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Type 2: Low carb cannot repair damaged beta cells
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<blockquote data-quote="Tophat1900" data-source="post: 2365996" data-attributes="member: 362123"><p>This is really just a continuation of the conversation on this thread below, except there are now two threads. </p><p></p><p><a href="https://www.diabetes.co.uk/forum/threads/why-wont-the-nhs-tell-you-the-secret-to-treating-diabetes.178134/page-24" target="_blank">https://www.diabetes.co.uk/forum/threads/why-wont-the-nhs-tell-you-the-secret-to-treating-diabetes.178134/page-24</a></p><p></p><p>In the link posted by the op is this for the treatment of T2</p><p></p><p><span style="font-size: 18px"><strong>ADA ALGORITHM FOR TREATMENT OF TYPE 2 DIABETES</strong></span></p><p><strong>The ADA algorithm for the treatment of type 2 diabetes advocates a stepwise therapeutic approach that is based upon reduction in the plasma glucose concentration and NOT upon known pathophysiological disturbances (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B49" target="_blank">49</a>). It dictates the initiation of therapy with lifestyle modification plus metformin to achieve an A1C < 7.0% (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F18/" target="_blank">Fig. 18</a>). If the goal is not reached or if secondary failure occurs, the ADA algorithm suggests one of three options: <em>1</em>) First is the addition of basal insulin, an option unlikely to be chosen by primary care physicians or most endocrinologists in the U.S. and unlikely to achieve the desired level of glycemic control based upon well-designed studies by experts in the field of insulin therapy (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B302" target="_blank">302</a>–<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B308" target="_blank">308</a>). Moreover, all of these insulin-based add-on studies have been associated with a high incidence of hypoglycemia and major weight gain (range 4.2–19.2 lbs, mean 8.5 lbs within 6–12 months or less) (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F19/" target="_blank">Fig. 19</a>). <em>2</em>) Second is the addition of a TZD, but this option is unlikely to be chosen because of the concerns raised in the ADA algorithm about this class of drugs. Thus, the ADA algorithm basically guides the physician to select a sulfonylurea as the choice for a second antidiabetic agent. Moreover, third party reimbursers like this option because sulfonylureas are inexpensive. Neither the GLP-1 analogs nor the DPP-4 inhibitors are included as an option in the ADA algorithm (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B49" target="_blank">49</a>). Since neither the sulfonylureas nor metformin exerts any effect to preserve β-cell function (see previous discussion and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F16/" target="_blank">Fig. 16</a>), the 20% of β-cell function that was present at the time of diagnosis of diabetes (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B40" target="_blank">40</a>–<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B42" target="_blank">42</a>) will largely have been lost by the time that combined sulfonylurea/metformin therapy has failed, and the majority of these patients will require insulin treatment. Insulin therapy is difficult for most primary care physicians, and even in the hands of experienced endocrinologists it is not easy to achieve and maintain an A1C <7%—let alone <6.5%—without significant hypoglycemia and weight gain (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B302" target="_blank">302</a>–<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B308" target="_blank">308</a>). Moreover, it is unclear why one would initiate insulin before exenatide, since insulin rarely decreases the A1C to <7.0% and is associated with significant weight gain and hypoglycemia (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B302" target="_blank">302</a>–<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B308" target="_blank">308</a>) (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F19/" target="_blank">Fig. 19</a>). Most recently, an ADA Consensus Statement has significantly revised the ADA therapeutic algorithm (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B309" target="_blank">309</a>). A two-tier approach is advocated, and sulfonylureas have been elevated into the first tier and are to be used if diet/exercise plus metformin fail to reduce the A1C to <7.0% (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F20/" target="_blank">Fig. 20</a>). From the pathophysiological standpoint, this represents a major step backward, since an overwhelming body of evidence-based medicine (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F16/" target="_blank">Fig. 16</a>) conclusively demonstrates that sulfonylureas do not preserve β-cell function and do not achieve durability of glycemic control. Although this algorithm is not the official policy statement of ADA, it is likely to be interpreted as such by most third-party payers. "</strong></p><p><strong></strong></p><p>The link you posted is all about ADA drug treatment for t2 diabetics. I could find no mention to low carb at all. If I missed it please point it out to me. </p><p></p><p>The article then states this below. This view imo is incorrect. Obesity is in my view mostly a sign of metabolic dysfunction. The ADA clearly believes it is a cause. </p><p><strong></strong></p><p><strong>"It is abundantly clear that the current epidemic of diabetes is being driven by the epidemic of obesity" </strong></p><p><strong></strong></p><p>[USER=422465]@Tannith[/USER] in regards to your copy n paste, it is clear you have posted fragments and it is not one copy n paste. The article is titled. </p><p></p><p><span style="font-size: 22px"><strong>From the Triumvirate to the Ominous Octet: A New Paradigm for the Treatment of Type 2 Diabetes Mellitus</strong></span></p><p></p><p><span style="font-size: 15px">It is not titled </span></p><p><span style="font-size: 15px"><strong>Type 2: Low carb cannot repair damaged beta cells</strong></span></p><p><span style="font-size: 15px"></span></p><p><span style="font-size: 15px">In fact I couldn't find any discussion on diet at all. Let alone a claim that low carb cannot do as you state. The article is about the ADA's algorithm drug therapy approaches. And a A1C goal of 7%</span></p><p><span style="font-size: 15px"></span></p><p><span style="font-size: 15px"></span></p><p><span style="font-size: 15px"></span></p><p></p><p><span style="font-size: 15px"><strong>Summary: Treatment.</strong></span></p><p><strong>Although this paradigm shift, which is based upon pathophysiology, represents a novel approach to the treatment of type 2 diabetes, it is substantiated by a vast body of basic scientific and clinical investigational studies. Because this algorithm is based upon the reversal of known pathophysiological defects, it has a high probability of achieving durable glycemic control. If the plasma glucose concentration can be maintained within the normal nondiabetic range, the microvascular complications of the disease, which are costly to treat and associated with major morbidity and mortality, can be prevented. Most importantly, this will enhance the quality of life for all diabetic patients.</strong></p><p><strong></strong></p><p>So, the goal of the ADA is jump straight to drugs and try to achieve an A1c goal of 7%... I did see maybe 6.5% being mentioned somewhere, but it's a long article. Either way, not a good outcome. And given the hostility and ignorance towards low carb by much of the medical world it doesn't surprise me that it isn't mentioned. </p><p></p><p></p><p>Tannith please point out anything I missed or got wrong. I am operating on zero coffee at the moment. </p></blockquote><p></p>
[QUOTE="Tophat1900, post: 2365996, member: 362123"] This is really just a continuation of the conversation on this thread below, except there are now two threads. [URL]https://www.diabetes.co.uk/forum/threads/why-wont-the-nhs-tell-you-the-secret-to-treating-diabetes.178134/page-24[/URL] In the link posted by the op is this for the treatment of T2 [SIZE=5][B]ADA ALGORITHM FOR TREATMENT OF TYPE 2 DIABETES[/B][/SIZE] [B]The ADA algorithm for the treatment of type 2 diabetes advocates a stepwise therapeutic approach that is based upon reduction in the plasma glucose concentration and NOT upon known pathophysiological disturbances ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B49']49[/URL]). It dictates the initiation of therapy with lifestyle modification plus metformin to achieve an A1C < 7.0% ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F18/']Fig. 18[/URL]). If the goal is not reached or if secondary failure occurs, the ADA algorithm suggests one of three options: [I]1[/I]) First is the addition of basal insulin, an option unlikely to be chosen by primary care physicians or most endocrinologists in the U.S. and unlikely to achieve the desired level of glycemic control based upon well-designed studies by experts in the field of insulin therapy ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B302']302[/URL]–[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B308']308[/URL]). Moreover, all of these insulin-based add-on studies have been associated with a high incidence of hypoglycemia and major weight gain (range 4.2–19.2 lbs, mean 8.5 lbs within 6–12 months or less) ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F19/']Fig. 19[/URL]). [I]2[/I]) Second is the addition of a TZD, but this option is unlikely to be chosen because of the concerns raised in the ADA algorithm about this class of drugs. Thus, the ADA algorithm basically guides the physician to select a sulfonylurea as the choice for a second antidiabetic agent. Moreover, third party reimbursers like this option because sulfonylureas are inexpensive. Neither the GLP-1 analogs nor the DPP-4 inhibitors are included as an option in the ADA algorithm ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B49']49[/URL]). Since neither the sulfonylureas nor metformin exerts any effect to preserve β-cell function (see previous discussion and [URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F16/']Fig. 16[/URL]), the 20% of β-cell function that was present at the time of diagnosis of diabetes ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B40']40[/URL]–[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B42']42[/URL]) will largely have been lost by the time that combined sulfonylurea/metformin therapy has failed, and the majority of these patients will require insulin treatment. Insulin therapy is difficult for most primary care physicians, and even in the hands of experienced endocrinologists it is not easy to achieve and maintain an A1C <7%—let alone <6.5%—without significant hypoglycemia and weight gain ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B302']302[/URL]–[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B308']308[/URL]). Moreover, it is unclear why one would initiate insulin before exenatide, since insulin rarely decreases the A1C to <7.0% and is associated with significant weight gain and hypoglycemia ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B302']302[/URL]–[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B308']308[/URL]) ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F19/']Fig. 19[/URL]). Most recently, an ADA Consensus Statement has significantly revised the ADA therapeutic algorithm ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/#B309']309[/URL]). A two-tier approach is advocated, and sulfonylureas have been elevated into the first tier and are to be used if diet/exercise plus metformin fail to reduce the A1C to <7.0% ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F20/']Fig. 20[/URL]). From the pathophysiological standpoint, this represents a major step backward, since an overwhelming body of evidence-based medicine ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/figure/F16/']Fig. 16[/URL]) conclusively demonstrates that sulfonylureas do not preserve β-cell function and do not achieve durability of glycemic control. Although this algorithm is not the official policy statement of ADA, it is likely to be interpreted as such by most third-party payers. " [/B] The link you posted is all about ADA drug treatment for t2 diabetics. I could find no mention to low carb at all. If I missed it please point it out to me. The article then states this below. This view imo is incorrect. Obesity is in my view mostly a sign of metabolic dysfunction. The ADA clearly believes it is a cause. [B] "It is abundantly clear that the current epidemic of diabetes is being driven by the epidemic of obesity" [/B] [USER=422465]@Tannith[/USER] in regards to your copy n paste, it is clear you have posted fragments and it is not one copy n paste. The article is titled. [B][/B] [SIZE=6][B]From the Triumvirate to the Ominous Octet: A New Paradigm for the Treatment of Type 2 Diabetes Mellitus[/B][/SIZE] [B][SIZE=4][/SIZE][/B] [SIZE=4]It is not titled [B]Type 2: Low carb cannot repair damaged beta cells[/B] In fact I couldn't find any discussion on diet at all. Let alone a claim that low carb cannot do as you state. The article is about the ADA's algorithm drug therapy approaches. And a A1C goal of 7% [B][/B] [B][/B][/SIZE] [SIZE=4][B]Summary: Treatment.[/B][/SIZE] [B]Although this paradigm shift, which is based upon pathophysiology, represents a novel approach to the treatment of type 2 diabetes, it is substantiated by a vast body of basic scientific and clinical investigational studies. Because this algorithm is based upon the reversal of known pathophysiological defects, it has a high probability of achieving durable glycemic control. If the plasma glucose concentration can be maintained within the normal nondiabetic range, the microvascular complications of the disease, which are costly to treat and associated with major morbidity and mortality, can be prevented. Most importantly, this will enhance the quality of life for all diabetic patients. [/B] So, the goal of the ADA is jump straight to drugs and try to achieve an A1c goal of 7%... I did see maybe 6.5% being mentioned somewhere, but it's a long article. Either way, not a good outcome. And given the hostility and ignorance towards low carb by much of the medical world it doesn't surprise me that it isn't mentioned. Tannith please point out anything I missed or got wrong. I am operating on zero coffee at the moment. [SIZE=4][/SIZE] [/QUOTE]
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