I had someone tell me today that they had heard on talk radio over the weekend that there was a vitamin cure for Parkinson's and that the medical and drug establishment had been suppressing it.
So what was that all about?
First, we have a study in fruit flies which have a mutant parkin gene. Fruit flies, not humans. A mutant gene which most people with Parkinson disease do not have-- it causes the rare condition of autosomal recessive juvenile parkinsonism. In vertebrates, the protein is a component of a multiprotein E3 ubiquitin ligase complex which in turn is part of the ubiquitin-proteasome system that mediates the targeting of proteins for degradation. In addition, physiological studies of skin fibroblast cells from persons with autosomal recessive juvenile parkinsonism show significantly decreased mitochondrial complex I activity and ATP production in the cells (source: Leiden Open Variation Database, per The Parkinson's Institute). It is not certain which abnormality produces clinical human disease, though most pathological evidence, showing alpha-synuclein problems thought related to ubiquitin deficits, favors the deficit in ubiquitin.
Currently, there is no evidence, pro or con, that vitamin K2 affects hereditary forms or indeed any form of Parkinson's disease. Dietary plant vitamin K1 is converted to animal vitamin K2 and then stored for use in the K2 form by all mammals. In humans, vitamin K2 primarily acts as a cofactor in the production of blood clotting factors, with a secondary role in calcium and bone metabolism. Vitamin K2 deficiency causes clotting problems, but not parkinsonism.
The fruit fly insect has ubiquitin, but it does not have basal ganglia, and has no coagulation system for vitamin K2 to act upon. Instead, vitamin K2 acts to promote mitochondrial metabolism, a metabolism which is decreased in fruit flies with the aberrant parkin gene. Because mitochondria serve aerobic energy needs, the pathology in fruit flies affects the flies' aerobic exercise capacity: they have trouble with their muscles of flight. Vitamin K2 improves aerobic mitochondrial energy production in those fruit flies, helping them to fly.
Could the parkin mutation also be causing disease in humans via defective mitichondrial metabolism in the brain? Perhaps. However, we have no evidence, pro or con, that the ordinary, adult, sporadic form of Parkinson's is related to any use by brain mitochondria of the parkin protein. And we have no evidence, from what I can see, that the fruit fly illness is due to a fruit fly brain degeneration. So we have no evidence that vitamin K2 has anything to do with ordinary adult human Parkinson's disease. If there is such evidence in the future, well, bring it on -- we'll use it gladly :). The research does give a new potential direction for human studies.
Did the man I spoke to have any idea that the research promising him a vitamin cure on the radio was work done in fruit flies? No, none at all. That detail was left out of the radio show report's cure claim. As was the fact that the cured illness was not phenotypic Parkinson's disease.
So, the use of a vitamin in a tangentially related genetic anomaly in insects (homologous gene, questionable homology of use of that gene), via media distortion, becomes an expectation of a vitamin curing human disease today. Media hype leads to hyperinflated expectations of a cure, before any true human testing has been done. This then leads to disappointment, which causes a few to claim cures are being withheld via conspiracy, and thus props up the business models of alternative patent vitamin medicine hucksters.
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ABSTRACT
Science. 2012 Jun 8;336(6086):1306-10. doi: 10.1126/science.1218632. Epub 2012 May 10.
Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency.
Vos M, Esposito G, Edirisinghe JN, Vilain S, Haddad DM, Slabbaert JR, Van Meensel S, Schaap O, De Strooper B, Meganathan R, Morais VA, Verstreken P.
VIB Center for the Biology of Disease, Leuven, Belgium.
Human UBIAD1 localizes to mitochondria and converts vitamin K(1) to vitamin K(2). Vitamin K(2) is best known as a cofactor in blood coagulation, but in bacteria it is a membrane-bound electron carrier. Whether vitamin K(2) exerts a similar carrier function in eukaryotic cells is unknown. We identified Drosophila UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson's disease that affects mitochondrial function. We found that vitamin K(2) was necessary and sufficient to transfer electrons in Drosophila mitochondria. Heix mutants showed severe mitochondrial defects that were rescued by vitamin K(2), and, similar to ubiquinone, vitamin K(2) transferred electrons in Drosophila mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K(2) that serves as a mitochondrial electron carrier, helping to maintain normal ATP production.
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