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I highly recommend the book “Could It Be B12” for all of you that have questions….it is a wealth of information. The author’s website is b12awareness dot o r g


If you have the MTHFD gene, there is a possibility it could lead to pernicious anemia too.


Thank you for the great post and information Dr. Kresser!

To those in doubt about the seriousness of B12 deficiency, I can tell you finding out the HARD WAY that you are deficient is horrible. In May 2007 when I was 30 I ended up in the hospital with a severe case a ataxia and nystagmus. I was in the hospital for 8 days, where I was initially diagnosed with MS. After almost every possible test available was performed on me (3 MRI’s, Cat Scan, Spinal Tap, blood tests every day, to name a few), they only thing that was wrong with me was a B12 level of 110, with sclerosis of the brain caused by the deficiency. Since then I’ve taken B12 shots every month, and have been much better. There was a period when I doctors were trying to wean me off of B12, but that caused me a severe metabolic imbalance, so I was back to B12 shots again.

Right now, after new B12 tests, it was discovered that even though with the monthly shots I take, my B12 level is still low (475), which dropped to (261) after 7 weeks with no B12 injection. So, in addition to being back to B12 shots (of the Cyanocobalamin kind), I’m also supplementing myself with sublingual Methylcobalamin. Hopefully this will increase my B12 levels back to normal (I hope at least to 600), while my doctors try to figure out again where in the process I seem to not be assimilating B12 (I’m a meat-eatrian, with no reason WHATSOEVER to be deficient).

Word of advice: The only reason why ((it seams)) I was not diagnosed with a B12 deficiency before, was because doctors had me labeled as having depression and anxiety, which was causing me to have low body weight -all bullshit!. They had me on medication which improved my mood, but physically I was still deteriorating. I had to end-up in the hospital for anyone to realize my B12 deficiency.

Anyhow, wish me luck! But seriously, if you’re vegetarian or vegan, or if you find yourself tired and achy all the time and unable to keep a decent weight, have your b12 level check -it is worth it!

Dr. Kesser: Are there any other tests I should demand from my Doctors? The only one I know they did, was Intrinsic Factor, and supposedly that one came negative. Any help would be appreciated!


Carole says

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Clinical Evaluation and DNA Extraction

Informed written consent was obtained from study participants under a protocol approved by the Institutional Review Board of the Mayo Clinic. Family members were evaluated by electrocardiography and echocardiography, with normal values based on body surface area and age. Medical records were acquired for the proband’s deceased siblings, as well as a detailed medical history for the extended family. Genomic DNA was extracted from either whole blood samples or paraffin-embedded cardiac tissue from biopsy (QIAamp DNA Mini Kit, QIAGEN, Inc).

Genotyping and Haplotype Analyses

We selected 3 polymorphic dinucleotide repeat markers spanning each of the 8 gene loci for autosomal dominant HCM: , and . Markers were identified from online genetic databases and maps (Map Viewer and GeneMap’ 99 [National Center for Biotechnology Information] and The Genome Database ) and amplified by the polymerase chain reaction (PCR), as previously described. Genotypes were scored and haplotypes were constructed with the goal of identifying the inheritance of an identical paternal and maternal haplotype among the siblings with cardiomyopathy.

Mutational Analyses

Once the haplotype analyses implicated the () as a candidate gene for autosomal recessive cardiomyopathy, mutational analyses of the gene were performed. Genomic structure was first determined by performing an online Human Genome Basic Local Alignment Search Tool (BLAST) search with mRNA sequence (GenBank accession number NM_000258 ), identifying a single genomic contig harboring (GenBank accession number NT_029949 ). Oligonucleotide primer pairs were designed for PCR amplification of coding and splice junction regions for the 6 translated exons of , by use of OLIGO 6.51 Primer Analysis Software (National Biosciences). PCR amplification and single-strand polymorphism (SSCP) analyses were performed as previously described. DNA cycle sequencing of exon 4 was performed with the use of a Thermo Sequenase kit (Amersham Life Sciences, Inc). Sequence homology between human essential light chain of myosin and homologous proteins was determined with the MaxHom multiple sequence alignment program on the PredictProtein server.

The family pedigree structure is shown in Figure 1 A. The proband (V.3) and his sister (V.4) were referred for cardiac evaluation after the death of 2 siblings. The oldest brother (V.1) developed dyspnea and peripheral edema at age 13 and died a year later after a thromboembolic event. The other brother (V.2) developed fatigue, cardiomegaly, and hepatomegaly at age 12 and died 2 years later after operation to remove an intracardiac thrombus. Intraoperative needle biopsies of both ventricles demonstrated mild-moderate myocyte hypertrophy and interstitial fibrosis. Echocardiograms were not available for either brother, but their medical records indicated they had cardiomyopathy with dilated atria, suggesting restrictive heart disease.

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