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#9621
08-14-2009, 09:36 PM
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Re: Vitamin B12 deficiency is commonly misdiagnosed.
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Hi Tam, I understand the brainfog. After general paralysis comes death in the b12 progression. This is too important to let money stand in the way. If you can't afford the starter kit just say so and since enough people have used my first order code I'll send you a starter kit. You sound like a person who needs it. Sorry I didn't get back to you sooner as this just barely was posted because your first few go through the moderator. Right now you are not in a position to know how much this can help your situation. You could be 75% better by January. If you decide to do this I will post how to send me your address.
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Freddd - Systems Analyst with websites coming soon on methylcobalamin and providing withdrawal planning and reasonable taper schedules for Oxycontin, MSContin, oxycodone, morphine, Valium and more at eztaper.com. 
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#9622
08-14-2009, 09:41 PM
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Re: Vitamin B12 deficiency is commonly misdiagnosed.
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I think that it is important for you to know that the active b12 sublinguals are 1000 to 10,000 times more effective than the cyanocobalamin patch. Doctors generally know nothing about active b12s and very little about b12 deficiency symptoms and wouldn't recognize it if hit in the face with it.
__________________
Freddd - Systems Analyst with websites coming soon on methylcobalamin and providing withdrawal planning and reasonable taper schedules for Oxycontin, MSContin, oxycodone, morphine, Valium and more at eztaper.com.
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#9623
08-14-2009, 09:46 PM
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Re: Vitamin B12 deficiency is commonly misdiagnosed.
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Would you mind sharing what steps you have taken to help with the brain fog? Thanks. Jeff
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#9624
08-14-2009, 09:59 PM
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Re: Vitamin B12 deficiency is commonly misdiagnosed.
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For most of your body, the bloodstream acts as a highway supplying oxygen and nutrients, and carrying away wastes. It also permits the free movement of things such as the cells of the immune system, hormones, and other messenger molecules. It does a lot of other things besides. However, certain organs which “do work” on the blood – eg lungs, heart, kidneys, liver – have two entirely separate supplies – the blood they need to keep them working, and the blood they are doing the work on. In the case of the heart, for instance, the blood being worked on (“pumped”) enters the right (“pulmonary”) side via the vena cava, and exits (to the lungs) via the pulmonary artery; it then re-enters on the left (“systemic”) side (the heart is two pumps, not one) via the pulmonary veins, and exits via the aorta http://www.biosbcc.net/doohan/sample/images/heart/0283circulation.jpg Confusingly, the heart is almost always pictured as though viewed through the chest wall, so that “right” means “body right”, as opposed to “image right”. However, the heart itself – being an organ (a muscle, in fact) needs its own blood supply in order to function. That is delivered via the coronary arteries (the first branch of the aorta), and exits via the coronary veins – the major part of the network shown here as a tracery over the outer surface of the heart: http://www.healinglightseries.com/IMAGES/Images-Heart/Heart.jpg The liver is a serious box of tricks; this: http://www.plim.org/liver.html lists six major functions (I was taught that there are seven), but it does literally hundreds of other things besides. The hepatic portal vein is the highway into the liver for the blood that is going to be “worked upon”; we spoke – see postings 9530 and 9534 – about the fact that the cobalamins (leaving supplementation aside) in the blood are mainly contained either within holotranscobalaminII or holohaptocorrin. {Some – drifting remains from dead cells - circulate for a short time attached to fragments of protein from the parent cell, but the particles are soon salvaged by holotranscobalaminIII} The process which forms holotranscobalaminII means that the substance has direct access to the bloodstream, and to needy cells, since all eukaryotic cells are equipped to receive it. Holohaptocorrin appears (please, somebody either tell me that this is wrong, or give me supporting references) to get into the bloodstream by simple diffusion, and is “welcomed” only by liver cells and by some cells of the reticuloendothelial system. Both holohaptocorrin and holotranscobalaminII are capable of being held as part of the liver’s “buffer”, since the liver’s cells have receptors which can identify both, and arrange for them to be “drawn in”; the same seems likely also to be the case for holotranscobalaminIII – but I can’t find any research - corroborative or otherwise - published on the Net. This statement, then, is unlikely to be correct (but I’d be happy to be proven wrong; all that I am after is as much correct information as possible about how the process actually works.): “it looks like it's certainly in a position to release it's stores of B12 (as well as fresh/recycled B12 from the intestine) directly into the blood” The buffer isn’t B12; it’s holohaptocorrin and holotranscobalaminII (and III – probably). HolotranscobalaminII and III are “real” B12 nailed to two proteins – transcobalaminII and III. Holohaptocorrin is any cobalamin, nailed to the protein haptocorrin. The liver cannot split these things apart, nor can it differentiate between “real” B12 and the other cobalamins. The process which does both of those things (ie discerning the identity of individual cobalamins, and transferring B12 {eventually} to transcobalaminII) is the haptocorrin, IF, trypsin, chymotrypsin, hydrochloric acid “dance” which occurs in the digestive system from the duodenum southwards. Ie the only way that the B12 “stored” in the liver can be released is via the enterohepatic circulation. As you are aware, I’m working on a paper which I hope will be accepted for publication by the PA Society (even if it isn’t, it’s broadening my knowledge!!), and one thing that has become blindingly clear is that the enterohepatic circulation is not a sideshow to dietary intake of B12. Enterohepatic circulation is the main act, and dietary intake is the sideshow. We need only a tiny amount of dietary input because we have evolved a system which feeds, salvages, cleans up, and returns the minuscule amount of B12 we have to our cells over and over again. In people without B12 Deficiency problems, significant numbers of the B12 molecules donated by their mothers when they were foetuses will probably still be circulating within them the day they die. “It also looks as though it could reabsorb some of the B12 circulating in the blood, via the hepatic artery.” Unless you are supplementing, there is no free B12 in your blood; only holotranscobalaminII and holohaptocorrin. If you are supplementing, then free B12 can be picked up by transcobalaminII molecules returning “empty” from needy cells. In Nature, our blood does not contain free B12, but that doesn’t mean that transcobalaminII will not latch on to it; here’s a good paper: http://www.ajcn.org/cgi/content/full/85/4/1057 and here’s the relevant statement: “The greatest increase in holo-TC was observed 24 h after ingestion of three 9-µg doses of vitamin B-12. Our results indicate that a vitamin B-12 absorption test based on measurement of holo-TC after administration of three 9-µg doses of vitamin B-12 should run for 24 h.” As indicated earlier, the liver certainly does latch on to holohaptocorrin and holotranscobalaminII; however, there is a clear limit to how much buffering it can handle, since – in times of plenty – we steadily jettison lots of “real” B12 in our faeces. As I have said before, what a pity the same isn’t true about our “real” storage system – adipose tissue!!
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#9625
08-14-2009, 10:14 PM
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Re: Vitamin B12 deficiency is commonly misdiagnosed.
Hi Kevin,
It seems rather a pity that we can't "get fat" with b12 in order to really have a storage system. I guess it was just not something that ever really came up naturally. I wonder how the "setpoint" is changed so we retain more b12 instead of discarding it. Have you come across a possible reason yet that my first dose of methylfolate and ever more afterwards has at least slowed down my excretion of b12 in the urine?
__________________
Freddd - Systems Analyst with websites coming soon on methylcobalamin and providing withdrawal planning and reasonable taper schedules for Oxycontin, MSContin, oxycodone, morphine, Valium and more at eztaper.com.
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#9626
08-15-2009, 01:03 AM
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Re: Vitamin B12 deficiency is commonly misdiagnosed.
Quote:
To keep it brief, here are the steps I have taken to help (actually pretty much eliminate) brainfog. 1. Take active B12s (three 5000mcg mb12 and one 3000mcg ab12 per day), of course. I also take all the basics that I can, but I am not sure in what way they helped or not with eliminating brainfog. 2. Avoid complex carbohydrates (bread, pasta, table sugar (sucrose is a two simple sugar molecules)). Simple sugars (honey, fruit) is okay. Theory is body is not properly digesting, so the bacteria in your gut feast on the complex carbs and produce toxins that are absorbed. Simple sugars do not need to be digested and are absorbed quickly. I would think that once fully healed, this would not be needed anymore. Personally, I can eat more complex carbs than I used to and still not have brainfog. 3. Use freeze dried adrenal gland. Link to what I use: http://www.iherb.com/Natural-Sources...ules/6138?at=0 I started with three a day before I had started active b12s. It helped my brain fog somewhat. Then I started one mb12 a day, and slowly tapered off the adrenal gland. Then for some reason, brain fog started coming back. Started adrenal gland and the brain fog disppeared pretty quickly. I do not really need this anymore now although I use it occasionally if I am stressed or have not gotten enough sleep for a couple of days. 4. Enzymes. I use these because I cannot really swallow pills. http://store.homefirst.com/bfont-siz...ductinfo/SBET/ This is a plant based enzyme pill. Wobenzyme (has pancreatic enzymes as well) would probably be more effective if you can swallow pills: http://www.iherb.com/Mucos-Pharma-Wo...ets/10831?at=0 I take 2 or 3 of the plant based enzymes at each meal. I do feel I need these less now, but I might start to enter the fog again if I stopped taking them at this point... Hope that helps! Let me know if you have any other questions... FYI, I will be outside the reach of a computer for most of the weekend, so would be slow to reply if you did have any questions.
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#9627
08-15-2009, 05:38 AM
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Re: Vitamin B12 deficiency is commonly misdiagnosed.
Dear Freddd and doveman,
“I wonder how the "setpoint" is changed so we retain more b12 instead of discarding it” Although there are hints of underlying reactions involving what are described as “calcium bridges” (between reactions, I assume), the main mechanism appears just to be one of quantities. It’s seen most clearly in the case of simple dietary deficiency - the likes of myself. If we stop taking in B12, there’s no reason to assume that there is any associated decrease in the input of other cobalamins – from plants, from oral bacteria, etc. The amount of holohaptocorrin passing through the digestive system therefore remains pretty steady. If the mechanism which gets holohaptocorrin into the bloodstream is nothing more elaborate than diffusion (and I’m still searching for something discussing the process definitively), then the amount of holohaptocorrin circulating in the blood will also remain steady (even though all new input only contains “b12 analogues”). HolotranscobalaminII and III already in the liver are – as I said at posting #9626 - “real” B12 attached to protein, so when they are excreted into the duodenum in the bile, they’ll eventually be processed in the same way as dietary B12 within protein (ie meat etc) is. The B12 they contain will therefore eventually re-enter the circulation as holotranscobalaminII once more; this is a biological process, and if there is no dietary B12 input, there will be more than enough IF etc to ensure that virtually all B12 held within HCII and III is trapped and re-cycled. “Virtually all” – there is bound to be some process inefficiency, but plenty of data exists to say that it is small, and becomes even smaller as time goes by and the cycle repeats itself. Something like 60% of the holohaptocorrin that was already in the system before the dietary supply was cut off contains “real” B12. When this re-enters the duodenum, it also will encounter a lot of IF etc. Certainly, there’s still a dietary holohaptocorrin throughput, but – since none of it contains “real” B12 - it does not attract the attention of IF, so there is a lot of IF to attend to the holohaptocorrin molecules which do contain B12. As always, this B12 ends up in the circulation, travelling as holotranscobalaminII. Inevitably, some of the “old stock” of holohaptocorrin (containing “real” B12) will be missed by IF etc; there is a risk that this will be lost in faeces; however, there is also a reasonable chance that it will be driven back into the circulation by diffusion. “Partly re-processed” B12 removed from transcobalaminII by haptocorrin also stands a good chance of re-entering the system – also by diffusion within holohaptocorrin. Once in the bloodstream, it passes through the cycle over and over again, so that – given time – nearly all of the B12 it contains will be retrieved. Thereafter, all of our B12 for circulating and for processing will be held in holotranscobalaminII, and none as holohaptocorrin. We’ll still be producing IF etc, but none of it will be consumed in reactions with holohaptocorrin, leaving a huge amount to deal with the transiting holotranscobalaminII; under such circumstances the process efficiency would - I suggest - be very high. There is an appealing, simple elegance to the processes I keep postulating; however, I awoke this morning with the certainty of a huge hole in my reasoning. At posting #9626, I said this to doveman: Quote:
With no IF, they were only going to get B12 into their bloodstreams via the 1% passive diffusion route (hence, presumably, the vast amounts of liver) However, onward transmission to needy cells requires the involvement of transcobalaminII (returning empty from a delivery run, the molecule can definitely pick up “free” B12 in the bloodstream – there’s plenty of research). All of the above implies either that there is some method of extracting B12 from carrier proteins without involving IF, or that there is free B12 in liver. At the moment, both seem unlikely. Any thoughts would be appreciated. "Have you come across a possible reason yet that my first dose of methylfolate and ever more afterwards has at least slowed down my excretion of b12 in the urine?" No; I've been concentrating on the mysteries of the enterohepatic circulation, and I'd imagine that what you are describing either goes on at cellular level, or is some trick being worked on the kidneys. If I come across anything, I'll certainly let you know.
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#9628
08-15-2009, 06:35 AM
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Re: Vitamin B12 deficiency is commonly misdiagnosed.
Quote:
Hi Kevin, Is there any reason to assume that bovine TC1, TC2 and TC3 are significantly different, if at all from human? Hemoglobin isn't. In that case the b12 is already bound for pickup. It's not like muscle meat that has the b12 in mitochondria that has to be digested to be separated. Flooding the intestine with raw beef liver worked so maybe that's because it was already prepared. Also, as we have demonstrated free active b12 is readily picked up by the cells once it is in the blood.
__________________
Freddd - Systems Analyst with websites coming soon on methylcobalamin and providing withdrawal planning and reasonable taper schedules for Oxycontin, MSContin, oxycodone, morphine, Valium and more at eztaper.com.
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#9629
08-15-2009, 06:51 AM
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Re: Vitamin B12 deficiency is commonly misdiagnosed.
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i placed order for the 4 items from iherb ... i was able to see that the organic market has them but more costly so until those arrive i just got a 1000 dose to take i still need to find a dr here who believes this is real so i can begin the disability application and maybe suppliment my incme until i can work again. i've applied for a couple jobs such as the person who sits and takes the tickets at the theater ... but 1; in this economy i just don't think it's likely they will hire someone who can only do one job when there is probable long list of those who can do much more 2; hubby is concerned about me getting any job combined with multiple physical therapy appts/dr appts each week. the emotional strain of this almost does me in some days ... i try to remember 1; i am not dying and 2; so many have done this for so much longer for various things with much less to hope for ... still some days i just feel so totally useless thank you so much for listening ... that means so very much. tamara
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#9630
08-15-2009, 03:03 PM
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Re: Vitamin B12 deficiency is commonly misdiagnosed.
Hi Kevin
Thanks for the explanation about the heart, very helpful. After singing the praises of pictures, that one I linked to actually got me a bit confused for a while, as it shows the stomach upstream from the intestine, which made me wonder how the B12 gets from the stomach to the intestine to bind with IF. But then I realised that as this is an accepted fact, it must just be that the picture's not as accurate as it could be. Now if I've understood the process correctly, B12 is released from IF in the enterocytes (in the small intestine) and then goes on to the liver. Is the B12 at this point still the same as the B12 that was released from protein in the stomach and does it continue on to the liver unbound or is it at this point where it binds to TCII and haptocorrin before continuing on to the liver? The hepatic portal vein is the highway into the liver for the blood that is going to be “worked upon”; we spoke – see postings 9530 and 9534 – about the fact that the cobalamins (leaving supplementation aside) in the blood are mainly contained either within holotranscobalaminII or holohaptocorrin. {Some – drifting remains from dead cells - circulate for a short time attached to fragments of protein from the parent cell, but the particles are soon salvaged by holotranscobalaminIII} The process which forms holotranscobalaminII means that the substance has direct access to the bloodstream, and to needy cells, since all eukaryotic cells are equipped to receive it. Holohaptocorrin appears (please, somebody either tell me that this is wrong, or give me supporting references) to get into the bloodstream by simple diffusion, and is “welcomed” only by liver cells and by some cells of the reticuloendothelial system. Sorry you've lost me there. If B12 does indeed bind to TCII and HC before reaching the liver, the blood going into the liver to be "worked upon" via the hepatic portal vein contains both holoTCII and holoHC, and I assume this blood then leaves the liver and enters the circulation still containing both. So I don't understand when you say holoTCII "has direct access to the bloodstream" whilst holoHC can only "get into the bloodstream by simple diffusion". The buffer isn’t B12; it’s holohaptocorrin and holotranscobalaminII (and III – probably). HolotranscobalaminII and III are “real” B12 nailed to two proteins – transcobalaminII and III. Holohaptocorrin is any cobalamin, nailed to the protein haptocorrin. The liver cannot split these things apart, nor can it differentiate between “real” B12 and the other cobalamins. The process which does both of those things (ie discerning the identity of individual cobalamins, and transferring B12 {eventually} to transcobalaminII) is the haptocorrin, IF, trypsin, chymotrypsin, hydrochloric acid “dance” which occurs in the digestive system from the duodenum southwards. Ie the only way that the B12 “stored” in the liver can be released is via the enterohepatic circulation. Does the liver build this buffer using that which has entered via the hepatic artery and is this the second supply to keep it working that you referred to, as opposed to the portal vein which supplies the blood it works on (and which I presume doesn't contribute to the buffer)? I'm afraid I don't understand your argument that the B12 stored in the liver needs to go through the enterohepatic circulation to be released, as if it could release the stored holoTCII directly into the bloodstream this could be taken up by cells without need of any further processing.
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So I feel I am building a more solid foundation to avoid brainfog. So, I can eat more complex carbs or use less enzymes and not develop brainfog. So that is good. I have not even had to take freeze dried adrenal gland for the past 2 weeks to keep off brainfog. And since the two go hand in hand for me, my energy is good as well.
