Perhaps a milder version?

Diabetes
People with diabetes may experience insulin shock if too much insulin is injected. This causes a rapid drop in blood sugar, a condition known as hypoglycemia. The reaction comes on rapidly and can lead to coma and even death. Sweating is a symptom of an insulin reaction, along with hunger, pallor, trembling, rapid heartbeat, weakness, and mood swings.

My dad is 80 years old and was told 7 or 8 years ago he was diabetic. I believe he had it for years before the diagnosis. There was a saying in the greater family between cousins, etc. that "a meal was not complete without something sweet". Craving sweets and excessive sweating have been the norm since the day I was born. Could there be a possible connection?

Mike

i take only regular 25/100s - a lot of them i'll grant you but i don't have dyskinesia. i had it on azilect, stalevo, CR, mirapex, and requip. It wasn't until i dropped stalevo and started pamelor that i didn't have dyskinesia on all that levo dopa if i didn't mix it with anything else dopaminergic.
i'm thinking that taking it in low frequent doses yields the best continuity, and that anything else over or under causes imbalances in more transmitters than just dopamiine.
nortriptyline isn't even really that much of an anticholinergic but i think it works. norepinephrine is also involved and these neuro transmitters are in both ends of our brains.....digestion and elimination require transmitters to move smoothly too.

It's easy for me to predict an off. i just have to eat the wrong food at the wrong time...or too much food. i take smaller amounts of sinemet at night but do not go off before i go to bed. i couldn't sleep, i have to be somewhere in between....a twilight of off and on.

i'm dense and can't figure out what your posts are about. i did talk to a scientist at wpc who believes insulin is involved with pd and other things. would you mind explaining it a little more in relation to pd?

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]


-----------------------------

1: Int J Neurosci. 1993 Mar-Apr;69(1-4):125-30.

The relationship between diabetes mellitus and Parkinson's disease.

Sandyk R.

NeuroCommunication Research Laboratories, Danbury, CT.

It has been reported that 50% to 80% of patients with Parkinson's disease have
abnormal glucose tolerance which may be further exacerbated by levodopa therapy.
Little is known about the impact of chronic hyperglycemia on the severity of the
motor manifestations and the course of the disease as well as its impact on the
efficacy of levodopa or other dopaminergic drugs. This issue, which has been
largely ignored, is of clinical relevance since animal studies indicate that
chronic hyperglycemia decreases striatal dopaminergic transmission and increases
the sensitivity of postsynaptic dopamine receptors. In addition, evidence from
experimental animal studies indicates that diabetic rats are resistant to the
locomotor and behavioral effects of the dopamine agonist amphetamine. The
resistance to the central effects of amphetamine is largely restored with
chronic insulin therapy. In the present communication, I propose that in
Parkinson's disease diabetes may exacerbate the severity of the motor disability
and attenuate the therapeutic efficacy of levodopa or other dopaminergic agents
as well as increase the risk of levodopa-induced motor dyskinesias. Thus, it is
advocated that Parkinsonian patients should be routinely screened for evidence
of glucose intolerance and that if found aggressive treatment of the
hyperglycemia may improve the response to levodopa and potentially diminish the
risk of levodopa-induced motor dyskinesias.

PMID: 8082998 [PubMed - indexed for MEDLINE]

----------------------------

1: Neurology. 2004 Sep 28;63(6):996-1001.

Diabetes mellitus and progression of rigidity and gait disturbance in older
persons.

Arvanitakis Z, Wilson RS, Schneider JA, Bienias JL, Evans DA, Bennett DA.

Rush Alzheimer's Disease Center, Rush University Medical Center, 600 S. Paulina,
Suite 1020E, Chicago, IL 60612, USA.

BACKGROUND: Parkinsonian-like signs, including rigidity, gait disturbance, and
bradykinesia, are common and progressive in old age and are associated with
morbidity and mortality. Few risk factors for these signs have been identified.
Diabetes mellitus, also a common chronic condition in old age and known to be
associated with physical and neurologic disability, may be associated with
parkinsonian-like signs. OBJECTIVE: To examine the relation of diabetes to four
parkinsonian-like signs. METHODS: Participants were 822 older Catholic clergymen
and women who were without clinically diagnosed Parkinson disease or dementia at
baseline. For up to 9 years, they had uniform annual evaluations, which included
a modified version of the motor portion of the Unified Parkinson's Disease
Rating Scale, from which previously established measures of four specific
parkinsonian-like signs were derived. Participants were evaluated for the
presence of diabetes, based on direct medication inspection and history.
RESULTS: Diabetes was present in 128 (15.6%) participants. In random effects
models controlling for age, sex, and education, diabetes was associated with
worsening rigidity (p < 0.01) and gait (p < 0.05), over an average of 5.6 years
of follow-up, but not with change in bradykinesia or tremor. The presence of
stroke did not substantially affect the association of diabetes with rigidity
but reduced the association of diabetes with gait to a trend (p = 0.08).
CONCLUSION: Diabetes may be a previously unrecognized risk factor for
progression of parkinsonian-like signs in older persons.

PMID: 15452289 [PubMed - indexed for MEDLINE]

1: Lancet Neurol. 2004 Mar;3(3):169-78.

Insulin and neurodegenerative disease: shared and specific mechanisms.

Craft S, Watson GS.

Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound
Medical Center, Department of Psychiatry and Behavioral Sciences, University of
Washington School of Medicine, Seattle, 98108, USA. scraft@u.washington.edu

Insulin has functions in the brain and dysregulation of these functions may
contribute to the expression of late-life neurodegenerative disease. We provide
a brief summary of research on the influence of insulin on normal brain
function. We then review evidence that perturbation of this role may contribute
to the symptoms and pathogenesis of various neurodegenerative disorders, such as
Alzheimer's disease, vascular dementia, Parkinson's disease, and Huntington's
disease. We conclude by considering whether insulin dysregulation contributes to
neurodegenerative disorders through disease-specific or general mechanisms.

PMID: 14980532 [PubMed - indexed for MEDLINE]

...i talked to Dr.Watson!

Thanks ! Overall do they refer to older onset?

Rick,
Please translate these papers to our less technical lot such as myself !
Or correct my understanding of them.
For me, these early researches are in line with recent papers, which were a subject of several threads on this forum in the last 3 weeks or so. Simply put, PD is thought to have a similar genetic fault as diabetics type 2 which prevent the cells from accepting glucose to fuel the cell. Further more it was suggested to use already approved diabetic 2 drugs to treat PD.
Alternatively, I speculated using ketonic diet to starve the body of glucose which forces the liver to make ketons, which is, accepted by brain cells as an alternative fuel.
cheers
Imad

Imad-
These studies were just the top of the pile, but they point out that insulin problems are part of PD for many or, even, all of us and that the gold standard that medicine offers us contributes to the problem.

The bigger issue, however, is that we, both patients and docs andscientists, have to get past the narrow focus of dopamine, substantia nigra, and neurology and look at PD for what it is - a system wide breakdown of homeostatic control. In normal language, we are dealing with the increasing loss of our ability to maintain our balance in every sense of the phrase.

Insulin is just one example. Think about it for a moment. One of the most powerful and dangerous chemicals in the body. It is a constant factor but its level is always in flux. It impacts every system in the body, including the brain, and not necessarily in a gentle manner. Among its roles is the control of glucose - too little or too much is deadly as well.

Yet, to consider what role it might have in PD is "thinking outside the box"! The box is too damn small!

It isn't just insulin. I could name you a dozen other things that are not in that box. The bottom line, however, is that we are dealing with an incredibly complex disorder. But medicine has relegated us to a narrow slot and wants us to stay there, albeit unconsciously.

The truth is that everything affects PD and PD affects everything. Insulin. Glucose. Adrenaline. Cortisol. Noradrenaline. Dopamine. Acetylcholine. Serotonin. Cytokines. On and on and every one a player.

Oddly enough, I don't see this as cause for despair. There are a dozen actors in the play but we don't have to remove them all to disrupt the show. Any two or three may well change our lives. But changing our lives can be very hard. If medicine (or society) truly wants to save us, what we really need is support in every sense of the word. We can do more for ourselves than the pills can, but only if we aren't dealing with what passes for modern life.

We gave at the office.