Treating Chronic Fatigue Syndrome (ME/CFS): Vitamin B12- When It Doesn’t Work by Fred

 

Treating Chronic Fatigue Syndrome (ME/CFS): Vitamin B12- When It Doesn’t Work by Fred

Vitamin B12 is one of the most frequently prescribed treatments in chronic fatigue syndrome (ME/CFS) yet it is not uncommon
for it to perform poorly or even to have negative effectsthus. Here Fred provides some of the reasons he believes B12 does not sometimes work in ME/CFS

  • Taking It in Tablet Form- Active b12 is taken as an oral tablet reducing its absorbtion to below 1%. A 1000mcg active b12 oral tablet might bind as much as 10mcg of b12. Again the b12 has to be squeezed through a keyhole that limits the amount and is subject to binding problems in the person whether genetic or acquired.
  • Taking It In An Inactive Form - they take an inactive b12, either cyanob12 or hydroxyb12. The research “validating” their use was primarily for reducing blood cell size in Pernicious Anemia, keeping the serum b12 level over 300pg/ml at the end of the period between injections. They make a statistically significant effect that can be seen in lab tests in a significant percentage of people compared to placebo. They do not heal most damage done by active b12 deficiencies and have little or no effect on the vast majority of symptoms. They may even block active b12 from receptor sites hindering the effects of real b12. They both cause a keyhole effect of having only a very limited amount (estimated at 10mcg/day) that can actually be bound and converted to active forms. They in no way increase the level of unbound active cobalamins which appear required for most healing.
  • Enzyme Problems – Some people are totally incapable of converting these to active forms because they lack the enzyme (see below)
  • Improper Usage – They take a sublingual tablet of active b12 and chew it or slurp it down quickly reducing absorbtionback to that same 1% and limited to binding capacity. With sublingual tablets absorbtion is proportionate to time in contact with tissues. I performed a series of absorbtion tests comparing sublingual absorbtion to injection via hypersensitive response and urine colorimetry. The sublingual b12s must be retained under the upper lip or tongue for 45 minutes to two hours for effectiveness with verified absorbtion ranging from 15% to 25% with urine colorimetry and by effect.
  • Wrong Brand – Of the many brands of sublingual methylb12 only some are very effective. Some are completely ineffective and some have a little effect. Of 10 brands of methylb12 systematically tested, 2 rated 5 stars with 5 hypersensitive testers. They were Enzymatic Therapy 1mg, and Jarrow Formulas 1 mg and 5mg. In addition Country Life Dibencozide rapy 1mg, and Jarrow Formulas 1 mg and 5mg. In addition Country Life Dibencozide (adenosylb12) also rated 5 stars. One brand of 5mg methylb12 rated ZERO stars, completely ineffective in all testers. The other 7 brands rated 1-3 stars. Solgar Metafolin (methylfolate) is one of two brands available and is superior to folic acid in every way.
  • Decayed Product – or injectable methylb12, if it is exposed to too much light (very little light actually is too much) it breaks down. Broken down methylb12 is hydroxyb12. It doesn’t work at healing brain/cord problems of those who have a presumed low CSF cobalamin level. That requires a flood of unbound methylb12 and adenosylb12 (2 separate deficiencies) that can enter by diffusion. Adenosyl12from sublinguals can ride along with injected methylb12.
  • They don’t take BOTH active b12s.
  • Low Dosage – they don’t take enough active b12s for the purpose, espcially amounts needed to penetrate CSF by diffusion.
  • Lack of methylfolate.
  • Lack of other critical cofactors.
  • Lack of basic cofactors.
  • Taking glutathione or glutathione generating cofactors that induce an active b12 deficien

Four Distinct Types of Vitamin B12 Deficiencies – Most people consider b12 deficiency to be a unitary thing. it isn’t. There are 4 distinct and different b12 deficiencies each with it’s own set of characteristics, and a person can have any combination of the 4. In addition is the definition of “deficiency” itself.

Each type of active b12 has it’s own deficiency symptoms. The results of shutting down the neuronal mitochondria are different from loosing myelin or slowing down impulses or lacking a wide variety of neural transmitters or who knows what other effects. Unless a CSF draw is done, there is no way to detect these deficiencies. There are no standards of what is “deficient” even if a draw is done. Pragmatically these deficiencies can both be detected and differentiated. For a variety of reasons I won’t go into now, I could make a case for ME being a CSF deficiency of largely methylb12 specifically for instance.

Potential Challenges To B12 Absorption

  • Can’t absorb b12 for a wide variety of reasons including IF insufficiency (Pernicious Anemia) of either genetic or autoimmune causality.
  • Can’t bind B12s for transport
  • Genetic Challanges
  • Decreased CSF cobalamin levels – hypothetical cause, confirmed problem
  • Lacking Enzyme to convert methylb12 to adenosylb12 – confimed, named cobalamin letter disease
  • Lacking Enzyme to convert adenosylb12 to methylb12 – confimed, named cobalamin letter disease
  • Lacking Enzyme to convert cyanocobalamin to methylb12 or adenosylb12 – confimed, named cobalamin letter disease
  • Lacking Enzyme to convert hydroxycobalamin to methylb12 or adenosylb12 – confimed, named cobalamin letter disease
  • Lacking Enzyme to convert glutathionylcobalamin to methylb12 or adenosylb12 – hypothetical cause, some evidence for problem
  • Lacking enough enzyme(s) to convert folic acid to sufficient methylfolate, – confirmed cause

Each of those can be overcome. On top of the genetic reasons, the methylb12 generated by bacteria is not all the same and some bacteria breeds may generate superior methylb12. This is totally unexplored but may account for some brand differences.

Personal Story -I personally appear to lack all of those enzymes for interconversion of forms of b12 and folic acid for instance and had all four b12 deficiencies. When I find something that works 5% of the time I find out why it doesn’t work 100% of the time. That’s engineering. Because my body is hypersensitive to these changes it’s very much like debugging software and I can know sometimes in hours or less what takes others weeks or months to find out. The information I am presenting here is a distillation of decades of experience and 6 years of active experimentation on myself and children. And I always do much reading to find why I should try some things or why they worked/didn’t work afterwards.

(Fred , a former and ME/CFS patient has developed a theory which suggests that a significant subset of ME/CFS patients have a hidden Vitamin B12 deficiency not treatable by standard B12 injections. This is presented for informational purposes only. Fred is not a medical professional and his proposal has not been evaluated by a medical professional; please confer with your medical professional before starting any treatment regime based on his ideas)

 

 

3 comments

{ 3 comments… read them below or add one }

Mimi June 15, 2012 at 10:27 am

Hi Fred,

Have you ever tried the B12 patch? If so, how did it work?

Mimi

Reply

Alan October 15, 2012 at 6:25 pm

im takeing methyl b-12 2500mcg by SOLARAY. Is this one you testing? do i need to trow this out?
thanks

Reply

hayley December 29, 2013 at 10:20 am

hi i can not have more then every 3 months, as it makes my ME/CFS much worse! i also have pernicious anemia (tests showed) i find it does not help in anyway, have had it weekly, monthly etc, but as soon as i have had it, within a day i am so poorly! so not fair it does not work for me as well!

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