Re: Is there a quick cause and effect for FBG?
- From: "GysdeJongh" <jongh711@xxxxxxxxx>
- Date: Mon, 11 May 2009 07:59:29 +0200
"Michael" <micoder@xxxxxxxxxxxxx> wrote in message
news:bjHNl.148077$641.41282@xxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
I am wondering if our FBG can be dramatically influenced by a previous
day's indiscretion?
Hi Michael,
here are my two, uh.... 1 cent, Madoff has the other :)
There are two very distinct ways to look at your FBG :
1) The way we look at our FBG
The FBG is, of course, also just a blood glucose value and if it is high we
worry about the damage this can cause to our body so we try to prevent it.We
do that by tweaking bedtime snacks as you know.We measure this FBG each
morning because we want to avoid any peaks in our blood glucose
values.Speaking for myself, I stoped measuring my FBG after about 1 year.I
knew what happed to my blood glucose after following the advice of good
people here.I do it in moderation.There are more important things to do in
life :)
2) The way your dokter looks at FBG
The reason your dokter wants to know your Blood Glucose value when you are
still Fasting is that it can be used diagnostically.Your body detects that a
new day has started, your liver converts glycogen to glucose and puts that
in your blood stream to pickup for your muscles.You have to work, kill a
dinosaur. __IF__ your muscles indeed pick up the glucose than your FBG
will be low and your dokter will conclude that, generally speaking, the
system is still working.If it is too high he will conclude that he has to
change something in your medication.As he expects T2 patients to deteriorate
slowly he wants to know the FBG only twice a year.This sampling frequency,
how often do you want to know the FBG, is the __BIG__ difference between
1) and 2) This is also the reason that SMBG is considered not necessary for
T2 by the medical profession ... :)
So at this point in time the answer of science and your dokter to your
question is of course : "no a few high carb snacks will have zero influence
on your FBG because it wil not influence your insulin resistance
dramatically".
Now it was noticed that this sytem depends on processes in your brain : the
endorphin system and your hypothalamus.It was noticed that mygrating birds
have to become insulin resistant each year to save glucose.There is now a
clinical trial going where they want to tweak the endorphin system to
prevent high FBG.Very beautiful.
This is also just 1 example of the use of animal models in medicine and it
proves that all the usual " JUST MICE AGAIN " cryers don't know how science
works.The active substance , Cycloset is a quick-release formulation of
bromocriptine mesylate, a dopamine agonist.
Here is the, free, article :
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1924849&blobtype=pdf
BMC Endocr Disord. 2007 Jun 25;7:3.
A randomized, double-blind, placebo-controlled trial to assess safety and
tolerability during treatment of type 2 diabetes with usual diabetes therapy
and either Cycloset or placebo.
BACKGROUND: Cycloset is a quick-release formulation of bromocriptine
mesylate, a dopamine agonist, which in animal models of insulin resistance
and type 2 diabetes acts centrally to reduce resistance to insulin- mediated
suppression of hepatic glucose output and tissue glucose disposal. In such
animals, bromocriptine also reduces hepatic triglyceride synthesis and free
fatty acid mobilization, manifesting decreases in both plasma triglycerides
and free fatty acids. In clinical trials, morning administration of Cycloset
either as monotherapy or adjunctive therapy to sulfonylurea or insulin
reduces HbA1c levels relative to placebo by 0.55-1.2. Cycloset therapy also
reduces plasma triglycerides and free fatty acid by approximately 25% and
20%, respectively, among those also receiving sulfonylurea therapies. The
effects of once-daily morning Cycloset therapy on glycemic control and
plasma lipids are demonstrable throughout the diurnal portion of the day (7
a.m. to 7 p.m.) across postprandial time points. METHODS/DESIGN: 3,095
individuals were randomized in a 2:1 ratio into a one year trial aimed to
assess the safety and efficacy of Cycloset compared to placebo among
individuals receiving a variety of treatments for type 2 diabetes.
Eligibility criteria for this randomized placebo controlled trial included:
age 30-80, HbA1c <or= 10%, diabetes therapeutic regimen consisting of diet
or no more than two hypoglycemic agents or insulin with or without one
additional oral agent (usual diabetes therapy; UDT). The primary safety
endpoint will test the hypothesis that the rate of all-cause serious adverse
events after one year of usual diabetes therapy (UDT) plus Cycloset is not
greater than that for UDT plus placebo by more than an acceptable margin
defined as a hazard ratio of 1.5 with a secondary endpoint analysis of the
difference in the rate of serious cardiovascular events, (myocardial
infarction, stroke, coronary revascularization or hospitalization for or
angina or congestive heart failure). Efficacy analyses will evaluate effects
of Cycloset versus placebo on change from baseline in HbA1c, fasting
glucose, body weight, waist circumference, blood pressure and plasma lipids.
DISCUSSION: This study will extend the current data on Cycloset safety,
tolerability and efficacy in individuals with type 2 diabetes to include its
effects in combination with thiazolodinediones, insulin secretagogues,
metformin, alpha-glucosidase inhibitors and exogenous insulin regimens.
TRIAL REGISTRATION: clinical trials.gov NCT00377676.
PMID: 17592632
PMCID: PMC1924849
hth
Gys
.
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