The campaign against saturated fats by the American Heart Association has been a tremendous error. The American Heart Association recommends that intake of saturated fats be severely limited. However, with biotin deficiencies and and underactivity of acetyl-CoA carboxylase fatty acids are not synthesized and saturated fatty acids are the first ‘non-essential’ fatty acids to be synthesized. Where there are long term biotin deficiencies, which I think are very prevalent, saturated fats become essential fatty acids. Profound depressions can result from lack of saturated fats in diets.
The supplemented fats must be animal fats. Butter and ghee are the most readily available animal fats. Butter must be eaten 3-4 times a day. Butter works quickly for depression. Purchased beef tallow is apparently not beef tallow. Purchased beef tallow melts at room temperature which beef tallow should not do.
I am leaving the question open as to whether saturated fats are bad for the heart, there is evidence that they are not, but many individuals will face the choice of absolutely crippling depressions and heart disease or more butter in the diet and perhaps statins.
Beta-oxidation is up-regulated in schizophrenia. Malonyl-CoA inhibits beta-oxidation. Malonyl-CoA is synthesized by acetyl-CoA carboxylase which is a biotin-dependent enzyme. With deficiencies in biotin due to dysregulation of the SMVT malonyl-CoA will not be synthesized which will lead to low levels of malonyl-CoA and increased beta-oxidation which is what is seen in schizophrenia.
Thyroid hormones have been extensively investigated in major depression but abnormalities in thyroid hormones have not been found. Still in terms of treating depression thyroid hormones have had attractions. Meta-analyses indicate that augmentation of anti-depressants with triiodothyronine (T3) or thyroxine (T4) and can be helpful in the treatment of refractory depression.
There are definite difficulties with thyroid function in major depression but the problem is too little iodine. With dysregulation of the sodium-dependent multivitamin transporter (SMVT) iodine transport is impaired. The SMVT transports iodine. The role of the SMVT in the transport of iodine has not been emphasized to the same extent as the role of the SMVT in the transport of biotin and pantothenic acid. As it turns out the SMVT plays a key role in iodide homeostasis which if upset can result in major depression despite normal levels of thyroid hormones.
As an augmentation strategy to anti-depressants iodine would be taken three times a day. The Tolerable Upper level Limit for iodine for adults is 1100 micrograms per day. Tests on thyroid function would have to be obtained. Abnormal levels of thyroid hormones as shown by tests on thyroid function must be avoided.
If iodine can augment anti-depressants in the treatment of major depression this would point to the SMVT as playing a key role in psychiatric illnesses.
With epigenetic dysregulations dysregulated transcription does not have to be body wide. With hypermethylated genes and histones isolated to only a few organs blood tests may be normal even though there are definite difficulties. MDs in a all probability would agree that blood tests would not pick up a lot epigenetic dysregulations but then MDs would say ‘what can we do about that?’ and continue to draw blood and do tests on blood.
The sodium-dependent multivitamin transporter (SMVT) also transports iodide. How important the SMVT is for iodide transport is not clear. Supplementing with biotin and pantothenic acid, however, could competitively block the transport of iodide by the SMVT. There is another transporter of of iodide, the sodium/iodide cotransporter, (SLC5A5) which is largely expressed in the thyroid. The SMVT is expressed in the digestive tract.
From Interaction of α-Lipoic Acid with the Human Na+/Multivitamin Transporter (hSMVT)
‘Furthermore, the equimolar replacement of NaCl with LiCl or lowering the pH of the uptake assay from pH 7.4 to pH 5.5 (generation of a proton gradient across the oocyte membrane) resulted in R-[3H]LA accumulation in hSMVT-expressing oocytes that was indistinguishable from that observed in control oocytes (Fig. 2E)’ Control oocytes lack the hSMVT. The SMVT is the sodium-dependent multivitamin transporter and LiCl is lithium chloride. The SMVT transports biotin, pantothenic acid and lipoate.
The hSMVT is pH sensitive. Sodium bicarbonate buffers pH. If dysregulation of the SMVT in a key to to bipolar disorder as is argued in the page on bipolar disorder then sodium bicarbonate could be a key to the treatment of bipolar disorder. Sodium bicarbonate would also supply sodium which is required for transport by the SMVT.
The sodium of sodium bicarbonate could raise blood pressure. Each dosage of sodium bicarbonate would have to be taken with a 24 ounce glass of water to prevent dehydration which could raise blood pressure.
Blood pressure would have to be monitored. Individuals with high blood pressure may simply not be able to take sodium bicarbonate.
Sodium bicarbonate would be taken with biotin and pantothenic acid where biotin and pantothenic acid would be taken away from each other. Lipoic acid would not be taken as lipoic acid could competitively block the transport of pantothenic acid and biotin by the SMVT. Lipoic acid is synthesized on residues so there is no need to take lipoic acid.
Acetyl-CoA carboxylase is a biotin-dependent enzyme that is involved in the synthesis of non-essential fatty acids. Supplementation with beef tallow or ghee could be helpful. Taurine would be supplemented to assist with digestion of fatty acids.
If sodium bicarbonate, biotin, pantothenic acid, beef tallow or ghee and taurine are effective in the treatment of bipolar disorder then sodium bicarbonate, biotin, pantothenic beef tallow or ghee and taurine acid would be infinitely preferable for the treatment of bipolar disorder than lithium and/or anti-convulsants.
Supplements on the ‘supplements to be avoided’ list on the Treatment page would also be avoided. See the page on bipolar disorder for more on the SMVT
In Friedreich ataxia iron-sulfur clusters are not formed, due to deficiencies in frataxin which results in iron accumulation in mitochondria. The relevant point is that problems in iron-sulfur cluster formation can be associated with iron accumulation in mitochondria and iron toxicity. The point I have been making is that there are difficulties in synthesizing iron-sulfur clusters in many neurological illnesses due to dysregulation of the transsulfuration pathway which synthesizes L-cysteine. L-cysteine supplies sulfur for iron-sulfur cluster formation.
Iron chelators are now being investigated as treatments for Alzheimer’s disease and Parkinson’s disease. If iron is being accumulated in cells in Alzheimer’s disease and Parkinson’s disease due to difficulties in iron-sulfur cluster formation then iron chelators would not be appropriate treatments. Iron-sulfur cluster formation is increased by supplemental iron. Iron chelators by decreasing iron would decrease iron–sulfur cluster formation leading to iron accumulation in mitochondria and iron toxicity.
Dr. Holick has underestimated the problems with vitamin D/calcium. Where Dr. Holick made a misstep though is that the form of the calcium supplement matters a whole lot. Only calcium hydroxapatite works. Calcium hydroxapatite has to be taken with taurine and vitamin D.
Over the last few decades there have been huge controversies about whether there are widespread vitamin D deficiencies and whether vitamin D supplementation could prevent many chronic illnesses. Dr. Michael Holick claims there is a vitamin D deficiency pandemic. Dr. Holick points to association of vitamin D deficiency with a myriad of acute and chronic illnesses including preeclampsia, childhood dental caries, periodontitis, autoimmune disorders, infectious diseases, cardiovascular disease, deadly cancers, type 2 diabetes and neurological disorders.
However, a umbrella study that addressed meta-analyses that addressed studies where vitamin D supplements were given did not show much effectiveness in terms of outcomes when vitamin D was supplemented.
Dr. Holick is a lot more right than wrong. Taurine is required for calcium homeostasis. See also this paper. See also this paper. With taurine deficiencies calcium homeostasis is upset. With taurine deficiencies individuals can develop severe cases of osteomalacia even where vitamin D levels are normal.
Very unfortunately supplementation with vitamin D alone is not enough to treat these dysregulations of calcium homeostasis. The umbrella study as to the efficacy of vitamin D supplementation alone is also correct. To treat dysregularities in calcium homeostasis due to deficiencies in taurine, L-taurine must be supplemented, calcium hydproxapatite must be supplemented and vitamin D must be supplemented.
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.