taurine, however, is a also a powerful activator of GABA A receptors and also modulates NMDA receptors. There might not be much biochemical advantage to acamprosate compared to taurine.

Taurine should be taken with flax seed oil and calcium hydroxyapatite. Taurine and filtered flax seed oil should be taken at the same time. Calcium was a particularly poor choice to complex acamprosate with. Only calcium hydroxapatite should be supplemented when there is mental illness.

Opioids or taurine, calcium hydroxapatite, and vitamin D for back pain?

Opioids are very frequently prescribed for back pain. Opioid addictions are a horrendous problem in the US and around the World. If a lot of back pain is due to a hidden osteomalicia then there could be a switch away from opioids to treat back pain to taurine, calcium hydroxapatite and vitamin D. Thousands and thousands of lives could be saved by switching to taurine, calcium hydroxapatite and vitamin D3. Mexico could be brought back from the abyss that drug cartels have brought Mexico to.

A point about a hidden osteomalacia is that in a hidden osteomalacia calcium homeostasis is dysregulated. Along with osteomalacia there would be a plethora of very negative psychological effects due to dysregulations in calcium homeostasis. People with back pain due to a hidden osteomalacia would not only be in physical pain but would also be in very serious psychological pain. Indeed back pain would be an indication that opioids should not be prescribed as individuals with back pain would be very prone to addiction to opioids due to the psychological pain that goes hand in hand with back pain.

The psychological pain associated with a hidden osteomalacia could be the driving force for addictions to opioids where there is back pain as opioids are not all that effective for the physical pain attendant on back aches.

If taurine, calcium hydroxapatite and vitamin D3 would be infinitely preferable for the treatment of back pain compared to opioids.

A secret of the ages

As it turns out lots of backaches are due to a hidden osteomalacia. With low levels of taurine fine control of calcium transport is lost. Calcium blood levels can be normal or just slightly low and one can still have a severe case of osteomalicia. Osteomalacia refers to a marked softening of the bones, most often caused by severe vitamin D deficiency. Severe vitamin D deficiencies can result in poor absorption of calcium which can lead to softening of the bones.

Taurine is required for calcium homeostasis. See also this paper. See also this paper. With taurine deficiencies fine control of calcium is lost which can lead to a hidden osteomalicia as calcium levels are normal or very near normal.

The treatment would be to take taurine, however, there is an added complication. Apparently the calcium-sensing receptor has become dysregulated. The calcium-sensing receptor is over-sensitive. With taurine deficiencies there can apparently be a kind of hypocalcemic hypercalciuria which can result in a hidden osteomalicia. The calcium-sensing receptor is antagonized by phosphate. Phosphate binds to the calcium-sensing receptor blocking the calcium-sensing receptor. Calcium must be taken with taurine to treat this hidden osteomalicia but the calcium in the calcium supplement must be bound to phosphate. That basically leaves calcium hydroxyapatite as the only acceptable calcium supplement. Calcium supplements not bound to phosphate are worse than useless for this hidden osteomalicia. Supplemental vitamin D would also be helpful.

An added complication is that taurine must be taken with filtered flax seed oil otherwise there is a spaced out feeling from the taurine. Taurine is needed for fat absorption. With taurine deficiencies there can be shortages of essential fatty acids which filtered flax seed oil taken with taurine can supply. Taurine and filtered flax seed oil should be taken at the same time for better absorption of fatty acids from filtered flax seed oil.

The bad news is that this is a very, very different view of backaches. New transformative ideas appear to be clearly wrong to the the vast majority of individuals, including MDs. The good news is that lots of backaches heretofore untreatable turn out to be very treatable. Osteomalacia can be cured.

Huge increase in anti-psychotic usage in bipolar disorder in recent years

In the treatment of bipolar disorder anti-psychotics have increasingly become more commonly prescribed, increasing from 12.4% of outpatient visits for bipolar disorder in the 1997-2000 period to 51.4% in the 2013-2016 period.

The page on bipolar disorder of this site both points to why lithium and anti-convulsants work at all while also pointing to why lithium and anti-convulsants are very inadequate treatments for bipolar disorder. Lithium and anti-convulsants target the SMVT but do so poorly where the dysregulation of the sodium-dependent multivitamin transporter (SMVT) is only one factor that gives rise to bipolar disorder.

Anti-psychotics are terrible drugs but many psychiatrists and patients find them preferable to lithium and anti-convulsants.

Ketogenic diets and beta-oxidation

A ketogenic diet is not advisable as a ketogenic diet would increase beta-oxidation. Low carbohydrate diets could result in weight loss but the side-effects are too great. No one would have weight problems if ketogenic diets improved health. Individuals could live with the bland ketogenic diets. Ketogenic diets, unless used to treat epilepsy, are ill advised. There still could be benefits from avoiding high glycemic foods, especially as long as ketosis is avoided.

Increased beta-oxidation sounds terrific. Rev up metabolism, increase energy, burn fats, loose weight, work hard, play hard, live life to the fullest. However increased beta-oxidation where there is already excessive beta oxidation due to decreases is biotin transport can lead to serious difficulties. See the page on bipolar disorder as to why there could be difficulties in biotin transport.

A warning sign that one should definitely avoid a ketogenic diet is if one is addicted to coffee, tea and/or sodas. Another warning sign that a ketogenic diet should be avoided is if one has any chronic illness.

In medicine ideas that should work but do not work are terrible ideas to put into practice. Ketogenic diets do not work in terms of overall health. Antioxidant supplements still make a lot of scientific sense outside the clinic but do not work and antioxidant supplements that deliver free antioxidants should be avoided. In medicine, a truth which is almost invariably correct, is that when the correct answer is not known then the provided ‘answers’ are usually very far from the truth and can be very dangerous. The best briefs in medicine are always fails in clinics.

Biotin and beta-oxidation

Acetyl-CoA carboxylase is a biotin-dependent enzyme that catalyzes the irreversible carboxylation of acetyl-CoA to produce malonyl-CoA. Malonyl-CoA inhibits the rate-limiting step in beta-oxidation of fatty acids. Malonyl-CoA inhibits fatty acids from associating with carnitine by regulating the enzyme carnitine acyltransferase.

Malonyl-CoA also plays a key role in chain elongation in fatty acid biosynthesis

Biotin supplementation would then both inhibit beta-oxidation and assist with chain elongation in fatty acid biosynthesis.

I have been arguing that increases is beta-oxidation that result from increased intakes of polyphenols can lead to difficulties in schizophrenia. Given the dual functions of malonyl-CoA in inhibiting beta-oxidation and assisting with fatty acid elongation if there is excessive beta-oxidation there would have to be difficulties in fatty acid elongation. Supplemental biotin would decrease beta-oxidation and increase fatty acid elongation which would be headed in the right direction. Biotin would not be supplemented at the same time as pantothenic acid as pantothenic acid is a competitive inhibitor of biotin transport.

Biotin is apparently necessary for the treatment of the negative symptoms of schizophrenia. Biotin, however, taken alone is not effective as with biotin there are still difficulties with fatty acid absorption. Negative symptoms of schizophrenia are due to dysregulation of fatty acid metabolism which is dysregulated in multiple ways in schizophrenia.

Cholesterol, taurine and Alzheimer’s disease

In Alzheimer’s disease there are high levels of homocysteine which points to the transsulfuration pathway (homocysteine to L-cysteine) being dysregulated in Alzheimer’s disease. Taurine is synthesized from L-cysteine. Taurine lowers LDL cholesterol levels. High LDL cholesterol levels, which increase the risk of Alzheimer’s disease, could be connected to the dysregulation of transsulfuration pathway as with dysregulation of the transsulfuration pathway there will be low levels of taurine which will increase cholesterol levels.

Polyphenols, homocysteine, Parkinson’s disease and Alzheimer’s disease

High homocysteine levels indicate the transsulfuration pathway (homocysteine to L-cysteine) is dysregulated. Taurine is synthesized from L-cysteine. Taurine is needed to form various bile acids. Bile acids are needed for fat absorption.

Polyphenols can increase beta-oxidation which can lead to serious difficulties if there are difficulties in the metabolism of fatty acids which are likely if there are high homocysteine levels.

Many illnesses for which polyphenols have been postulated to be treatments are associated with high levels of homocysteine, however, where there are high homocysteine levels there could be difficulties in fatty acid metabolism. Increasing levels of polyphenols, which increase beta-oxidation, would be contradicted where there are difficulties in fatty acid metabolism.

Polyphenol supplements are frequently suggested as treatments for Alzheimer’s disease and Parkinson’s disease, however, both Alzheimer’s disease and Parkinson’s disease are associated with high homocyteine levels whereby there could be difficulties in fatty acid metabolism. Polyphenol supplements could worsen Alzheimer’s disease and Parkinson’s disease. In the treatment of Alzheimer’s disease polyphenols have been full of promise but have failed to deliver effective treatments.

Caffeine pills have nowhere near the same effect as coffee. There must be more to the effects of coffee than caffeine and that something more is the polyphenol contents of coffee and the effect of those polyphenols on beta-oxidation.

Iron and Alzheimer’s disease

Iron overload in various regions of the brain has been postulated to be involved in the pathological mechanism of Alzheimer’s disease. Iron overload in the brain may very well be involved in the etiology of Alzheimer’s disease but iron overload in the brain in Alzheimer’s disease would not be due to too much iron in the diet.

A meta-analysis indicates that serum iron levels are significantly lower in Alzheimer’s disease patients than in healthy controls. Another meta-analysis also indicates that serum iron is significantly lower in patients with Alzheimer’s disease than in healthy controls.

Loss of control over iron metabolism rather that just ‘too much iron’ could be why iron can have negative effects in Alzheimer’s disease. Treatment in AD would demand that control be regained over iron metabolism. Iron chelators have been proposed as a treatment for Alzheimer’s disease. Iron chelators, however, would not be useful in terms of regaining control over iron metabolism. Iron chelators could have negative effects in AD.