For serum levels of iron, there is also the concern about free iron, such as is added to cereal, being worse than iron that is naturally occurring. But I've understood it to be hemosiderin iron that is the culprit in CCSVI, following the leakage of red blood cells across the blood-brain barrier.
A benefit from bloodletting in CCSVI could also be due to the retirement of older blood cells that are banged up, and the production of new blood cells that might function better in conditions of turbulent flow and/or stasis.
Polymorphisms in the genes coding for iron binding and transporting proteins, in the presence of local iron overload, might be responsible for suboptimal iron handling. This might account for the significant variability peculiar to MS phenotypes, particularly affecting MS risk and progression paving the way for personalized pharmacogenetic applications in the clinical practice.
Genetically some of us are better and some of us are worse at iron binding and transporting iron out of our brains. The local iron overload is in the brain as a result of hemosiderin leakage (CCSVI theory) or neuron degeneration (MS theory) but both theories agree that there is iron overload in the brain. Because people with progressive disease are genetically worse at removing iron from their brains, it might be that this ability is among the determinants of whether we have a relapsing-remitting course or a progressive course. This is a very fundamental difference and, if we are RR, we want to stay RR as long as possible and not go SP; and maybe there are strategies such as blood-letting or iron chelation by taking green tea supplements or the deferoxamine as used in thalessemia.
The difference is to stop looking at iron accumulation in the brain as a side-effect of neurodegeneration (MS theory), and start looking at it as a contributor to damage. And if CCSVI is contributing to the iron accumulation, then getting CCSVI venoplasty is a great start.