Many illnesses, such as schizophrenia, Alzheimer’s disease, Parkinson’s disease and bipolar disorder are associated with oxidant stress. Yet, increasing levels of free antioxidants by supplementing with more than RDA amounts of vitamin E, beta-carotene and vitamin C does not treat these illnesses.
Increasing levels of free antioxidants via supplmentation could be much worse than useless. Before iron can be absorbed iron must be reduced from Fe3+ to Fe2+. Antioxidants like vitamin C, vitamin E , beta-carotene and quercetin could one way or other promote the reduction of Fe3+ to Fe2+ in the gastrointestinal tract which would increase absorption. The goal, however, is to delay iron absorption as long as feasible.
There is oxidant stress in lots of illnesses but this could be due to dysregulation of selenoproteins and dysregulation of iron metabolism which would not be fixed by increasing levels of free antioxidants with supplemental vitamin C, vitamin E , beta-carotene, quercetin etc.
Supplementing with free antioxidants could be associated with very subtle but serious mineral dysregulations which would basically be undiagnosable.
High levels of homocysteine are associated with increased risks for a number of illnesses. Hyperhomocysteinemia is a risk factor far osteoporosis, Alzheimer’s disease, Parkinson’s disease, stroke, cardiovascular disease, cancer, aortic aneurysm, hypothyroidism and end renal stage disease among other illnesses. I would add schizophrenia and bipolar disorder.
I have been arguing that high homocysteine levels point to the transsulfuration pathway being dysregulated. That there are so many illnesses associated with high homocysteine combined with the ineffectiveness of folic acid in reducing risk ratios for various illnesses point to high homocysteine levels being a proxy for other dysregulated biological processes. I have been arguing than high homocysteine levels are associated with increased risks for epigenetic dysregulations.
Folic acid supplementation, which reduces homocysteine levels, does not decrease risk ratios for the various illnesses that high homocysteine levels are associated with, for example, cardiovascular illnesses. Folic acid is ineffective as homocysteine must be metabolized through the transsulfuration pathway. Increasing remethylation of homocysteine to L-methionine does not fix the transsulfuration pathway leaving folic acid ineffective in decreasing risk ratios for various illnesses. Very unfortunately increasing levels of L-cysteine through supplementation with N-acetyl-L-cysteine, cysteine, cystine or lipoic acid also does not work where such supplementation can be very dangerous.
Elevated circulating levels of branched-chain amino acids have been associated with insulin resistance where decreased degradation of branched-chain amino acids could be what is leading to elevated circulating levels of branched-chain amino acids. Metabolic syndrome is associated with insulin resistance.
Methylcrotonyl CoA carboxylase and propionyl-CoA carboxylase are two biotin-dependent enzymes in the branched-chain amino acid degradation pathway. Dysregulation of the sodium-dependent multivitamin transporter which transports biotin could dysregulate the branched-chain amino acid degradation pathway leading to high levels of circulating branched-chain amino acids and insulin resistance.
Insulin resistance is present in 52% of individuals with bipolar disorder. Insulin resistance develops is brains of individuals with Alzheimer’s disease. In China in individuals with schizophrenia the prevalence of insulin resistance is 37.2% Both disease processes and drugs used to treat these illnesses could increase insulin resistance in theses illnesses. A commonality among these illnesses could be dysregulation of the sodium-dependent multivitamin transporter both by disease processes and drugs used to treat these illnesses.
Biotin supplementation decreases hyperglycemia, normalizing glucose levels, in patients with non-insulin dependent diabetes. There is reduced hyperglycemia is diabetic patients taking biotin.
The sodium-dependent multivitamin transporter transports both biotin and pantothenate. Pantothenate is needed to synthesize coenzyme A which is closely tied to the actions of biotin-dependent enzymes. Biotinylation of the sodium-dependent transporter reduces transport by the sodium-dependent multivitamin transporter. High levels of biotin could decrease transport of pantothenate by the sodium-dependent multivitamin transporter. A combination of pantothenic acid and biotin where 500 mg. of pantothenic acid is taken once a day away from supplemental biotin and 5 mg of biotin is taken three times a day could word work better in controlling hyperglycemia than biotin alone.
Only the abundance of biotinylated 3-methylcrotonyl-CoA carboxylase (holo-MCC) and propionyl-CoA carboxylase (holo-PCC) can distinguish between biotin-deficient and biotin-sufficient individuals. Methylcrotonyl CoA carboxylase and propionyl-CoA carboxylase could be particularly sensitive to biotin deficiencies.
Low levels of vitamin D are associated with schizophrenia, bipolar disorder Alzheimer’s disease and Parkinson’s disease. Vitamin D is a fat soluble vitamin. Bile acids are required for fat absorption. Taurocholic acid is a bile acid that is a conjugate of cholic acid with taurine. Taurochenodeoxycholic acid is a bile acid formed in the liver by conjugation of chenodeoxycholic acid with taurine. Taurine increases absorption of vitamin D.
There are low levels of vitamin D in schizophrenia, bipolar disorder, Alzheimer’s disease and Parkinson’s disease due to dysregulation of taurine synthesis in these illnesses attendant on dysregulation of the transsulfuration pathway which synthesizes L-cysteine from which taurine is synthesized.
Supplementation with vitamin D in these illnesses heretofore has not helped much as difficulties in fat absorption have not been addressed. Taurine, which regulates calcium homeostasis besides aiding in fat absorption, taurine would be taken with vitamin D, vitamin K and calcium carbonate to address low levels of vitamin D where there are chronic illnesses. Vitamin K is also a fat soluble vitamin whose abosoprtion could be impaired by low levels of taurine.
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.