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Undiagnosed: Numbness After Consuming Carbohydrates
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<blockquote data-quote="ChetRoi" data-source="post: 1755163" data-attributes="member: 468700"><p>From Dionne:</p><p>“</p><p>Unfortunately still no explanation ....</p><p>“</p><p>“</p><p>Hello, I just wanted to second Lamont D's suggestion of fasting....</p><p>“</p><p></p><p>Hi Dionne, thanks for the reconnect—</p><p></p><p>I have had an initial visit with an immunologist; first-round testing has uncovered no autoantibodies. More testing to follow, perhaps with pre/post carb challenges, which up to this point hasn’t been done.</p><p></p><p>Exercise just after eating carbs is not something I have tried but I do know that a prolonged fast of carbs (keto diet) does seem to give me a few meals/days without much numbness after eating carbs.</p><p></p><p>I will make note of the channelopathy possibility for my clinicians, and I will read more about this myself.</p><p></p><p>With regard to fasting, I am currently 160 pounds (11.4 stone) and 5’ 10”, and I lose weight easily so I must be careful about reduced calorie dieting.</p><p></p><p>I have just completed a new round of dietary challenges and learned that food cholesterol still has a significant numbing affect, albeit much less sensitivity than with carbohydrates. So, my eating choices are now even more reduced.</p><p></p><p>The apparent connective tissue inelasticity presents as medial (and to lesser extent, lateral) epicondylitis, carpal tunnel, cubital tunnel, and general muscle/ligament inelasticity evidenced by torn L and R medial menisci, torn L biceps tendon, torn L rotator cuff, and easily strained back and shoulder muscles, all in the absence of strenuous exercise. The chronic inelasticity symptoms have been largely relieved with Adenosylcobalamin (bioactive B12) supplements. The connective tissue pain returns when Adenosylcobalamin repletion is reduced or interrupted.</p><p></p><p>Some new information:</p><p></p><p>My youngest daughter, largely bed-ridden and under pain management for ten years, was just diagnosed with Hypermobile Ehlers-Danlos Syndrome. There are now 14 known subtypes of EDS but this type has not yet had genetic allele errors identified. Hypermobile EDS' inheritance pattern is autosomal dominant meaning each child has a 50% chance of having the defect when just one parent carries the “bad” genes. I will nonetheless be tested for EDS-related genetic defects but judging only by the clinical presentation, it appears to originate from my wife’s side off the family.</p><p></p><p>A new round of amino acid testing by a biochemical geneticist revealed nothing except to confirm my body is in a state of ketosis. :-/</p><p></p><p>In the next 30 days, more testing to come with the immunologist, an endocrinologist, and the biochemical geneticist.</p><p></p><p>With regard to my B12 deficiency/malabsorption/pathway blockage problem, you should be aware that the widely used serum B12 test would not show any pathology as a result of B12 not being absorbed into the cells. This was the case for me.</p><p></p><p>Adequate levels of B12 are essential for proper metabolic processing of at least carbs and food cholesterol. The MMA (urine or blood), serum Homocysteine and folate tests will provide this information, allowing one to rule out a B12 cellular-level dysmetabolism connection.</p><p></p><p>In my case, the bioactive B12s—both Methylcobalamin and Adenosylcobalamin—demonstrably mitigate the post-carb numbness, and to a significant degree.</p><p></p><p>From my latest medical write-up:</p><p>“</p><p>As has been reported in the scientific literature, high-dose vitamin B-12 can overcome pathway deficits in some patients, perhaps related to the more recent finding that B-12 cofactors Methylcobalamin (MeCbl) or Adenosylcobalamin (AdoCbl) may have a significant stabilizing effect on the MMACHC (cobalamin C) protein. In this patient’s case, repletion and ongoing titration with MeCbl and AdoCbl, and B-9 Methylfolate (MeFolate) in therapeutic doses begun in 2014 initially resulted in dramatic biochemical and clinical improvement.</p><p></p><p>However, accumulated neurologic deficits have progressed to the severe level with a January 2018 Dx of severe SMPN with axonal features and denervation. Nonetheless, in mid-2016, adoption of a fat-oriented very low carb ketogenic diet to bypass the dysfunctional carbohydrate metabolic pathway has further slowed accumulating deficits. Currently, MeCbl is administered subQ: 0.45 cc every day @ 25 mg/mL. AdoCbl and MeFolate are given orally @ 1.5 mg and 1.6 mg, respectively, every day.</p><p></p><p>Importantly, a diagnostic clue may be found in the lack of effectiveness of the standard-of-care Cyanocobalamin (CyCbl) and the dramatic therapeutic response to B-12 cofactor repletion (MeCbl, AdoCbl). It may indicate the end stage cobalamin pathway reduction is never realized because from a CyCbl administration for the patient neither the cytoplasm methylation to form MeCbl, nor mitochondrial adenosylation to form AdoCbl occurs. Alternatively, it may suggest the effectiveness of the MeCbl repletion is also a function of the applied cellular methylation by influencing gene expression. For example, hypermethylation is a process now known to improve some systemic diabetes manifestations.</p><p>“</p><p></p><p>Looking ahead toward new investigative paths, here is a list of (my top four) candidates. Again, from my monthly medical summary document:</p><p></p><p>“</p><p>Best Lay Differential Assertions on the Pathology</p><p></p><p>Over the past several years, in discussion with physicians, four of the most likely disease candidates have driven much of the diagnostic testing.</p><p></p><p>1) A late-onset inborn error of B-12 metabolism, subclinical until the 6th decade of life, interrupting the cobalamin pathway before final reduction to its cofactors in the lysosome. This explanation correlates best with the clinical features: the presence of the characteristic B-12 deficiency triad of neurological, hematological, and psychiatric symptoms; dramatic clinical response to B12 cofactors MeCbl and AdoCbl but not standard of care CyCbl; foamy transformed macrophages; connective tissue disturbances; chronic low alkaline phosphatase (may suggest the liver is not storing B-12--a B-12 recycling failure); dysfunctional carbohydrate and cholesterol metabolism due to insufficient B-12 thereby giving rise to interrupted cellular signaling; severe neurological complications upon disease progression; and other manifestations.</p><p></p><p>Further, the clinical phenotype is consistent with an error of cobalamin recycling/transport: subacute onset and slow progression; multi-system involvement; a decrease in motor and sensory NCV; distal axonopathy; muscle weakness, fasciculations, ataxia; initially thrombocytopenia, then developing pancytopenia; and psychiatric disturbances.</p><p></p><p>2) Paraneoplastic Syndrome (PNS). The PNS effect has likely been present since birth. Initially a cyst perturbing the B-12 and perhaps other nutrient pathways, it evolved into an RCC circa 2010 having multi-system effects due to the secretion of hormones and cytokines by an immune response or from the tumor itself.</p><p></p><p>A 1.3 cm renal mass extending from the lower pole of the R kidney, cryoablated in Nov 2016. The mass was observed 10 years earlier on a CT scan as a cyst. Four days after cryoablation, chronic hip dermal lesions spontaneously resolved suggesting a paraneoplastic response, consistent with the patient’s dysmetabolism syndrome. A PET scan of June 2017 for evidence of renal cancer found no indication of neoplasm. A carbohydrate challenge in August 2017 demonstrated a less severe acute dysmetabolic reaction. Of late, chronic thrombocytopenia and transient cytopenias may have stabilized.</p><p></p><p>3) A small intestine bacterial overgrowth, inhibiting absorption of B-12. Multiple past infections of Candida Albicans; past stomach parasitic infection from unwashed fruit; one year living in rural Southeast Asia, sometimes consuming local food.</p><p></p><p>A carbohydrate dysmetabolism that in this patient introduces a greater systemic disturbance than a food cholesterol dysmetabolism is consistent with a SIBO clinical phenotype. However, a 2017 SIBO test (hydrogen only) was negative.</p><p></p><p>4) A storage disease, possibly lysosomal. Cobalamin utilization depends on its efficient transit through the intracellular lysosomal compartment and subsequent delivery to the cytosol and mitochondria. Lysosomal dysfunction may impair lysosomal cobalamin transport. Enzymopathy could result in the improper catabolism of carbohydrates and cholesterol with the resulting accumulation of organelle debris disrupting the cellular uptake of cobalamin.</p><p></p><p>Foamy transformed macrophages, typical in lysosomal storage disorders and B12 deficiency, were present in a 2012 rib lesion biopsy of an exceedingly rare bone xanthoma, subsequently resected. However, a hepatic transplant physician expressed the opinion, upon reviewing the results of the liver biopsy, that neither a storage disease nor a primary hepatic condition was a likely cause of the metabolic dysfunction.</p><p>“</p><p></p><p>I'll pass on more information after the upcoming consults. Take care.</p></blockquote><p></p>
[QUOTE="ChetRoi, post: 1755163, member: 468700"] From Dionne: “ Unfortunately still no explanation .... “ “ Hello, I just wanted to second Lamont D's suggestion of fasting.... “ Hi Dionne, thanks for the reconnect— I have had an initial visit with an immunologist; first-round testing has uncovered no autoantibodies. More testing to follow, perhaps with pre/post carb challenges, which up to this point hasn’t been done. Exercise just after eating carbs is not something I have tried but I do know that a prolonged fast of carbs (keto diet) does seem to give me a few meals/days without much numbness after eating carbs. I will make note of the channelopathy possibility for my clinicians, and I will read more about this myself. With regard to fasting, I am currently 160 pounds (11.4 stone) and 5’ 10”, and I lose weight easily so I must be careful about reduced calorie dieting. I have just completed a new round of dietary challenges and learned that food cholesterol still has a significant numbing affect, albeit much less sensitivity than with carbohydrates. So, my eating choices are now even more reduced. The apparent connective tissue inelasticity presents as medial (and to lesser extent, lateral) epicondylitis, carpal tunnel, cubital tunnel, and general muscle/ligament inelasticity evidenced by torn L and R medial menisci, torn L biceps tendon, torn L rotator cuff, and easily strained back and shoulder muscles, all in the absence of strenuous exercise. The chronic inelasticity symptoms have been largely relieved with Adenosylcobalamin (bioactive B12) supplements. The connective tissue pain returns when Adenosylcobalamin repletion is reduced or interrupted. Some new information: My youngest daughter, largely bed-ridden and under pain management for ten years, was just diagnosed with Hypermobile Ehlers-Danlos Syndrome. There are now 14 known subtypes of EDS but this type has not yet had genetic allele errors identified. Hypermobile EDS' inheritance pattern is autosomal dominant meaning each child has a 50% chance of having the defect when just one parent carries the “bad” genes. I will nonetheless be tested for EDS-related genetic defects but judging only by the clinical presentation, it appears to originate from my wife’s side off the family. A new round of amino acid testing by a biochemical geneticist revealed nothing except to confirm my body is in a state of ketosis. :-/ In the next 30 days, more testing to come with the immunologist, an endocrinologist, and the biochemical geneticist. With regard to my B12 deficiency/malabsorption/pathway blockage problem, you should be aware that the widely used serum B12 test would not show any pathology as a result of B12 not being absorbed into the cells. This was the case for me. Adequate levels of B12 are essential for proper metabolic processing of at least carbs and food cholesterol. The MMA (urine or blood), serum Homocysteine and folate tests will provide this information, allowing one to rule out a B12 cellular-level dysmetabolism connection. In my case, the bioactive B12s—both Methylcobalamin and Adenosylcobalamin—demonstrably mitigate the post-carb numbness, and to a significant degree. From my latest medical write-up: “ As has been reported in the scientific literature, high-dose vitamin B-12 can overcome pathway deficits in some patients, perhaps related to the more recent finding that B-12 cofactors Methylcobalamin (MeCbl) or Adenosylcobalamin (AdoCbl) may have a significant stabilizing effect on the MMACHC (cobalamin C) protein. In this patient’s case, repletion and ongoing titration with MeCbl and AdoCbl, and B-9 Methylfolate (MeFolate) in therapeutic doses begun in 2014 initially resulted in dramatic biochemical and clinical improvement. However, accumulated neurologic deficits have progressed to the severe level with a January 2018 Dx of severe SMPN with axonal features and denervation. Nonetheless, in mid-2016, adoption of a fat-oriented very low carb ketogenic diet to bypass the dysfunctional carbohydrate metabolic pathway has further slowed accumulating deficits. Currently, MeCbl is administered subQ: 0.45 cc every day @ 25 mg/mL. AdoCbl and MeFolate are given orally @ 1.5 mg and 1.6 mg, respectively, every day. Importantly, a diagnostic clue may be found in the lack of effectiveness of the standard-of-care Cyanocobalamin (CyCbl) and the dramatic therapeutic response to B-12 cofactor repletion (MeCbl, AdoCbl). It may indicate the end stage cobalamin pathway reduction is never realized because from a CyCbl administration for the patient neither the cytoplasm methylation to form MeCbl, nor mitochondrial adenosylation to form AdoCbl occurs. Alternatively, it may suggest the effectiveness of the MeCbl repletion is also a function of the applied cellular methylation by influencing gene expression. For example, hypermethylation is a process now known to improve some systemic diabetes manifestations. “ Looking ahead toward new investigative paths, here is a list of (my top four) candidates. Again, from my monthly medical summary document: “ Best Lay Differential Assertions on the Pathology Over the past several years, in discussion with physicians, four of the most likely disease candidates have driven much of the diagnostic testing. 1) A late-onset inborn error of B-12 metabolism, subclinical until the 6th decade of life, interrupting the cobalamin pathway before final reduction to its cofactors in the lysosome. This explanation correlates best with the clinical features: the presence of the characteristic B-12 deficiency triad of neurological, hematological, and psychiatric symptoms; dramatic clinical response to B12 cofactors MeCbl and AdoCbl but not standard of care CyCbl; foamy transformed macrophages; connective tissue disturbances; chronic low alkaline phosphatase (may suggest the liver is not storing B-12--a B-12 recycling failure); dysfunctional carbohydrate and cholesterol metabolism due to insufficient B-12 thereby giving rise to interrupted cellular signaling; severe neurological complications upon disease progression; and other manifestations. Further, the clinical phenotype is consistent with an error of cobalamin recycling/transport: subacute onset and slow progression; multi-system involvement; a decrease in motor and sensory NCV; distal axonopathy; muscle weakness, fasciculations, ataxia; initially thrombocytopenia, then developing pancytopenia; and psychiatric disturbances. 2) Paraneoplastic Syndrome (PNS). The PNS effect has likely been present since birth. Initially a cyst perturbing the B-12 and perhaps other nutrient pathways, it evolved into an RCC circa 2010 having multi-system effects due to the secretion of hormones and cytokines by an immune response or from the tumor itself. A 1.3 cm renal mass extending from the lower pole of the R kidney, cryoablated in Nov 2016. The mass was observed 10 years earlier on a CT scan as a cyst. Four days after cryoablation, chronic hip dermal lesions spontaneously resolved suggesting a paraneoplastic response, consistent with the patient’s dysmetabolism syndrome. A PET scan of June 2017 for evidence of renal cancer found no indication of neoplasm. A carbohydrate challenge in August 2017 demonstrated a less severe acute dysmetabolic reaction. Of late, chronic thrombocytopenia and transient cytopenias may have stabilized. 3) A small intestine bacterial overgrowth, inhibiting absorption of B-12. Multiple past infections of Candida Albicans; past stomach parasitic infection from unwashed fruit; one year living in rural Southeast Asia, sometimes consuming local food. A carbohydrate dysmetabolism that in this patient introduces a greater systemic disturbance than a food cholesterol dysmetabolism is consistent with a SIBO clinical phenotype. However, a 2017 SIBO test (hydrogen only) was negative. 4) A storage disease, possibly lysosomal. Cobalamin utilization depends on its efficient transit through the intracellular lysosomal compartment and subsequent delivery to the cytosol and mitochondria. Lysosomal dysfunction may impair lysosomal cobalamin transport. Enzymopathy could result in the improper catabolism of carbohydrates and cholesterol with the resulting accumulation of organelle debris disrupting the cellular uptake of cobalamin. Foamy transformed macrophages, typical in lysosomal storage disorders and B12 deficiency, were present in a 2012 rib lesion biopsy of an exceedingly rare bone xanthoma, subsequently resected. However, a hepatic transplant physician expressed the opinion, upon reviewing the results of the liver biopsy, that neither a storage disease nor a primary hepatic condition was a likely cause of the metabolic dysfunction. “ I'll pass on more information after the upcoming consults. Take care. [/QUOTE]
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