Lotus97
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I thought for the people who can't process folinic acid the folinic acid builds up and blocks methylfolate. The reason I was asking about people who could normally process it was because I thought maybe since the dose of folinic acid was so high that even they wouldn't be able to process it quickly enough. Also, I thought you said something about folinic acid staying in the system a long time and you considered even 800 mcg kind of high. I don't have time to reread this thread right now (but I do intend to) so I'm sorry if I'm misstating what you said.Why do you think folinic acid blocks methylfolate? In 81% at least it appeared to not. If all goes well folinic acid is buffered and converted to methylfolate. Folinic acid is not only for nucletoides. It is storage form in the cell for folatea. Would expect much of it goes to methylfolate IF all is working well and no MTHFS defect. The really high dose are for cns penetration and saturation. Just like the r eally high doses if methylfolate used by some in these forums.
I've heard people talking about CNS before in the methylation forums, but I don't know what they mean (other than it being short for central nervous system). Actually, you and Adreno were talking about that in relation to neurotransmitters recently in that other thread. Do I remember correctly? I read through so much information in such a short amount of time it's hard for me to remember everything. Is that what people are referring to when they say "neurological healing"? I don't know what that means specifically. That's something independent of methylation I assume? I guess Leucovorin can be used sort of like Deplin as a treatment for depression.
http://link.springer.com/article/10.1023/A:1015271927517
Low folate is associated with poorer response to selective serotonin reuptake inhibitors (SSRIs) in majordepressive disorder (MDD). Folate supplementation in MDD has been studied in other settings with promising results. The objective of this study was to assess the efficacy of methylfolate as an adjunctive treatment among adults with MDD and inadequate response to an SSRI. Twenty-two adults (59% female; mean age 45.2 ± 11.0 years) with DSM-IV MDD, partial or nonresponse to an SSRI after at least 4 weeks of treatment, and a 17-item Hamilton Depression Rating Scale (HAM-D-17) score ≥ 12 were enrolled in this 8-week prospective open trial. Exclusion criteria included current use of anticonvulsants or psychotropics other than an SSRI, or B12 deficiency. Leucovorin (folinic acid), which is metabolized to methylfolate, was added to SSRIs at 15–30 mg/day. Folate levels rose from 28 ± 19 ng/mL to 301 ± 203 ng/mL (p < 0.001). HAM-D-17 scores among the 16 completers decreased from 19.1 ± 3.9 to 12.8 ± 7.0 (p < 0.01). However only 31% of completers and 27% of the intent-to-treat (ITT) sample achieved response (≥50% reduction in HAM-D-17 scores), and only 19% of completers and 18% of the ITT sample achieved remission (HAM-D-17 ≤ 7). Leucovorin appears to be modestly effective as an adjunct among SSRI-refractory depressed individuals with normal folate levels. The application of leucovorin as an adjunct in the setting of refractory depression deserves further study.