picante
Senior Member
- Messages
- 829
- Location
- Helena, MT USA
Happy New Year to everybody! I'm looking for people who understand Naviaux et al's analysis of sphingolipid problems, and I want to know if anyone else has noticed this connection:
I've just gotten my OAT results from Great Plains, showing a high level of tricarballylic acid (the 9th metabolite on the list). The explanation says that this could be from fumonisins, a group of mycotoxins found in corn. (Well, sigh! I avoid anything corn-based like the plague because these foods & vitamins make my guts miserable.)
But this is the part that got my attention:
Next I found this: https://en.wikipedia.org/wiki/Fumonisin_B1#Toxicodynamics
So that brings us to Naviaux et al's observation that their ME/CFS study group has impaired sphingolipid metabolism.
Are some of us suffering from fumonisin toxicity? Or could our tricarballylic acid be high for some other reason, having to do with Naviaux's sphingolipid analysis?
Do Naviaux et al even mention tricarballylic acid in their paper? Is it something they measured?
I've just gotten my OAT results from Great Plains, showing a high level of tricarballylic acid (the 9th metabolite on the list). The explanation says that this could be from fumonisins, a group of mycotoxins found in corn. (Well, sigh! I avoid anything corn-based like the plague because these foods & vitamins make my guts miserable.)
But this is the part that got my attention:
Tricarballylic acid is an inhibitor of the enzyme aconitase and therefore interferes with the Krebs cycle. The main symptoms of aconitase deficiency are myopathy and exercise intolerance. [Me! Me!]
Next I found this: https://en.wikipedia.org/wiki/Fumonisin_B1#Toxicodynamics
Because of their similarity, fumonisins are able to inhibit sphingosine-sphinganin-transferases and ceramide synthases and are therefore competitive inhibitors of sphingolipid biosynthesis and metabolism.
So that brings us to Naviaux et al's observation that their ME/CFS study group has impaired sphingolipid metabolism.
Are some of us suffering from fumonisin toxicity? Or could our tricarballylic acid be high for some other reason, having to do with Naviaux's sphingolipid analysis?
Do Naviaux et al even mention tricarballylic acid in their paper? Is it something they measured?