You must understand that we are talking about something that your docs don't know about but that is making your life hell while shortening it. It has been known since 1930 that ldopa can cause hyperglycemia. But in 1930 ldopa was a useless compound. When it became the "gold standard" in 1967 that earlier work was brushed aside because the addition of the carbidopa formulation theoretically fixed the problem. Unfortunately, while it did give the numbers desired in the bloodstream, nobody looked to see what was happening in muscle tissue. Why muscles? Because that's where 90% of glucose activity happens...

Then in 2004 a paper was published that I ran across a few weeks ago and that set bells to ringing:

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.


Like rosebud and others, I had been dealing with some very freaky symptoms and had been blaming H pylori, but as I looked into this things began to fall into place. The picture is still unfolding, but something very important is here.