Targets for Glycemic Control

In the paper

“Similarly, both fasting plasma glucose (FPG) and postprandial plasma glucose (PPG) are directly correlated to the risk of complications, with some evidence that PPG might constitute a stronger independent risk factor for CV complications (4)(5)(6)(7)(8)(9)(10).”

What the sources say

• Partly supported

  The Results and Discussion report that preprandial, before-breakfast, and postprandial glucose measures were associated with risk of retinopathy progression. They do not assess cardiovascular complications or show that postprandial glucose is a stronger independent risk factor; the Discussion instead identifies mean blood glucose as the primary determinant of retinopathy risk. Page numbers are unavailable in our copy. (LLM, conf=0.88)

  cites [4] 4. Service FJ, O'Brien PC. The relation of glycaemia to the risk of development and progression of retinopathy in the diabetic control and complications trial. Diabetologia 2001;44:1215-20. sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [5] 5. Coutinho M, Gerstein HC, Wang Y, et al. The relationship between glucose and incident cardiovascular events. A metaregression analysis of published data from 20 studies of 95,783 individuals followed for 12.4 years. Diabetes Care 1999;22:233-40. source
• ?Not checked — no full text of the sourcecites [6] 6. Levitan EB, Song Y, Ford ES, et al. Is nondiabetic hyperglycemia a risk factor for cardiovascular disease? A meta-analysis of prospective studies. Arch Intern Med 2004;164:2147-55. source

In the paper

“In the DCCT cohort, there was a significant reduction in CV outcomes (42%), nonfatal myocardial infarct (MI), stroke and CV death (57%), as well as all-cause mortality (33%) in previously intensively treated participants compared with those who were previously in the standard arm (17)(18)(19).”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.

  cites [17] 17. Nathan DM, Cleary PA, Backlund JY, et al. Intensive diabetes treatment and car- diovascular disease in patients with type 1 diabetes. N Engl J Med 2005;353:2643- 53. sourceExperimental — accuracy not yet measured
• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [18] 18. Writing Group for the DCCT/EDIC Research Group, Orchard TJ, Nathan DM, et al. Association between 7 years of intensive treatment of type 1 diabetes and long- term mortality. JAMA 2015;313:45-53. sourceExperimental — accuracy not yet measured
• Partly supported

  The Conclusions (page unavailable) mention 42% fewer CVD outcomes and 57% fewer major cardiovascular events, but identify those figures as earlier follow-up results. For the paper’s 30-year follow-up, the Results report reductions of 30% and 32%, respectively; the 32% reduction was not statistically significant (P = 0.07). The passages found do not report a 33% reduction in all-cause mortality. (LLM, conf=0.88)

  cites [19] 19. Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Inter- ventions and Complications (EDIC) Study Research Group. Intensive diabetes treatment and cardiovascular outcomes in type 1 diabetes: The DCCT/EDIC study 30-year follow-up. Diabetes Care 2016;39:686-93. sourceExperimental — accuracy not yet measured

In the paper

“Subsequent observational data from long-term follow up after termination of randomization periods of both the DCCT and UKPDS cohorts showed a persistence of significant microvascular benefits and also demonstrated an emergence of beneficial effect on CV outcomes attributed to intensive glycemic control.This has been termed as”

What the sources say

• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [14] 14. Writing Team for the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group. Effect of inten- sive therapy on the microvascular complications of type 1 diabetes mellitus. JAMA 2002;287:2563-9. sourceExperimental — accuracy not yet measured
• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [15] 15. Martin CL, Albers J, Herman WH, et al. Neuropathy among the diabetes control and complications trial cohort 8 years after trial completion. Diabetes Care 2006;29:340-4. sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [16] 16. Holman RR, Paul SK, Bethel MA, et al. 10-Year Follow-up of intensive glucose control in type 2 diabetes. New Engl J Med 2008;359:1577-89. source

In the paper

“If an A1C target ≤7.0%cannot be achieved with a FPG target of 4.0-7.0mmol/L and PPG target of 5.0-10.0mmol/L, further FPG lowering to 4.0 to 5.5 mmol/L and/or PPG lowering to 5.0-8.0 mmol/L may be considered, but must be balanced against the risk of hypoglycemia [Grade D, Level 4 (38) for FPG target for type 2 diabetes; Grade D, Consensus for FPG target for type 1 diabetes; Grade D, Level 4 (38,40”

What the sources say

• ?Not checked — no full text of the sourcecites [38] 38. Woerle HJ, Neumann C, Zschau S, et al. Impact of fasting and postprandial gly- cemia on overall glycemic control in type 2 diabetes Importance of postpran- dial glycemia to achieve target HbA1c levels. Diabetes Res Clin Pract 2007;77:280-5. source
• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [40] 40. Monnier L, Colette C, Dunseath GJ, et al. The loss of postprandial glycemic control precedes stepwise deterioration of fasting with worsening diabetes. Diabetes Care 2007;30:263-9. sourceExperimental — accuracy not yet measured

In the paper

“There was significant reduction in the incidence of major microvascular events in the intensive control group, mainly through a 21% relative reduction in nephropathy (23); however, no beneficial effect of intensive glucose lowering was found on major CV events or allcause mortality either during the trial or the subsequent median observational follow up of 5.4 years (24).”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [23] 23. ADVANCE Collaborative Group, Patel A, MacMahon S, et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med 2008;358:2560-72. sourceExperimental — accuracy not yet measured
• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [24] 24. Zoungas S, Chalmers J, Neal B, et al. Follow-up of blood-pressure lowering and glucose control in type 2 diabetes. New Engl J Med 2014;371:1392-406. source

In the paper

“Although, nontraditional glycemic targets, such as fructosamine and glycated albumin, have also been associated with CV outcomes and mortality in a cohort study (51), the broader utility of such targets and their correlation with A1C has not yet been established.”

What the sources say

• Supported

  The Discussion reports that fructosamine and glycated albumin were associated with coronary heart disease, ischemic stroke, heart failure, and death in a community-based cohort. Citation (51) follows the cohort-study finding; the subsequent statement about broader utility and correlation with A1C is not attributed to this source. (LLM, conf=0.93)

  cites [51] 51. Selvin E, Rawlings AM, Lutsey PL, et al. Fructosamine and glycated albumin and the risk of cardiovascular outcomes and death. Circulation 2015;132:269- 77. source

In the paper

“During a median follow up of 5.6 years, there was a nonsignificant reduction in the primary outcome (first occurrence of a major CV event), but the progression to albuminuria was significantly reduced in the intensive-treatment participants, with 9.1% of participants having significantly reduced progression compared to 13.8% in the standard therapy group.”

What the sources say

• Supported

  The Abstract reports a median follow-up of 5.6 years and a lower, nonsignificant rate of the primary cardiovascular outcome with intensive therapy (hazard ratio 0.88; P = 0.14). Table 3, reproduced in the Discussion, reports any increase in albuminuria in 9.1% of the intensive-therapy group versus 13.8% of the standard-therapy group (P = 0.01). (LLM, conf=0.94)

  cites [25] 25. Duckworth W, Abraira C, Moritz T, et al. Glucose control and vascular compli- cations in veterans with type 2 diabetes. N Engl J Med 2009;360:129-39. source
• ?Not checked — no full text of the sourcecites [26] 26. Moritz T, Duckworth W, Abraira C. Veterans Affairs diabetes trial-corrections. N Engl J Med 2009;361:1024-5. source

In the paper

“Such multifactorial interventions have recently been suggested to lead to not only significant microvascular and CV benefits but also mortality reduction in the 21-year follow up of the Steno-2 study (34).”

What the sources say

• Supported

  The Discussion reports significant risk reductions in microvascular complications and says reduced mortality resulted from fewer incident cardiovascular events and cardiovascular deaths. The Cardiovascular disease section also reports a lower risk of cardiovascular events in the intensive-therapy group. The supplied passages do not specify page numbers. (LLM, conf=0.93)

  cites [34] 34. Gaede P, Oellgaard J, Carstensen B, et al. Years of life gained by multifactorial intervention in patients with type 2 diabetes mellitus and microalbuminuria: 21 years follow-up on the Steno-2 randomised trial. Diabetologia 2016;59:2298- 307. source

In the paper

“In people with type 2 diabetes, an A1C ≤6.5% may be targeted to reduce the risk of CKD [Grade A, Level 1A (23)] and retinopathy [Grade A, Level 1A (21)], if they are assessed to be at low risk of hypoglycemia based on class of antihyperglycemic medication(s) utilized and the person's characteristics [Grade D, Consensus].”

What the sources say

• Supported

  The citation to this paper is attached to the CKD-risk portion of the sentence; retinopathy has a separate citation, and the hypoglycemia-risk qualification is labeled consensus. The Results (p. 2) report that intensive control achieved a mean A1C of 6.5% and reduced new or worsening nephropathy. The End Points section (p. 4) defines nephropathy to include albuminuria and serious renal outcomes. (LLM, conf=0.88)

  cites [23] 23. ADVANCE Collaborative Group, Patel A, MacMahon S, et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med 2008;358:2560-72. source
• Partly supported

  The Results report less retinopathy progression with intensive glycemic therapy (7.3% versus 10.4%); the intensive group's median A1C at one year was 6.4%. However, the Methods specify a target below 6.0%, not ≤6.5%, so this study supports intensive control for retinopathy but does not directly test the cited threshold. CKD and the hypoglycemia-risk qualification have separate attributions in the citing sentence. (LLM, conf=0.84)

  cites [21] 21. The ACCORD Study Group and ACCORD Eye Study Group. Effects of medical thera- pies on retinopathy progression in type 2 diabetes. New Engl J Med 2010;363:233-44. sourceExperimental — accuracy not yet measured

In the paper

“In addition, several insulin treat-to-target trials have safely used dose titration protocols in individuals not at target A1C to reach lower than”

What the sources say

• Partly supported

  Study Procedures (page not available) describes dose titration toward fasting self-monitored plasma glucose of 4.4–5.6 mmol/L in insulin-naïve people with type 2 diabetes, and Results > Hypoglycaemia reports that severe events were infrequent. The paper does not support the sentence’s other specified fasting ranges, a type 1 diabetes protocol, or a protocol targeting both fasting and 2-hour postprandial glucose. (LLM, conf=0.86)

  cites [41] 41. Bolli GB, Riddle MC, Bergenstal RM, et al. New insulin glargine 300 U/ml com- pared with glargine 100 U/ml in insulin-naive people with type 2 diabetes on oral glucose-lowering drugs: A randomized controlled trial (EDITION 3). Dia- betes Obes Metab 2015;17:386-94. sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [42] 42. Gerstein HC, Yale JF, Harris SB, et al. A randomized trial of adding insulin glargine vs. avoidance of insulin in people with type 2 diabetes on either no oral glucose- lowering agents or submaximal doses of metformin and/or sulphonylureas. The Canadian INSIGHT (Implementing New Strategies with Insulin Glargine for Hyperglycaemia Treatment) study. Diabet Med 2006;23:736-42. source
• ?Not checked — no full text of the sourcecites [43] 43. Yki-Järvinen H, Juurinen L, Alvarsson M, et al. Initiate insulin by aggressive titra- tion and education (INITIATE): A randomized study to compare initiation of insulin combination therapy in type 2 diabetic patients individually and in groups. Diabetes Care 2007;30:1364-9. source
• Supported

  The study protocol (page unavailable) describes dose titration toward FPG 4.0–5.5 mmol/L in people with poorly controlled type 2 diabetes. The Hypoglycaemia section reports no severe episodes, supporting the safety characterization for this trial. This paper supplies the type 2 diabetes, 4.0–5.5 mmol/L example, not the other targets listed in the broader sentence. (LLM, conf=0.88)

  cites [44] 44. Yki-Järvinen H, Kauppinen-Mäkelin R, Tiikkainen M, et al. Insulin glargine or NPH combined with metformin in type 2 diabetes: The LANMET study. Diabetologia 2006;49:442-51. source
• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [45] 45. Davies M, Storms F, Shutler S, et al. Improvement of glycemic control in sub- jects with poorly controlled type 2 diabetes: Comparison of two treatment algo- rithms using insulin glargine. Diabetes Care 2005;28:1282-8. sourceExperimental — accuracy not yet measured
• Partly supported

  The trial summary (p. 1) and Study protocol and treatment (p. 2) support the use of insulin dose titration in people with type 2 diabetes above the A1C goal. Its FPG target was ≤5.5–5.6 mmol/L, not a stated range of 4.5–5.5 mmol/L; mean FPG at the end of the trial was 6.5–6.7 mmol/L. This paper does not establish the other type 1 diabetes or combined FPG/2-hour PG targets listed in the claim. (LLM, conf=0.86)

  cites [46] 46. Riddle MC, Rosenstock J, Gerich J. The treat-to-target trial: Randomized addi- tion of glargine or human NPH insulin to oral therapy of type 2 diabetic patients. Diabetes Care 2003;26:3080-6. sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [47] 47. Heller S, Buse J, Fisher M, et al. Insulin degludec, an ultra-longacting basal insulin, versus insulin glargine in basal-bolus treatment with mealtime insulin aspart in type 1 diabetes (BEGIN Basal-Bolus Type 1): A phase 3, randomised, open- label, treat-to-target non-inferiority trial. Lancet 2012;379:1489-97. source

In the paper

“In most people with type 1 or type 2 diabetes, an A1C ≤7.0% should be targeted to reduce the risk of microvascular [Grade A, Level 1A (1,2,22,23)] and, if implemented early in the course of disease, CV complications [Grade B, Level 3 (23)].”

What the sources say

• ?Not checked — no full text of the sourcecites [1] 1. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998;352:837-53. source
• ?Not checked — no full text of the sourcecites [2] 2. The Diabetes Control and Complications Trial Research Group. The relation- ship of glycemic exposure (HbA1c) to the risk of development and progres- sion of retinopathy in the diabetes control and complications trial. Diabetes 1995;44:968-83. source
• Partly supported

  The Results and Conclusions report that intensive glycemic control reduced retinopathy progression in people with established type 2 diabetes, supporting the microvascular portion of the claim. The Methods specify an intensive A1C target below 6.0%, not a recommended target of ≤7.0% for most people with either type of diabetes. The paper does not report that early implementation reduces cardiovascular complications; its discussion of early treatment concerns the effect on the eyes. (LLM, conf=0.88)

  cites [22] 22. Action to Control Cardiovascular Risk in Diabetes Follow-On (ACCORDION) Eye Study Group and the Action to Control Cardiovascular Risk in Diabetes Follow-On (ACCORDION) Study Group. Persistent effects of intensive glycemic control on retinopathy in type 2 diabetes in the Action to Control Cardiovas- cular Risk in Diabetes (ACCORD) follow-on study. Diabetes Care 2016;39:1089- 100. sourceExperimental — accuracy not yet measured
• Partly supported

  The Results (p. 2) show that intensive glucose control reduced major microvascular events in patients with type 2 diabetes, primarily through fewer cases of nephropathy. The study did not include people with type 1 diabetes, and the Discussion (pp. 11–12) reports no significant reduction in major cardiovascular events. It does not establish a cardiovascular benefit from starting the target early in the disease course. (LLM, conf=0.89)

  cites [23] 23. ADVANCE Collaborative Group, Patel A, MacMahon S, et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med 2008;358:2560-72. sourceExperimental — accuracy not yet measured

In the paper

“The salient results of this study include: increased survival for a median of 7.9 years; 8.1 years longer median time before first CV event; and reduction in all microvascular complications, except for peripheral neuropathy, for participants in the intensive-therapy group compared to the conventional therapy group.”

What the sources say

• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [34] 34. Gaede P, Oellgaard J, Carstensen B, et al. Years of life gained by multifactorial intervention in patients with type 2 diabetes mellitus and microalbuminuria: 21 years follow-up on the Steno-2 randomised trial. Diabetologia 2016;59:2298- 307. source

In the paper

“Most of the large outcome trials conducted so far have been mostly based on preprandial glucose and A1C targets, with limited evidence of a long-term benefit of targeting PPG alone (49,50).”

What the sources say

• Partly supported

  The Discussion says earlier intervention studies paid no attention to controlling postprandial hyperglycemia, and that this trial’s limited follow-up prevented evaluation of clinical events. That supports the point about limited long-term outcome evidence, but the paper does not establish that most large trials used preprandial glucose and A1C targets. (LLM, conf=0.85)

  cites [49] 49. Esposito K, Giugliano D, Nappo F, et al. Regression of carotid atherosclerosis by control of postprandial hyperglycemia in type 2 diabetes mellitus. Circulation 2004;110:214-19. sourceExperimental — accuracy not yet measured
• Partly supported

  The Conclusions (page not specified) call HEART2D the first study to examine whether reducing postprandial glucose affects cardiovascular outcomes and report no difference between prandial and basal strategies. They also discuss large trials using A1C goals, but do not establish that most large outcome trials used preprandial glucose targets. HEART2D targeted A1C in both arms, so it did not test targeting PPG alone. (LLM, conf=0.84)

  cites [50] 50. Raz I, Wilson PW, Strojek K, et al. Effects of prandial versus fasting glycemia on cardiovascular outcomes in type 2 diabetes: The HEART2D trial. Diabetes Care 2009;32:381-6. sourceExperimental — accuracy not yet measured

In the paper

“When A1C values are higher, the major contribution is the FPG levels, but as the A1C value approaches the target value of ≤7.0%, there is a greater contribution from PPG values (37-39).”

What the sources say

• ?Not checked — no full text of the sourcecites [37] 37. Monnier L, Lapinski H, Colette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of type 2 diabetic patients: Variations with increasing levels of HbA(1c). Diabetes Care 2003;26:881-5. source
• ?Not checked — no full text of the sourcecites [38] 38. Woerle HJ, Neumann C, Zschau S, et al. Impact of fasting and postprandial gly- cemia on overall glycemic control in type 2 diabetes Importance of postpran- dial glycemia to achieve target HbA1c levels. Diabetes Res Clin Pract 2007;77:280-5. source
• Partly supported

  The Results (page not available) show that basal hyperglycemia contributed more at higher A1C levels, while the postprandial contribution was relatively greater at lower levels after treatment intensification. But the baseline trend was not statistically significant, and the Conclusions caution that treatment type can matter more than A1C alone. The claim omits those qualifications and extends the pattern toward ≤7.0%, a range not represented at baseline. (LLM, conf=0.86)

  cites [39] 39. Riddle M, Umpierrez G, DiGenio A, et al. Contributions of basal and postpran- dial hyperglycemia over a wide range of A1C levels before and after treatment intensification in type 2 diabetes. Diabetes Care 2011;34:2508-14. sourceExperimental — accuracy not yet measured

In the paper

“Evidence also supports the use of multifactorial risk-reduction strategies in addition to A1C control for CV prevention, including blood pressure (BP) and lipid targets; CV prevention medications; physical activity and other healthy behaviours; as well as smoking cessation (see Cardiovascular Protection in People with Diabetes chapter, p. S162).”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [34] 34. Gaede P, Oellgaard J, Carstensen B, et al. Years of life gained by multifactorial intervention in patients with type 2 diabetes mellitus and microalbuminuria: 21 years follow-up on the Steno-2 randomised trial. Diabetologia 2016;59:2298- 307. sourceExperimental — accuracy not yet measured

In the paper

“These trials-the DCCT in type 1 diabetes (11), the Kumamoto trial (12) and the UKPDS (1,13) in type 2 diabetes-confirmed that improved glycemic control significantly reduced the risk of microvascular complications, but had no significant effect on CV outcomes.”

What the sources say

• ?Not checked — no full text of the sourcecites [11] 11. The Diabetes Control and Complications Trial Research Group, Nathan DM, Genuth S, et al. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes melli- tus. N Engl J Med 1993;329:977-86. source
• ?Not checked — no full text of the sourcecites [12] 12. Ohkubo Y, Kishikawa H, Araki E, et al. Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with non-insulin-dependent diabetes mellitus: A randomized prospective 6-year study. Diabetes Res Clin Pract 1995;28:103-17. source
• ?Not checked — no full text of the sourcecites [1] 1. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998;352:837-53. source
• ?Not checked — no full text of the sourcecites [13] 13. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabe- tes Study (UKPDS) Group. Lancet 1998;352:854-65. source

In the paper

“Similarly, there was a significant reduction in MI (15% to 33%) and all-cause mortality (13% to 27%) in the UKPDS cohort in participants who had been originally randomized to intensive treatment (16).”

What the sources say

• ?Not checked — no full text of the sourcecites [16] 16. Holman RR, Paul SK, Bethel MA, et al. 10-Year Follow-up of intensive glucose control in type 2 diabetes. New Engl J Med 2008;359:1577-89. source

In the paper

“The initial data from the Diabetes Control and Complications Trial (DCCT; type 1 diabetes) (2) and the United Kingdom Prospective Diabetes Study (UKPDS; type 2 diabetes) (3) demonstrated a curvilinear relationship between A1C and diabetes complications, with no apparent threshold of benefit, although the absolute reduction in risk was substantially less at lower A1C levels.”

What the sources say

• ?Not checked — no full text of the sourcecites [2] 2. The Diabetes Control and Complications Trial Research Group. The relation- ship of glycemic exposure (HbA1c) to the risk of development and progres- sion of retinopathy in the diabetes control and complications trial. Diabetes 1995;44:968-83. source
• ?Not checked — no full text of the sourcecites [3] 3. Stratton IM, Adler AI, Neil HA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): Prospective observational study. BMJ 2000;321:405-12. source

In the paper

“Evidence indicates that improved glycemic control reduces the risk of both microvascular and CV complications.”

What the sources say

• ?Not checked — no full text of the sourcecites [11] 11. The Diabetes Control and Complications Trial Research Group, Nathan DM, Genuth S, et al. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes melli- tus. N Engl J Med 1993;329:977-86. source
• ?Not checked — no full text of the sourcecites [12] 12. Ohkubo Y, Kishikawa H, Araki E, et al. Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with non-insulin-dependent diabetes mellitus: A randomized prospective 6-year study. Diabetes Res Clin Pract 1995;28:103-17. source
• ?Not checked — no full text of the sourcecites [1] 1. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998;352:837-53. source
• ?Not checked — no full text of the sourcecites [13] 13. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabe- tes Study (UKPDS) Group. Lancet 1998;352:854-65. source

In the paper

“More intensive glucose control, A1C ≤6.5%, may be sought in people with a shorter duration of diabetes and longer life expectancy, especially in those people who are on treatment with antihyperglycemic agents with a low risk of hypoglycemia.”

In the paper

“An A1C target ≤8.5% may be more appropriate in people with type 1 and type 2 diabetes with limited life expectancy, higher level of functional dependency and a history of repeated severe hypoglycemia with hypoglycemia unawareness.”

In the paper

“Intensive glucose control with lowering A1C values to ≤7.0% in both type 1 and type 2 diabetes provides strong benefits for microvascular complications and, if achieved early in the disease with avoidance of hypoglycemia and glucose variability as part of a multifactorial treatment approach, likely provide a significant CV benefit.”

In the paper

“Data from a meta-analysis suggest that people with type 2 diabetes who receive intensive glucose lowering therapy have a reduced risk of the composite major adverse CV events (MACE) and MI, with no significant effect on the risk of total mortality, cardiac death, stroke and CHF (28).”

What the sources say

• ?Not checked — no full text of the sourcecites [28] 28. Fang HJ, Zhou YH, Tian YJ, et al. Effects of intensive glucose lowering in treat- ment of type 2 diabetes mellitus on cardiovascular outcomes: A meta-analysis of data from 58,160 patients in 13 randomized controlled trials. Int J Cardiol 2016;218:50-8. source

In the paper

“In order to achieve an A1C ≤7.0%, people with diabetes should aim for: a. FPG or preprandial PG target of 4.0 to 7.0 mmol/L and a 2-hour PPG target of 5.0-10.0mmol/L [Grade B, Level 2 (2) for type 1; Grade B, Level 2 (1) for type 2 diabetes]”

What the sources say

• ?Not checked — no full text of the sourcecites [2] 2. The Diabetes Control and Complications Trial Research Group. The relation- ship of glycemic exposure (HbA1c) to the risk of development and progres- sion of retinopathy in the diabetes control and complications trial. Diabetes 1995;44:968-83. source
• ?Not checked — no full text of the sourcecites [1] 1. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998;352:837-53. source

In the paper

“However, management strategies that would minimize glucose variability and their impact on hard clinical outcomes remain to be determined before these novel measurement targets of glucose quality can systematically be incorporated into clinical practice guidelines.”

In the paper

“Higher glycemic targets are also appropriate for functionally dependent adults of any age or individuals with limited life expectancy and little likelihood of benefit from intensive therapy.”

In the paper

“Correlation between A1C and estimated mean glucose values A1C values (%) 5.5-6.5 6.5-6.9 7.0-7.47.5-7.98.0-8.5 Estimated mean glucose (mmol/L) 6.2-7.7 7.8-8.5 8.6-9.3 9.4-10.1 10.2-10.9”