Are you diabetic, glucose intolerant, syndrome X!!!!!

reverett123 · 12-09-2011, 11:17 AM

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:

Originally Posted by Conductor71

Oh boy, Rick...what you gotten us into? lol While sudden potassium is an obvious explanation for these episodes, I hadn't ruled out insulin as eating or digesting food seems to play a role for me. Whatever is going on, it blocks the synthesis or more like something is missing or depleted during episode because I can try a triple dose of levodopa and I get nothing.
I have noticed episodes occur when stomach is empty. Oddly, I feel like I digest and metabolize food much more quickly than I used to but cannot take off extra weight. I know we often have slower digestion/constipation and urinary frequency, but I have more a sudden parasympathetic reaction resulting in both urge to urinate and have bm - not normal I feel really empty after like cleaned out empty...this is my turning point then I normalize. If I don't have the hyper motility and bathroom trip, this brain fog and weakness eventually responds to intake of a little food. I try to nibble on something healthy and/or with potassium like banana, cheese, or sunflower seeds though I respond more to turning back on with the potassium rich snacks.

What Rick and I are experiencing is more like a paralysis. With normal PD freezing we definitely have muscular contraction. With this, I have no sense of muscle tone or connection with my legs; they don't feel numb. For example, using a walker or being behind a shopping cart poses more risk than benefit.

I don't know if Rick experiences this but I have what I have dubbed princess and the pd moment...when I am coming around on meds but not quite on I have a heightened tactile sensitivity where I can sense if I am sitting on a thread or if someone touches me I get really irritated. Yet if I put weight on more affected side or my son happens to jump on me, I am irritated by the contact but the weight seems to trigger something that brings me back on sooner.

Can insulin cause anything like this? I have described this to my neuro who scratches his head and says not PD, while the endocrinologist I saw nearly laughed me out of the examining room. All levels were normal on my blood work and 24 urine capture, therefore I was making it all up.

I thought for awhile this was thyroid related but have norm levels despite being treated for hypothyroidism in my early 20's. I also have symptoms of this weight gain, hair loss (eyebrows and lashes), plus near diabetic bad dry feet...still doctors will not put me on trial low dose thyroid supplement.

Whatever is going on, I am so fed up as I don't think it is necessarily PD. It's really debilitating and unpredictable as I can think i am making a quick stop at Target and be trapped there for two hours.

Incidentally, I agree that there needs to be insulin measure. I have had the fasting glucose tolerance test at least three times. I was told levels were a little off but no need for treatment though I was symptomatic for hypoglycemia (my dad is hypoglycemic and has had bilateral hand tremor since he was a young man) but labs are normal so untreated.

I am far from a hypochondriac though doctors seem to think otherwise. I lose good portions of my mornings to this and I cannot go anywhere alone with my toddler son. Why would I make up symptoms? I suppose they think I like to sit in an office with a nausea inducing glob of sugar in my belly only to be poked four times. Yep, that's my idea of a fun four hours! Why do doctors not weigh in our symptoms anymore? So frustrating.

Laura

reverett123 · 12-09-2011, 11:21 AM

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]

Conductor71 · 12-09-2011, 11:26 AM

yes, we are the PD equivalent of My Dinner with André!

whatever the beastie is I want it gone.....

Laura

reverett123 · 05-04-2012, 05:13 PM

I'm going to bump this up due to its current relevence.

Conductor71 · 05-07-2012, 09:23 PM

Quote:

Originally Posted by reverett123

I'm going to bump this up due to its current relevence.

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.

reverett123 · 05-09-2012, 06:06 PM

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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