B12 insufficiency/MS

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B12 insufficiency/MS

Postby lyndacarol » Sun Jun 01, 2014 12:06 pm

I propose a forum dedicated to vitamin B12 deficiency (starting with the definition from the book, Could It Be B12? by authors Sally M. Pacholok, RN, BSN and Jeffrey J. Stuart, D.O. and the list of the signs and symptoms starting with, from the following article: "… peripheral neuropathy, the commonest neurological manifestation of vitamin B12 deficiency…"). The connection between MS and B12 was made long ago, as published in 1992 in the Journal of Neurology, Neurosurgery, and Psychiatry:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC489070/

"Multiple sclerosis and vitamin B12 metabolism"

… It is remarkable that, despite the fact that the age range is so different, the sex, racial and geographical distribution of MS and PA [pernicious anemia – the extreme form of B12 deficiency] are similar. Thus PA is a higher prevalence in northern Europe compared with Southern Europe in tropical areas, a diminishing prevalence from the north to the south of the UK and a higher incidence in white than black North Americans. The female-to-male ratio in both disorders is 1-3:1. Najim Al-Din et al have also drawn attention to some similarities in the HLA associations of MS and PA.…


There are many footnotes to support these statements.

Must watch: "Everything You Want Your Doctor to Know about Vitamin B12"

http://www.youtube.com/watch?v=BvEizypoyO0

I highly recommend this 50-minute documentary from the filmmaker Elissa Leonard, featuring Sally M. Pacholok, RN, BSN & her husband Jeffrey J. Stuart, D.O. (authors of the book, Could It Be B12? An Epidemic of Misdiagnoses); Lawrence Solomon, M.D., hematologist with Yale Medical School; Ralph Green, M.D., hematologist at UC Davis; and Donald Jacobsen, PhD, at the Cleveland Clinic (Homocysteine Research Lab).

@1:23 "The neurological manifestations well precede the hematological manifestations."

@1:46 "In 1948 scientists isolated a red crystalline pigment and named it vitamin B12. It is a primordial molecule responsible for the health of all the DNA in all our cells. The Framingham Offspring Study suggests 40% of Americans have suboptimal B12."
Cardinal Signs of Anemia Due to Vitamin B12 Deficiency:
Fatigue
Shortness of breath
Dizziness
Pale/yellowish skin
Swollen tongue that may appear dark red
Weight loss
Diarrhea
Numbness or tingling in your hands and legs
Muscle weakness
Irritability
Unsteady movements
Mental confusion or forgetfulness

Signs and Symptoms of B12 Deficiency:
#1 Peripheral Neuropathy
Tingling/Numbness
Sore Mouth or Tongue
Fatigue
Anxiety
Irritability
Depression
Weakness
Abnormal Gait
Mental Impairment
Visual Disturbances
Migraine
Orthostatic Intolerance
Chest Pain
Tachycardia
Difficulty Breathing
Edema
Elevated Homocysteine
Elevated MMA
Stomach and G.I. Problems
Blood Abnormalities
Neurological Lesions
Limb Movement Disorders
Psychosis
Thoughts of Suicide

Risk factors for B12 deficiency:
Vegetarian Diet
Pregnancy
Age over 50
Low Stomach Acid
Celiac Disease
Food Allergies
Eating Disorders Parasites
Use of Acid-Blockers
Use of Oral Birth Control Pills
Use of Metformin
Nitrous Oxide Anesthesia
Pernicious Anemia
Autoimmune Disorders
Pancreatic Insufficiency
Stomach Surgery
Intestinal Bacterial Overgrowth
Peptic Ulcer
Transcobalamin Deficiency


Here is more background information on the documentary: http://b12awareness.org/2013/01/21/2013 ... completed/
Last edited by lyndacarol on Tue Jun 03, 2014 8:38 am, edited 2 times in total.
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Re: B12 insufficiency/MS

Postby jimmylegs » Sun Jun 01, 2014 1:19 pm

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Re: B12 insufficiency/MS

Postby lyndacarol » Sun Jun 01, 2014 5:16 pm

As posted elsewhere by another – there are many common agents that reduce blood levels of vitamin B12:

http://www.mayoclinic.org/drugs-supplem ... b-20060243

Use cautiously in people taking the following agents, as they have been associated with reduced absorption or reduced serum levels of vitamin B12: ACE inhibitors, acetylsalicylic acid (aspirin), alcohol, antibiotics, anti-seizure agents, bile acid sequestrants, chloramphenicol, colchicine, H2 blockers, metformin, neomycin, nicotine, nitrous oxide, oral contraceptives, para-aminosalicylic acid, potassium chloride, proton pump inhibitors (PPIs), tobacco, vitamin C, and zidovudine (AZT, Combivir®, Retrovir®).
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Re: B12 insufficiency/MS

Postby lyndacarol » Mon Jun 02, 2014 8:01 am

Just to round up some pertinent information posted earlier in various locations:

A B12 deficiency can develop at any time in a person's life!

Go back to your family doctor and ask him to investigate a possible B12 deficiency. Your doctor will need to run a full panel of tests (NOT just the one blood test for B12). By the way, ask for a copy of your test results and keep your own file of them at home.


Posted by NHE, on May 29, 2014, undiagnosed-f54/topic24840.html#p225790:
In addition to watching the documentary, be sure to read the book "Could It Be B12?"
http://b12awareness.org/could-it-be-b12 ... diagnoses/

To eliminate B12 as a possibility, your doctor will need to run a full panel of tests.

These include...

• serum B12
• RBC folate
• urinary methylmalonic acid (uMMA)
• fasting homocysteine
• unsaturated B12 binding capacity

The tests should be run after not taking either B12 or folate supplements for at least 72 hours.

Posted by NHE, on May 30, 2014, undiagnosed-f54/topic24840.html#p225802:
Here's a paper which states that oligoclonal bands are found in B12 deficiency.

Magnetic resonance imaging (MRI), cranial computerized tomography (CCT), evoked potentials and cerebrospinal fluid (CSF) analysis in five patients with funicular myelosis.
Neurosurg Rev. 1987;10(3):209-11. http://www.ncbi.nlm.nih.gov/pubmed/3502675

Five Patients with vitamin B12 deficiency were examined by means of MRI, CCT, VEP, BAEP, EEG, and CSF. In 3 patients medianus-SEP and EMG/ENG were recorded as well. Partly, findings of MRI, CCT, VEP, BAEP, SEP, and CSF were similar to those in multiple sclerosis. This is not very surprising considering that the central nervous system lesions in vitamin B12 deficiency consist of disseminated demyelination. Because of this all these investigative techniques must be considered non-specific. Appraisal of findings is only possible in connection with the case history, clinical findings, and supplementary diagnostic measurements.
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Re: B12 insufficiency/MS

Postby lyndacarol » Tue Jun 03, 2014 8:08 am

Let me reiterate the link posted by NHE and recommend that everyone consider:

http://b12awareness.org/could-it-be-b12 ... diagnoses/

I have only begun to go through the information there. So far, I find it superb, especially the Signs and Symptoms list (http://b12awareness.org/about-b12/signs ... -children/).

And please note that multiple sclerosis is the second entry in this list: http://b12awareness.org/about-b12/disor ... europathy/
Last edited by lyndacarol on Thu Jun 05, 2014 2:46 pm, edited 1 time in total.
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Re: B12 insufficiency/MS

Postby NHE » Thu Jun 05, 2014 2:50 am

Vitamin B12 is used to convert homocysteine to methionine via methylation. As such, low vitamin B12 levels are associated with high homocysteine. Homocysteine is a toxic amino acid which has been widely reported to be associated with cardiovascular disease, e.g., high blood pressure, stroke, atherosclerosis, etc. The following paper discusses the association of high levels of homocysteine with lower cognitive scores and reduced cerebral white matter volume. So, if you're feeling a bit off and your MS doc tells you that you have white matter atrophy, then tell them to check your B12 and homocysteine levels. It's not always MS.


Associations between elevated homocysteine, cognitive impairment, and reduced white matter volume in healthy old adults.
Am J Geriatr Psychiatry. 2013 Feb;21(2):164-72.

    OBJECTIVES: Elevated homocysteine has emerged as a risk factor for cognitive impairment even in healthy elderly persons. Reduced brain volume and white matter hyperintensities also occur in healthy elderly as well, but the interrelationships between these have not been well studied. We report these interrelationships in non demented, relatively healthy, community-dwelling older adults from a single East Asian population.

    METHODS: Two hundred twenty-eight right-handed participants age 55 years and above were evaluated. Persons with medical conditions or neurological diseases other than well-controlled diabetes mellitus and hypertension were excluded. Participants underwent quantitative magnetic resonance imaging of the brain using a standardized protocol and neuropsychological evaluation. Plasma homocysteine, folate, vitamin B(12), and markers for cardiovascular risk: blood pressure, body mass index, fasting blood glucose, and lipid profile were measured.

    RESULTS: Elevated homocysteine was associated with reduced global cerebral volume, larger ventricles, reduced cerebral white matter volume, and lower cognitive performance in several domains. Elevated homocysteine was associated with reduced white matter volume (β = -20.80, t = -2.9, df = 223, p = 0.004) and lower speed of processing (β = -0.38, t = -2.1, df = 223, p = 0.03), even after controlling for age, gender, and education. However, the association between homocysteine and lower speed of processing disappeared after controlling for white matter volume. Elevated homocysteine was not associated with white matter hyperintensity volume or with hippocampal volume. Although homocysteine and folate levels were correlated, their effects on white matter volume were dissociated.

    CONCLUSION: In non demented, relatively healthy adults, elevated homocysteine is associated with lower cognitive scores and reduced cerebral white matter volume. These effects can be dissociated from those related to white matter hyperintensities or reduced folate level.
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Re: B12 insufficiency/MS

Postby jimmylegs » Thu Jun 05, 2014 9:27 am

and, you can ask for this check (the first thing i did in 2006) and STILL have them say nope, you're not deficient, EVEN if you have a blatant outright deficiency (as i did) BUT which doesn't show up on their computer systems (because trend graphs don't readily calculate text such as "no level detected")
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Re: B12 insufficiency/MS

Postby lyndacarol » Thu Jun 05, 2014 10:20 am

Review of history and my conjecture on it:
#1. In Good Calories Bad Calories by Gary Taubes (page 319):
The notion of a carbohydrate-restricted diet based exclusively on fatty meat was publicized after World War I by the Harvard anthropologist-turned-Arctic-explorer Vilhjalmur Stefansson, who was concerned with the overall healthfulness of the diet, rather than its potential for weight loss. Stefansson had spent a decade eating nothing but meat among the Inuit of northern Canada and Alaska. The Inuit, he insisted, as well as the visiting explorers and traders who lived on this diet, were among the healthiest if not the most vigorous populations imaginable.

Among the tribes with whom Stefansson lived and traveled, the diet was primarily caribou meat, "with perhaps 30 percent fish, 10 percent seal meat, and 5 or 10 percent made up of polar bear, rabbits, birds and eggs."

Initially, I attributed the virtual nonexistence of MS among the Inuit to the dietary exclusion of carbohydrates, i.e., foods that trigger insulin secretion. Now I believe it is not what the Inuit didn't eat, it is what the Inuit did eat that accounts for low MS prevalence… animal-based foods which are high in B12.


#2. As previously discussed (general-discussion-f1/topic6044.html), this case of "Remission of multiple sclerosis post-liver transplantation" (http://www.ncbi.nlm.nih.gov/pubmed/15595263) has a connection to the discussion here.

A Caucasian woman with MS received an urgent liver transplant for fulminant liver failure at the age of 59. Her Extended Disability Scale Score (EDSS) pretransplant was 5.0 and clinically she had cerebellar and brainstem dysfunction. Post-transplant immunosuppression consisted of tacrolimus, mycophenolate mofetil and tapering corticosteroids that were discontinued after 1.5 years. Post-transplant her EDSS decreased to 2.0 and after three years she is clinically asymptomatic with only very mild dysarthria on neurologic examination. Long-term maintenance immunosuppression consists of low dose tacrolimus.

I am now convinced that the transplanted liver was a new source of vitamin B-12.

The liver/liver capsule element of Dr. Wahls' program seems to fit as well, as does her recommendations for bone broth.

Further support for this is here: http://www.jdmdonline.com/content/12/1/17

Clinically overt features of vitamin B12 deficiency manifest by 5–10 years owing to the large body stores in the liver mainly that are not quickly depleted [28].

#3. Hepatomegaly (enlargement of the liver) and splenomegaly (enlargement of the spleen) are listed as signs/symptoms of B12 deficiency (Could It Be B12? Page 300). Since chronic pancreatitis is also listed in the B12 deficiency criteria list (page 303), I suspect that the pancreas can also be enlarged and secrete excess insulin.

#4. Vitamin D is good for us, but perhaps it is the liver with its B12 in cod liver oil (and not the vitamin D) that is responsible for the benefits to some people with MS. I think I will be replacing my vitamin D capsule with cod liver oil.
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Re: B12 insufficiency/MS

Postby NHE » Thu Jun 05, 2014 9:12 pm

Here's a paper of possible interest depicting enhancing white matter lesions in the brain and spinal chord due to B12 deficiency. Free full text.

Cobalamin deficiency: clinical picture and radiological findings.
Nutrients. 2013 Nov 15;5(11):4521-39.

    Vitamin B12 deficiency causes a wide range of hematological, gastrointestinal, psychiatric and neurological disorders. Hematological presentation of cobalamin deficiency ranges from the incidental increase of mean corpuscular volume and neutrophil hypersegmentation to symptoms due to severe anemia, such as angor, dyspnea on exertion, fatigue or symptoms related to congestive heart failure, such as ankle edema, orthopnea and nocturia. Neuropsychiatric symptoms may precede hematologic signs and are represented by myelopathy, neuropathy, dementia and, less often, optic nerve atrophy. The spinal cord manifestation, subacute combined degeneration (SCD), is characterized by symmetric dysesthesia, disturbance of position sense and spastic paraparesis or tetraparesis. The most consistent MRI finding is a symmetrical abnormally increased T2 signal intensity confined to posterior or posterior and lateral columns in the cervical and thoracic spinal cord. Isolated peripheral neuropathy is less frequent, but likely overlooked. Vitamin B12 deficiency has been correlated negatively with cognitive functioning in healthy elderly subjects. Symptoms include slow mentation, memory impairment, attention deficits and dementia. Optic neuropathy occurs occasionally in adult patient. It is characterized by symmetric, painless and progressive visual loss. Parenteral replacement therapy should be started soon after the vitamin deficiency has been established.
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Re: B12 insufficiency/MS

Postby NHE » Thu Jun 05, 2014 9:50 pm

This paper represents the potential problem of misdiagnosis of MS instead of B12 deficiency. The mean B12 levels in the MS cohort were 342.64 ± 210.66 pg/mL. As such, some of the MS patients were down around 132 pg/mL which is definitely deficient. The typical range for serum B12 is around 247-925 pg/mL. Homocysteine in the MS patients was also sky high at 22.73 ± 11.63 μmol/L. The standard range is 4-12 µmol/L. It's interesting that Inf-beta increased homocysteine by nearly 5 µmol/L though those patients not on Ifn treatment were still quite high. It suggests a potential role of Ifn-beta in increasing B12 deficiency risks.


Homocysteine, vitamin B12 and folate levels in Iranian patients with Multiple Sclerosis: a case control study.
Clin Neurol Neurosurg. 2013 Sep;115(9):1802-5.

    BACKGROUND: Recently, homocysteine (Hcy), folate, and vitamin B12 have been proposed to have several roles on MS pathogenesis.

    OBJECTIVE: We performed this study to determine the role of serum levels of Hcy, vitamin B12, and folate in patients with relapsing remitting MS (RRMS) and compared them with healthy controls.

    METHODS: We recruited 75 RRMS patients and 75 subjects as controls with the same age and sex. Homocysteine was measured using fluorimetric high-performance liquid chromatography. Plasma folate and vitamin B12 levels were measured through ion-capture method.

    RESULTS: Mean plasma levels of vitamin B12, folate, and Hcy in cases were 342.64 ± 210.66 pg/ml, 9.74 ± 4.77 ng/ml, and 22.73 ± 11.63 μM/L, respectively, which showed significant difference in comparison with the controls. In addition, there were significant correlations between mean serum Hcy levels and duration of disease (r=0.2, p=0.05) and treatment with interferon (r=0.21, p=0.01). In cases, Hcy level was higher among those on β interferon (24.56 ± 11.87 vs. 19.71 ± 10.75, p=0.01).

    CONCLUSIONS: We concluded that serum levels of vitamin B12 and folate decreased in RRMS patients, but Hcy levels increased significantly. It seems necessary to conduct prospective trials to determine whether the treatment with supplements and correct biomarker levels in the early stage of the disease can change the course of the disease. We recommend regular checking of the serum level of Hcy in patients who use disease-modifying drugs.
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Re: B12 insufficiency/MS

Postby MamaCat » Fri Jun 06, 2014 10:03 am

Thanks for all this info. Reading up and learning, but I am far from educated about this. I know that in some cases the serum B12 can be low-normal and a person still have a B12 deficiency. Is it possible for the serum B12 to be high-normal and a person still be deficient, or does that rule out the need for further testing, in your opinion?

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Re: B12 insufficiency/MS

Postby NHE » Fri Jun 06, 2014 3:10 pm

MamaCat wrote:Thanks for all this info. Reading up and learning, but I am far from educated about this. I know that in some cases the serum B12 can be low-normal and a person still have a B12 deficiency. Is it possible for the serum B12 to be high-normal and a person still be deficient, or does that rule out the need for further testing, in your opinion?


According to the authors of "Could It Be B12?" the urinary methylmelonic acid test (uMMA) is an indicator of how your body is processing B12. If the uMMA result is high, then there's a problem with B12 somewhere in its metabolic pathway.
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Re: B12 insufficiency/MS

Postby standingtall » Sat Jun 14, 2014 10:34 pm

It surely is posted elsewhere, but what can be done to improve b12 utilization in the body. My b12 was low initially via blood test , but now remains very high despite stopping b12 supplementation. I am convinced of at least a strong correlation between ms progression and the bodies declining ability to process b12.
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Re: B12 insufficiency/MS

Postby NHE » Sun Jun 15, 2014 12:23 am

standingtall wrote:It surely is posted elsewhere, but what can be done to improve b12 utilization in the body. My b12 was low initially via blood test , but now remains very high despite stopping b12 supplementation. I am convinced of at least a strong correlation between ms progression and the bodies declining ability to process b12.

If you're not processing B12 correctly, methylmalonic acid and/or homocysteine will be high. Have you been tested to check their levels?
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Re: B12 insufficiency/MS

Postby standingtall » Mon Jun 16, 2014 5:40 am

Yes, I have been tested. But before I give the data, let me tell my B12 story. About 3 months after my first MS attack with all symptoms subside and just prior to diagnosis of MS I tested low on B12. I do not have that exact data, but I think it was in the 20pg/ml range. This was in the fall of 2010. The doc prescribed B12 injections for a few weeks, but the B12 did not increase. I have no recollection or data on hand about mma or hcy at that time. Post B12 injections, the doctor suggested that I begin 1mg sublingual methylcobalamin which I did. Then in the course of addressing the B12 deficiency, I got the MS diagnosis and the B12 concern sort of went out the window for the doctors. You know, the old MS patient shuffle where every disfunction or symptom is pinned to the MS diagnosis.
I continued to take the B12 supplements anyway, because I could tell a real difference in my energy level when I took them twice daily. When I missed the supplements a few times, I felt very tired and fatigued. Approximately, a year later I got another B12 check myself and the level continued to be on the low side at 82pg/ml. I then switched from the 1mg supplement to a 5mg supplement.
After making the B12 dosage change, I felt great. Best I had felt in probably 10 years. After about a year, I did another B12 recheck myself. This time the level was 3300pg/ml, I could not believe it. I dropped the dosage back to the 1mg amount, and after 3 month recheck it remained about the same. I stopped the supplementation altogether, except for a small amount I get in my multi and after 3 more months the level had dropped down to 1271. I can't afford to pay for too much blood work on my own, and the docs I had at the time wouldn't order it so I was doing this without Dr. supervision. I did not think to check mma or hcy at the time, duh? Recheck of B12 in 2013 was 1078pg/ml. During this time, when I reduced or stopped the B12 supplementation I noticed that my energy level was much reduced. This continues today.
Finally in April 2014, B12 was 781pg/ml. Homocysteine was 5.1umol and methylmalonic acid was 113nmol. I switched primary physicians this year and I think I finally found a good one, as he checked everything. Although he was not very intrigued by my B12 story.
Sorry for the long story, but I still believe I have B12 issues. I do not understand the mechanism that would cause such a deficiency in B12, preventing it from coming up with supplementation. Then only to be followed by an extended period of high B12, preventing it from coming down. Also, the physical benefits of supplementation were tangible and had to be more than coincidence. I will stop here, but feel at least for me that unraveling this mystery holds much of the key for everything I have been battling for the last four years. Maybe the B12 issue is a symptom of what else is going on with my body, but I just don't think so.
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