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Message: <blockquote data-quote="Oldvatr" data-source="post: 1796524" data-attributes="member: 196898">Thank you.  Looking at the dates of this research then it is before the recent moves to tackle T2D such as diet and lifestyle changes, and also before the market release of the latest SU drugs, that have improved glycemic control for us.  The reports you link to are not actual proof as to cause of the decrease in beta cell function, and merely document the effects of the then current treatment regimes.In fact NICE themselves have published a meta analysis of 10 RCT trials that show that not one SU drug on the market at the time had any significant effect on reducing BGL levels and were less effective in this task than Metformin.  I repeat this is not necessarily the case for todays PWD who have better tools available to deal with high bgl levels such as eat to meter, LC diets, avoiding processed foods. etc.  The Gliclazide drug referred to by the OP is of the same family as the older SU drugs, but not of the same class,  Add to that the obvious problem with these trials in that the diet being used is based on Eatwell#1 then it is clear that the participants on oral meds would not be able to achieve good bgl control so the [beta cell] mortality due to hyperglycemia is NOT eliminated  as a significant causal effect,  IMO the value of these older studies reflect a methadology failure and are no longer Gold Standard evidence. I think the hypothesis remains unproven,  I do accept that even today the use of lifestyle improvement is only applicable to a few PWD who are proactive, and that the general class of PWD remain in the older treatment regimes, and will still unfortunately 'progress' to  negative outcome.  My own experience with Gliclazide so far has been positive and my beta cell function has improved, not reduced, due to my current lifestyle, I have been using Glic for about 6 years now, with 4 years at maximum dose and very high bgl levels in the 30's (mmol/l, that is).  So I  was experiencing the classic progression as described in those reports, but I have stepped back from that brink and significantly reduced my Glic dose from 320mg to 40 mg a day. At the end of the day, a DX of LADA does involve treatment with insulin an inevitable matter so we are at best discussing a temporary stopgap measure.  I think that if there is an adverse effect from SU then it will not make any significant difference to that outcome in the timescale, but may be a QOL choice for the OP to make.</blockquote>

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