Sodium dependent transport in very common with the sodium-dependent multivitamin transporter only one example. Sodium is also required for the transport of vitamin C by sodium-dependent vitamin C transporter 1 and sodium dependent vitamin C transporter 2 .
Why would sodium-dependent transport in the gut be especially prone to dysregulation? Sodium-dependent transport is regulated transport. When the gut epigenome goes awry regulated transport can become dysregulated and a large part of regulated transport in the gut is sodium-dependent. With regulated transport there is an opening for DNA hypermethylation to have a large effect. Transport by passive diffusion may not be so susceptible to dysregulation when the gut epigenome goes awry.
The first order of business would be to re-regulate the gut epigenome. TET enzymes and JmjC domain proteins are vitamin C and iron dependent enzymes. Both iron and vitamin C would be required to re-regulate TET enzymes and JmjC domain proteins in the gut.
Vitamin C and iron, however, cannot be taken at the same time. Vitamin C complexes with iron which would make iron unavailable in the gut even though iron absorption can be increased by vitamin C. Iron from iron carbonyl would be taken at bedtime five or so hours after the last vitamin C dosage of the day. Vitamin C can also interfere with copper absorption so copper from copper gluconate would also be taken at bedtime. Only trace minerals that are available in the gut can be supplemented. There are some excellent chelated minerals on the market all of which must be avoided.
One of the difficulties in any epigenetic approach to illnesses is to select which hypermethylated genes are the relevant hypermethylated genes. In a range of illnesses there could be excess DNA hypermethylation of genes associated with sodium dependent transport. Given this is the case this would clearly be relevant to the etiology such illnesses..