[reverett123]

This deserves more attention than it got with the soft title I put on it, so here it is. One study never followed up on, but if verified then it is a ticking bomb.


1: J Appl Physiol. 2004 Dec;97(6):2339-46. Epub 2004 Jul 16.

Levodopa with carbidopa diminishes glycogen concentration, glycogen synthase
activity, and insulin-stimulated glucose transport in rat skeletal muscle.

Smith JL, Ju JS, Saha BM, Racette BA, Fisher JS.

Dept. of Biology, St. Louis University, 3507 Laclede Ave., St. Louis, MO 63103,
USA. smithjl@slu.edu

We hypothesized that levodopa with carbidopa, a common therapy for patients with
Parkinson's disease, might contribute to the high prevalence of insulin
resistance reported in patients with Parkinson's disease. We examined the effects
of levodopa-carbidopa on glycogen concentration, glycogen synthase activity, and
insulin-stimulated glucose transport in skeletal muscle, the predominant
insulin-responsive tissue. In isolated muscle, levodopa-carbidopa completely
prevented insulin-stimulated glycogen accumulation and glucose transport. The
levodopa-carbidopa effects were blocked by propranolol, a beta-adrenergic
antagonist. Levodopa-carbidopa also inhibited the insulin-stimulated increase in
glycogen synthase activity, whereas propranolol attenuated this effect.
Insulin-stimulated tyrosine phosphorylation of insulin receptor substrate (IRS)-1
was reduced by levodopa-carbidopa, although Akt phosphorylation was unaffected by
levodopa-carbidopa. A single in vivo dose of levodopa-carbidopa increased
skeletal muscle cAMP concentrations, diminished glycogen synthase activity, and
reduced tyrosine phosphorylation of IRS-1. A separate set of rats was treated
intragastrically twice daily for 4 wk with levodopa-carbidopa. After 4 wk of
treatment, oral glucose tolerance was reduced in rats treated with drugs compared
with control animals. Muscles from drug-treated rats contained at least 15% less
glycogen and approximately 50% lower glycogen synthase activity compared with
muscles from control rats. The data demonstrate beta-adrenergic-dependent
inhibition of insulin action by levodopa-carbidopa and suggest that unrecognized
insulin resistance may exist in chronically treated patients with Parkinson's
disease.


PMID: 15258132 [PubMed - indexed for MEDLINE]

[reverett123]

1 diabetes) or HHNS (if you have type 2 diabetes).

Early signs of hyperglycemia in diabetes include:

* Increased thirst
* Headaches
* Difficulty concentrating
* Blurred vision
* Frequent urination
* Fatigue (weak, tired feeling)
* Weight loss
* Blood glucose more than 180 mg/dL

Prolonged hyperglycemia in diabetes may result in:

* Vaginal and skin infections
* Slow-healing cuts and sores
* Decreased vision
* Nerve damage causing painful cold or insensitive feet, loss of hair on the lower extremities, and/or erectile dysfunction
* Stomach and intestinal problems such as chronic constipation or diarrhea

[lurkingforacure]

Whoa, and our neuro calls all of these "secondary symptoms of PD". Lots have wondered whether the meds cause so-called PD symptoms, this to me seems like a classic case of one med causing a whole host of problems for which more meds are needed. Am I wrong?

[reverett123]

I'm just digging into this, but it seems that sinemet has a short term effect of low blood sugar and a long term effect of high. The list of symptoms in all the books are for norms so who knows what the effects on a stressed out PWP might be. And what do you suppose the effect is on the BBB?

This may be the reason for "symptom creep" over the last forty years.

[pacem]

So, would a stabilization of the glucose by taking chromium picolinate be a quick solution? What about Mucuna? Would that have the same effect as the synthetic meds?

[rosebud]

I've posted twice, and lost both..

I'm not cosmiclly connected tonight...will try again tomorrow. Ah yes...I was just tagged as diabetic. I'm thinking of changing my username to candy-queen

[Curious]

Rose..double check and be sure you check the Remember me box when you logged in.

I'm sorry you lost your posts. Happens to me too..I hit the preview post button, then forget to hit the Submit Reply one.

[rosebud]

My common observation is that my levodopa gets converted to adrenaline when I have an abundance of glucose running loose in my system. It t akes 32 minutes for my sinemet cr to hit my system. Sometimes it goes where it's supppose to go, sometimes it doesn't. I have noticed a correlation between The onset of my meds, and a tsunami of adrenaline coming down the road. If I have the zip to do it, I get out of bed in the morning like a bat out of hell the minute I hit that 32 minute mark.

Now I have noticed that if my blood sugar is over 6 (that's about 108 for you in the U.S.) It's a lot trickier to get things under control. Above 7 and I may as well have stayed in bed....oh ya, I am in bed because I can't friggin walk!
(and I should have saved the medication as they will not kick in and only make the situation worse.) Meds only work well, when blood glucose readings are low and stable. The paradox is, levodopa drives up your Blood sugar levels so you can't win. This situation gets worse over time. Your neuro want's to increase your meds (cuz that's what Neuro's do.) They have a little perscription pad and a pen and that's their sole means of dealing with you, preferably in 15 minutes or less.

I have more to say but I have to get up and move a bit to work off my dinner.

[reverett123]

I would be interested in knowing if anyone else has a similar pattern as to when their legs simply stop working and it is a struggle to even take one step. Brain fog is also a part of it. And a damnable need to urinate.

It is not present when I first get up and take my first round. If I am on by the 45 minute mark, then it won't be a factor all morning. However some mornings nothing works right and after an hour of waiting, I may have to deal with it for a couple of hours. The variable seems to be whether my stomache is working or not. I don't know if that is cause or a second symptom of a bigger cause.

Sometimes it will show up early afternoon, but it is most common near bedtime. Say 80%.

Because of the brain fog and because eating protein first thing in the morning usually blocks it, I suspect low blood sugar in the morning. But that doesn't hold up in the other time periods since I have eaten.

However,if it is being caused by sinemet then the timing makes more sense. An hour after my first one unless an egg stabilizes the glucose while blocking part of the med.

As the day wears on and sinemet builds up to a maximum level at bedtime? Is hypoglycemia the trigger?

[rosebud]

I am trying a new approach this morning, I cannot acccept that what is wrong with my body is un-correctable. My first line of defence (or off the Fence) is good nutrition. I am not tooo far into the diabetic label to be salvaged from the claws of doubt and destruction! My second line of defence is exercise. Get the glucose into those muscles and burn it like the masterful machine it is.
I will see where that takes me. Last night I started...have no clue what my blood sugar is at the moment. If you don't hear from me again, I probably killed myself (unintentionally .....not talking the serious mental stuff...although I am mental at times). We are creative by nature...and obsessive by aculturation, or possibly just personality disorder. The creative parts build great scenerios of possibilities, then we adopt them...dangerous stuff. Rick -you have so many possibilities going on at any one time you'll need several lifetimes with PD to pursue them all. Gotta love that overactive brain though. I have the same problem as my daughter said last night."can't you go watch TV or something for awhile..."