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Message: <blockquote data-quote="Oldvatr" data-source="post: 1460571" data-attributes="member: 196898">I am not sure what it is about the logic you are using in your thread, but something is setting off my alarm bells.  I think it is this assertion <<< It's not much of a leap to suggest an LCHF diet increases IR or at least won't bring it down.It may be that an intense workout should be combined with carbs and protein.>>> that i find I disagree with, but not sure why.If we go back to basic principles, then I find that defining Insulin as the storage hormone is acceptable.  So IR means that the body does not store glucogen or lipids as efficiently as it should.  One of the diagnostic pointers to diabetes is high levels of glucose in the blood, with unexplained weight loss.  So for a T2D then for example, having high bgl that does not start to reduce by the 2hr PP after a meal would show that either insulin is not being produced or there is resistance.So if a diet regime leads  to improved response times to mealtime bgl levels, then this might indicate lessening of the IR, in terms of carb glucose storage in the muscles.  The other form of IR is mainly felt by T1D, and seems to be triggered by eating high levels of fat (pizza effect).  Again this IR seems to delay the response to insulin being administered thus prolonging the PP peak.  Either way it might be possible to devise a diagnostic method to measure this increase or decrease in PP response to give an indication of IR being made worse or better.  However, RH colleagues will have to wait for a different method than this.It would need a stable medication regime, and probably involve a period of fasting followed by a standardised meal that can be repeated.   In fact it is sounding like the GTT test used in diagnosis.We cannot use meds reduction as an indicator of reducing IR since changes in carb intake will prompt this reaction anyway, without necessarily being linked to changes in IR.  Similarly weight gain / loss, although linked to IR, has too many variables to control in order to isolate the insulin response.  Like wise the actual meter reading of bgl is a poor method due to too many variables.  So unless we can find a way of home testing for insulin levels in the blood then  we are stuck.  Maybe CGM technology will help here/Remember that IR in T2D is mainly acting as a bouncer on the gateway to the muscle cells.  Exercise needs insulin to be absent in order to effectively deal with bgl levels.  So when there is high IR then the excess insulin hangs around for a while until excreted, and this will make exercise after a meal or snack less effective.  Some meds like Gliclazide boost levels of insulin in the blood and in this case act as a sledgehammer to force feed the fat cells with the excess bgl, and also opens up the lipid storage pathway to the adipose fatcells hence bypassing the muscle storage that is locked out by IR.It was generally accepted that T1D did not suffer IR, which has been regarded mainly as a T2D problem, but recent studies have discovered the Pizza Effect which can affect T1D, but it is not so common. <a href="https://www.ncbi.nlm.nih.gov/pubmed/12112937" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/12112937</a><a href="https://www.ncbi.nlm.nih.gov/pubmed/8462382" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/8462382</a>There is another thread on this site that is related to this topic.<a href="http://www.diabetes.co.uk/forum/threads/why-isnt-hyperinsulinemia-talked-about-more.120514/" target="_blank">http://www.diabetes.co.uk/forum/threads/why-isnt-hyperinsulinemia-talked-about-more.120514/</a></blockquote>

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