Thanks for the post and link. This is a good review.
I am going to present four abstracts at the Movements Disorders meeting in Nice this fall. We have been investigating neurodegeneration involving disregulation of the Cupin superfamily and the metabolic "cycle" involved in human health and aging.
Taurine is a major end product in both the exogenous and endogenous pathways. The author was somewhat correct on the pathways to taurine.
We have focused deeply on these pathways because of a rare gene mutation that attacks children. During the research we realized that the disorder was the Rosetta Stone for neurodegeneration.
Taurine deficiency is a serious problem in human aging as well as numerous diseases, however the upstream metabolites that convert to taurine are far more critical for the prevention of neurodegeneration. These are cysteamine and hypotaurine. Hypotaurine is produced from two different dioxygenase pathways to taurine. One is cysteine and the other cysteamine. Both cysteramine and hypotaurine are necessary reactive oxygen species scavengers in the brain, whereas taurine is not.
The cysteamine part of the cycle is the endogenous portion from the breakdown of coenzyme A. This is being researched now in Parkinson's and Huntington's disease. The initial Huntington's RCT failed to show disease reversal, however it was too short. It did show a dramatic increase in brain derived neurotrophic factor (BDNF). This was probably the most important finding.
The cysteine portion is more of an exogenous pathway to hypotaurine and taurine. Cysteine can be increased by dietary intake such as eggs or by supplement with NAC.
We have found an older metabolite that fulfills the endogenous part of the cycle. This is Pantethine and has been researched for almost 60 years (well over 600 papers and hundreds of RCTs). It was the frontline hypercholesterolemia agent prior to statins. Further, pantethine lowered LDL, raised HDL, lowered triglycerides and improved platelet clotting function. It did not lower LDL as much as statins. That was the marketing appeal of statins. Unlike statins, Pantethine's action did not involve the disruption of the mevalonate pathway. Pantethine breaks down after oral ingestion in the lumina of the intestine to pantothenate and cysteamine. Cysteamine is the critical agent to support the endogenous portion of the hypotaurine to taurine pathway. Both cysteamine and pantethine have shown other therapeutic benefits including protection in malaria infection, radiation treatment and brain infarct.
Sadly, because of statin marketing, pantethine research has slowed dramatically in the past 15 years. This is tragic for those suffering from metabolic disorders and those who are also taking statins. I will go on record as saying when the time comes, statins will be seen as the worse of bad drugs. The controversy over Vioxx and Tamiflu will pale in comparison. The first lawsuits have already been filed over statin caused type 2 diabetes. The longterm neurological damage has yet to be assessed.
I am not a doctor and this is not medical advice. Pantethine can be found on Amazon (active agent Pantesin). My wife and I began taking it three years ago at a dose of 450mg TID.
I'll be able to post much more after the meeting and also our submissions of other IRBs and NIH R01 applications.
For those who are interested in problems with disrupting the mevalonate pathway there is this link:
Statin Damage to the Mevalonate Pathway.
Thanks for the article. This was eye-opening...
“There are now compelling explanations for the many reports of aggressiveness, hostility, sensitivity, paranoia, homicidal ideation, road rage like reactions, profound depression, suicidal ideation and even suicides associated with the use of statin drugs.”