Freddd
Senior Member
- Messages
- 5,184
- Location
- Salt Lake City
People without any symptoms and who have no startup of methylation or anything else with the Deadlock Quartet find 800mcg of L-methylfolate quite sufficient and no need for any additional potassium by symptoms (none applicable). For me, I had hindered healing and cell formation my whole life. For me, it’s like all the tissues built during these years have to be rebuilt.
I have no idea if that is the case but that could account for that high potassium, getting rid of faulty cells built with workaround methods and replacing them with healthy cells. After I develop all those lesions in the first days of folate deficiency (however arrived at) when my folate levels return to full functionality the lesions have healthy tissue grow under them and they slough off. What happens with the equally rapidly induced IBS with the induced folate deficiencies (also injected quantites of broken down by light MeCbl (HyCbl and AquaCbl equilibrium in some percentage). Does that too from lesions that are then sloughed off by new tissues built underneath?. That happens to my angular cheilitis as well. When it starts it is like fissures opening up. When it heals it heals from underneath and sloughs off the whole damaged layer.
A current research question revolves around why so many people don’t develop IF or parietal cell antibodies until AFTER PA starts up. That of course is opposite the way that had been assumed for decades. It appears to me that autoimmune problems get triggered in the more severe methyl trap or maybe methyl trap with faulty mitochondria, not in partial methylation block. This is an unknown area so who knows.
The recent discovery of quad helix DNA in cancer cells points right at that MeCbl-l-methylfolate DNA replication point. Something goes wrong and bam! So where in the system breakdown does this happen?
I have no idea if that is the case but that could account for that high potassium, getting rid of faulty cells built with workaround methods and replacing them with healthy cells. After I develop all those lesions in the first days of folate deficiency (however arrived at) when my folate levels return to full functionality the lesions have healthy tissue grow under them and they slough off. What happens with the equally rapidly induced IBS with the induced folate deficiencies (also injected quantites of broken down by light MeCbl (HyCbl and AquaCbl equilibrium in some percentage). Does that too from lesions that are then sloughed off by new tissues built underneath?. That happens to my angular cheilitis as well. When it starts it is like fissures opening up. When it heals it heals from underneath and sloughs off the whole damaged layer.
A current research question revolves around why so many people don’t develop IF or parietal cell antibodies until AFTER PA starts up. That of course is opposite the way that had been assumed for decades. It appears to me that autoimmune problems get triggered in the more severe methyl trap or maybe methyl trap with faulty mitochondria, not in partial methylation block. This is an unknown area so who knows.
The recent discovery of quad helix DNA in cancer cells points right at that MeCbl-l-methylfolate DNA replication point. Something goes wrong and bam! So where in the system breakdown does this happen?