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12-09-2011, 11:17 AM | #61 | |||
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In Remembrance
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First, I must repeat that blood sugar levels are not the point. In fact, they are irrelevant to what I am trying to convey other than that they give a clumsy way of monitoring insulin levels and the latter is very important because of its effect on potassium levels. Those, in turn, determine whether or not our nerves and muscles work.
Second, there is the concept of what are known as "periodic paralyses" - a family of conditions both inherited and acquired numbering some two dozen and counting. Only discovered about thirty years ago, they are still a rich field of discovery. In what I am looking at, potassium is at the center, but other electrolytes can cause their own problems. That's why they are a "family". Third, in the case of potassium and/or PD the problem can be too much of the electrolyte ("hyperkalemic") or too little ("hypokalemic") as well as where it is at a given time (cell or plasma?). Our bodies need a certain amount to be in the plasma to make things work right. But if you are one of the "fortunate few" you may have trouble maintaining that distribution since certain things can trigger the cells to suck up the potassium from the plasma. Insulin, not glucose, is one of the main triggers. It seems obvious that most PWP don't have the struggle that Laura and I have, but that doesn't mean that it is not relevant to PD. After all, we may be way out at the end of a spectrum of some sort. And there is another factor in the form of the renin-aldosterone-angiotensin axis which also regulates potassium levels and has an ill-defined role in PD as well. It really will make your head spin. But the really interesting part is that if this is a factor, it may be curable. The contribution from the RAA axis most commonly results from a benign tumor on one of the adrenal glands and is easily removed. It is worth looking at but it is another one of those "between the cracks" things that makes the doc role his eyes. Quote:
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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12-09-2011, 11:21 AM | #62 | |||
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In Remembrance
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1. Nervenarzt. 2011 Apr;82(4):511-20; quiz 521.
[Muscle channelopathies. Myotonias and periodic paralyses]. [Article in German] Jurkat-Rott K, Lerche H, Lehmann-Horn F. Abteilung für Neurophysiologie, Universität Ulm, Albert-Einstein-Allee 11, 89081, Ulm. karin.jurkat-rott@uni-ulm.de The myotonias and familial periodic paralyses are muscle channelopathies. They have in common an impaired muscle excitation that is caused by mutations in voltage-gated Na(+), K(+), Ca(2+), and Cl(-) channels. Membrane hyperexcitability usually results in myotonic stiffness; with increasing membrane depolarization hyperexcitability can be transiently turned into hypoexcitability causing transient weakness as in severe myotonia. Hypoexcitability due to long-lasting depolarization that inhibits action potential generation is the common mechanism for the periodic paralyses. Interictally, the ion channel malfunction may be compensated, so that specific exogenous or endogenous provocative factors are required to produce symptoms in the patients. An especially obvious triggering agent is the level of serum potassium, the ion decisive for resting membrane potential and degree of excitability. Periodic paralysis mutations for which the ion channel malfunction is not fully compensated interictally cause progressive myopathy. PMID: 21484581 [PubMed - indexed for MEDLINE]
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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12-09-2011, 11:26 AM | #63 | |||
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Senior Member
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yes, we are the PD equivalent of My Dinner with André!
whatever the beastie is I want it gone..... Laura |
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05-04-2012, 05:13 PM | #64 | |||
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In Remembrance
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I'm going to bump this up due to its current relevence.
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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05-07-2012, 09:23 PM | #65 | |||
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Senior Member
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Here we have some just published research. Geez, you don't say that PD could somehow involve the endocrine system??!??
Clinical features of Parkinson disease when onset of diabetes came first: A case-control study. No full text but worth scanning related citations... The conclusion is what counts: CONCLUSIONS: Onset of diabetes before the onset of PD appears to be a risk factor for more severe PD symptoms. These findings support the hypothesis that diabetes has a role in the etiopathogenesis of PD. Neurologists should be aware of the potential impact of diabetes on overall PD management. |
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05-09-2012, 06:06 PM | #66 | |||
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In Remembrance
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What if the Ldopa in mucuna is a red herring and it works via its glycemic action?
Abstract: Mucuna pruriens is used extensively for its medicinal value for the treatment of diabetes mellitus in Nigeria. This study investigated the anti-diabetic activity of Mucuna pruriens on the blood glucose levels and the histopathology of the pancreas. To achieve this, Acute toxicity studies of the plant extract was determined. Doses of 100, 200 and 400 mg/kg bw of the extract were administered orally daily for 21 days to alloxan-induced diabetic Wistar rats. Metformin was used as a standard anti-diabetic drug and given by gavage. The fasting blood glucose levels were determined at intervals of three days. Premininary phytochemical screening revealed the presence of flavonoids, saponin, tannins, cardiac glycosides, triterpenes and reducing sugars. The LD50 of the extract of Mucuna pruriens was found to be 2154 mg/kg. The study showed that there was a significant reduction (p<0.05) in the fasting blood sugar levels in alloxan-induced diabetic treated groups that received 100, 200 and 400 mg/kg of the extract orally, with a maximum reduction (p<0.01) of 161.83±18.2, 153.67±13.8 and 133.83±10.4 recorded in the groups treated with 100, 200 and 400 mg/kg. The histopathological studies of the pancreas of diabetic animals revealed the degeneration of pancreatic Islet cells, but with the restoration of pancreatic Islet cells in the pancreas of diabetic group treated with various doses of the plant extract. The implications of the results obtained in the present study provide the scientific rationale for the use of Mucuna pruriens as anidiabetic agent. View Abstract View PDF View HTML Cite this Reference: E.D. Eze, A. Mohammed, K.Y. Musa and Y. Tanko, 2012. Evaluation of Effect of Ethanolic Leaf Extract of Mucuna pruriens on Blood Glucose Levels in Alloxan-Induced Diabetic Wistar Rats. Asian Journal of Medical Sciences, 4(1): 23-28.
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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"Thanks for this!" says: | lurkingforacure (05-09-2012) |
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