As someone who has avoided type II diabetes by restricting carbohydrates, my guess is that the excess deaths in those trials agressively lowering blood glucose, were most likely a side effect of the pharmceuticals used, rather than a consequnce of lower glucose per se.  This conclusion assumes that the "agressive treatment" was mainly through drugs, and not through carbohydrate restriction.

More drugs at higher doses, including insulin itself, can be expected to increase detrimental effects, as well as more positive ones.  For some people, the increased negative side effects overwhelmed the positive effects of lower blood glucose.

The trial should have had an arm with placebo drugs and carb restriction to lower glucose. 

 Art Davidson 

 

 

I was just reading a comment in Physicians First Watch regarding the sub-set of patients with positive spot urine mircoalbumenia and aggressive management of HbgA1C. So I do indeed beleive that cookie cutter medicine probably is not the best variety.

The mechanism of disease is the critical factor, not just blood glucose.  You can make blood glucose as normal as you want by giving enough insulin, but insulin is a 2 edged sword.  It cause deposition of lipids and is pro inflammatory>  You have to change the mechanism of the disease to make the body anti inflammatory - so agents such as TZDs and fish oils that affect lipids and increase insulin sensitivity reverse the disease process.

A a fellow I showed in my research project that tight glucose control (A1C<7.0) was correlated with a greater incidence of in stent restenosis partciluliarly in women (presented Aug 2001). My hypothesis was that higher insulin levels used to achieve lower A1C would act as a growth factor for cellular hyperplasia within the stent. I think insulin also promotes cellular hyperplasia in vascular tissue and due to it's mass causes luminal obstruction, diffusely as in "small diabetic" vessels which are actually small lumens or as a component of plaque volume in focal plaque. Insulin or insulin sensitization may also lead to plaque vulnerability and or hypercoaguability and thus more events. The disparate findings between accord and advance may be related to the mechanism of glucose lowering; increasing insulin levels with secretagogous and or  insulin vs insulin sensitizers. Also insulin sensitizers appear not to have class effect as evidenced by Avandia vs Glucophage for example. Vascular tissue sensitized to insulin may receive more insulin "effect". Varying Sensitization mechanisms may account for the difference between Avandia and other insulin sensitizers.

Dear Dr TOPOL

I FIND VERY INTERESTING THE TOPOLOG.

PLEASE CAN YOU WRITE IN ENGLISH WHAT ARE ARE YOU SAYING.

BECAUSE IT IS DIFFICULT FOR FRANCOPHON PEOPLE TO UNDERSTAND ALL WHAT ARE YOU SAYING.

IT WILL BE MORE EASIER WHEN WE HAVE THE WRITING

THANK YOU VERY MUCH

 

Dr Nadhem HAJLAOUI, INTERVENTIONAL CARDIOLOGIST, ASSISTANT PROFESSOR.

MILITARY HOSPITAL OF TUNIS