soulfeast
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oh this may be how FA/PGA form competes with the other forms as per yasko.
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Another warning about high folic acid intake by Dr. Victor Herbert
Folate absorption occurs primarily in the upper half of the small intestine. Megaloblastic anemia from folic acid deficiency responds readily to daily oral folate doses as low as 100 to 200 μg of PGA (pteroylglutamic acid). In general, however, 400 μg to 1000μg (1mg) is administered and is usually sufficient to correct deficiency, even in malabsorption states. My general approach is to give 1 mg daily for the first week, except in situations of severe malabsorption, when I administer 2 to 5 mg daily for the first week. I ensure that cobalamin deficiency is not coexistent and may initially co-administer 100 μg of cobalamin. After the first week, I treat with 100 μg orally daily. Full replenishment of folate stores can be achieved within several weeks of oral therapy. Maintenance should be with 400μg folic acid orally daily. If the underlying cause can be reversed, maintenance therapy can be stopped.
Adverse effects can occur from folate treatment with 1 or more mg of PGA daily. This is because at such doses substantial amounts of PGA, which is an oxidized, shelf-stable and thus preferred pharmaceutical form of folic acid, are absorbed by diffusion without being first reduced as is desirable by alimentary tract enzymes to human-cell-usable tetrahydrofolic acid. This absorbed unreduced PGA then blocks cell uptake of tetrahydrofolate, and can actually produce folate deficiency, as Prof. John Scotts group at Trinity Medical College in Dublin, Ireland showed in a large and excellent study of fertile Irish females. Also, giving folic acid to cobalamin-deficient patients will conceal the hematologic abnormalities of the B12 deficiency while allowing subacute combined degeneration of the spinal cord to proceed untreated to irreversibility. One must therefore always look for coexistent vitamin B12 deficiency in all patients for whom folate therapy is proposed.
:worried: This is what concerns me about Dr. V's protocol: I get benefits in terms of calming, but I don't want to get even more folate deficient!
So low RBC FA could be caused by low FA which causes or helps cause lw methionine which causes low homocysteine which FA needs to stay in the cell.
If this is the case, and I am reading this right, then wouldnt it be helpful to also supplement with methionine?
Yes, I know Dr. V gives some people methionine supps. But I'd be careful about taking it if you're not sure. After amino acid i.v. (19) my methionine (plasma) was quite high and I felt lousy. Methionine is abundant in red meat.
This protocol differs from Yasko in that he is not trying to compensate for genetic polymorphisms. The idea of the 5:2 is mostly to balance the ANS. You are getting much more B12 and FA than you supposedly need if everything is working -- which it isn't, we all know that too well. Apparently, for some reason, even if we have enough of this stuff in our diets, we are not using it properly. One reason could be that stress messes up the system (duh!). It increases oxidative stress such as free radical damage, it uses up glutathione, it shunts the transulfuration pathway, it diverts resources from rebuilding into catabolism. V's theory, as I understand it, is to calm the SNS & increase PNS activity in order to be able to get the other stuff to work properly.I am also wondering about folks who are MTR ++ (like me). I think this means I guzzle up B12 too fast. Would I need a higher ratio of B12 to FA than the 5:2 calls for? ?
His book on Energy - The Essence Of Environmental Health is all about expanding the capacity of the ANS to handle stressors, whether environmental toxins or exercise or emotions, and most of it focuses on how to reduce stressors so that the body can balance itself. (BTW, I'm not recommending the book: I'm actually finding it boring and can't seem to finish it).
Even though I'm concerned about long term impacts of high FA (PGA) as a potential cause of hypo-methylation, in the short term, I need to calm down my system.
Since FA (PGA) is water soluble, it won't hang around forever. The next thing to research though is how long does it hang around? And is there anything that binds it if we want to clear it out?
Yes, I know Dr. V gives some people methionine supps. But I'd be careful about taking it if you're not sure. After amino acid i.v. (19) my methionine (plasma) was quite high and I felt lousy. Methionine is abundant in red meat.
This protocol differs from Yasko in that he is not trying to compensate for genetic polymorphisms. The idea of the 5:2 is mostly to balance the ANS. You are getting much more B12 and FA than you supposedly need if everything is working -- which it isn't, we all know that too well. Apparently, for some reason, even if we have enough of this stuff in our diets, we are not using it properly. One reason could be that stress messes up the system (duh!). It increases oxidative stress such as free radical damage, it uses up glutathione, it shunts the transulfuration pathway, it diverts resources from rebuilding into catabolism. V's theory, as I understand it, is to calm the SNS & increase PNS activity in order to be able to get the other stuff to work properly.
His book on Energy - The Essence Of Environmental Health is all about expanding the capacity of the ANS to handle stressors, whether environmental toxins or exercise or emotions, and most of it focuses on how to reduce stressors so that the body can balance itself. (BTW, I'm not recommending the book: I'm actually finding it boring and can't seem to finish it).
Even though I'm concerned about long term impacts of high FA (PGA) as a potential cause of hypo-methylation, in the short term, I need to calm down my system.
Since FA (PGA) is water soluble, it won't hang around forever. The next thing to research though is how long does it hang around? And is there anything that binds it if we want to clear it out?
On another track here.. is creatine a sign soley of methylation or can it be created in other ways? Can you create the products of methylation without methylation?
6.5 Elimination by route of exposure
Oral
Following oral administration of single 0.1 to 0.2 mg doses
of folic acid in health adults, only a trace amount of the
drug appears in urine . Following administration of large
doses, the renal tubular reabsorption maximum is exceeded and
excess folate is excreted unchanged in urine. Small amounts
of orally administered folic acid have been recovered from
faeces. About 0.05 mg/day of normal body folate stores is
lost by a combination of urinary and faecal excretion and
oxidative cleavage of the molecule.
10.1 General principles
In case of massive ingestion gastric lavage or induced
vomiting could be considered if seen within 1 to 2 hours
after ingestion. Activated charcoal should be given
repeatedly in view of the enterohepatic circulation of
folic acid.
10.5 Elimination
Adequate hydration would be sufficient to eliminate the
drug through the kidneys.
My low creatinine levels showed I was not methylating well, and I am guessing that folate was functionally insufficient. This became evident when added 5 mg methyl B12 daily for awhile and ending up with very high methionine, high glycine, high sarcosine, and a miserable liver.When nutrients are diverted for scavenging or are inactivated alone or in combination, methylation will become inadequate under stress. If hydroxocobalamin is insufficient or dysfunctional, then methylation cannot proceed. When GSH is insufficient or dysfunctional, hydroxocobalamin is dysfunctional. In either instance, folate becomes functionally insufficient, even when levels are elevated, because it is saturated with methyl groups and aldehydes. This condition is called the folate trap.
Creatine V puts this last among methylation priorities because once the methyl group is used to make creatine it cannot be recycled.
I am guessing that the reason I continued to have high serum folic acid on Rich's S. Five protocol, was due to this explanation in V's patent:
My low creatinine levels showed I was not methylating well, and I am guessing that folate was functionally insufficient. This became evident when added 5 mg methyl B12 daily for awhile and ending up with very high methionine, high glycine, high sarcosine, and a miserable liver.
Maybe this is why we are all stressed out!
Climacteric. 2008 Oct;11(5):397-403.
Norepinephrine activity, as measured by MHPG, is associated with menopausal hot flushes.
Dormire SL, Bongiovanni R.
The University of Texas at Austin, School of Nursing, Austin, Texas 78664-1499, USA.
Abstract
OBJECTIVES: Baseline norepinephrine levels, as measured by a metabolite (plasma 3-methoxy-4-hydroxyphenolglycol, MHPG), have been reported to increase in women who experience hot flushes. However, norepinephrine is also discharged in a counter-regulatory attempt to increase brain glucose as normal daily variations occur. .... [rest of abstract deleted]
PMID: 18781484
Here's my argument. Let me know what you think?
Once we get low brain glucose, experienced as fatigue and brain fog, our body compensates by increasing norepinephrine to raise brain glucose, leading our heart to start pounding and our pulse to race. We experience the feeling of stress, and the fatigue that inevitably comes after it. Increase NE leads to increased oxidative stress. Extra demands are put on methylation to break down the norepinephrine and to handle the damage from increased stress hormones. In the end, we become deficient in folates, B12, cortisol and DHEA, and glutathione.
Could one become MORE b12 and MORE FA "deficient" in the process of the scavenging? Asking for a reason. I was using for a week or so and started having irritability (FA deficiency sign) and more creepies (possible methyl B12 deficiency sign.. which has been helped by adding methyl b12).
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