Transcript · English → Indonesian
Exploring Drug Repurposing in Cancer Treatment
Begitu pasien berada dalam kondisi ketosis nutrisi ini, hal itu
membuka serangkaian, rangkaian obat baru yang mungkin
sudah, eh, dibuang, tak berhasil. Itulah seluruh bidang
pemanfaatan ulang
obat sekarang.
Mm.
Namun, begitu tubuh berada dalam kondisi fisiologis baru ini, hal-hal yang
dikira tidak efektif menjadi sangat efektif.
Jadi sekali lagi, itu bidang baru yang akan terbuka, eh, seiring
hasilnya begitu informasi ini makin tersebar luas.
Dan Anda juga menyebutkan, um, albendazol dalam ceramah Anda.
Apakah itu juga punya, a, a, aspek penghambat glutamin?
Ya, itu ada di makalah kami juga. Itu hal menarik lainnya.
Obat parasit. Saya tidak tahu soal ivermektin karena
ada banyak
muatan politis mengenainya. Jadi saya tidak— Saya bilang ke lab,
"Kami takkan melakukannya," karena kami tidak mau dapat, dapat,
eh, kena amukan seseorang. Tapi, tetapi albendazol,
fenbendazol,
um, aku berkata, "Kenapa sih... Kenapa..." Orang meminumnya dan mereka,
dan kau mendengar
orang berkata, "Yah, aku sembuh dari kankerku dengan ini
dan itu." Jadi aku, aku,
Aku mendalaminya dan berkata, "Kenapa, kenapa obat parasit bekerja
melawan sel kanker?"
Dan ternyata parasit memakai fosforilasi
tingkat substrat mitokondria di dalam jaringan.
Dan, dan albendazol, fenbendazol ini membunuh
parasit-parasit ini.
Jadi kucoba pada sel kanker, dan benar saja, obat itu
menargetkan substrat mitokondria dan glikolisis.
Mm.
Jadi kini kita tahu mekanismenya kenapa obat parasit bisa bekerja.
Tapi kanker bukanlah parasit.
Mm.
Semua orang ini bilang kanker itu parasit. Itu bukan parasit.
Parasit dan tumor memakai jalur metabolisme yang sama, dan obat yang
bekerja melawan parasit bisa sangat efektif melawan kanker,
dan itulah yang
mulai kita lihat, terutama dalam ketosis nutrisi.
Ya.
Benar, 'kan? Bisakah kamu bayangkan ini?
Ya. Ya, itu— Oh, maaf, lanjutkan.
Hm, jadi ivermectin sebenarnya bekerja pada jalur
kematian sel
mitokondria, jalur Bcl-2/Bax, Bad.
Jadi itu sebenarnya membantu mendorong jalur kematian sel.
End of transcript · 297 words · machine translated
Original transcript (English)
Once you put the patient in this state of nutritional ketosis, it opens up a whole array, a new array of drugs that may have been, uh, thrown out, not worked. That's called the whole field of repurposing drugs now.
Mm. But once the body is in this new physiological state, things that were thought to be ineffective become super effective. So again, that's a whole new field that will open, uh, as the results once this information gets out more.
And you mentioned, um, albendazole in your talk as well. Does that have a, a, a glutamine blocking aspect to it as well? Yes, that's in our paper also. That's another interesting thing. Parasite medications. I don't know about ivermectin because there was a lot
of political stuff about that. So I didn't-- I said to the, the lab, "We're not gonna do that," because we didn't wanna get, get, uh, get the wrath from somebody. But, but albendazole, fenbendazole, um, I said, "Why the hell... Why..." People have taken that and they,
and you hear people say, "Well, I got my rid of my cancer with this and that." So I, I, I did a dive on it and I said, "Why, why parasite medications work against cancer cells?"
And it turns out that the parasites use mitochondrial substrate-level phosphorylation in the tissue. And the, and these albendazole, fenbendazole kill these parasites. So I tried it on the cancer cell, and sure, sure as hell, they, it, it
targets the mitochondrial substrate and glycolysis. Mm. So we have a mechanism now why parasite medications are working. But cancer is not a parasite. Mm.
All these people say cancer is a parasite. It's not a parasite. Parasites and tumors use a common metabolic pathway, and a drug that works against parasites can be very effective against cancer, and that's what we begin to see, especially under nutritional ketosis.
Yeah. Right? Can you imagine this? Yeah. Yeah, that-- Oh, sorry, go on. Um, so ivermectin, it actually works on the mitochondrial cell death
pathway, the Bcl-2/Bax, Bad pathway. So it actually helps push the cell death pathway.
