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<blockquote data-quote="Neohdiver" data-source="post: 1101267" data-attributes="member: 258692"><p>I have not personally taken gliclazide (or any of the other sulfonylureas) - and my doctor would need to do a lot of arm twisting to get me to. Just to get my biases out there up front.</p><p></p><p>Our healthy glucose metabolism is a perfectly balanced on-demand system. When carbohydrates come in, your body takes stock and says, "Hmm . . . I need X quantity of insulin to help transport that glucose where it needs to go, and pumps out quantity X pretty much instantaneously to pair with the glucose and transport it across the blood vessel walls so it can go where it is needed to provide energy. When you are insulin resistant (Type 2, primarily), your body may well send out quantity X of insulin but insulin resistance means that it doesn't work very well. As a result the glucose increases in the bloodstream faster than the insulin can remove it (the spikes) - and it takes longer to clean up the remnants (dropping to your baseline much more slowly). When you are insulin insufficient (Type 1, from the start, and often Type 2 in later stages), your body may know you need quantity X, but it isn't able to produce it, so it sends out less (or none at all) to pair with the glucose.</p><p></p><p>Either way the quantity of glucose overwhelms the insulin - because the insulin doesn't work well or there isn't enough of it, or both.</p><p></p><p>Metformin works on insulin resistance (although our understanding of exactly how it does that is changing). It makes the insulin we have work better.</p><p></p><p>Sulfonylureas work on the opposite end of the problem by coaxing the pancreas to make and secrete insulin. </p><p></p><p>You'd think both would solve the problem - but there are risks associated with having too much insulin (added insulin or the sulfonylureas) that are non-existent with medications that merely make the insulin that is present work more efficiently (like Metformin). Because our natural insulin production system is an on-demand system, a "dumb" system that continuously adds insulin even when there are no carbs coming in is not the best substitute. When the added insulin (produced continuously - rather than on-demand) does what it does best - helping the glucose out of the bloodstream to where it is needed for energy, it can take too much out. The "dumb" steady-state secretion system doesn't understand that your blood glucose is not intended to go below a certain level. It's like the old (US?) joke about the boy scout helping a resistant little old lady across the road - it just keeps helping the blood glucose across the road (blood vessel walls), whether it needs/wants to go or not. The result can be a hypo. Just guessing from the timing of your side effects that that might be what you're talking about.</p><p></p><p>Of course, if hypos aren't the unpleasant side effects you're experiencing, feel free to ignore this post <img src="data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7" class="smilie smilie--sprite smilie--sprite1" alt=":)" title="Smile :)" loading="lazy" data-shortname=":)" /></p></blockquote><p></p>
[QUOTE="Neohdiver, post: 1101267, member: 258692"] I have not personally taken gliclazide (or any of the other sulfonylureas) - and my doctor would need to do a lot of arm twisting to get me to. Just to get my biases out there up front. Our healthy glucose metabolism is a perfectly balanced on-demand system. When carbohydrates come in, your body takes stock and says, "Hmm . . . I need X quantity of insulin to help transport that glucose where it needs to go, and pumps out quantity X pretty much instantaneously to pair with the glucose and transport it across the blood vessel walls so it can go where it is needed to provide energy. When you are insulin resistant (Type 2, primarily), your body may well send out quantity X of insulin but insulin resistance means that it doesn't work very well. As a result the glucose increases in the bloodstream faster than the insulin can remove it (the spikes) - and it takes longer to clean up the remnants (dropping to your baseline much more slowly). When you are insulin insufficient (Type 1, from the start, and often Type 2 in later stages), your body may know you need quantity X, but it isn't able to produce it, so it sends out less (or none at all) to pair with the glucose. Either way the quantity of glucose overwhelms the insulin - because the insulin doesn't work well or there isn't enough of it, or both. Metformin works on insulin resistance (although our understanding of exactly how it does that is changing). It makes the insulin we have work better. Sulfonylureas work on the opposite end of the problem by coaxing the pancreas to make and secrete insulin. You'd think both would solve the problem - but there are risks associated with having too much insulin (added insulin or the sulfonylureas) that are non-existent with medications that merely make the insulin that is present work more efficiently (like Metformin). Because our natural insulin production system is an on-demand system, a "dumb" system that continuously adds insulin even when there are no carbs coming in is not the best substitute. When the added insulin (produced continuously - rather than on-demand) does what it does best - helping the glucose out of the bloodstream to where it is needed for energy, it can take too much out. The "dumb" steady-state secretion system doesn't understand that your blood glucose is not intended to go below a certain level. It's like the old (US?) joke about the boy scout helping a resistant little old lady across the road - it just keeps helping the blood glucose across the road (blood vessel walls), whether it needs/wants to go or not. The result can be a hypo. Just guessing from the timing of your side effects that that might be what you're talking about. Of course, if hypos aren't the unpleasant side effects you're experiencing, feel free to ignore this post :) [/QUOTE]
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