Search
Search titles only
By:
Search titles only
By:
Home
Forums
New posts
Search forums
What's new
New posts
New profile posts
Latest activity
Members
Current visitors
New profile posts
Search profile posts
Log in
Register
Search
Search titles only
By:
Search titles only
By:
New posts
Search forums
Menu
Install the app
Install
Reply to Thread
Guest, we'd love to know what you think about the forum! Take the
Diabetes Forum Survey 2024 »
Home
Forums
Diabetes Discussion
Ask A Question
Undiagnosed: Numbness After Consuming Carbohydrates
JavaScript is disabled. For a better experience, please enable JavaScript in your browser before proceeding.
You are using an out of date browser. It may not display this or other websites correctly.
You should upgrade or use an
alternative browser
.
Message
<blockquote data-quote="ChetRoi" data-source="post: 1736014" data-attributes="member: 468700"><p>Until a few months ago, I used the FatSecret app to track all my food consumption. I did this for almost three years. I have not encountered a single physician who thought it useful to review the reports, although it has helped me.</p><p></p><p>I describe the carb reaction at the end of my initial post. Also, here is the rest of that which I tried to post but was denied because the post was too lengthy:</p><p></p><p><u>What We Know</u></p><p></p><p>1) Indications of sub-clinical long-term illness; manifestations are consistent with a prolonged B-12 deficiency.</p><p>a) Congenital heart murmur as a toddler; chronic manual proprioception errors beginning as a toddler and continuing into adulthood.</p><p>b) Recurrent infections since late 1960s: sinusitis has not re-established since MeCbl repletion began.</p><p>c) Severely diminished or absent deep tendon reflexes first noticed by a clinician in the late 1970s.</p><p>d) Presence of B-12 deficiency triad of neurological, hematological, and psychiatric symptoms.</p><p>e) Progressive, painless, severe SMPN with axonal features; B ulnar entrapment across R elbow. EMG/NCV indicates denervation.</p><p>f) Two cobalamin transport genes have heterozygous mutations: TCN1 (rs526934, genotype AG) and TCN2 (rs1801198, genotype CG).</p><p>g) Chronic abnormal platelets; thrombocytopenia for at least five years. Other cytopenias transient.</p><p>h) Enlarged abdominal lymph nodes, splenomegaly, NAFLD, renal cell carcinoma (cryoablated).</p><p>i) 2017 liver biopsy showed glycogenated nuclei and trace positive iron stain in macrophages. Portal tracts contain a sparse lymphocytic infiltrate.</p><p>j) Foamy transformed macrophages, seen in B-12 deficiency, was present in a 2012 tissue biopsy of an exceedingly rare bone xanthoma of the L 10th rib; excised.</p><p><em>“The lesion of interest is present in the tissue biopsy and comprises cytologically [benign] spindle cells arranged in a somewhat haphazard fashion resembling fibrous histiocytoma. These are in many respects overshadowed by <u>sheets of foamy macrophages</u> resulting in a xanthomatous appearance. Given the relatively nonspecific nature of xanthomatous change, I suspect it likely that this represents an example of fibrous dysplasia given the location.”</em></p><p></p><p>2) Immediate and dramatically effective therapeutic response to MeCbl and AdoCbl repletion; ultra high dosage required; disease progression continues but at a slower pace as long as carb consumption is minimal (target of less than 25 grams/day). Deficits accumulation occurs within days if repletion is interrupted. Standard of care CyCbl is ineffective.</p><p></p><p>3) The syndrome defines a progressive disease provoking a metabolic dysfunction.</p><p>a) About an hour or so after consuming carbohydrates, an acutely arising distal-to-proximal numbness begins that can advance into the torso—presumed to be a biochemical interruption of neuronal cellular signaling due to macronutrient dysmetabolism. B-12 is required to metabolize both carbohydrates and food cholesterol.</p><p>b) The glycemic load of the carbohydrates consumed predicts the extent and intensity of the distal numbness and rigidity</p><p></p><p><u>What We are Doing</u></p><p></p><p>1) Treatments. Regardless of the etiology of the disease, two facts have emerged in its management.</p><p>First, as previously discussed, a dramatically positive reaction occurs when taking methylcobalamin and adenosylcobalamin, both methylation cofactors of B12. These benefits are lost if repletion is interrupted. Note that cyanocobalamin--unmethylated B12--is ineffective. </p><p>Second, neurological deficits are acutely exacerbated by <em>any</em> carbohydrate consumption. </p><p>The following are the only treatments known to possibly help this unidentified disease.</p><p>a) Daily ultra high dosage repletion of B12 cofactor vitamins, and the B9 cofactor vitamin.</p><p>b) A very low carbohydrate (less than 25 grams/day), moderate protein, and high fat (Ketogenic) diet.</p><p>c) Light weight lifting to maintain muscle mass given both disease and possible wasting effect of ketogenic diet.</p><p>Bicycle riding to reduce loss of leg strength.</p><p></p><p>I am seeing a different endocrinologist in June. Perhaps she will have some ideas.</p></blockquote><p></p>
[QUOTE="ChetRoi, post: 1736014, member: 468700"] Until a few months ago, I used the FatSecret app to track all my food consumption. I did this for almost three years. I have not encountered a single physician who thought it useful to review the reports, although it has helped me. I describe the carb reaction at the end of my initial post. Also, here is the rest of that which I tried to post but was denied because the post was too lengthy: [U]What We Know[/U] 1) Indications of sub-clinical long-term illness; manifestations are consistent with a prolonged B-12 deficiency. a) Congenital heart murmur as a toddler; chronic manual proprioception errors beginning as a toddler and continuing into adulthood. b) Recurrent infections since late 1960s: sinusitis has not re-established since MeCbl repletion began. c) Severely diminished or absent deep tendon reflexes first noticed by a clinician in the late 1970s. d) Presence of B-12 deficiency triad of neurological, hematological, and psychiatric symptoms. e) Progressive, painless, severe SMPN with axonal features; B ulnar entrapment across R elbow. EMG/NCV indicates denervation. f) Two cobalamin transport genes have heterozygous mutations: TCN1 (rs526934, genotype AG) and TCN2 (rs1801198, genotype CG). g) Chronic abnormal platelets; thrombocytopenia for at least five years. Other cytopenias transient. h) Enlarged abdominal lymph nodes, splenomegaly, NAFLD, renal cell carcinoma (cryoablated). i) 2017 liver biopsy showed glycogenated nuclei and trace positive iron stain in macrophages. Portal tracts contain a sparse lymphocytic infiltrate. j) Foamy transformed macrophages, seen in B-12 deficiency, was present in a 2012 tissue biopsy of an exceedingly rare bone xanthoma of the L 10th rib; excised. [I]“The lesion of interest is present in the tissue biopsy and comprises cytologically [benign] spindle cells arranged in a somewhat haphazard fashion resembling fibrous histiocytoma. These are in many respects overshadowed by [U]sheets of foamy macrophages[/U] resulting in a xanthomatous appearance. Given the relatively nonspecific nature of xanthomatous change, I suspect it likely that this represents an example of fibrous dysplasia given the location.”[/I] 2) Immediate and dramatically effective therapeutic response to MeCbl and AdoCbl repletion; ultra high dosage required; disease progression continues but at a slower pace as long as carb consumption is minimal (target of less than 25 grams/day). Deficits accumulation occurs within days if repletion is interrupted. Standard of care CyCbl is ineffective. 3) The syndrome defines a progressive disease provoking a metabolic dysfunction. a) About an hour or so after consuming carbohydrates, an acutely arising distal-to-proximal numbness begins that can advance into the torso—presumed to be a biochemical interruption of neuronal cellular signaling due to macronutrient dysmetabolism. B-12 is required to metabolize both carbohydrates and food cholesterol. b) The glycemic load of the carbohydrates consumed predicts the extent and intensity of the distal numbness and rigidity [U]What We are Doing[/U] 1) Treatments. Regardless of the etiology of the disease, two facts have emerged in its management. First, as previously discussed, a dramatically positive reaction occurs when taking methylcobalamin and adenosylcobalamin, both methylation cofactors of B12. These benefits are lost if repletion is interrupted. Note that cyanocobalamin--unmethylated B12--is ineffective. Second, neurological deficits are acutely exacerbated by [I]any[/I] carbohydrate consumption. The following are the only treatments known to possibly help this unidentified disease. a) Daily ultra high dosage repletion of B12 cofactor vitamins, and the B9 cofactor vitamin. b) A very low carbohydrate (less than 25 grams/day), moderate protein, and high fat (Ketogenic) diet. c) Light weight lifting to maintain muscle mass given both disease and possible wasting effect of ketogenic diet. Bicycle riding to reduce loss of leg strength. I am seeing a different endocrinologist in June. Perhaps she will have some ideas. [/QUOTE]
Verification
Post Reply
Home
Forums
Diabetes Discussion
Ask A Question
Undiagnosed: Numbness After Consuming Carbohydrates
Top
Bottom
Find support, ask questions and share your experiences. Ad free.
Join the community »
This site uses cookies. By continuing to use this site, you are agreeing to our use of cookies.
Accept
Learn More.…