I also have high levels of legionella in the water. Is this a thing for CFS/ME or just a coincidence?
It's a pity we barely have any data on the CSF. This is where we would have to look for viral residues and parasites.
Why has nothing happened to the trypanosomes theory since then? Or has it? Even a single confirmation in the CSF of any kind of trypanosome would be progress. Is it possibly another parasite and the sequencing results are just confounded by the CFS/ME pathology, which is similar to the sleeping sickness pathology?
None of the effective treatment options for sleeping sickness seem to be a possibility in the western world. Fexinidazole is available in the Democratic Republic of the Congo. Although it was
approved by the EMA, it's only applicable to countries outside the EU. What a hybris... this reminds me of Ivermectin. It's ok when poor countries take it for decades, but as soon as Europeans are supposed to take it, we'll discredit its safety profile. Next, Suramin seems to be effective in the blood, but not in the CSF, and it's also toxic. It would be helpful to understand Suramin's mechanism of action.
One theory is that it's just the G6PD inhibition that helps (
10.1111/j.1432-1033.1996.0592h.x). In this case, fava beans could have therapeutic effects. But it's unclear if it can cross the BBB and it's very harmful for people with G6PD deficiency.
The disruption of glycolysis is also a speculated mechanism of action because trypanosomes depend on high amounts of glucose. Consistently, hypoglycemia has shown a mild therapeutic effect (
10.3390/tropicalmed5010014). The insulin analog synthalin showed promising efficacy. The keto diet could help reduce the elevated glycolytic activity in CFS/ME patients and the energy supply of the parasite all along, but not eliminate the problem. The brain still relies on certain amounts of glucose for its function. But after a long period of keto diet, when the brain adapted to BHB as a fuel source, hypoglycemia might not be as harmful anymore.
Suramin also inhibits thymidine kinase, which is a target for many herpes virostatics (
diva2:1071945). Adenosine kinase would be the other target identified by the same researcher. Within this model, he found
Smyrnium olusatrum (aka Alexanders) and its active compound isofuranodiene to show efficacy. But it's unclear to me how much of the fruits or plants you would have to eat to reach the IC50. I don't think it can cross the BBB anyway. A microfluidic encapsulation could circumvent this.
Suramin also interacts with P2X7, a driver of autism and Alzheimer's disease. Kudzu and its active compound puarine also downregulate P2X7 and its pain induction (
10.1016/j.burns.2012.08.013). But I don't think that P2X7 is part of trypanosome pathology. It's probably just a coincidence because Suramin interacts with many enzymes. It's still worth a shot though.
What about natural sources of Suramin? Suramin is a colorless version of
Trypan Blue. This is synthesized from
Toluidine. This is found in pine oil, where it has been originally found. However, it's unlikely that pine oil contains sufficient amounts of it. Trypan Blue probably is as toxic or even more toxic than Suramin. This is why Suramin normally is given as a slow infusion. Either way, it can not cross the BBB.
I already mentioned Ivermectin (pmid:
23135008), but it won't work against the chronic type in the CNS due to its limited BBB permeability.
Another option might be Quercetin (
10.1128/AAC.48.3.924-929.2004;
10.1016/j.exppara.2010.10.011;
10.1021/acsomega.0c01818). It has a good safety profile and could be taken long-term. It can cross the BBB (
10.1155/2016/2986796), though liposomal delivery could even improve this further.
Another idea is the support of the immune innate system that the trypanosomes evade. But I leave this for another time.
