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You would be better off taking folate rather than folic acid, which is a synthetic substance, High intakes of folic acid have been associated with cancer, they can mask a low B12. Also, regarding B12 there are a couple of paragraphs above that read: “A high intake of folic acid might mask detection of vitamin B12 deficiency and lead to a deterioration of central nervous system function in the elderly. In one study, consumption of folic acid in excess of 400 micrograms per day among older adults resulted in significantly faster rate of cognitive decline than supplement nonusers. (11) Another study found a higher prevalence of both anemia and cognitive impairment in association with high folic acid intake in older adults with a low vitamin B12 status. (12) As vitamin B12 deficiency is a common problem for many older adults, these studies suggest that high folic acid intake could cause serious cognitive consequences in the elderly.

Despite the risks associated with high levels of folic acid intake, it is well established that adequate folate intake from the consumption of folate-rich foods is essential for health. Folate aids the complete development of red blood cells, reduces levels of homocysteine in the blood, and supports nervous system function. It is well known for its role in preventing neural tube defects in newborns, so women of childbearing age must be sure to have an adequate intake prior to and during pregnancy.

Excellent sources of dietary folate include vegetables such as romaine lettuce, spinach, asparagus, turnip greens, mustard greens, parsley, collard greens, broccoli, cauliflower, beets, and lentils. (13) Not surprisingly, some of the best food sources of folate are calf’s liver and chicken liver.”


Lan says

How long does B12 from an injection stay in the body? ND says could be around and affect blood test result after 2.5 months; MD says it can only be around 2-3 weeks.

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I don’t know about blood tests, but I’ve heard some people say that for them, the effects only last one day.

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Hi Lan, the real answer is “it depends”. Thus, the half-life of stored B12 is over 200 days. The half-life of injected B12 is different, and it depends upon how it is administered. IV injected material seems to have a half-life of around 16 hours. Thus a 1 mg dose would be almost totally gone (less than 4 ug left) by 9 days. IM injected material lasts slightly longer, but probably not much. Topically administered material in b12oils would be longer due to the depot effect of the skin. IM injected material given 4-6 weeks apart doesn’t actually top up areas such as the brain or restock the liver, because if it did, you would only need to have 3 or 4 injections every 4-5 years, In stead the IM injected material give you this massive peak and trough effect. What is also important is that the B12 has to be around to saturate any “free” transcobalamin (holotranscobalamin), as this is the protein that is required in order to get cellular uptake. Only about 25% of protein bound B12 in serum is bound to TC.


Should have said that the symptoms of low B12 and low iron can be very similar. Having both at the same time is a real drag!

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Can anyone tell me how long it might take to go from 342 to 239? Is it possible to have your B12 drop dramatically over 2 months? I started weekly shots about 6 weeks ago and then 3 weeks later was switched to bi-weekly. I get the shots on Friday. By the Monday/Tuesday of the week I am scheduled to get a shot, I am so cloudy, tired, can’t think. The doctor (who practices integrative medicine and is 100% on board with my treatment) thinks it is odd that I “respond so dramatically” to the shots. Any ideas?


Hi Moongirl,

Yes it is for all sorts of reasons. What it comes down to is you need to increase your input. The 5 star sublinguals will do you FAR better than weekly or less injections. Also some other items will help heal you thoroughly so you won’t suffer damage from this. If you were responding very strongly to 5 star methylb12, that is entirelu normal and expected. That anyone responds strongly to cyanocbl is a 1 in a million experience. It doesn’t last That is the problem with cyanocbl along with that it works very poorly compared to mb1w2 and adb12 of suitable quality.

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Freddd, I think it is great that you are doing all this work and spreading the word. I have to admit though that I get a little confused when I am reading your replies to others regarding all the other inefficiencies that can arise from treating the B12. I see you told someone that you are currently writing up instructions. I’d love to know when that is ready. I found the sublingual methyl-b you recommend at my local natural food store. I would like to start taking it after I get my levels re-drawn and after the doc tests me for intrinsic factor antibodies (this week.) I am also having my D retested as that was extremely low at 11. I am ready to beat this thing and get my life back. Moon


goofy_mom says

Hi Freddd, I am 38 and would describe myself as a healthy person until few months ago when my neck started bothering me. Went to neurologist who sent me to physical therapy which didnt help. In few weeks, I started feeling tingling in right arm and leg and face. They did MRI to rule out MS and fortunately it was negative. I was a vegetarian for years and had low B12 11 years ago when I did monthly b12 shots for 6 months. I just got b12 checked out and it was 362 and doc says its “in range” but all my symptoms are there which makes me feel its too low. I started liquid 1000mcg b12 of generic brand today but came across this and very hopeful that trying your suggested will help. I need to start with the following based on your article. I already take potassium supplement and slow releasing iron + multi-vitamin. Will any of these interfere with the basic remedy described below: Jarrow Formulas, Methyl B-12, 5000 mcg Enzymatic Therapy, B12 Infusion Solgar, Folate Metafolin Folic Acid, 800 mcg

This forum has given me a ray of hope. Please answer so I can order it from Goofy_mom


Thank you so much on this information! I had been extremely worried when my doctors were told me I needed an appointment with my PCP immediately about this.I’m only 19. As a child I was in an out of the hospitals. We had discovered that I have Crohns disease, Rheumatoid Arthritis and Sjogrens Disease an then I had just found out I had this. Not to be a negative Nancy but I thought three diseases were enough but now this. My first visit to my adult rheumotologist was deeply concerned about me being able to sleep an awful amount of hours an still exhausted, also I guess she had noticed that it was very hard for me to come up with words or I would just forget what we were saying. I have recently noticed that I can stare at once spot an just blank out. Has anyone had thisproblem? Personally, being a nursing student an still only a child this is very hard for me to grasp.Also has anyone heard of other methods than shots? I’m taking Humera (the worst injection in the world) and its making me want to never have an injection again! Thanks!


Mary, I am reading a book called, “Could It Be B12?” and it talks about how even Bipolar can be in some cases caused by B12 deficiency. The book is written by a nurse and her husband who is a doctor. Also, B12 does affect nerves. So I would get that book and read it and see if you can find a doc to test you before you start taking a vitamin supplement. Maybe her doc would test you? Good luck Mary. Be your own advocate and be strong in caring for your own health. I wish I had known about B12 when I was 15.


Mary Wright says

Hi my name is Mary I’m only 15, but my mother has suffered from sezures for 20 years hers started when she hit her head on a pole. We don’t know what type of sezures she has yet or what to give her but last November I had a sezure and since I have been having them (when there was 350 lbs. of pressure on my jaw). I’m going to try and keep this as short as possible i don’t want to waste your time, but we just found out that she is low on B 12. We believe that I may be too. Due to the fact that I have been diagnosed as bipolar for many years and ADHD and asthma ect. I have always been very independent so sezures scare me. Do you profesionaly think there could be any connection to her sezures and her deficiancy in B12? We are hopeing that if we find her solution we will find mine. There aren’t too many neurologists that take any intrest in dealing with kids.- thank you for your time


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Figure 3.

Targeting ubiquitin-dependent degradation of cyclin E. F-box protein FBW7 specifically recognizes two separate phosphodegrons in cyclin E and targets cyclin E for ubiquitin-dependent proteasome degradation by the SCF-FBW7 E3 ligase complex. The phosphorylation of both amino- and carboxy-terminal degrons in cyclin E is catalyzed by GSK3 and CDK2 and creates two separate binding sites for FBW7. Both mitogenic and antiproliferative signals exert their effect on the cell cycle through cyclin E ubiquitylation by inhibiting the activity of GSK3 or stimulating the expression of FBW7, respectively.

Cyclin D is phosphorylated at T286, a site analogous to T380 in cyclin E, and T286 phosphorylation promotes cyclin D destruction ( Diehl et al. 1998 ). Multiple F-box proteins, such as Fbxo41, Fbxw8, SKP2, and Fbxo31, have been implicated in targeting cyclin D for destruction, but the E3 ligase responsible remains to be definitively identified ( Kanie et al. 2012 ). Promoting the destruction of both D- and E-type G 1 cyclins by GSK3-mediated phosphorylation, however, could allow cells to effectively couple the PI3K–AKT pathway to G 1 cell cycle control. T286-phosphorylated cyclin D1 can also be recognized and stabilized in the nucleus by Pin1, a prolyl isomerase that regulates the function of proteins by causing conformational change of their S/T-phosphorylated forms ( Liou et al. 2002 ).

Progression through G 1 phase is also controlled by other E3 ligases. In particular, the anaphase-promoting complex (APC), which promotes the ubiquitin-dependent proteasomal degradation of multiple mitotic regulatory proteins, remains active in G 1 phase to suppress accumulation of mitotic cyclins until cyclin-E–CDK2 is activated at the G 1 /S transition.

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Some CKIs are also regulated by the ubiquitin–proteasome pathway. Again, this regulation involves phosphorylation of these CKIs, which provides a mechanism linking extracellular signaling to the G 1 cell cycle control machinery.

In Saccharomyces cerevisiae , a single CDK, Cdc28, forms multiple B-type cyclin–CDK complexes to drive both S phase and mitosis. Cdc28 is inhibited by Sic1, a CKI that is unrelated in sequence to either the p21 or INK4 family of CKIs. Sic1 is targeted for ubiquitylation ( Fig. 4 ) following phosphorylation by the G 1 cyclin–CDK complex Cln–Cdc28 ( Schwob et al. 1994 ). Inactivation of Sic1 rescues the inviability of yeast cells lacking the G 1 cyclins Cln1, Cln2, and Cln3 ( Schneider et al. 1996 ), and mutation of CDK phosphorylation sites in Sic1 causes stabilization of Sic1 and blocks DNA replication. These observations indicate that the primary function of these three G 1 cyclins, once mitogenically activated, is to promote Sic1 ubiquitylation to bring about the G 1 /S transition. Phosphorylated, but not unmodified, Sic1 binds to the F-box protein Cdc4, which, through a linker protein, Skp1, brings Sic1 to the Cul1 (also known as Cdc53)–Roc1 (also known as Rbx or Hrt1) E3 ligase complex for ubiquitylation by the E2 enzyme Cdc34 ( Feldman et al. 1997 ; Skowyra et al. 1997 ). Nine sites in Sic1 are phosphorylated, and each contributes to Cdc4 binding, with any six being required ( Nash et al. 2001 ). This multisite phosphorylation requirement makes Sic1 ubiquitylation ultrasensitive to the level of G 1 CDK activity, enabling cells to measure the strength of mitogens and set the level of CDK activity that determines the timing of DNA replication. It transforms a gradual accumulation process, such as protein synthesis during G 1 phase, into an irreversible switch for the onset of DNA replication. Sic1 is also phosphorylated by its target, the B-type cyclin–CDK complex Clb5–CDK1, which may ensure irreversibility of the G 1 /S transition once DNA replication has been initiated.

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