BCDHLMOP

L & P not too bad though.

I don't have Parkinson's but ACDHIJLNOPQ

wonder what other diseases these indicate?

CBAD

HMOP

Kevin

BCHLOP
(Like Ron, I shuffle, mostly before morning meds. I only fall when I do something stupid, like trying to change directions suddenly when running, or attempting the "snowplow" stop when cross-country skiing )

12 Respondents:

***********alertness (8)
B**********muscle strength (10)
C***********coordination (11)
D********brain fog (8)
E**zombie like (2)
F*headaches (1)
G*double vision (1)
H**********Inability to walk (10)
I*****salt/sweets (5)
J*abdominal distress (1)
Kcolitis (0)
L****ringing in ears (4)
M*******urinary problems (7)
Nskin eruptions (0)
O***********painful shoulders and neck muscles (11)
P********memory problems (8)
Q******sudden or excessive sweating (8)



The symptoms are for reactive hypoglycemia - a rare form of hypoglycemia where blood sugar values stay within normal limits and which makes your doctor tell that you are imaging it.

Remember, research has shown that as much as 80% of us have weird glucose problems

Interesting, Rick. Those symptoms don't seem to relate to me. Have some short term memory problems from artane, though, and other symptoms like aches and pains have other obvious causes.

found this:

Metabolism. 1987 Apr;36(4):351-5.
Effects of supplemental chromium on patients with symptoms of reactive hypoglycemia.

* Anderson RA,
* Polansky MM,
* Bryden NA,
* Bhathena SJ,
* Canary JJ.

To determine if chromium (Cr) is involved in hypoglycemia, eight female patients with symptoms of hypoglycemia were supplemented with 200 micrograms of Cr as chromic chloride for three months in a double-blind crossover experimental design study. Chromium supplementation alleviated the hypoglycemic symptoms and significantly raised the minimum serum glucose values observed two to four hours following a glucose load. Insulin binding to red blood cells and insulin receptor number also improved significantly during Cr supplementation. These data suggest that impaired Cr nutrition and/or metabolism may be a factor in the etiology of hypoglycemia.

PMID: 3550373 [PubMed - indexed for MEDLINE]

Diabetes Res Clin Pract. 2005 Sep;69(3):305-8. Epub 2005 Feb 23.
Pioglitazone prevents reactive hypoglycemia in impaired glucose tolerance.

* Arii K,
* Ota K,
* Suehiro T,
* Ikeda Y,
* Nishimura K,
* Kumon Y,
* Hashimoto K.

Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, Kochi 783-8505, Japan. ariik@med.kochi-u.ac.jp

A 42-year-old woman with hypoglycemic symptoms that occurred several hours after a meal visited our hospital. The hypoglycemic symptoms appeared when she was 37 years old, and her plasma glucose level had been assessed as less than 60 mg/dL when she experienced the symptoms. One year before, she had been diagnosed with reactive hypoglycemia by 75 g-oral glucose tolerance test (OGTT), which showed a normal glucose tolerance (NGT) pattern, and had begun taking an alpha-glucosidase inhibitor and nutritional treatment. A 75 g-OGTT on admission showed hypoglycemia at 240 min after glucose loading, excessive insulin secretion and an impaired glucose tolerance (IGT) pattern. A euglycemic-hyperinsulinemic clamp study demonstrated decreased insulin sensitivity. Therefore, we suspected that she had reactive hypoglycemia associated with insulin resistance and treated her with 15 mg/day pioglitazone. Her hypoglycemic symptoms completely disappeared after treatment with pioglitazone; insulin sensitivity in a euglycemic-hyperinsulinemic clamp study improved. Another 75 g-OGTT revealed that the excessive insulin secretion and hypoglycemia at 240 min after glucose loading had disappeared, and glucose tolerance was normalized from an IGT pattern to an NGT pattern. Thus, we believe that pioglitazone is effective for reactive hypoglycemia and aggravated glycemic metabolism associated with insulin resistance.

PMID: 16098929 [PubMed - indexed for MEDLINE]

Endocrine Practice
Issue: Volume 11, Number 2 / March-April 2005
Pages: 97 - 103
URL: Linking Options

INSULIN AUTOIMMUNITY AND HYPOGLYCEMIA IN SEVEN WHITE PATIENTS

Ananda Basu A1, F. John Service A1, Liping Yu A2, Don Heser A1, Laura M. Ferries A3, George Eisenbarth A2

Abstract:

Objective: To report the clinical, biochemical, and immunologic characteristics of 7 white patients with the rare disorder of hyperinsulinemic hypoglycemia in association with spontaneously generated high titers of antibodies to human insulin.

Methods: We reviewed the clinical data, history, and symptoms of the 7 study patients and summarized the biochemical findings during a spontaneous episode of hypoglycemia. Insulin antibody binding was measured in all patients, and antibody affinity, capacity, and clonality were analyzed in 4. A mixed meal study was conducted in 2 patients. A potential mechanism for postprandial hypoglycemia is presented.

Results: In all 7 patients (6 women and 1 man), symptoms were neuroglycopenic, occurring primarily postprandially but during fasting in some patients. During hypoglycemia, concentrations of insulin, proinsulin, and, in most patients, C peptide considerably exceeded those observed in patients with insulinoma. These concentrations were spuriously elevated as a result of interference by the autoantibodies in the immunoassays. No patient had evidence of an insulinoma on various radiologic localization procedures directed at the pancreas. Insulin antibodies showed a high percentage of binding to human insulin--50 to 90%. Heterogeneity of antibodies regarding clonality and antibody binding sites was noted; some patients had polyclonal and some had monoclonal IgG class antibodies. Most patients had two categories of binding sites: high affinity/low capacity and low capacity/high affinity. Although the mechanism for postprandial hypoglycemia remains conjectural, prolonged elevations of postprandial concentrations of total and free insulin are consistent with the putative mechanism of a buffering effect of insulin antibodies.

Conclusion: Insulin autoimmune hypoglycemia, although rare in any racial group and especially in white subjects, can be readily detected by high titers of insulin antibodies. Such a determination should be done in all patients undergoing evaluation for hypoglycemia. (Endocr Pract. 2005;11:97-103)

are you taking sinemet? if so, type (CR or standard), dose, schedule?

-Rick

Answer part A = BCDHLMOP
Sinemet
1 25/100 CR 3 times a day
1 25/100 Regular 3 times a day
prior to DBS 25/250 Regular 6 or 7 times a day

but i have taken sinemet, reg 25/100 in small doses.

i currently take mucuna w/ lodosyn for when i need or want to go do something. you could say i take it on as needed basis which is typically 2-4 x day, tho sometimes i skip a day. i think it is similar in effect to sinemet, perhaps a bit smoother - because it is a wole food, natural product. i consider it a drug as well and try to keep use to a minimum.

Ibken, have you tried the mucuna without the carbidopa? There's probably something similar to carbidopa in mucuna pruriens, which makes it three times more effective than sinemet (as seen in a clinical trial).