B-12 - The Hidden Story

[nina_online]

Fred: Symptoms of adenosylB12 and methylB12 deficiency?

Fred, in your personal story forum, you say that there are distinctive symptoms of adenosyl- versuls methyl-cobalamin deficiency.

I was wondering if you could elaborate on that and list symptoms. Your symptom list at http://forums.aboutmecfs.org/showthread.php?t=167&page=2
doesn't differentiate.

I am so happy for you that you got healthy; sad that your years of illness could be due/exacerbated in part to fortification of foods by cyanocobalamin.

Thanks,
Nina

 

[Freddd]

Fred, in your personal story forum, you say that there are distinctive symptoms of adenosyl- versuls methyl-cobalamin deficiency.

I was wondering if you could elaborate on that and list symptoms. Your symptom list at http://forums.aboutmecfs.org/showthread.php?t=167&page=2
doesn't differentiate.

I am so happy for you that you got healthy; sad that your years of illness could be due/exacerbated in part to fortification of foods by cyanocobalamin.

Thanks,
Nina

Hi Nina,

I can only make a partial differentiation as like most people I needed both and I appear to have some limited conversion capacity.

The adenosylb12 populates mitochondria and oxidizes fuel into ATP. Severe muscle fatigue went away. Tender spots and knots in muscles went away. Muscles that contract until exhausted and then cease contracting and just be sore and exhausted recovered. Burning muscle pain had already recovered from mb12 but that would have been affected if adb12 was first. My muscles recovered in all sorts of ways, reduced pain, grew, healed and became exercise tolerant with adb12. My muscles came back more densely. My energy increased massively with adb12. My neurology became more funtional and mood improved with adb12, after months of being saturated with mb12. I invite you to try these things and pay careful attention as to what affects which things. Mb12 affected mood, most neurology not affected by neuronal mitochondria, personality, energy neurological pain, neurological and neuropsychiatric healing and healing of most all tissues, ie endothelial, epithelial, neurological, blood, immune, except muscles. So burning bladder, burning tongue, dermatitis, inflammed stomach, intestines, lungs all got better with mb12.

If I had taken adb12 first I might have had a broader range of things it affected but I took mb12 first by 9 months. Both adb12 and mb12 affected things in two steps. They both had their effects at 1-25mg on body an nervous system and they both had a separate set of effects at 50mgs, after the body had been saturated for months, which diffuses into CSF and has a non linear discontinuous threshold effect at about that level for at least some people upregulating neurological healing and saturating neuronal mitochondria.

 

[nina_online]

Excellent. The adenosyl symptoms/benefits you list (muscle and energy-related) are exactly what I need to address. MB12 (along with MTHFolate) has resolved my sensory overload and hypervigilance. I had no idea B12 affected energy and muscle development, which is where I am lacking now (I posted on another forum about supplements for muscle development and the only recommendation was creatine).

By the way, my sister and I both took glutathione/ATP shots. Our glutathione levels went up but ATP never did. I wonder if that could be due to a lack of AdenosylB12.

I'm so glad you are posting this info about adenosylB12. A lot of us know about the importance of methylB12, and it is a mainstay of biochemical approaches to autism, but adenosyl is not so well known. In fact, I called my (rather sophisticated) compounding pharmacy asking for it today, and the person who answered, a doctor no less, had never heard if it.

I'm going to start taking the Country Life AdB12 as soon as I can find it.

 

[Freddd]

Excellent. The adenosyl symptoms/benefits you list (muscle and energy-related) are exactly what I need to address. MB12 (along with MTHFolate) has resolved my sensory overload and hypervigilance. I had no idea B12 affected energy and muscle development, which is where I am lacking now (I posted on another forum about supplements for muscle development and the only recommendation was creatine).

By the way, my sister and I both took glutathione/ATP shots. Our glutathione levels went up but ATP never did. I wonder if that could be due to a lack of AdenosylB12.

I'm so glad you are posting this info about adenosylB12. A lot of us know about the importance of methylB12, and it is a mainstay of biochemical approaches to autism, but adenosyl is not so well known. In fact, I called my (rather sophisticated) compounding pharmacy asking for it today, and the person who answered, a doctor no less, had never heard if it.

I'm going to start taking the Country Life AdB12 as soon as I can find it.

Hi Nina,

The brands and products specified can all be had at competitive prices and fast delivery from www.iherb.com or many other online stores. I was surprised too. I was clued into the adenosylb12 by bodybuilders. Good luck and good health.

 

[Freddd]

These are the two specific defects leading to inability to make adenosylcobalamin in the brain. Again, treatment of cbl B is only 40% effective when treated with hydroxyb12. Why don't they use their brain and use adenosylb12 for trewatment instead of hydroxyb12? Carnitine is also suggested for use to aid the functinality. This is beginning to sound like obstinate stupidity on the part of those insisting that the only treatment is hydroxyb12.

Cobalamin C disease is concermed with homocysteine (mb12) rather than mma as for these two. Cobalamin D is concerned with a combination of a/b and c so a person has 2 defects affecting inability to synthecize both forms of active b12s.


cblA- They have the best prognosis because the biochemical and
clinical abnormalities reverse in about 90% of patients when they are
provided pharmacological doses of hydroxy-cobalamin (OH-cbl)
injections.
cblB- Equal fractions of affected patients are alive and well, alive and
impaired or deceased. Age of onset of symptoms can help
prognosticate, those with later onset tend to have a more benign course.
About 40% of these patients will respond with a drop in MMA level
when given pharmacological doses of OH-cbl injections.
Missing Enzyme
& Location:
Cobalamin A (cblA) deficiency: defect in the mitochondrial cobalamin
reductase. These patients are unable to make adenosylcobalamin.
Cobalamin B (cblB) deficiency: defect of mitochondrial cob(I)alamin
adenosyltransferase and the patients are unable to make
adenosylcobalamin

http://66.102.1.104/scholar?hl=en&lr...n+mitochondria


Patients with congenital malabsorption develop megaloblastic anemia and failure to thrive in the first years of life and may later develop a myelopathy.2-3 In the first months of life, most patients with TCII deficiency present with severe megaloblastic anemia, failure to thrive, and diarrhea, but neurological involvement is not present at diagnosis.2-3 On the basis of complementation studies performed in cultured skin fibroblasts, failure in the synthesis of cellular AdoCbl and/or MetCbl has been divided into disease groups, Cbl A to Cbl H.1, 4 Isolated increased levels of MMA in the blood and urine characterizes Cbl A, Cbl B, and Cbl H diseases. Most of these patients present in infancy with recurrent episodes of ketoacidosis without megaloblastic anemia. Hyperhomocysteinemia and hypomethioninemia without methylmalonic aciduria characterize Cbl E and Cbl G diseases. Most patients who have these 2 diseases present in the first months of life with megaloblastic anemia, poor feeding, and, if their disease is not promptly diagnosed, with various neurological deficits such as tonus abnormalities or seizures. Cobalamin C, Cbl D, and Cbl F diseases are due to defective synthesis of both MetCbl (resulting in hyperhomocysteinemia and hypomethioninemia) and AdoCbl (resulting in methylmalonic aciduria). Most of these patients present in the neonatal period with feeding difficulties, failure to thrive, neurological deterioration, and megaloblastic anemia. In addition, they may have renal and liver failure, cardiomyopathy, pneumonia, and retinopathy.3, 5
http://archneur.ama-assn.org/cgi/con...ull/60/10/1457

Our patients presented no evidence of having defective vitamin B12 supplies, malabsorption, or transport since they had normal vitamin B12 and TCII levels in their serum. Despite the absence of megaloblastic anemia and the presence of normal vitamin B12 serum levels, they were both clearly affected with a neurological form of vitamin B12 deficiency only diagnosed by the demonstration of homocystinuria and methylmalonic aciduria. Patient 1 exhibited a subacute combined degeneration of the spinal cord, which is highly suggestive of a vitamin B12 deficiency. Nevertheless, the diagnosis of functional vitamin B12 deficiency had been long delayed because of normal serum vitamin B12 levels although a metabolic investigation of the cellular vitamin B12 status had not been performed.
The metabolic disorder of these sisters can probably be included in the Cbl C group, although no complementation studies were done with fibroblasts from patients identified with Cbl D or Cbl F. First, Cbl C is the most common of these diseases; to our knowledge, only 2 cases in a sibship have been reported as Cbl D disease and fewer than 10 cases as Cbl F disease.6 Second, in contrast to fibroblasts from patients with Cbl F, which accumulate excess unmetabolized cyanocobalamin, fibroblasts from our patient had a low incorporation of cyanocobalamin (in accordance with our findings in other patients with Cbl C disease) compared with healthy control subjects. Similar therapeutic approaches are proposed for these 3 groups of Cbl disease and aim to normalize all metabolite values including methionine levels


Most patients with Cbl C disease respond biochemically and clinically when treated with high-dose systemic hydroxocobalamin.7-11 As with pernicious anemia, myelopathy and peripheral neuropathy improved more slowly and less completely than cortical signs (Table 3). Because this treatable condition can lead to death or irreversible neurological damage, it requires prompt diagnosis and treatment. This article emphasizes the need, at any age, for extensive investigation of the vitamin B12 status in patients with neurological symptoms whose clinical picture is consistent with vitamin B12 deficiency and in whom the serum vitamin B12 level is normal.

This article is a must read. It is free.

 

[Freddd]

And More:

Department of Digestive Diseases, VA Medical Center, West Haven, CT 06516, USA.
All of vitamin B12 in nature is of microbial origin. Cobalamin, as vitamin B12 should correctly be termed, is a large polar molecule that must be bound to specialized transport proteins to gain entry into cells. Entry from the lumen of the intestine under physiological conditions occurs only in the ileum and only when bound to intrinsic factor. It is transported into all other cells only when bound to another transport protein, transcobalamin II. Congenital absence or defective synthesis of intrinsic factor or transcobalamin II result in megaloblastic anemia. The Immerslund-Graesbeck syndrome, a congenital defect in the transcellular transport of cobalamin through the ileal cell during absorption, also presents with megaloblastic anemia, but with accompanying albuminuria. In most bacteria and in all mammals, cobalamin regulates DNA synthesis indirectly through its effect on a step in folate metabolism
, the conversion of N5-methyltetrahydrofolate to tetrahydrofolate, which in turn is linked to the conversion of homocysteine to methionine. This reaction occurs in the cytoplasm, and it is catalyzed by methionine synthase, which requires methyl cobalamin (MeCbl), one of the two coenzyme forms of the vitamin, as a cofactor. Defects in the generation of MeCbl (cobalamin E and G diseases) result in homocystinuria; affected infants present with megaloblastic anemia, retardation, and neurological and ocular defects. 5'-Deoxyadenosyl cobalamin (AdoCbl), the other coenzyme form of cobalamin, is present within mitochondria, and it is an essential cofactor for the enzyme Methylmalonyl-CoA mutase, which converts L-methylmalonyl CoA to succinyl CoA. This reaction is in the pathway for the metabolism of odd chain fatty acids via propionic acid, as well as that of the amino acids isoleucine, methionine, threonine, and valine. Impaired synthesis of AdoCbl (cobalamin A or B disease) results in infants with methylmalonic aciduria who are mentally retarded, hypotonic, and who present with metabolic acidosis, hypoglycemia, ketonemia, hyperglycinemia, and hyperammonemia. Megaloblastic anemia does not develop in these children because adequate amounts of MeCbl are present, but the effect of methylmalonic acid on marrow stem cells may give rise to pancytopenia. Congenital absence of reductases in the cytoplasm, which normally reduce the cobalt atom in cobalamin from its oxidized to its reduced state (cobalamin C and D diseases), results in impaired synthesis of both MeCbl and AdoCbl. Both methylmalonic aciduria and homocystinuria therefore develop in these children, and they present with megaloblastosis, mental retardation, a host of neurological and ocular disorders, and failure to thrive; however, they do not have hyperglycinemia or hyperammonemia. A similar biochemical profile and clinical presentation is also seen in cobalamin F disease, which results from a defect in the release of cobalamin from lysosomes, following receptor-mediated endocytosis of the transcobalamin II-cobalamin complex into cells. It is important to recognize these inborn errors of cobalamin absorption, transport, or function as soon after birth as possible, because most respond (in some patients more fully than others) to parenteral administration of cobalamin. Delays in diagnosis can lead to grave clinical consequences.
PMID: 8775094 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/8...gdbfrom=pubmed

This gives a good breakdown of the many variations of the lettered cobalamin diseases. The presumed "late onset" forms are not well defined and are considered rare, or perhaps merely rarely recognized.

 

[Freddd]

And Folate -

Cobalamin deficiency in the newborn usually results from cobalamin deficiency in the mother. Megaloblastic anaemia, pancytopenia and failure to thrive can be present, accompanied by neurological deficits if the diagnosis is delayed. Most cases of spina bifida and other neural tube defects result from maternal folate and/or cobalamin insufficiency in the periconceptual period. Polymorphisms in a number of genes involved in folate and cobalamin metabolism exacerbate the risk. Inborn errors of cobalamin metabolism affect its absorption, (intrinsic factor deficiency, Imerslund-Gräsbeck syndrome) and transport (transcobalamin deficiency) as well as its intracellular metabolism affecting adenosylcobalamin synthesis (cblA and cblB), methionine synthase function (cblE and cblG) or both (cblC, cblD and cblF). Inborn errors of folate metabolism include congenital folate malabsorption, severe methylenetetrahydrofolate reductase deficiency and formiminotransferase deficiency. The identification of disease-causing mutations in specific genes has improved our ability to diagnose many of these conditions, both before and after birth.
http://www.ncbi.nlm.nih.gov/pubmed/1...gdbfrom=pubmed


Cobalamins are essential biological compounds structurally related to haemoglobin and the cytochromes. Although the basic cobalamin molecule is only synthesized by micro-organisms, all mammalian cells can convert this into the coenzymes adenosylcobalamin (AdoCbl) and methylcobalamin (MeCbl). AdoCbl is the major form in cellular tissues, where it is retained in the mitochondria. MeCbl predominates in blood plasma and certain other body fluids such as breast milk; in cells MeCbl is found in the cytosol. Inherited disorders of cobalamin metabolism are single gene defects, transmitted as recessive traits. They affect absorption, transport or intracellular metabolism of cobalamin. At least 12 different mutations are known, including defects or deficiencies of IF, IF-receptor and TCII, MM-CoA mutase and of the various reductases and synthases required for synthesis of AdoCbl and MeCbl. These have been designated cblA to cblG. Abnormalities are detectable by urine and plasma assays of methylmalonic acid and homocysteine, and plasma and erythrocyte analysis of cobalamin coenzymes, which can reveal deficiencies of MeCbl or AdoCbl. Fibroblast studies discriminate between closely similar defects. In man, AdoCbl is required in only two reactions: the catabolic isomerization of MM-CoA to succinyl-CoA and interconversion of alpha- and beta-leucine. MeCbl is required in the anabolic transmethylation of homocysteine to methionine. Intestinal absorption of cobalamin requires the glycoproteins TCI and IF from the stomach and IF-cobalamin receptors in the ileum. Cobalamin is transported to cells bound to a polypeptide, TCII, is captured by surface receptors and absorbed by endocytosis. The complex is then split in the lysosomes, cobalamin is released and the coenzymes are synthesized. In plasma, 80-90% of the cobalamin is bound to TCI, whose function is uncertain. Megaloblastic anaemia at birth or in the first few weeks of life is a rare but serious event. Myelopathy and developmental delay, with or without seizures may also occur without anaemia. If urine and light-protected blood samples are collected and sent to an appropriate metabolic unit, an inborn error of cobalamin metabolism, including TCII deficiency in which the serum B12 may be normal, can quickly be diagnosed. IF deficiency or Imerslund-Gräsbeck disease usually presents with signs of cobalamin deficiency within the first year of life and can be diagnosed by absorption studies. Current treatment involves dietary protein restriction and/or parenteral OHCbl and the prognosis is very variable. Since lack of MeCbl leads to depressed DNA synthesis affecting rapidly dividing cells in the brain and elsewhere, treatment with this coenzyme should be considered at the earliest stage in appropriate cases.(ABSTRACT TRUNCATED AT 400 WORDS)

http://www.ncbi.nlm.nih.gov/pubmed/8...gdbfrom=pubmed

 

[Freddd]

These three specualtive papers by Carmen Wheatley are quite interesting in approaching the biochemical interactions of b12 and glutathione. Unfortunately there are from the viewpoint of hyroxycobalamin.



A scarlet pimpernel for the resolution of inflammation? The role of supra-therapeutic doses of …
C Wheatley - Medical Hypotheses, 2006 - Elsevier
... A scarlet pimpernel for the resolution of inflammation? ... Carmen Wheatley Corresponding
Author Contact Information , E-mail The Corresponding Author , E-mail The ...
Cited by 9 - Related articles - Web Search - All 4 versions

[CITATION] The return of the Scarlet Pimpernel: cobalamin in inflammation II—cobalamins can both selectively …
C WHEATLEY - Journal of Nutritional & Environmental Medicine, 2007 - Informa Healthcare
Cited by 2 - Related articles - Web Search - BL Direct

Cobalamin in inflammation III—glutathionylcobalamin and methylcobalamin/adenosylcobalamin coenzymes …
C WHEATLEY - Journal of Nutritional & Environmental Medicine, 2007 - informaworld.com
... Email: wheatley.carmen@googlemail.com ... In two previous hypothesis papers, A Scarlet Pimpernel for the Resolution of Inflammation? ...
__________________

 

[Freddd]

And vitamin e and fatty acids play a part.

Excretion of methylmalonic acid by vitamin E-deficient patients and decreased labeling of adenosylcobalamin (AdoCbl) from cyanocobalamin in vitamin E-deficient rats suggest an interaction of vitamins E and B-12. We studied this interaction in two human cell culture systems: foreskin fibroblasts and a hepatoma cell line (HepG2). We measured radiolabeling of AdoCbl and methylcobalamin from [57Co]hydroxycobalamin for 6 d in the presence and absence of linoleate (an oxidative stressor) and alpha-tocopherol. In both cell types, labeling of AdoCbl was lower in the presence of linoleate unless alpha-tocopherol was present. The decrease was accentuated by peroxidized linoleic acid; AdoCbl synthetic rate was inversely associated with thiobarbituric acid-reactive compound concentration. Subcellular partitioning of labeled cobalamin revealed less in mitochondria in the linoleate-stressed cells that were not treated with alpha-tocopherol. We conclude that lipoperoxidation reduces mitochondrial AdoCbl formation and that alpha-tocopherol exerts a protective effect in oxidatively stressed cells. We suggest that this subcellular deficiency in AdoCbl may be one mechanism by which vitamin E deficiency leads to neurologic injury. The mechanism seems primarily to involve an alteration in intracellular cobalamin distribution with perhaps a minor effect upon enzymes of AdoCbl synthesis.
http://grande.nal.usda.gov/ibids/ind...s&therow=74607
__________________

 

[Freddd]

Here is a presentation by James A. Neubrander MD on autism, methylb12 and adenosylb12 in which he distinguishes between b12 deficiency and b12 dependency. He also discusses the biochemistry of many of the same supplements that I use in the high dose active b12 protocol. He also talks about the "over methylator" idea and how it leads to wrong conclusions in avoidance of methylb12 in favor of hydroxybcobalamin. I think this is a must read paper. He also places the neurological "non-regression" point after 3-4 years of high dose mb12 therapy for at least some of the autistic kids. He also describes the reduction of startup effects as a new equilibrium is achieved and the body adjusts to that. It is my opinion that adults can decide to tolerate the startup effects that would cause concern in non-verbal autistic children and their concerned parents who don't know what exactly is going on. His reported incidence of actual detrimental side effects is totally minimal and then the method is to back off the concentration of the injectable solution a bit as a titration method.
http://www.hbot4u.com/autismdoc2.pdf

I have been reading Dr. Neubrander all along and adopted many of his ideas and found them to be productive of results for CFS/FMS/ME/CFIDS and neurological problems of many varieties. The subcutaneous injections of high concentration (20-25mg/ml) methylb12 solution is directly from his work. It does work better.

 

[Freddd]

Active B12 Protocol - Part 1

ACTIVE COBALAMIN TESTS, TRIALS AND PROTOCOLS
Version 1.0, 08/15/09 – PART 1

I’ve been involved in the insurance, individual and group health business at various levels since 1972. I started out setting up plans for individuals and companies and ended up designing and writing software for insurers, consulting, plan design and monitoring plans for trustees. I even did some of the preliminary actuarial and statistical work for an early dental plan at age 13 in 1961. I’ve been involved in this most of my life. I’m not a doctor. I was plagued with health problems my whole life and when they got so bad I could no longer work, I set out to solve my problems. In 2002 I took on myself as a client and devoted my fulltime efforts to this task. I look at the internet as a huge distributed processing supercomputer that integrates both the minds of many people with the digital capabilities and research access of computers. This has been done with the cooperation of literally thousands of people in person and remotely with hundreds reporting their individual trials in detail. Additional people are starting every day and generally having predictable results.

All of these tests, trials and protocols are based on the effects of having significant amounts of unbound active b12s circulating in the body. The effects are often rapid and very obvious. People without symptoms have no effects. If a person feels “energized”, and nothing else, that is still significant even if they didn’t feel fatigued in the first place. This can’t happen if there were no empty b12 receptor sites accepting one of the active b12s. I know plenty of people who had no discernable effects at all from any quantity of either or both active b12s. All effects are considered a positive response. Dr. Neubrander makes the distinction between b12 deficiency and b12 dependency. The distinction for me is that while 10mcg a day is enough for me to not be technically deficient as with most people, for some reason my body is dependent upon 30mg/day for proper functioning and neurological health.

The amounts of active b12s used here have generally not been researched. Combining them with many other items hasn’t been researched. Protocols combining both active b12s have not been researched. The protocols acceptable to insurance companies are generally based on 1mg of injected cyanocobalamin each month or 1mg of injected hydroxycobalamin each 3 months after several “loading” doses as therapy for pernicious anemia. The more general and neurological effects of low but not desperately low levels of b12 have generally not been widely studied nor have the therapies effective for these conditions. B12 dependency has not been studied. The protocols would be considered as experimental for insurance purposes. As I have been told by researchers that no protocol with so many items could possibly be approved by an institutional review board for research it is likely to remain experimental for the indefinite future no matter how well it actually works.


WHAT ARE REASONABLE EXPECTATIONS? – The good, the bad and the ugly

ALL of these can happen if the necessary cofactors are also present. Until they are, symptoms may remain relatively unchanged. Changes will often be detected as starting within the first few doses of a newly added cofactor if that is a key cofactor. However, they may not start until the last necessary cofactor is present. That does not mean the previously started ones are not necessary. For some specific thing to heal may take 1000 steps. On 999 of those steps it is still not healed. Only after the final step will a specific thing be healed. There are many dependencies. Some symptoms may require changes in neurological functioning, biochemical functioning, mitochondrial functioning, epithelial healing, endothelial healing and neurological healing, both peripheral and central. This can start in minutes and finish in years. Active b12s are immediately active. There is no significant time required for it to work its way through a series of biochemical keyholes. There is no way to assure that any specific improvement may occur in any specific person. A return of sexual functionality for instance, may occur over months to years. There is no big signal saying “I’m back”. It may return as gradually as it went away. Without challenging the functionality one would never know it has returned. Most, but not all, of the symptoms on the list can correct partly to fully with both active b12s and cofactors.

END PART 1

 

[Freddd]

Active B12 Protocol - Part 2

Version 1.0, 08/15/09 – PART 2


· Active b12s will do everything that inactive cobalamins are proven to do for Pernicious Anemia and anything else.
· Active b12s put approximately 100 to 10,000 times as much active b12, 99+% unbound, into the serum as do inactive cobalamins. This causes a much faster diffusion into the tissues needing them and much faster response. As these are unbound b12s they are excreted more quickly and must be renewed daily for continued high level benefit. At least as much b12 will be bound depending upon biological limits. Three days without methylb12 and many people will begin to have return of symptoms. Three weeks without adenosylb12 and many people will start seeing some return of those symptoms.
· Active b12s produce much quicker results, often starting within 10 minutes for some kinds of symptoms.
· With active b12s mitochondria can start putting out more energy in 10 minutes.
· With active b12s neurological functioning can start changing in under 1 hour.
· With active b12s, hallucinations, if caused by deficiency, can diminish or disappear within hours.
· With active b12 moods can be affected, often starting within one hour.
· Muscle pains can start diminishing within days.
· Burning muscle pain can be gone in 10 days.
· Muscle spasms and knots can start diminishing within weeks.
· Muscles can become normal starting within weeks.
· Muscles can gain exercise tolerance, at the diminished level at which they are starting out within weeks and can grow and heal in response to exercise normally thereafter. Reasonable exercise is a must to stimulate healing of muscles and restoration of exercise capacity. One half to one percent a day increase appears to be a rate most can tolerate. One percent a day for a year is 37x increase. ½ percent a day for a year is 6x increase. This can apply to weight lifted or feet walked or minutes on the Nordic Track.
· Sores at corners of mouth can be gone within weeks.
· Irregular heartbeats, palpitations, tachycardia, may become pivot point symptom helping you home in on missing factors. For me it was B-Right twice a day AND 50mg of zinc daily after most other things were in place.
· Dermatitis and other skin problems can start normalizing over weeks to months.
· Red burning tongue can be normal within weeks.
· Burning mouth can be normal within weeks.
· Teeth hypersensitive to hot and cold can tend towards normal in months.
· Multiple chemical sensitivity can diminish over weeks to years
· Allergies and asthma can diminish over months to years
· Hair can return to neuropathic slick legs over months, usually finer and not as much, but some return
· Chronic and acute headaches can diminish and disappear over months to years
· Sleep disorders can diminish and disappear of weeks to months, dependent upon all necessary cofactors
· Sexual dysfunctions of a number of causes may correct over a period of time.
· Abnormal cells on PAP smear may return to normal in future on new tests.
· Coarsened skin texture and dark coarse hair in some neuropathic skin areas can return to normal over months to years
· Inability to focus eyes can disappear in days.
· Vertigo can disappear within days to years
· Ability to balance on one foot may return in months to years.
· Burning bladder can be gone within weeks
· Brainfog can start diminishing within hours dependent upon many factors being present. This often progresses in steps as additional cofactors are added.
· Neurological pain can start diminishing, fading over months to years.
· IBS can start changing in weeks if irritating foods are stopped, often dairy or gluten, subject to individual identification.
· Neurological degeneration – subacute combined degeneration may require larger injectable doses to stop it once it has started. Even more frequent larger doses may be needed to reverse it.
· Autoimmune problems do not appear to reverse. They appear to remain generally unchanged once started.
· Neuropsychiatric changes can heal over months to years with sufficient doses, may occur in several dose and/or cofactor dependent stages. This does not mean that “the old you” from “before” is going to come back. If you have gone through personality and mood changes on the way down you will change again on the way back. Flattened affect may become a new “normal” though not the same as “before”. Personality will be more “normal” but not the same as “before”. The brain relearns as it rebuilds. Mood can become very volatile during these changes. Anger and sadness often become prominent at first as a person begins to see how badly damaged they have been and how their life has been damaged and is in shambles. Coming to grips with this seems to be part of the healing process. It wasn’t easy for me or anybody I know who has gone through it. Those around us have seen it all along. We get to see it as we come out of it. It may have taken 20-30 years of deterioration and been relatively invisible. Coming out is much more rapid and hence quite visible.
· Memory and cognitive changes can be reversed in days to years. This does not mean that memory of the impaired period is regained. I have 20 years lost in the fog. Just call me Rip Van Winkle. It means that when you make a lunch date for next week you can remember to show up.
· Most symptoms attributable to CFS/FMS/ME/CFIDS can be gone within a year of all necessary factors being present.
· Severe neurological symptoms take longer.
· Comorbidity is uncovered.A person may have any number of other unrelated conditions that has overlapping symptoms and so is invisible until these have been removed. When 150 symptoms go away and 25 remain what the 25 relate to may become much more obvious. I know one person who uncovered cerebellular paraneoplastic syndrome just as an example.
· People have been able to come out of wheelchairs in weeks to months where the cause has been subacute combined degeneration which is often not diagnosed or mis diagnosed.
· Some processes that had been on “hold” may start up. For example my male pattern baldness stopped progressing for 20 years and has started up again. Conceivably it could be some other disease processes as well.
· Dropfoot and toe dragging can disappear in days to months.
· Numbness of feet and legs can diminish in days to months. Normal feeling may never return but functionality with enough feeling and motor control for normal functioning and reduced falls can return in months including motor control and location sense of individual toes. Regenerating nerves can be painful.

END PART 2

 

[Freddd]

Active B12 Protocol - Part 3

Version 1.0, 08/15/09 – PART 3


THREE HOUR QUESTIONAIRE AND SINGLE DOSE REPONSIVENESS TEST – ESTIMATED 60% DETECTION

This is the screening test and questionnaire detection method. It is far from complete or perfected at this point. It misses an estimated 40% of people who could potentially benefit. When the list of symptoms, signs and co-correlates is used as a questionnaire it can pick out persons who are likely to benefit. Though this has not been used on a large enough scale to determine the most significant items or set of items, several trends are seen. There are several clusters of symptom patterns. They might appear with named clustering such as FMS or CFS or without names such as a combination of IBS and asthma and multiple chemical sensitivity. These appear most predictive when they cut across types of symptoms. Clustering of endothelial tissue symptoms across body areas such as GI AND Lung AND Skin AND Oral AND bladder. Other clustering examples include endothelial tissue AND CNS neurological AND peripheral neurological. Lots of symptoms, all peripheral neurological don’t appear any more significant than only a few peripheral neurological. Generally, the more symptoms across more bodily areas however defined, the more likely to be one or more b12 deficiencies. People without symptoms generally have no discernable response at all. A meeting can be held based on people having certain symptoms or groups of symptoms. A short presentation can be made and informed consent forms signed. Then the questionnaires can be handed out along with one each of a 1mg methylb12 and 3mg adensoylb12 along with directions to put under upper lip for as long as possible exceeding 45 minutes. After people are done with the questionnaire based on entry conditions another short presentation can be made concerning effects of the active b12 tablets. Then people fill out the exit questionnaire that asks for what the effects are. They can be invited back for a follow-up session or go directly into that for those who responded or think they might if given more time and cofactors.



CAUTIONS

1. Can reverse Botox for approximately 24 hours.
2. Some people feel really good, best in years and then crash the next day, especially if they overdo because of how good they feel
3. Some people, especially those on cyanocobalamin injections or daily 1mg oral for years, have an extremely powerful reaction, sometimes causing fear and paranoia about active b12s.
4. People whose normal reaction to most things is anxiety will react with anxiety.
5. Symptoms may intensify, or at least the perception of them may intensify.


PEOPLE MISSED

1. People who don’t respond within 1.5 hours. Some people need a series of doses over a longer period to respond due to the nature of their symptoms.
2. People who don’t recognize a subtle response until they get home and realize that their mood has changed or they feel better or that driving was easier or whatever.
3. People who don’t respond without methylfolate or B-complex.
4. People who don’t respond without certain other basic or critical cofactors present
5. People who need a saturation dose of active b12s to enter CNS/CSF for response.





MINIMIZED ONE MONTH TRIAL TO DETECT ACTIVE COBALAMIN RESPONSIVNESS – ESTIMATED 80% DETECTION TRIAL




Needed items:

1) Jarrow 5000mcg methylb12 (brand specific because of comparative tests showing it to be one of two most outstanding brands and tests verifying absorbtion at 15%-25% compared to injections. Jarrow 1mg and 5mg produced strong differential effects over all other brands of 10 tested except Enzymatic Therapy 1mg. 60 tablets

2) Jarrow B-Right - a modest strength b-complex with multiple coenzyme b-vitamins and absolutely no cyanob12, suitable for twice a day usage. B-Right comes as 100 capsules with microencapsulated inositol to prevent stomach irritation sometimes caused by b-vitamins.

3) Country Life Dibencozide 3mg - Adenosylb12, tested as 5 stars, also tested for absorbtion at 15%-25% compared to injection - 60 tablets

4) Solgar methylfolate 800mcg - One of only 2 brands of methylfolate available as a vitamin, half the price of the competition. Several prescriptions brands exist. Exclusive manufacturer of methylfolate restricting what vitamin companies can produce a product and requiring strict quality controls meeting pharmaceutical standards, 100 tablets

5) Potassium - to prevent hypokalemia caused by a sudden burst of healing. If person is on Furosomide (Lasix) or several other diuretics this is very important. If potassium is on the low end of scale (3.5-4), it’s also important. Normal supplement is 99-100mg. 1-3 a day of these is usually enough to prevent problem though some need more as well as dietary choices like bananas. Monitor this with your doctor, especially the first 90 days following initial startup and critical factor additions.

6) Omega3 fish oils. EPA & DHA are the two active factors. Some people suggest a specific ratio between these works best. It is generally agreed that they ought to total in excess of 500mg/day. I take 1800mg/day. I take the Costco house brand and have no specific suggestions as to brand, source or ratios. These are essential to heal the myelin which is one kind of damage that occurs with b12 deficiencies.

END PART 3

 

[Freddd]

Active B12 Protocol - Part 4

Version 1.0, 08/15/09 – PART 4

I am one of the more extreme cases of cobalamin lettered diseases surviving to adulthood as most are thought to die as children, along with my 3 children. Before antibiotics none of us would have survived childhood. It appears that none of us can convert cyanob12 to either active form. None of us can interconvert active cobalamin forms to each other sufficiently and none of us can convert folic acid sufficiently to methylfolate. We all need SAM-e and L-carnitine for normal functioning. Further it appears that all of us have difficulty getting sufficient amounts of both active b12s into the CSF. I don't think that most people have all of those things going on but there has never been any widespread testing for all of the above though each has been individually defined. I have posted near this the descriptions of Cobalamin A, B, C, D etc diseases which specify the cobalamin conversion problems and define them by what enzymes are missing. The problems of getting cobalamins into the CSF are just starting to be looked at in terms of CFS/FMS/CFIDS/ME, Alzheimer’s etc but the markers are not well defined. We have determined pragmatic tests that appear to get at the problems and the test is also the therapy.

The above list of supplements, because they use the active substances make no assumptions about a person’s ability to convert inactive substances such as cyanob12, hydroxyb12, folic acid, B6 or calcium pantothenate to the active coenzyme forms. This allows most everybody to respond if they are deficient regardless of genetic status in these matters. It may be that the people who develop the most and most severe symptoms are exactly the ones who can't make one or more of the conversions. It was so for me and my children. So a recent study using cyanob12, folic acid and b6 to prevent Alzheimer’s was quite possibly doomed to failure because of its underlying false assumptions.

The tests then to be performed are as follows. This is to glean maximum information as to what is going on and to be able to see symptom regressions to earlier forms when they occur, and to guide future supplement choices for fine tuning.

Additional basic supplements would be Vitamins A, D, E, C, plus Zinc 50mg, Calcium, CoQ10, magnesium, trace minerals, lecithin, Alpha Lipoic Acid. These would allow healing to continue once started and maximize effects. Caution is advised with CoQ10 as at certain stages of healing it has produced sizable increases in blood pressure in some participants. It would not hurt to start the basics at the same time but are not part of most basic test of principle if a person wants to do only the absolute minimum. I suggest a high gamma E 8 factor complex but can’t offer any hard evidence for it at this time. The NOW Foods Gamma E complex appears excellent. They are required to continue the 100% TRIAL.

There are many additional supplements that may be of benefit, especially chromium GTF, possibly green tea extract, grape extract and other similar substances. The effects of other amino acids are not fully explored yet and may make large differences for some people. Then there are supplements like Pregnenolone which is a hormone precursor, DHEA, 5-HTP and others. Do some research on these and decide for yourself if they might be worth a trial. They may even be terribly important keys for some people. Some of these are restricted in some countries. Carnitine can only be ordered into Canada with a form from your doctor. This is a work in progress, not finished. It has such profound effects for so many people I don’t feel that I can hold it up the 90% effects waiting for the last 10%. I think those will come about by the sharing of information of those who try such things. The effect of the internet is to allow us to run 100,000 experiments in parallel and find out in a few years what could otherwise take centuries.


Alerts:
1) CoQ10 can cause substantial increase in blood pressure during early stages of healing in some persons taking methylb12. The effects with Adenosylb12 are unknown.

2) Methylb12 can reverse Botox injections for about 24 hours per dose. The effects of Adenosylb12 are unknown in this.

3) Methylb12 can obscure the course of tetanus by preventing neurological effects thereby delaying diagnosis and treatment. The effects of Adenosylb12 are unknown in this.



1 - Print out list of symptoms or insert in spreadsheet like Excel and score by present condition and by each prior ten year interval, or other periods as make sense. Each symptom can be scored on a scale of 0-7, 0 being none, 7 being worst possible. As some of the symptoms are later stages of earlier symptom progressions this shows up by scoring for presence in earlier decades and seeing what comes and goes. Add person’s additional symptoms that are not already on the list. Most chronic symptoms become ignored after 10 or 20 years of being told they don't matter by doctor after doctor. Be sure to include everything.

2 - Take supplements to following schedule

END PART 4

 

[Freddd]

Active B12 Protocol - Part 5

Version 1.0, 08/15/09 – PART 5


Week 1

If additional vitamin, mineral, supplement basics are chosen, split between morning and evening meals.

Methylb12 - In morning after breakfast one tablet under tongue and/or upper lip (break tablet) making last as long as possible. 45 minutes gives approximately 15% or better absorbtion duplicating 750mcg injection of methylb12. Two hour duration gives approximately 25% absorbtion duplicating 1250mcg methylb12 injection. It affects melatonin timing.
Note immediate and daylong effects.

1 methylfolate with morning meal


With morning and evening meal 1 B-Right capsule, 1 potassium tablet or capsule, more if muscles spasms while relaxed occur. Call doctor and get tested for potassium. In addition, all other basic vitamins and minerals taken should be divided between morning and evening meals.

Note effects each day. The first doses of methylb12 may have all the subtlety of a sledge hammer. I was literally floored for an hour by my first dose and it faded over about 3 weeks. There often will be an increase in inflammatory responses, intensification of symptoms, and/or a regression of symptoms to earlier stages, activation of not noticed symptoms etc. This is entirely normal and expected. ANY response should be considered a positive response. Those that normally respond with anxiety will do so and need additional support during the first dose especially. Anxiety is a normal b12 deficiency symptom which many have. There are a number of theories as to why this worsening or intensifying of symptoms. Dr Myhill says toxins are being purged. Dr Wheatley in the "scarlet pimpernel" speculative papers says that b12 is involved in regulating inflammation and that first it increases and then decreases. When it does happen don't let the person be scared off. Those who have been on substantial cyanob12 doses for years often have the most intense and fearful reactions. As methylb12 reaches a new equilibrium in the body, the effect fades. Higher doses get it over with faster. Lower doses draw it out for much longer. There is NOT linear proportionality of intensity with increased doses. A 5mg sublingual isn’t significantly more intense than 1 1mg sublingual.

At end of week score symptoms again.



Week 2 - Week 4

If additional vitamin, mineral and supplement basics are chosen, split between morning and evening meals.

Dibencozide (adenosylb12) - In morning after breakfast, before methylb12, one tablet under upper lip making it last as long as possible. 45-120 minutes gives approximately 15%-25% or absorbtion duplicating 450-750mcg injection of methylb12 via colorimetry.

Note: Take note of initial effect on first day, it may not be duplicated on additional days. Adenosylb12 is not lost as quickly once it enters mitochondria.

Methylb12 - In morning after breakfast one tablet under tongue and/or upper lip (break tablet) making last as long as possible. 45 minutes gives approximately 15% or better absorbtion duplicating 750mcg injection of methylb12. Two hour duration gives approximately 25% absorbtion duplicating 1250mcg methylb12 injection. It affects melatonin timing

1 methylfolate with morning meal

With morning and evening meal 1 B-Right capsule, 1 potassium, and additional supplements.

At end of each week score symptoms again.

END PART 5

 

[Freddd]

Active B12 Protocol - Part 6

Version 1.0, 08/15/09 – PART 6


Week 5 - Day 1

Do everything as in weeks 2-4.

Then a onetime test now that equilibrium has been reached on active b12s at normal levels.

At some time during day: Take 10 Jarrow 5mg methylb12 over a period of 90-120 minutes, adding two tablets every little while making each tablet last at least 45 minutes saturating oral cavity. This will duplicate the effects of a 7.5mg SC injection of methylb12 which is a suprathreshold dose for neural healing as suggested by Japanese studies. A darkening of the urine anywhere from dark yellow to orange or pink will be observed verifying absorbtion at 15% or better and functioning of one specific kind of kidney tubule. Assuming kidneys are functioning correctly, if this much cobalamin is being absorbed it will be visible. Note all effects. This will probably not be anywhere near as powerful as initial dose but any noticeable effect appears to indicate a reduced CSF cobalamin level (pragmatically based hypothesis) of methylb12 and will affect previously not affected symptoms, especially neurological and neuropsychiatric or increase effect, for several hours or longer.

Week 5 - Day 2

Do everything as in weeks 2-4.

Then a onetime test now that equilibrium has been reached on active b12s at normal levels.

Take 17 Country Life 3mg dibencozide tablets over a period of 90-120 minutes, adding 3-4 tablets in multiple locations every little while making each tablet last at least 45 minutes saturating oral cavity. This will duplicate the colorimetry effects of a 7.5-10mg SC injection of methylb12 which is a suprathreshold dose for neural healing as suggested by Japanese studies. A darkening of the urine anywhere from dark yellow to orange or pink will be observed verifying absorbtion at 15% or better and functioning of one specific kind of kidney tubule. If kidneys are functioning normally this much cobalamin will be visible if it is absorbed. Note all effects. This will probably not be anywhere near as powerful as initial dose but any noticeable effect will indicate a reduced CSF level (pragmatically based hypothesis) of adenosylb12 in neural mitochondria and will affect previously not affected symptoms or increase effect, for several hours or longer. The effects of dibencozide are more subtle than methylb12 generally. Might affect perceptual "brightness", mood, energy and harder to put into words type things. ANY effects should be noted even if difficult to describe.


A person with NO effects at all to any of these doses and no effect over the month is probably not functionally deficient. This 80% test does not detect everybody. Those requiring any or all of the critical cofactors to have any response may have a very minimal or no response.

Reorder time has come. All the basics should be added if they were not already present. After the rest of the basics, the critical cofactors should be added 1 or 2 at a time, perhaps a week apart.


EVALUATION OF 5 WEEK TRIAL – Active B12s


1. If there is any effect, even if unpleasant, continue to 100% detection trial and add all basics and then start adding critical cofactors and evaluate and repeat large dose tests.
2. If there is no effect at all, realize that as this is incomplete it misses around 20% of those who could benefit by taking the basics and critical cofactors not previously included. Re-evaluate 3 months after adding last item and repeat large dose test.
3. If there is ANY additional effect from 50mg challenge dose of methylb12, titrate to 25mg per day of methylb12 as 5 times 5mg doses. After equilibrium is reached, 3 months or so try both 25mg single dose for 2 hours and 50 mg dose for 2 hours at different times. If 25mg single dose makes a difference continue on this daily until equilibrium is reached and no daily effect noted. Then try 50mg dose in 2 hours. If this makes a difference, ANY difference, talk to doctor about 7.5-10.0mg methylb12 injections. This 7.5-10mg injection is a suprathreshold dose that appears to cause more methylb12 to enter the CSF/CNS for an effect on the Central Nervous System. This is the approximate dose that may be required to stop certain types of degeneration such as subacute combined degeneration, but not necessarily limited to it, once started if the cause is a Cerebral Spinal Fluid b12 deficiency. There is some evidence that damage from other causes such as toxins and diabetic neuropathy may also respond. In my case 3x10mg or 4x7.5mg subcutaneous mb12 injections per day are required to reverse foot numbness, loss of position sense and motor control of lower leg and foot and toes.
4. If there is ANY additional effect from 51mg challenge dose of adenosylb12, titrate to 24mg/day, single dose and multiple doses as in number 3 above. When equilibrium is reached and no further daily effect is noticed at either single dose or multiple doses, try the 51mg challenge dose. Find what frequency will maintain this in equilibrium. It may very well be a single dose per week to a single dose per month. As adenosylb12 achieves its effects locked into place in the mitochondria it doesn’t diminish as rapidly as methylb12. If methylb12 injections are taken I have found that the adenosylb12 , once every 5-7 days, can be maintained by taking 15mg (or whatever you determine maintains CSF equilibrium for you) as single dose 2 hours following 7.5mg SC injection or at any time during day if 30mg/day of mb12 in several SC injections is taken. It appears to join with the mb12 in riding the diffusion gradient into the CSF.


• ZONE 3A1 – Methylb12 injection, 7.5mgs SC to 25mgs SC per dose, 1-2 doses per day or 50-60mgs sublingual (Jarrow) saturating oral cavity for 90-120 minutes, 1-2 doses per day. Brain and cord healing, energy and mood, appears dependent upon sufficient methylfolate being present. Neurological deterioration stops, limited amount of healing

• ZONE 3A2 – Methylb12 injection, 7.5mgs SC to 25mgs SC per dose, 3-4 doses per day or 50-60mgs sublingual (Jarrow) saturating oral cavity for 90-120 minutes, 3-4 doses per day. Substantial brain and cord healing, energy and mood, appears dependent upon sufficient methylfolate being present.

• ZONE 3B1 – Adenosylb12 sublingual (Country Life), 42-60mgs per dose saturating oral cavity for 90-120 minutes, 1 dose per week to 1 dose per month. Brain and cord healing, energy and mood, but different from methylb12 was achieved with adenosylb12

• ZONE 3B2 – Adenosylb12 sublingual (Country Life), 15mgs per dose under upper lip for 90-120 minutes, 1 dose per day to 1 dose per week taken in conjunction with 7.5mg mb12 injection, allowing diffusion into CSF with mb12. Brain and cord healing, energy and mood, but different from methylb12 was achieved with adenosylb12


END PART 6

 

[Freddd]

Active B12 Protocol - Part 7

Version 1.0, 08/15/09 – PART 7



NEAR 100% DETECTION TRIAL

This includes all the essentials and basics


Then further evaluation should be made. Additional CRITICAL "showstopper" cofactors are:

1) FOR ENERGY, ADENOSYLB12 REINFORCEMENT in ATP cycle - Only one may be needed or all or any combination may be needed for maximum effect. L-carnitine fumarate & Alpha Lipoic Acid (ALA) was the most potent one for me, like a sledge hammer, followed by Creatine & d-Ribose. As energy production affects mood these all also affect mood. Lack of neuronal mitochondrial function is little explored.
· L-carnitine (person needs to try each form, fumarate and acetyl to find most effective for them, increased my aerobic capacity. Could provoke heavy duty response
· Alpha Lipoic Acid - carnitine "helper"
· Creatine – involved in later stages of ATP cycle
· D-ribose – involved in later stages of ATP cycle
ADDITIONAL THERAPUTIC DEVICES
There are two electronic devices available that may have a beneficial effect. One is the ReBuilder, sold for the purpose of re-establishing nerve channels and is a modified TENS & EMS unit. I and some others have had benefit from it, at the very least significantly reduced neurological pain. The other is also a modified TENS unit and is called The Slightest Touch and is sold as an orgasm augmentation unit, a “toy”, not as a therapy device and is not tested or claimed as such. It does appear to work however, in much the same way as the ReBuilder And when used as directed appears to produce the claimed results, and more. It is also more fun to apply as directed. It appears to do at least some of the same things as the ReBuilder at least to the extent of re-establishing certain neurological pathways when used as directed. A footbath that comes up to the lower calf will also stimulate the same nerve pathways with the ReBuilder or use with stick on TENS electrodes. The ReBuilder is more versatile and costs more. There may be other devices of benefit with neuropathies using the same or different principles.

DIFFERENT ENERGY AND EXERCISE PROBLEMS
· getting sustained exercise started, first 15 minutes
· keeping exercise going into the aerobic period after 15 minutes or so
· energy recovery after exercise
· muscle recovery after exercise
The various cofactors listed are involved in these different stages of energy and exercise. All of them may be needed. This list is not complete. There are other factors that affect these, sometimes very indirectly. Chromium GTF and vitamin E affect blood sugar. Other things can affect glycogen storage. This is often where the fine tuning is required.

2) Energy and mood METHYLB12 REINFORCMENT, methylator reinforcement, DNA methionine/homocysteine cycle.
· SAM-e, like a sledge hammer for me, titration from 100mg or less may be needed for heavy duty responder, 200-400mg appears adequate for most
· TMG - TriMethylGlycine, smoothed out the effects of l-carnitine for me,
· DMG – DiMethylGlycine may be preferable for some people instead of TMG; individual trial only can determine that.
These are "showstoppers" because either b12 alone may have only minimal effects without one or more, in unknown combinations, of these various items. The one most recently added may have a huge effect but only because the other three needed were already present. I would suggest adding only one or two at a time to avoid too powerful responses. I found that ALA and carnitine, ribose and creatine, with SAM-e all by itself and TMG added in shortly after carnitine to be a workable ordering. If you want to see what is needed, i.e. ribose, after starting all factors try discontinuing only that for a while and do the start and stop several times to see if it has an effect on the whole. Ribose didn't have an effect for me early on but does now with the other factors already present. Some people have found ribose to be far less subtle.

For me, Of the 175+ symptoms I used to have on that list I have 27 of them left, mostly from neurological damage from long term deficiency or a car crash in 1972. And those are generally far diminished from the way they were.

FACTORSTO AVOID
· Glutamine & NAC (n-acetyl cysteine) as precursors to glutathione,
· Un-denatured whey as precursor to glutathione
· Any form of glutathione, oral or IV infusion (Myers cocktail optional ingredient)
· Precursors of several varieties as ingredients to separate multi ingredient supplements including such as NAG – n-acetyl glutamine and various forms of cysteine.
If a person has been taking hydroxycobalamin and using glutathione then many symptoms merely remain in place. If a person has been taking active b12s, especially methylb12 then taking glutathione causes within a couple of days hard onset of previous b12 deficiency symptoms. With glutathione this happens far more quickly than if a person merely quits taking active b12 or changes to inactive cobalamins. Further the amount of b12 visible in the urine goes way up within hours. The hypothesis is that glutathione reacts chemically with the methylb12 forming glutathionylcobalamin, an inactive form. This inactive form then needs a specific enzyme, which may be lacking in some people, to convert it back to methylb12 and/or adenosylb12 in the cell. This forces the active b12 through a keyhole limiting the amount of active b12 available. Those lacking the requisite enzymes can’t convert. Further, the active b12 is converted to a form that appears preferred for kidney excretion.


1) Serum cobalamin test -
· A low result indicates b12 deficiency in a general sense even if the symptoms are too subtle to be seen yet.
· A higher result means you have more b12 in your serum the moment it was taken. There is no level that means that a person may not have b12 responsive symptoms. In some studies people with over 1500pg/ml had b12 responsive symptoms.
2) uMMA
· A high level means that the biochemical process involving adenosylb12 generating ATP broke at a specific place generating MMA instead of ATP
· A low level does not mean that you have sufficient adenosylb12
3) Hcy
· A high level indicates that homocysteine is not getting changed back into methionine properly, probably because of a lack of methylb12, but also possibly a lack of methylfolate or p-5-p
· A low level does not indicate sufficient methylb12, methylfolate or p-5-p

All three of these tests can alert a person to certain problems but totally lack the ability to say that there are no active b12 responsive deficiency symptoms. Further they are totally incapable of detecting CSF/CNS level deficiencies that may exist independently of bodily deficiencies. They are completely incapable of “ruling out” b12 deficiency and yet are used that way every day.


END PART 7

 

[Cynthia]

B12 shots

SYMPTOMS, SIGNS AND CO-CORRELATES OF METHYLB12, ADENOSYLB12, METHYFOLATE AND SELECTED COFACTOR DEFICIENCIES
LAST UPDATE - Version 1.01, 08/02/09


This is an international list of symptoms. One might think that b12 deficiency is b12 deficiency. Not according to the lists that appear in various countries. One of the factors appears to be which forms of inactive cobalamins are used in the country as vitamins and for therapy. The UK which uses hydroxyb12 has a substantially different list than the USA which uses cyanob12. The UK list reflects that they also define ME as a disease and that is not done in the USA. A list from India with a lot of vegetarians has different priorities than either the USA or UK in which meat eaters predominate.

Further, instead of just saying peripheral neuropathies - paresthesias for instance, the various paresthesias are broken out giving a person more opportunity to recognize or understand what is being asked for. Further, it allows tracking and progression over time. B12 deficiencies don't cause sudden numbness of the feet. This might take months to years to develop going through a progression of paresthesias. Further, symptoms which the patient might report and signs that the doctor might note are both given giving the appearance of redundency. In a computerized scoring system it makes no difference. Some people will recognize it one way, others might use more technical terms. What's important is that they recognize it. I have also included specific unique descriptions that might catch a few additional people. Then the list has been expanded by all the symptoms that respond to the active b12s. This is a much broader list than what responds to inactive cobalamins. Then there are the co-correlates such as various autoimmune diseases that have a high correlation with low b12 but no causality determined and which once occurring, do not change back. On shear numbers, I had 185 of the nearly 300 symptoms, signs and co-correlates in every category prior to 05/21/03. I'm down to about 27 now.

mouth sensitive to hot and cold
sore burning tongue
beef-red tongue, possibly smoother than normal
sore mouth, no infection or apparant reason
teeth sensitive to hot and cold
canker sores
burning bladder (no UTI)
painful urgency (no UTI)
burning urethra (no UTI)
burning muscle
accumulating muscle pains following exertion
sore muscles
lack of muscle recovery after exercise
exercise does not build muscle
extremely sore neck muscles reversing normal curvature of neck
exercise deblitates for up to a week, making things much worse
painfully tight muscles, especially legs and/or arms
frequent muscle spasms anywhere in body
muscle pain especially around attachment points to bones
Eighteen severely tender muscle spots of FMS
Bursitis
dyspepsia - sick stomach, nausea, regurgitation, vomiting, bloating, not emptying
flatulence
altered bowel habits
abdominal pain
loss of appetite for meat, fish, eggs, dairy, the only b12 contining foods, nutrient specific anorexia
intermittent constipation
intermittant diarrhea
irritable bowel syndrome
Crohns disease (direction of causality if any not established)
Celiac disease (direction of causality if any not established) - gluten sensitivity
Dairy sensitivity
sores, ulcers and lesions along entire GI tract or any part
anorexia
Bullimia
reduced libido - loss of sexual desire
loss of orgasmic intensity
unsatisfying orgasms
inability to orgasm
loss and/or change of genital sensations - "gloved" loss of sensation
burning genital skin sensation
unable to become aroused
reduced testosterone

paleness
rapid heart rate
heart arythymias
shortness of breath
heart palpitations
weak pulse
congestive heart failure
arteriosclerosis
Widespread pain throughout body
Hypothyroid (direction of causality if any not established)
High homocysteine
High urinary MMA

dizziness - even unable to walk
vertigo

irritable
depression
SAD - Seasonal Affective Disorder
mental slowing
personality changes
chronic malaise
poor concentration
moodiness
tiredness
mood swings
memory loss
listlessness
impaired connection to others
mentally fuzzy, foggy, brainfog
psychosis, including many of the most florid psychosis seen in literature, megoblastic madness
Alzheimer's
delirium
dementia
paranoia
delusions
hallucinations
strange "smells" that are not present like linen being ironed, burnt odors or tidal flats etc
strange "sounds" that are not present, rustlings, mummurings, detonations etc
deja vu experiences
anxiety or tension
nervousness
mania
impaired executive function
cognitive impairment
memory impairment
Hypersensitivity to touch
Hypersensitivity to odors
Hypersensitivity to tastes
Hypersensitivity to clothing texture
Hypersensitivity to chemicals
Hypersensitivity to body malfunctions, symtoms
Hypersensitivity to sounds and noises
Hypersensitivity to light and visual stimuli
Hypersensitivity to blood sugar changes
Hypersensitivity to internal metabolic changes
Hypersensitivity to temperature changes
Hypersensitivity to foods
mild to extremely severe fatigue
continuous extremely severe fatigue
easy fatiguability
severe abnormal fatigue up to and including apparent paralysis leading to death
spastic paralysis
weakness

sleep disorders
non restorative sleep
lack of dreaming
Night terrors
Prolonged hypnogogic state transitioning to sleep
Sleep paralysis
alteration of touch all over body, normal touch can be unpleasant and painful
alterations and loss of taste
alterations and loss of smell
loss of smell and taste of strawberries specifically
loss or alteration of smell and taste of potato chips specifically
roughening and increased raspiness of voice, mb12 can smooth it outin mid word
blurring of vision - can be sudden onset and sudden return
dimmed vision - usually not noticed going into it because change can be very slow or present for life
Visual impairment can be seen; ophthalmological exam may show bilateral visual loss
optic atrophy
optic neuritis
optic neuropathy
centrocecal scotomata
intolerance to bright light
diminished hearing - gradual onset or present for life, sudden return possible
unclear hearing, garbled
tinnitus - ringing in ears
always feeling cold
intolerance to loud sounds
intolerance to multiple sounds
inability to pick pick out one voice amongst many
Brainstem or cerebellar signs or even reversible (with mb12) coma may occur
neural tube defect not caused by folate deficiency or child with it
demyelinated areas on nerves
subacute combined degeneration
axonial degeneration of spinal cord
unsteadiness of gait
ataxic gait, particularly in dark
positive Romberg
positive Lhermittes
neuropathies, many types
progressive bilateral neuropathies
demyelination of nerves - white spots on nerves on MRIs
loss of detail and sensual aspects of touch all over body
paresthesias in both feet - burning, tingling,cobwebs, wet, hairs, pain, numbness, etc
paresthesias in both legs - burning, tingling, cobwebs, wet, hair, pain, numbness, etc
paresthesias in both hands - burning, tingling, cobwebs, wet, hairs, pain, numbness, etc
paresthesias in both arms - burning, tingling, cobwebs, wet, hairs, pain, numbness, etc
Loss of position sense is the most common abnormality (or vibration sense)
Loss of vibration sense is the most common abnormality (or position sense)
Loss of sense of joint position
hands feel gloved with loss of sensitivity
feet feel socked by loss of sensitivity
trembling
neuropathic bladder
unable to release bladder, mild to severe
urinary incontenance - occasionally to frequently
fecal incontinance - occasionally to frequently
sudden electric like shocks/pains shooting down arms, body, legs shooting down from neck movement
standing with eyes closed, a slight nudge or bump causes loss of balance
most patients have signs of both spinal cord and peripheral nerve involvement
The effect on reflexes is quite variable
Motor impairment may range from only mild clumsiness to a spastic paraplegia
clumsiness
slowed nerve impulses
decreased reflexes
difficulty swallowing
brisk reflexes
decreased deep tendon reflex
toes turn up instead of down in reflex to sole stimulation
Positive bilateral Babinski reflex
Foot Drop
impaired white blood cell response
poor resistance to infections
easy bruising
pronounced anemia
macrocytic anemia
megablastic anemia
pernicious anemia
decreased blood clotting
low hematocrit
MCV > 92-94 first warning, MCV > 97-100 alert
elevated MCH (Mean Corpuscular Hemoglobin)
elevated LDH
big fat red cells (when said this way usually with happy or healthy modifying it completely misinterpreting results of MCV
platelet dysfunction, low count
white cell changes, low count
hypersegmented neutrophils
migraine headache cycles
headaches
inflamed epithelial tissues - mucous membranes, skin, GI, vaginal, lungs, bladder
inflamed endothelial tissues - lining of veins and arteries, etc
high CRP without infection
mucous becomes thick, jellied and sticky
dermatitis herpetiformis, chronic intensely burning itching rash
frequent infected follicles
Seborrheic dermatitis
dandruff
eczema
dermatitis
skin on face, hands, feet, turns brown or yellow if anemia occurs
poor hair condition
thin nails
transverse ridges on nails, can happen as healing starts
splits/sores at corners of mouth
Hyperhidrosis - excessive sweating
Bariatric surgery
glutathione, glutathione producing supplements such as NAC/glutamine
Dilantin,
tegretol and some other medications
Relatives, grandparant, parent, sibling, child, grandchild ever needing b12 shots or supplement
coma
seizures
brain atrophy with ileal tuberculosis preventing b12 absorbtion


MEN
erectile disfunction
low sperm count
poor sperm motility
Poor sperm quality
Zero sperm count


WOMEN
post partum depression
post partum psychosis
False positive pap smears, noncancerous cellular changes
menstrual symptoms
Frequent miscarriage
child with neuro tube defects
PMS


STARTING AS INFANT OR CHILD
delayed myelination
failure to thrive
autism
delayed speech
depression
frequent or continuous toncilitis
frequent strep
frequent pneumonia
frequent longlasting supposed viral illnesses that linger and linger and linger
everything goes to the lungs for extended periods
headaches
growing pains
skin problems
dandruff
allergies
asthma
continuous swolen glands in neck
low grade fever for years
Night terrors
Prolonged hypnogogic state transitioning to sleep
Sleep paralysis
seizures
coma

Hi Fredd...
New here, but saw this on the B12. I've been giving myself shots for years now. My dr. explained it wasn't just for fatigue, but for my sensitive nerves. Plus, I need the B12 to hold in my iron. So, I'm also taking a capsule called Trinsicon..I'm getting lots of B12. I see your list of many things I can relate to. I have to say, there is one "huge" difference I've noticed since I started B12...besides my iron levels..and that is I don't have panic attacks anymore. Now, I'm not sure if this is something that the B12 has done for me or not.
Also, there was a lady asking how to buy B12..my ins. covers it...3 dollars is all. My nurse taught me how, and my husband in case I need him to help. I usually give it in the top of my legs, more so than the hips, because I have large numb areas on my legs..but..have noticed that I am starting to get numb areas on my hips. Just a little MS thing. Thanks for sharing all of this on B12, it's very interesting...the B12 has helped me. Cynthia

 

[Freddd]

Hi Fredd...
New here, but saw this on the B12. I've been giving myself shots for years now. My dr. explained it wasn't just for fatigue, but for my sensitive nerves. Plus, I need the B12 to hold in my iron. So, I'm also taking a capsule called Trinsicon..I'm getting lots of B12. I see your list of many things I can relate to. I have to say, there is one "huge" difference I've noticed since I started B12...besides my iron levels..and that is I don't have panic attacks anymore. Now, I'm not sure if this is something that the B12 has done for me or not.
Also, there was a lady asking how to buy B12..my ins. covers it...3 dollars is all. My nurse taught me how, and my husband in case I need him to help. I usually give it in the top of my legs, more so than the hips, because I have large numb areas on my legs..but..have noticed that I am starting to get numb areas on my hips. Just a little MS thing. Thanks for sharing all of this on B12, it's very interesting...the B12 has helped me. Cynthia

Hi Cynthia,

If the shots you are getting aqre cyanob12 they are not helping much. Methylb12 injections, which I take are an easy 1000 timkes more effective, really. Also, as I do subcutaneous injections, much easier and virtuallyt painless. I use a 31 gauge short needle (5/16"). I do 3 x 10mg or 4x7.5mg daily and it first stopped the spread of numbness and then reversed it. Let's talk about this. I think you can do a lot better.

 

[winston]

B12

Hi Fredd, I am new here and very curious about the B12 treatment that gave you such a good recovery. I am a 60 year old female and first got ill in 2001. It was more CFS than FMS. I tried every treatment I could find and only until I did the Atlas Profilax did I start to recover. That was about 3 years ago and it took about 18 months to be 90% well. Something is still wrong, I can't exercise much. I tried weight training and within 1 hour I was exhausted. I tried pilates on a reformer and within 1 hour I was exhausted and it lasted sometimes 3 days. What caught my attention was the symptom of "sore tongue". My tongue has been so sore, like it has been burned and my tongue is swollen. Do you think this treatment could work for me? Should it be started with the Country Life Dibencozide. I have been on the wrong B12 you talked about. I am not excited about getting worse before getting better. I don't have a Dr. who can help. I am not as ill as I was 8 years ago but I am not well. I am married to a dentist and I have had lots of mercury fillings in my mouth, he took them all out. Had a hair analysis and the mercury was off the charts. My husband never uses mercury fillings but he does remove them from his patients and he probably had mercury in all the shirts that I have been washing for years. Thank you for all you are doing.

Lena