My response, written in about half an hour, from the top of my head:
You aren’t accounting for the ability of fungi to travel. Fungi like candida albicans can extend hyphae to extend spatially into surrounding tissues. This is why, for example, fungal arthritis is a thing, they can move over time in the body and into different areas post-invasion, so it’s not just exposed areas that are expected to be affected. Cryptococcus neoformans can use the “seed cell” morphotype to go smaller to a few microns in size, so they can get into tighter spots over time. Also, c. neoformans can travel in white blood cells. Look up the “trojan horse” mechanism, unfortunately this is a real thing.
This is using diagnosis and age metrics so survivorship bias is possible. We don’t count the people who didn’t make it to the older cohorts. For an infection where disease progression is slower, time is indeed a factor, so it’s expected the cancers would be different.
Looks like you’re restating the conclusion here. But p53 is involved in the genetic repair response that fungi like candida albicans can trigger via mycotoxin damage, for example. If you elaborate further I can try to understand your point.
Immunosuppressed individuals are likely already on immunomodular regimes, which might include anti-fungal and other things to address the fungi that are responsible for the common cancers. The fact that immunosuppressed get super weird cancers is still aligned with the large variety of fungal pathogens. The fungi world has exotica too, we actually don’t even know the full spectrum of fungal species on earth (there are too many variants). The consistency in cancer hallmarks, as well as the variations, is equally matched by the consistency of fungi, as well as fungi variations.
I don’t know enough (yet) to respond.
Canadian oncologist Dr. William Makis uses a protocol with ivermectin, fenbendazole and mebendazole with testimonials posted publicly. By categorical definition, -azole class drugs are anti-fungal. Not everyone can plan, fund and execute trials, so this shouldn’t be used against the fungal theory. For what it’s worth Dr. Makis has participated in trials. To your other point about mass treatments of anti-fungals and an expected miraculous curing of hundreds of thousands of patients by now: Fungal infections may be localized in different areas of the body. Fluid dynamics, physics and bioavailability are some reasons why the drugs may not reach 100% coverage in the body. I know this because my ACL rupture from a sports injury needed surgery to heal, as blood circulation didn’t reach the ACL directly. Some drugs may not be able to cross barriers where the fungi can.
Looks like an appeal to the crowd and doesn’t address the fungal theory directly. Aside from that, scientific consensus can be wrong with many historical examples available.
I think the fungal theory is very likely something that oncology has missed.
My response, written in about half an hour, from the top of my head:
You aren’t accounting for the ability of fungi to travel. Fungi like candida albicans can extend hyphae to extend spatially into surrounding tissues. This is why, for example, fungal arthritis is a thing, they can move over time in the body and into different areas post-invasion, so it’s not just exposed areas that are expected to be affected. Cryptococcus neoformans can use the “seed cell” morphotype to go smaller to a few microns in size, so they can get into tighter spots over time. Also, c. neoformans can travel in white blood cells. Look up the “trojan horse” mechanism, unfortunately this is a real thing.
This is using diagnosis and age metrics so survivorship bias is possible. We don’t count the people who didn’t make it to the older cohorts. For an infection where disease progression is slower, time is indeed a factor, so it’s expected the cancers would be different.
Looks like you’re restating the conclusion here. But p53 is involved in the genetic repair response that fungi like candida albicans can trigger via mycotoxin damage, for example. If you elaborate further I can try to understand your point.
Immunosuppressed individuals are likely already on immunomodular regimes, which might include anti-fungal and other things to address the fungi that are responsible for the common cancers. The fact that immunosuppressed get super weird cancers is still aligned with the large variety of fungal pathogens. The fungi world has exotica too, we actually don’t even know the full spectrum of fungal species on earth (there are too many variants). The consistency in cancer hallmarks, as well as the variations, is equally matched by the consistency of fungi, as well as fungi variations.
I don’t know enough (yet) to respond.
Canadian oncologist Dr. William Makis uses a protocol with ivermectin, fenbendazole and mebendazole with testimonials posted publicly. By categorical definition, -azole class drugs are anti-fungal. Not everyone can plan, fund and execute trials, so this shouldn’t be used against the fungal theory. For what it’s worth Dr. Makis has participated in trials. To your other point about mass treatments of anti-fungals and an expected miraculous curing of hundreds of thousands of patients by now: Fungal infections may be localized in different areas of the body. Fluid dynamics, physics and bioavailability are some reasons why the drugs may not reach 100% coverage in the body. I know this because my ACL rupture from a sports injury needed surgery to heal, as blood circulation didn’t reach the ACL directly. Some drugs may not be able to cross barriers where the fungi can.
Looks like an appeal to the crowd and doesn’t address the fungal theory directly. Aside from that, scientific consensus can be wrong with many historical examples available.
I think the fungal theory is very likely something that oncology has missed.