B-12 - The Hidden Story

[Lou]

quote by Freddd: "I'm trying to figure out how to make preventing and healing of all these diseases routine, not defending the kind of research that got us into this place initially. The same as Rich."

And man, are some of us ever grateful. It seems sometimes our culture has simply gotten away from 'the expericence of things'. We go on vacations and spend half our time taking photos(how bout just enjoy the trip for a change?), we watch T.V. to replace untold number of possible experiences, and much of religion has replaced the experience of God with faith in God. Okay, I'm getting a little off track.

But about the grateful part, it's just amazing to me what the two of you do here trying to help us. I count myself as terribly lucky the day I found PR. Even luckier the two of you found it.

 

[richvank]

Hi Rich,

So this will take the folic acid right into where to could do the worst damage? So an otherwise possibly beneficial looking innovation could be a catastrophe waiting to happen for 20% or whatever of population unable to utilize folic acid at all? Adb12 doesn't have any problem getting into the cell or mitochondria as is easily demonstrable, entering in 5 minutes after it hits the tissue. And 15-25% absorbtion is no slouch compared to all sorts of things. 1% passive absorbtion is the pits. I'm not sure what problem this is supposed to solve. It only soves a problem compared to cyancbl or hydroxcbl or any form taken orally. Putting folic acid into my brain sounds like a terrible idea. Talk about a Trojen horse, this is it. Putting folic acid in it is a terrible choice. Now I am properly frightened of ever trying this item. Thank you for the information. If it induces severe folate deficiency in susceptable folks can they be sued do you think? Maybe you have never been hit with a slegehammer folate deficiency but I have.

Hi, Freddd.

Maybe there has been a misunderstanding. I don't advocate taking folic acid liposomally. Even for people who don't have an intolerance of folic acid, as you've reported, I don't think it's the best form of folate to take. So I think we agree on that.

The reason I brought up this whole liposomal subject is that I know that you have gone to some great lengths to get coenzyme forms of B12 into the cells, and especially into the brain.
I'm just suggesting that using liposomal methyl B12 and liposomal adenosyl B12 may help in doing that. That's all. I'm not advocating any particular product that is currently on the market. I just thought that you might want to consider this mode of application as a possibility. Maybe it's possible to do it with something that's already on the market, and maybe not.
That's it.

Best regards,

Rich

 

[Freddd]

Hi, Freddd.

Maybe there has been a misunderstanding. I don't advocate taking folic acid liposomally. Even for people who don't have an intolerance of folic acid, as you've reported, I don't think it's the best form of folate to take. So I think we agree on that.

The reason I brought up this whole liposomal subject is that I know that you have gone to some great lengths to get coenzyme forms of B12 into the cells, and especially into the brain.
I'm just suggesting that using liposomal methyl B12 and liposomal adenosyl B12 may help in doing that. That's all. I'm not advocating any particular product that is currently on the market. I just thought that you might want to consider this mode of application as a possibility. Maybe it's possible to do it with something that's already on the market, and maybe not.
That's it.

Best regards,

Rich

HI Rich,

I appologize for the misunderstanding. I didn't think that you were suggesting such. I see all sorts of supplements, and for that matter medications, for which the only excuse is "marketing". I'm sort of shocked that somebody would include folic acid in this kind of invasive package. I think perhaps it has a great potential in delivering mb12/adb12 to the brain for healing. On the other hand the well known problem that 20% or so of population can't utilize folic acid at all would kind of be a warning that it's not a good idea to put it in a delivery package that delivers it into the worst possible places.

At this point I don't know what I think.

 

[adreno]

Here are two more studies of liposomal encapsulation of curcumin:

J Agric Food Chem. 2009 Oct 14;57(19):9141-6.
Evaluation of an oral carrier system in rats: bioavailability and antioxidant properties of liposome-encapsulated curcumin.
Takahashi M, Uechi S, Takara K, Asikin Y, Wada K.
Source

United Graduate School of Agricultural Science, Kagoshima University, Kagoshima, Japan.
Abstract

To enhance the curcumin absorption by oral administration, liposome-encapsulated curcumin (LEC) was prepared from commercially available lecithins (SLP-WHITE and SLP-PC70) and examined for its interfacial and biochemical properties. A LEC prepared from 5 wt % of SLP-PC70 and 2.5 wt % of curcumin gave a good dispersibility with 68.0% encapsulation efficiency for curcumin, while those from SLP-WHITE did not. Moreover, the resulting LEC using SLP-PC70 was confirmed to be composed of small unilamellar vesicles with a diameter of approximately 263 nm. The resulting LEC was then examined for its effect on bioavailability in Sprague-Dawley (SD) rats. Three forms of curcumin [curcumin, a mixture of curcumin and SLP-PC70 (lecithin), and LEC] were then administered orally to SD rats at a dose of 100 mg curcumin/kg body weight. The pharmacokinetic parameters following curcumin administration were determined in each form. Pharmacokinetic parameters after oral administration of LEC were compared to those of curcumin and a mixture of curcumin and lecithin. High bioavailability of curcumin was evident in the case of oral LEC; a faster rate and better absorption of curcumin were observed as compared to the other forms. Oral LEC gave higher C(max) and shorter T(max) values, as well as a higher value for the area under the blood concentration-time curve, at all time points. These results indicated that curcumin enhanced the gastrointestinal absorption by liposomes encapsulation. Interestingly, the plasma antioxidant activity following oral LEC was significantly higher than that of the other treatments. In addition, the plasma curcumin concentration was significantly correlated to plasma antioxidant activities, and enhanced curcumin plasma concentrations might exert a stronger influence on food functionality of curcumin. The available information strongly suggests that liposome encapsulation of ingredients such as curcumin may be used as a novel nutrient delivery system.

PMID:
19757811

Cancer Chemother Pharmacol. 2007 Jul;60(2):171-7. Epub 2006 Oct 19.
Comparison of systemic availability of curcumin with that of curcumin formulated with phosphatidylcholine.
Marczylo TH, Verschoyle RD, Cooke DN, Morazzoni P, Steward WP, Gescher AJ.
Source

Cancer Biomarkers and Prevention Group, Department of Cancer Studies and Molecular Medicine, University of Leicester, Robert Kilpatrick Clinical Sciences Building, Leicester Royal Infirmary, Leicester, LE2 7LX, UK. thm3@le.ac.uk
Abstract
PURPOSE:

Curcumin, a major constituent of the spice turmeric, suppresses expression of the enzyme cyclooxygenase 2 (Cox-2) and has cancer chemopreventive properties in rodents. It possesses poor systemic availability. We explored whether formulation with phosphatidylcholine increases the oral bioavailability or affects the metabolite profile of curcumin.
METHODS:

Male Wistar rats received 340 mg/kg of either unformulated curcumin or curcumin formulated with phosphatidylcholine (Meriva) by oral gavage. Rats were killed at 15, 30, 60 and 120 min post administration. Plasma, intestinal mucosa and liver were analysed for the presence of curcumin and metabolites using HPLC with UV detection. Identity of curcumin and metabolites was verified by negative ion electrospray liquid chromatography/tandem mass spectrometry.
RESULTS:

Curcumin, the accompanying curcuminoids desmethoxycurcumin and bisdesmethoxycurcumin, and the metabolites tetrahydrocurcumin, hexahydrocurcumin, curcumin glucuronide and curcumin sulfate were identified in plasma, intestinal mucosa and liver of rats which had received Meriva. Peak plasma levels and area under the plasma concentration time curve (AUC) values for parent curcumin after administration of Meriva were fivefold higher than the equivalent values seen after unformulated curcumin. Similarly, liver levels of curcumin were higher after administration of Meriva as compared to unformulated curcumin. In contrast, curcumin concentrations in the gastrointestinal mucosa after ingestion of Meriva were somewhat lower than those observed after administration of unformulated curcumin. Similar observations were made for curcumin metabolites as for parent compound.
CONCLUSION:

The results suggest that curcumin formulated with phosphatidylcholine furnishes higher systemic levels of parent agent than unformulated curcumin.

PMID:
17051370

I'm aware that it doesn't automatically mean that the same applies to B12, but I do think the idea looks intriging. Here's yet another study showing liposomal curcumin to attenuate seizures in rats; that would heavily suggest that the curcumin gets into the CNS:

http://www.ncbi.nlm.nih.gov/pubmed/22044441

Anyway, is there any reason why a liposomal encapsulation can't be used sublingually? Would the liposomes get absorped through the mucous membrane? Isn't that what the liposomal spray does; that is combine liposomal and sublingual application?

 

[maddietod]

HI Rich,
On the other hand the well known problem that 20% or so of population can't utilize folic acid at all....

Freddd - Is there any published research about this? I spent yesterday researching and didn't come up with anything. I won't get any traction with my family with "Well, this guy in my webgroup says..."

I'm curious about "well known" and "20% or so."

Thanks,

Madie

 

[Freddd]

Freddd - Is there any published research about this? I spent yesterday researching and didn't come up with anything. I won't get any traction with my family with "Well, this guy in my webgroup says..."

I'm curious about "well known" and "20% or so."

Thanks,

Madie

HI Madie,

I've seen it around at various numbers,as low as 15% and as high as 20+%, a narrow range. This comes up in discussing the genetic influenced F.A. utilizaration in research. That is where I've seen it over and over It is totally ignored by those who are trying to prove that folic acid does something. For that one needs to look at the outcomes to see the percentage for who F.A. wasn't effective, but that varies considerably. Next time I come across a reference I'll post it. I've seen it posted by other people a number of times around this board. Rich might know.

If you use google scholar and search for "unconverted folic acid" you will get lots of hits and then look for the ones that give a genetic percentage.


I was getting sicker and sicker for decades and was close to dying when I found the mb12 and started it. My parents, step parents, siblings wouldn't believe a word of it. They were convinced it was all in my head. Trying to convince them I was really sick got no traction. My sister is a pediatricican and is anti vitamin. Trying to convince family members of anything ariund these illnesses can be a frustrating waste of time and effort for many.

 

[Freddd]

Meriva curcumin is oral (capsule) based. You can find it on iHerb.

I am unwilling to carry out your experiment because: 1) I have enough side effects from 5mg mb12 and 3mg adb12 already, and 2) I don't have the biochemical knowledge to evaluate whether such an experiment is valid. Is the color of urine a valid measure of how much nutrient has been delivered into cells? Is it independent of water intake, kidney function, or other variables?

I do know that liposomal encapsulation is a hot thing in pharmacology, and that research has shown it to be superior in delivering drugs/nutrients into cells. This is because, as Rich has explained, the liposomes allow the drug/nutrient to enter through the cell membrane.

My main point is, that I cannot accept your offhand dismissal of the superiority of liposomal delivery over sublingual route, without seeing any data on this. I have just not seen any evidence that sublingual absorption is significantly better than oral, for any drug/nutrient. If anyone knows of such research, I'd like to see it. And even if it is superior to oral, we still need comparisons with liposomal delivery, before we can make any conclusions.

I'm not interested in defending any research, product, or method of delivery. I'm interested in finding out which is the most effective.

Hi Adreno,

Is the color of urine a valid measure of how much nutrient has been delivered into cells? Is it independent of water intake, kidney function, or other variables?

What comes out in the urine clearly isn't delivered to the cells. So, on the very first dose of Metafolin the just notiicable amount visible in urine of mb12 doubled. Each time I go into paradoxical folate deficiency the amount of b12 in the urine goes up a lot, some multiples of a just noticable difference. When I took glutathione with 30mg of mb12 unchanged, the amount of b12 in my urine went up to a level approximating that of 160mg with metafolin. So clearly folic acid, folinic acid, vegetable folate, glutathione and NAC all increase urine output of b12 a lot thereby decreasing the amount available to cells.

If you consider the strartup effects of mb12 and adb12 that you have experienced, that is the evidence it gets into the cells in ample amounts.

It is independent of water intake. The water just makes it more or less dilute, changes the color density, not the hue. Nothing else we normally eat causes such a magenta color in urine. It is the balance between yellow and magenta that remains unchanged as long as the subject takes the same vitamins etc at the same time each day.

Kidney function is a relevant item. Large doses of b12 are used to test the specific functioning of one type of kidney tubile, the only type that excretes b12. If that is not working then a person is in serious trouble. Otherwise it is consistant from day to day at whatever level it works. Each persons color is only compared to that person's urine color under the other conditions.

 

[richvank]

Freddd - Is there any published research about this? I spent yesterday researching and didn't come up with anything. I won't get any traction with my family with "Well, this guy in my webgroup says..."

I'm curious about "well known" and "20% or so."

Thanks,

Madie

Hi, Madie.

Here's an abstract of a paper showing a wide range in the rate of the initial reaction of DHFR, which is necessary for the utilization of folic acid. Only a small number of people were studied, though. You can get the full paper free at PubMed. Since then,there have been some papers about homozygous polymorphisms in DHFR that have very serious consequences. Perhaps heterozygosity for the same polymorphisms would account for slow reaction of folic acid. I haven't had time to study these later papers yet.

Rich

Proc Natl Acad Sci U S A. 2009 Sep 8;106(36):15424-9. Epub 2009 Aug 24.
The extremely slow and variable activity of dihydrofolate reductase in human liver and its implications for high folic acid intake.
Bailey SW, Ayling JE.
Source

Department of Pharmacology, University of South Alabama, 307 North University Boulevard, Mobile, AL 36688, USA.
Abstract

Numerous clinical trials using folic acid for prevention of cardiovascular disease, stroke, cognitive decline, and neural tube defects have been completed or are underway. Yet, all functions of folate are performed by tetrahydrofolate and its one-carbon derivatives. Folic acid is a synthetic oxidized form not significantly found in fresh natural foods; to be used it must be converted to tetrahydrofolate by dihydrofolate reductase (DHFR). Increasing evidence suggests that this process may be slow in humans. Here we show, using a sensitive assay we developed, that the reduction of folic acid by DHFR per gram of human liver (n = 6) obtained from organ donors or directly from surgery is, on average, less than 2% of that in rat liver at physiological pH. Moreover, in contrast to rats, there was almost a 5-fold variation of DHFR activity among the human samples. This limited ability to activate the synthetic vitamer raises issues about clinical trials using high levels of folic acid. The extremely low rate of conversion of folic acid suggests that the benefit of its use in high doses will be limited by saturation of DHFR, especially in individuals possessing lower than average activity. These results are also consistent with the reports of unmetabolized folic acid in plasma and urine.

PMID:
19706381

 

[aquariusgirl]

so sorry.. can't read the entire thread.. is there a commercially available form of lipoceutical b12? or do you have to make it yourself using leicithin?
thanks

 

[Freddd]

so sorry.. can't read the entire thread.. is there a commercially available form of lipoceutical b12? or do you have to make it yourself using leicithin?
thanks

Hi Aquariusgirl,

There was a link back no more than about 10-20 posts. However, it is a adenosylb12 with folic acid which might cause all sorts of problems for those who can't utilize folic acid. As sublingual mb12 and adb12 demonstrably work excellently at getting in the cells by diffusion and there isn't much improvement possible there, the advantage might be to getting into the brain but the folic acid might be dangerous in that way for those in whom folic acid blocks methylfolate. I would be interested in seeing some folks test it but nbot if they have a problem with folic acid.

 

[Nielk]

I wasn't sure where to post this but, I just picked up a copy of my labwork done a couple of weeks ago when I had Vertigo here in Florida.
On the phone, they had told me that everything is normal but these are the results that are out of the norm:

B12 - 1445 (normal 211-911)
Folate Serum - >24 (normal 5.38-17.0)

What does this mean? I have too much B12 in my blood? I thought that's not possible because the body flushes out the extra it doesn't need.

In addition,
Bun/Creatinine ratio - 41.6 (normal 6.0 - 25.0)
Neurophil% - 39.4 (normal 44.0 - 76.0)
Lymphocyte - 50.7 (normal 15.0 - 43.0)

I am hoping that Rich or Fredd or anyone can explain what these mean?

This doctor I went to for the first time. I'm just visiting here in Florida.

 

[Freddd]

en

I wasn't sure where to post this but, I just picked up a copy of my labwork done a couple of weeks ago when I had Vertigo here in Florida.
On the phone, they had told me that everything is normal but these are the results that are out of the norm:

B12 - 1445 (normal 211-911)
Folate Serum - >24 (normal 5.38-17.0)

What does this mean? I have too much B12 in my blood? I thought that's not possible because the body flushes out the extra it doesn't need.

In addition,
Bun/Creatinine ratio - 41.6 (normal 6.0 - 25.0)
Neurophil% - 39.4 (normal 44.0 - 76.0)
Lymphocyte - 50.7 (normal 15.0 - 43.0)

I am hoping that Rich or Fredd or anyone can explain what these mean?

This doctor I went to for the first time. I'm just visiting here in Florida.

Hi Neilk,

As far as the cobalamin goes, it means you have more than average in you blood. However, it is not an amount that means you should be asymptomatic of b12 deficiency symtpms. The average person in the USA with the average blood level also has an average amount of enlarged red cells and maybe 50 or more b12 deficiency symptoms that are considered non-specific and hence meaningless. Most of those symptoms would be ones that cyanocbl and/or hydroxcbl given in the "accepted" ways don't affect so officially they are not b12 deficiency symptoms and they become meaningless mystery disease. If the population were taking 1mg/day of methylb12 sublingually the average would be very different and this board would have a few dozen people with unknown problems. The problem is that certain types of liver disease cause the liver to be unable to remove cobalamin from the blood and accumulate it and so the level in the serum is much higher. Yours is rather low for somebody taking a useful amount of mb12/adb12 that will work to heal these diseases.

As far as the folate levels meaning, it to has it's interpretative roots based on inactive folic acid. Folic acid accumulates unchanged by those of us unable to convert it and hence elevated serum folate at least could resoanbly be expected to be high for somebody with paradoxical folate deficiency because it is not consumed by processes. I'm sure Rich can give you a lot more info.

SOme of the things that are affected by low methylfolate and low active b12 in the blood are MCV, MCH, platelet count, multisegment neutraphils and a few other things.

 

[richvank]

I wasn't sure where to post this but, I just picked up a copy of my labwork done a couple of weeks ago when I had Vertigo here in Florida.
On the phone, they had told me that everything is normal but these are the results that are out of the norm:

B12 - 1445 (normal 211-911)
Folate Serum - >24 (normal 5.38-17.0)

What does this mean? I have too much B12 in my blood? I thought that's not possible because the body flushes out the extra it doesn't need.

In addition,
Bun/Creatinine ratio - 41.6 (normal 6.0 - 25.0)
Neurophil% - 39.4 (normal 44.0 - 76.0)
Lymphocyte - 50.7 (normal 15.0 - 43.0)

I am hoping that Rich or Fredd or anyone can explain what these mean?

This doctor I went to for the first time. I'm just visiting here in Florida.

Hi, NeilK.

The serum B12 often comes out normal or high in PWMEs. This means that you do not have an absolute B12 deficiency. However, it does not detect a functional B12 deficiency, which s present in ME/CFS. Most of the B12 in the serum has been rejected by the cells and is bound to haptocorrin. Eventually the liver cells will import this and recycle it via the bile, back to the gut, for possible reabsorption into the blood, bound to transcobalamin. The B12 that is bound to haptocorrin is not available to the cells in general. Only the newly absorbed fraction that is bound to transcobalamin is normally absorbed by the cells in general.

Your serum folate is also elevated, but this test does not indicate what form it is. It could be folic acid, and you may be having difficulty converting it to the chemically reduced, active forms of folate that are used by the body. Normally, 5-methyl tetrahydrofolate is the most abundant folate form in the blood.

Given that you have ME/CFS, I think it is likely that you have a partial methylation cycle block, which is caused by the functional B12 deficiency, which in turn is caused by glutathione depletion.

It isn't possible to interpret the BUN/creatinine ratio without knowing the values for BUN and creatinine individually. Depending on them, it could be a kidney problem, or it could be that because of ME/CFS, you are burning protein at a higher than normal rate, and/or you are making less creatine (and hence creatinine) than normal because of a methylation deficit. Methylation is needed to make creatine.

Percentages of white blood cells are not easy to interpret without the absolute white cell counts. The percentage shift that you had could be caused by an increase in lymphocyte count, or a decrease in neutrophil count. Those indicate different things.

If you could get the methylation pathways panel from Health Diagnostics run, it would give you a clearer picture. The conventional B12 and folate tests are not very helpful in ME/CFS.

Best regards,

Rich

 

[Nielk]

Thank you so much, both Fredd and Rich for your time and interpretation.
We are so lucky to have you on this forum and you give of yourself so freely to all of us.
I REALLY appreciate it!

I'm going to try to get the methylation pathways panel. I'm going back home (NY) next week. The problem is that like we discussed before, NY residents are not allowed to
get this test from Health Diagnostics in NJ. I will try to figure it out how to get it done.

By the way, Rich, my Creatinine level shows 0.5 (normal 0.4 - 1.4) and BUN shows 20.8 (normal 6.0 - 25.0)

The way I understand it my blood might have a high level of B12 and Folate Serum but, it doesn't go to my cells because of partial methylation block - but, the only way to really find out is to get the methylation panel test.

Thank you so much,
Nielk

 

[aquariusgirl]

thanks freddd. yeah, not interested in any supp with folic acid in it. Just donated my bottle of folic acid to goodwill.

I use methyl B12 but I do wonder about ppl with lots of amalgam fillings using a lot of sublingual B12 ....if they might be methylating mercury ...

 

[richvank]

***Hi, NeilK

I'm going to try to get the methylation pathways panel. I'm going back home (NY) next week. The problem is that like we discussed before, NY residents are not allowed to
get this test from Health Diagnostics in NJ. I will try to figure it out how to get it done.

***O.K.

By the way, Rich, my Creatinine level shows 0.5 (normal 0.4 - 1.4) and BUN shows 20.8 (normal 6.0 - 25.0)

***O.K. My guess is that your kidneys are O.K., your creatinine is low-normal because of a partial methylation cycle block, and your BUN is high-normal because glutathione depletion has made it difficult for your cells to burn carbs and fats for fuel. They are thus burning protein at a higher rate than normal, and this is producing urea at a higher rate than normal, hence the elevated BUN ("blood urea nitrogen").

The way I understand it my blood might have a high level of B12 and Folate Serum but, it doesn't go to my cells because of partial methylation block - but, the only way to really find out is to get the methylation panel test.

***Yes, I'd say that's pretty much it.

Thank you so much,
Nielk

***You're welcome.

***Rich

 

[Freddd]

thanks freddd. yeah, not interested in any supp with folic acid in it. Just donated my bottle of folic acid to goodwill.

I use methyl B12 but I do wonder about ppl with lots of amalgam fillings using a lot of sublingual B12 ....if they might be methylating mercury ...

HI Aquariusgirl,

I agree with Cutler on this mb12/mercury thing. He says that IF mb12 can methylate mercury it does so in mcg quantities, potentially destroying all the methylb12 in a persons body causing massive mb12 deficiency symptoms and that it these mcg of mercury are methylate they are then removed by the liver and excreted with a 71 day serum halflife, a 1% a day decrease. Applied to large doses of Mb12 that means it would take about 5 to 10 years to clear the mercury from the body without ever reaching toxic levels of methylmercury. It would reach a maximum in 2-3 years. I posted the results of a model here on a mercury oriented thread abour 2 years ago.

 

[aprilk1869]

If I remember right, someone was asking about the percentage of the population with MTHFR mutations. Here is a small study that tested for C677T.

Effect of oral hormone replacement therapy on plasma homocysteine levels

Background. Various inherited or acquired conditions can lead to mild or severe hyperhomocysteinemia, which has toxic effects on the vascular endothelium. It has been reported that hormone replacement therapy is associated with decreased homocysteine plasma levels, but this is still a controversial issue.

Purpose. To compare homocysteine plasma levels in women before and after 3 months of oral hormone replacement therapy.

Methods. Twenty-four women were selected to take part in the study. Blood samples were collected immediately before hormone replacement therapy (cyclic association of 2 mg of estradiol valerate and 1 mg of cyproterone acetate) and three months after the beginning of hormone replacement therapy. Samples collected before hormone replacement therapy were used as controls. Plasma homocysteine levels and the presence of C677T mutation in the methylene tetrahydrofolate reductase gene were evaluated in all participants.

Results. The methylene tetrahydrofolate reductase gene mutation was detected in 8 women (33.3%) in heterozygosis, in 3 (12.5%) in homozygosis, and 13 women (54.2%) did not present the mutation. No significant differences were observed in homocysteine levels before and after three months of oral hormone replacement therapy, regardless of the C677T genotype. Conclusions. The results obtained indicate that homocysteine plasma levels are not affected after three months of oral hormone replacement therapy.

http://onlinelibrary.wiley.com/doi/10.1080/00016340600676136/abstract

 

[Deepak]

Hello Fredd,

I am sorry I did not know you needed to keep the other thread short so am reposting my queries here.


vitamin C, calcium, omega 3 is available in India. Magnesium is not so I ordered it last month from iherb. I also ordered nattokinase as i read in some places that thick blood can be a problem in Fibromyalgia and natto helps in breaking down the fibrin.

I have some questions

1 ) So you are saying I should take Metafolin + Jarrow Methylb12 5mg + Enzyamtic Therapy 1mg B12 infusion + Source Naturals Dibencozide daily ?? Should I take the dose mentioned on the bottles ?

2) You mention that one should also take potassium. We do not get plain potassium supplements here so could you tell me which one I can order from iherb?

3 ) What about the other co-factors you mention - should I do that later - for eg Sam-e , L-carnitine fumarate ??

4) Is this protocol ok to do even though one has regular b12 blood levels ? Is there a danger of too much ??

5) Is it ok to take LDN while on your protocol ?

6) Could tender or poky feelings in the scalp be related to b12 ? ( I did read the list of symptoms you listed and it seems this could be one )


Thanks so much.

Love,
Deepak

 

[Rosebud Dairy]

@ Nielk

In some people, once on the FAP, a potassium drop can be felt very notably as dizziness/vertigo/tinnitus. Give yourself some high potassium foods, making sure they are not high folate foods, and if it improves, then you won't need labs to tell you what is going on. If you have a mineral supplement containing potassium, which you may already be taking by now, try that when the vertigo begins. My own dizziness is accompanied by being very nauseated, and almost clammy, but definitely lightheadedness.