Hi Jenny, Nicky, Others:

Coenzyme Q10: A Review of Essential Functions and Clinical Trials -
http://tinyurl.com/bf4pg

This article is generally good in it's description of CoQ10's
pharmacology, how it relates to cardiovascular disease, it's connection
to the older sulphonylureas, as well as to cholesterol lowering drugs.
A larger portion of the article was related to CoQ10 (ubiquinone Q10)and
cardiovascular trials and it generally positive effects.

Page 8 of this article mentions that fully solublized softgel capsules
are the most bioavailable form of CoQ10.

The drugs that impact HMG-CoA such as the statins are frequently
discussed on this newsgroup. On the other hand I haven't seen anything
that mentions the impact of sulphonylureas on CoQ10.
Drug interactions:
"Beta-blockers have shown to decrease endogenous serum CoQ10 levels by
inhibiting CoQ10-dependent enzymes.51 Furthermore, CoQ10 supplementation
has been reported to reduce insulin requirements in diabetes mellitus.
Additionally, some oral hypoglycemic agents including glyburide,
acetohexamide, and tolazamide have also been shown to decrease
endogenous CoQ10 levels. Therefore, diabetic patients taking CoQ10 may
require dosage adjustments of hypoglycemic agents.54"
#54 Kishi T, Kishi H, et al. Bioenergetics in clinical medicine. Studies
on coenzyme Q and diabetes mellitus. J Med 1976;7:307-321.
scholar.google.com citations for the above article -
http://tinyurl.com/aydlq.  I did not find later studies that supported
this 1976 study.

A scholar.google.com search for sulfonylureas+CoQ10 -
http://tinyurl.com/dzm4e.

"Mitochondrial Function in Beta-cell Insulin Secretion
It has been recognized for a number of years that pre- and type 2
diabetic patients have an impaired ability of the pancreatic beta-cells
to secrete insulin.13,14 The homeostasis of glucose and insulin is based
on the ATP generated by glucose in the beta-cell. Glucose-stimulated
insulin secretion (GSIS) has been characterized by its pulsatile
nature as generated by oscillations in the ATP/ADP ratio.15 A series of
steps must be completed inside and outside the mitochondria before
insulin can be secreted (Figure 3). ...
Treatment Strategies CoQ10
Although most of the focus has been placed on the qualitative (genetic)
aspects of type 2 diabetes pathogenesis, the information presented
shows that mitochondrial dysfunction leading to diabetes is somewhere
along a continuum from increased oxidative stress to heterogeneous and
homogeneous disease. Treatment strategies that focus on decreasing
oxidative stress as well as increasing mitochondrial function might
present important options. One treatment agent that might have clinical
significance is coenzyme Q10 (CoQ10)." Mitochondrial Factors/Diabetes -
http://www.thorne.com/pdf/journal/7-2/mitochondrial_factors.pdf

Mitochondrial Medicine – Molecular Pathology of Defective Oxidative
Phosphorylation - http://www.annclinlabsci.org/cgi/content/abstract/31/1/25
"... the presence of a mutation of the mtDNA in the pancreatic ß-cell
impairs adenosine triphosphate (ATP) generation and insulin synthesis."

Frank

http://www.findarticles.com/p/articles/mi_m0MDR/is_1_8/ai_n6178372/

In this case history, published in the Journal of Diabetic Nursing,
there was the interesting information that the patient incorrectly
diagnosed as MODY was using "tiny" amounts of insulin long after the
period in which the "honeymoon" of type 1 should have been over.  The
patient also had normal C-peptide levels years after diagnosis and NO
evidence of DKA even with extremely high blood sugars at diagnosis.

But reading further you see that her treatment when they thought she was
a Type 1 was only two shots of Lispro a day--no basal at all, which may
explain why her A1c was high.

Unfortunately, in the same article the "improvement in control" achieved
with the sulfonylurea drug only brought her to 6.6%, which is still too
high according to the AACE standards.

One wonders what a basal/bolus insulin regimen might have done for her.
But in the UK, they seem to be WAY behind on using the newer insulin
regimens.

Her father, misdiagnosed as a Type 2, also was found to have the same
MODY gene. The grandparents has NO history of diabetes, which since this
is an autosomal dominant genetic syndrome suggests one of them had
undiagnosed MODY. A good reason to be careful in dismissing a MODY
diagnosis just because "no one in the family had it."

The father, btw, was controlled on tiny doses of repaglinide (Prandin) a
beta cell stimulator that is NOT a sulfonylurea.

--Jenny

http://www.geocities.com/lottadata4u  Diabetes Info

http://www.alt-support-diabetes.org/newlydiagnosed.htm Get Your Blood
Sugar Under Control

Given that people in their 80s are those most likely to have a heart
attack, I don't see why you'd want to give them a drug that affects
cardiac receptors in a negative way.

For people in the 50s, the problem with the PPAR drugs (Actos/Avandia)
is the swelling and fat gain, the long term effects of which really
aren't known.

I just read up on Repaglinide (Prandin) another beta stimulator which is
not a Sulf, but the problem here is that the only studies described in
the Prescribing Information are of patients taking it for one year and
there is a tiny, but troubling increase in cardiovascular "events"
compared to a sulf.  Since the time horizon here is FAR too short to
know the real effect on cardiovascular health, the jury has to be out
about this drug, and the related Starlix, too.

The worrisome thing to me is that when you take these drugs, you take
them every day, possibly several tablets a day, for the rest of your
life. This makes it vital to understand the very long-term effects, but
the drug approval process rarely studies a drug for more than 2 years.
--Jenny

http://www.geocities.com/lottadata4u  Diabetes Info

http://www.alt-support-diabetes.org/newlydiagnosed.htm Get Your Blood
Sugar Under Control

That's your choice.  I'm still grateful for Jenny's sharp eye.

Susan

Excellent implied advice. I'll apply it immediately to this
post.

Cheers, Alan, T2, Australia.
d&e, metformin 2x500mg

You sound to me like someone new to diabetes who is confused and wants
to find the official gold seal of approval which identifies those whose
opinions can be trusted. It would be rather nice if the world was as
simple as that :-)

Speaking as someone who trains students to be research scientists,
although not in the field of medicine, I would like to point out that
one of the first things a research student has to learn is that
qualifications are no guide. Some people who have the right
qualifications are simply not well educated enough in certain details
to handle a particular topic. Sometimes a topic is in a transitory
state and the best qualified people are at sea unless they're fiercely
up to date (which they rarely are). Sometimes they're being paid a lot
of money to put forward, or at least appear to put forward, a
particular point of view. Sometimes the topic in question is
controversial and there are a number of well supported but widely
divergent views on it.

And so on. In the end you simply have to rely on looking carefully at
how well the data supports the arguments presented, and how well the
arguments presented hang together. If that's all we diabetics could
rely on then few of us would have the talent or training to do it.

Fortunately there is a very important source of data on diabetes which
is available to us here but which is ignored by many researchers
because it doesn't come from a laboratory under controlled conditions,
and that is the reports of diabetics who are carrying out their own
experiments on themselves. Since I became diabetic I've carried out
lots of my own experiments on what I can eat and how various things
affect my blood glucose readings. I've probably plotted about 100
graphs by now of my own blood sugar responses to various things.

Some papers and books about diabetes, and some posters here, confirm
what I have observed in myself, explain it, and suggest further
experiments to me which turn out as they predicted. I tend to take
those people seriously. Some papers, books, and posters here suggest
things which are contradicted by my own observations on my own
diabetes. I tend to disregard those.

You do have something with which you can test the validity of the
opinions of various authorities and posters: your own blood glucose
meter. The people you should respect are those who can explain what
you have observed about your own diabetes, and whose suggestions turn
out to work for you. That's more important than any formal
qualifications.

I have no idea what Jenny's formal qualifications are, and I don't
much care, because in the year or so I've reading them she has shown
in her postings here enough intelligence and education on diabetic
topics to earn my respect and admiration. She is also one of those
whose postings have helped me to bring my own blood sugar readings
down and to reduce some of the diabetic complications I was already
suffering from, so she has also earned my gratitude.

Thanks, Jenny :-)