alex3619
Senior Member
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- Logan, Queensland, Australia
Ok, my protocol at the time of the conference was this:
During this general time frame I was also using a range of other factors, including B1 and B3, chromium picolinate, a range of antixoxidants including C, E and (I think) lipoic, pycnogenol (the original), and a bunch of other stuff (edit: including CoQ10). What I discussed in the paper was an attempt to minimize my protocol, rather than the full protocol I had found by experiment. I will have to sort through my notes.
The chief side effect was severe and intractable daily headaches. Nothing touched them. What use is more energy if you cannot get out of bed with an intense headache? Fatigue was also not improved by my protocol. Fatigue and energy are only weakly correlated in my view. You can fix one without the other being fixed. Our fatigue and lack of energy are not the same.
I was also taking folic acid not methyl folate. The whole methyl folate issue was not even on my radar then.
I will be very busy today so might not have much time available till mid week to do more.
The theoretically sufficient hypercitricemia daily protocol is currently:
4-8g alanine (depending on body mass) in two doses twelve hours apart.
2-4 g glycine (depending on body mass) in two doses twelve hours apart.
High dose vitamin B complex (optimal dosage not yet determined).
Magnesium and Potassium Phosphates (optimal dosage not yet determined).
Magnesium (chelated - optimal dosage not yet determined).
The alanine is to inhibit PK. It should not be taken close to bedtime. The dose
should start off small and be pyramided in 2-4g increments every 3-4 days.
The more severely affected the patient is, the smaller the increments should
be. This is because the initial effect of the alanine is to induce an
increase in hemolysis. This effect should be neutralized once citric acid
levels decline.
The glycine is a nutritional supplement but also to assist cell membrane
survival under low ATP conditions. The B complex is a general supplement and
includes many cofactors for the affected pathways. It may be preferable to
change this to a high dose multi-vitamin and mineral supplement, but so far
this has not proved necessary. The phosphates are to boost PFK and
G3PD activity, as well as slow the degeneration of 2,3 BPG. Magnesium is
included as a cofactor for PFK as well as a nutritional supplement to help
restore magnesium levels. Potassium is primarily included as a supplement to
help restore potassium levels. It may be necessary to include vitamin D3 if
there is any evidence of phosphate diabetes.
Individual nutritional requirements may necessitate the use of other
supplements. Otherwise, other supplements seem to be optional, at least
theoretically. However, personal experience using alanine shows that it has
minimal or no effect unless other factors are present and most of these have
already been mentioned. Other cofactors are still under investigation.
The treatment is expected to produce significant initial results, but will
have to be maintained to continue producing these results. It is hoped that
eventually this treatment might lead to a permanent correction of the problem,
but it might not. The concern is that although 2,3 BPG levels can be boosted,
restoring tissue oxygen supplies, many non-erythrocytic tissues will have
elevated PFK. This means that these tissues will continually overproduce citric
acid to block the PFK. Some of this will still flow over to block PFK in
erythrocytes. Over time this problem might be self-correcting, as improved
oxygen supply should reduce the rate of PFK synthesis. However, it is also
possible that permanent changes in PFK levels may result in a permanent
tendency to hypercitricemia.
During this general time frame I was also using a range of other factors, including B1 and B3, chromium picolinate, a range of antixoxidants including C, E and (I think) lipoic, pycnogenol (the original), and a bunch of other stuff (edit: including CoQ10). What I discussed in the paper was an attempt to minimize my protocol, rather than the full protocol I had found by experiment. I will have to sort through my notes.
The chief side effect was severe and intractable daily headaches. Nothing touched them. What use is more energy if you cannot get out of bed with an intense headache? Fatigue was also not improved by my protocol. Fatigue and energy are only weakly correlated in my view. You can fix one without the other being fixed. Our fatigue and lack of energy are not the same.
I was also taking folic acid not methyl folate. The whole methyl folate issue was not even on my radar then.
I will be very busy today so might not have much time available till mid week to do more.
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