Selenium and osteoporosis

Selenium intake in a dose-response manner is negatively correlated with osteoporosis. Compared with the lowest quartile tho odds ratios of osteoporosis were 0.72, 0.72 and 0.47 for the second, third and fourth quartiles of dietary Se intake, respectively. See also this paper.

In my paper on osteoporosis on the Osteoporsis page I argue that the transsulfuration pathway is dysregulated in osteoporosis. Dysregulation of the transsulfuration pathway would dysregulate selenium metabolsim as the food form of selenium, selenomethionine is metabolized via the transsulfuration pathway. Se-methylselenocysteine can be metabolized by kynurenine aminotransferase whereby Se-Methyl-L-selenocysteine + H2O <=> Pyruvate + Ammonia + Methaneselenol. Kynurenine aminotransferase is an enzyme that is not in the transsuluration pathway whereby Se-methylselenocysteine is the prefecred form of supplemental selenium as selenium from Se-methylselenocysteine is biovailable. Dosages of Se-methylselenocysteine should not exceed 200 micrograms a day. More is not better.

Taking supplemental taurine lowers blood pressure in humans

Taurine lowers blood pressure in humans by increasing synthesis of hydrogen sulfide, which is a vasodilator, through increasing activities of cystathionine beta-synthase and cystathionine gamma-lyase, the two enzymes in the transsulfuration pathway. Cystathionine beta-synthase and cystathionine gamma-lyase synthesize hydrogen sulfide. A meta-analysis indicates that taurine lowers blood pressure in clinically relevant amounts. Taurine also decreases homocysteine levels in humans. There is also lots of evidence from animals than taurine lowers total cholesterol. Research points to taurine as being the factor for Japanese longevity which could be due to taurine lowering various cardiovascular risk factors. The actions of taurine are more pronounced when taurine is taken on an empty stomach.

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 fat absorption 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 absorption. Increasing levels of polyphenols, which increase beta-oxidation, would be contradicted where there are difficulties in fatty acid absorption and 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 absoption. 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.

DHA and Alzheimer’s disease

Docosahexaenoic acid (DHA) levels are low in Alzheimer’s disease. DHA is synthesized from alpha-linoelic acid which is an essential fatty acid which must be obtained from the diet. For DHA to be synthesized from alpha-linoelic acid, alpha linoleic acid must first be absorbed.

A meta-analysis indicates that homocysteine levels are significantly high in Alzheimer’s disease. High homocysteine levels in Alzheimer’s disease indicate the transsulfuration pathway is dysregulated in Alzheimer’s disease as homocysteine is not being metabolized to L-cysteine which is what the transsulfuration pathway does.

With low levels of L-cysteine there will be low levels of taurine. Taurine is synthesized from L-cysteine. Taurine is needed for the formation of bile acids which are needed for fat absorption. With alpha-linoelic acid not absorbed in Alzheimer’s disease due to low levels of taurine synthesis of DHA will be impaired in Alzheimer’s disease which is what is seen is Alzheimer’s disease. Effectiveness of supplementation with DHA in Alzheimer’s disease could be limited due to a failure to absorb DHA due to low levels of taurine in Alzheimer’s disease.

Taurine only poorly crosses the blood-brain barrier. However, to assist with essential fatty acid absorption taurine does not have to cross the blood-barrier. Taurine by enhancing fat absorption can enhance brain function.

Homotaurine has has been shown to be a promising therapy for Alzheimer’s disease. In Alzheimer’s disease taurine could be taken with with fatty acid supplements high in alpha linoelic acid, such as lignan free flax seed oil. Lignans are polyphenols so flax seed oil with lignans is avoided.

In schizophrenia all paths lead to the transsulfuration pathway

With a dysregulation of the transsulfuration pathway (homocysteine to L-cysteine) sufficient L-cysteine for iron-sulfur cluster formation is not synthesized. Sulfur for iron-sulfur cluster biogenesis is derived from L-cysteine. Supplemental iron increases levels of iron-sulfur proteins. Supplemental iron can partly compensate for dysregulation of the transsulfuration pathway in schizophrenia. Selenomethionine, the food form of selenium is metabolized by enzymes in the transsulfuration pathway. Metabolism off Se-methylselenocysteine by-passes the transsulfuration pathway whereby Se-methylselenocysteine can provide bioavailable selenium for individuals with schizophrenia. Taurine is synthesized from L-cysteine. With L-cysteine not synthesized appropriately taurine will not be synthesized at appropriate levels. Taurine is needed to form various bile acids, With low levels of taurine there will not be sufficient taurine conjugated bile acids. Fat absorption requires bile acids. With low levels of taurine due to low levels of L-cysteine fat absorption will be impaired. Supplemental taurine and supplemental essential fatty acids will compensate for low levels of taurine due to low levels of L-cysteine which are in turn due to dysregulation of the transsulfuration pathway. Taurine by sparing L-cysteine will also increase levels of L-cysteine.

An Important Warning: No supplements that contain L-cysteine or L-methionine should be supplemented. And no supplements that reduce cystine to L-cysteine, such as lipoic acid, should be supplemented. See the Treatment page for supplements that can be of assistance in the treatment of schizophrenia.