Guia ADA Diabetes Mellitus 2013

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Guia ADA Diabetes Mellitus 2013

  1. 1. Standards of Medical Care inDiabetesd2013AMERICAN DIABETES ASSOCIATIONDiabetes mellitus is a chronic illnessthat requires continuing medical careand ongoing patient self-managementeducation and support to prevent acutecomplications and to reduce the risk oflong-term complications. Diabetes care iscomplex and requires multifactorial riskreduction strategies beyond glycemic con-trol. A large body of evidence exists thatsupports a range of interventions toimprovediabetes outcomes.These standards of care are intendedto provide clinicians, patients, researchers,payers, and other interested individualswith the components of diabetes care,general treatment goals, and tools to eval-uate the quality of care. Although individ-ual preferences, comorbidities, and otherpatient factors may require modification ofgoals, targets that are desirable for mostpatients with diabetes are provided. Spe-cifically titled sections of the standardsaddress children with diabetes, pregnantwomen, and people with prediabetes.These standards are not intended to pre-clude clinical judgment or more extensiveevaluation and management of the patientby other specialists as needed. For moredetailed information about management ofdiabetes, refer to references (1–3).The recommendations included arescreening, diagnostic, and therapeuticactions that are known or believed tofavorably affect health outcomes of patientswith diabetes. A large number of theseinterventions have been shown to be cost-effective (4). A grading system (Table 1),developed by the American Diabetes Asso-ciation (ADA) and modeled after existingmethods, was utilized to clarify and codifythe evidence that forms the basis for therecommendations. The level of evidencethat supports each recommendation islisted after each recommendation usingthe letters A, B, C, or E.These standards of care are revisedannually by the ADA’s multidisciplinaryProfessional Practice Committee, incor-porating new evidence. For the currentrevision, committee members systemati-cally searched Medline for human stud-ies related to each subsection andpublished since 1 January 2011. Recom-mendations (bulleted at the beginningof each subsection and also listed inthe “Executive Summary: Standards ofMedical Care in Diabetesd2013”) wererevised based on new evidence or, insome cases, to clarify the prior recom-mendation or match the strength of thewording to the strength of the evidence.A table linking the changes in recom-mendations to new evidence can be re-viewed at http://professional.diabetes.org/CPR. As is the case for all positionstatements, these standards of care werereviewed and approved by the ExecutiveCommittee of ADA’s Board of Directors,which includes health care professionals,scientists, and lay people.Feedback from the larger clinicalcommunity was valuable for the 2013revision of the standards. Readers whowish to comment on the “Standards ofMedical Care in Diabetesd2013” areinvited to do so at http://professional.diabetes.org/CPR.Members of the Professional PracticeCommittee disclose all potential finan-cial conflicts of interest with industry.These disclosures were discussed at theonset of the standards revision meeting.Members of the committee, their em-ployer, and their disclosed conflicts ofinterest are listed in the “ProfessionalPractice Committee for the 2013 ClinicalPractice Recommendations” table (seep. S109). The ADA funds developmentof the standards and all its position state-ments out of its general revenues anddoes not use industry support for thesepurposes.I. CLASSIFICATION ANDDIAGNOSISA. ClassificationThe classification of diabetes includesfour clinical classes:c Type 1 diabetes (results from b-celldestruction, usually leading to absoluteinsulin deficiency)c Type 2 diabetes (results from a pro-gressive insulin secretory defect on thebackground of insulin resistance)c Other specific types of diabetes due toother causes, e.g., genetic defects inb-cell function, genetic defects in in-sulin action, diseases of the exocrinepancreas (such as cystic fibrosis), anddrug- or chemical-induced (such as inthe treatment of HIV/AIDS or after or-gan transplantation)c Gestational diabetes mellitus (GDM)(diabetes diagnosed during pregnancythat is not clearly overt diabetes)Some patients cannot be clearly clas-sified as type 1 or type 2 diabetic. Clinicalpresentation and disease progression varyconsiderably in both types of diabetes.Occasionally, patients who otherwisehave type 2 diabetes may present withketoacidosis. Similarly, patients with type1 diabetes may have a late onset and slow(but relentless) progression of diseasedespite having features of autoimmunedisease. Such difficulties in diagnosis mayoccur in children, adolescents, andadults. The true diagnosis may becomemore obvious over time.B. Diagnosis of diabetesFor decades, the diagnosis of diabetes wasbased on plasma glucose criteria, eitherthe fasting plasma glucose (FPG) or the2-h value in the 75-g oral glucose toler-ance test (OGTT) (5).In 2009, an International ExpertCommittee that included representativesof the ADA, the International Diabetesc c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c cOriginally approved 1988. Most recent review/revision October 2012.DOI: 10.2337/dc13-S011© 2013 by the American Diabetes Association. Readers may use this article as long as the work is properlycited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.care.diabetesjournals.org DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 S11P O S I T I O N S T A T E M E N T
  2. 2. Federation (IDF), and the EuropeanAssociation for the Study of Diabetes(EASD) recommended the use of the A1Ctest to diagnose diabetes, with a thresholdof $6.5% (6), and the ADA adopted thiscriterion in 2010 (5). The diagnostic testshould be performed using a method thatis certified by the NGSP and standardizedor traceable to the Diabetes Control andComplications Trial (DCCT) reference as-say. Although point-of-care (POC) A1C as-says may be NGSP certified, proficiencytesting is not mandated for performingthe test, so use of these assays for diagnosticpurposes could be problematic.Epidemiological datasets show a sim-ilar relationship for A1C to the risk ofretinopathy as has been shown for thecorresponding FPG and 2-h PG thresh-olds. The A1C has several advantages tothe FPG and OGTT, including greaterconvenience (since fasting is not required),evidence to suggest greater preanalyticalstability, and less day-to-day perturbationsduring periods of stress and illness. Theseadvantages must be balanced by greatercost, the limited availability of A1C testingin certain regions of the developing world,and the incomplete correlation betweenA1C and average glucose in certain indi-viduals. In addition, HbA1c levels may varywith patients’ race/ethnicity (7,8). Somehave posited that glycation rates differ byrace (with, for example, African Americanshaving higher rates of glycation), but this iscontroversial. A recent epidemiologicalstudy found that, when matched for FPG,African Americans (with and without dia-betes) indeed had higher A1C than whites,but also had higher levels of fructosamineand glycated albumin and lower levels of1,5 anhydroglucitol, suggesting that theirglycemic burden (particularly postpran-dially) may be higher (9). Epidemiologicalstudies forming the framework for recom-mending use of the A1C to diagnose diabe-tes have all been in adult populations.Whether the cut point would be the sameto diagnose children or adolescents withtype 2 diabetes is an area of uncertainty(3,10). A1C inaccurately reflects glycemiawith certain anemias and hemoglobinopa-thies. For patients with an abnormal hemo-globin but normal red cell turnover, such assickle cell trait, an A1C assay without inter-ferencefromabnormalhemoglobinsshouldbe used (an updated list is available at www.ngsp.org/interf.asp). For conditions withabnormal red cell turnover, such as preg-nancy, recent blood loss or transfusion, orsome anemias, the diagnosis of diabetesmust employ glucose criteria exclusively.The established glucose criteria forthe diagnosis of diabetes (FPG and 2-hPG) remain valid as well (Table 2). Just asthere is less than 100% concordance be-tween the FPG and 2-h PG tests, there isno perfect concordance between A1C andeither glucose-based test. Analyses of theNational Health and Nutrition Examina-tion Survey (NHANES) data indicate that,assuming universal screening of the un-diagnosed, the A1C cut point of $6.5%identifies one-third fewer cases of undiag-nosed diabetes than a fasting glucose cutpoint of $126 mg/dL (7.0 mmol/L) (11),and numerous studies have confirmedthat at these cut points the 2-h OGTTvalue diagnoses more screened peoplewith diabetes (12). However, in practice, alarge portion of the diabetic population re-mains unaware of its condition. Thus, thelower sensitivity of A1C at the designatedcut point may well be offset by the test’sgreater practicality, and wider applicationof a more convenient test (A1C) may actu-ally increase the number of diagnoses made.As with most diagnostic tests, a testresult diagnostic of diabetes should berepeated to rule out laboratory error,unless the diagnosis is clear on clinicalgrounds, such as a patient with a hyper-glycemic crisis or classic symptoms ofhyperglycemia and a random plasmaglucose $200 mg/dL. It is preferablethat the same test be repeated for confir-mation, since there will be a greater likeli-hood of concurrence in this case. Forexample, if the A1C is 7.0% and a repeatresult is 6.8%, the diagnosis of diabetes isconfirmed. However, if two different tests(such as A1C and FPG) are both above thediagnostic thresholds, the diagnosis of di-abetes is also confirmed.On the other hand, if two differenttests are available in an individual and theresults are discordant, the test whose resultis above the diagnostic cut point should berepeated, and the diagnosis is made basedon the confirmed test. That is, if a patientmeets the diabetes criterion of the A1C (tworesults $6.5%) but notthe FPG (,126 mg/dL or 7.0 mmol/L), or vice versa, that per-son should be considered to have diabetes.Since there is preanalytical and ana-lytical variability of all the tests, it is alsopossible that when a test whose result wasabove the diagnostic threshold is re-peated, the second value will be belowthe diagnostic cut point. This is leastlikely for A1C, somewhat more likely forFPG, and most likely for the 2-h PG.Barring a laboratory error, such patientsare likely to have test results near themargins of the threshold for a diagnosis.The health care professional might opt toTable 1dADA evidence grading system for clinical practice recommendationsLevel ofevidence DescriptionA Clear evidence from well-conducted, generalizable RCTs that are adequatelypowered, including:c Evidence from a well-conducted multicenter trialc Evidence from a meta-analysis that incorporated quality ratings in theanalysisCompelling nonexperimental evidence, i.e., “all or none” rule developed by theCentre for Evidence-Based Medicine at the University of OxfordSupportive evidence from well-conducted RCTs that are adequately powered,including:c Evidence from a well-conducted trial at one or more institutionsc Evidence from a meta-analysis that incorporated quality ratings in the analysisB Supportive evidence from well-conducted cohort studiesc Evidence from a well-conducted prospective cohort study or registryc Evidence from a well-conducted meta-analysis of cohort studiesSupportive evidence from a well-conducted case-control studyC Supportive evidence from poorly controlled or uncontrolled studiesc Evidence from randomized clinical trials with one or more major or three ormore minor methodological flaws that could invalidate the resultsc Evidence from observational studies with high potential for bias (such as caseseries with comparison with historical controls)c Evidence from case series or case reportsConflicting evidence with the weight of evidence supporting the recommendationE Expert consensus or clinical experienceS12 DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 care.diabetesjournals.orgPosition Statement
  3. 3. follow the patient closely and repeat thetesting in 3–6 months.The current diagnostic criteria fordiabetes are summarized in Table 2.C. Categories of increased riskfor diabetes (prediabetes)In 1997 and 2003, the Expert Committeeon Diagnosis and Classification of Diabe-tes Mellitus (13,14) recognized an inter-mediate group of individuals whoseglucose levels, although not meeting cri-teria for diabetes, are nevertheless toohigh to be considered normal. These per-sons were defined as having impaired fast-ing glucose (IFG) (FPG levels 100 mg/dL[5.6 mmol/L] to 125 mg/dL [6.9 mmol/L])or impaired glucose tolerance (IGT) (2-hvalues in the OGTT of 140 mg/dL [7.8mmol/L] to 199 mg/dL [11.0 mmol/L]). Itshould be noted that the World HealthOrganization (WHO) and a number ofother diabetes organizations define the cut-off for IFG at 110 mg/dL (6.1 mmol/L).Individuals with IFG and/or IGT havebeen referred to as having prediabetes,indicating the relatively high risk for thefuture development of diabetes. IFG andIGT should not be viewed as clinicalentities in their own right but rather riskfactors for diabetes as wellas cardiovasculardisease (CVD). IFG and IGT are associatedwith obesity (especially abdominal or vis-ceral obesity), dyslipidemia with high tri-glycerides and/or low HDL cholesterol, andhypertension.As is the case with the glucose mea-sures, several prospective studies thatused A1C to predict the progression todiabetes demonstrated a strong, continu-ous association between A1C and sub-sequent diabetes. In a systematic review of44,203 individuals from 16 cohort stud-ies with a follow-up interval averaging 5.6years (range 2.8–12 years), those with anA1C between 5.5 and 6.0% had a substan-tially increased risk of diabetes with 5-yearincidences ranging from 9 to 25%. An A1Crange of 6.0–6.5% had a 5-year risk of de-veloping diabetes between 25 to 50% andrelative risk (RR) 20 times higher comparedwithan A1Cof5.0%(15). Ina community-based study of black and white adultswithout diabetes, baseline A1C was astronger predictor of subsequent diabetesand cardiovascular events than was fast-ing glucose (16). Other analyses suggestthat an A1C of 5.7% is associated withdiabetes risk similar to that in the high-risk participants in the Diabetes PreventionProgram (DPP) (17).Hence, it is reasonable to consider anA1C range of 5.7–6.4% as identifying in-dividuals with prediabetes. As is the casefor individuals found to have IFG andIGT, individuals with an A1C of 5.7–6.4%should be informed of their increased riskfor diabetes as well as CVD and counseledabout effective strategies to lower their risks(see Section IV). As with glucose measure-ments, the continuum of risk is curvilinear,so that as A1C rises, the risk of diabetes risesdisproportionately (15). Accordingly, inter-ventions should be most intensive andfollow-up particularly vigilant for thosewith A1Cs above 6.0%, who shouldbe con-sidered to be at very high risk.Table 3 summarizes the categories ofprediabetes.II. TESTING FOR DIABETES INASYMPTOMATIC PATIENTSRecommendationsc Testing to detect type 2 diabetes andprediabetes in asymptomatic peopleshould be considered in adults of anyage who are overweight or obese (BMI$25 kg/m2) and who have one or moreadditional risk factors for diabetes (Table4). In those without these risk factors,testing should begin at age 45. (B)c If tests are normal, repeat testing at leastat 3-year intervals is reasonable. (E)c To test for diabetes or prediabetes, theA1C, FPG, or 75-g 2-h OGTT are appro-priate. (B)c In those identified with prediabetes,identify and, if appropriate, treat otherCVD risk factors. (B)For many illnesses, there is a major dis-tinction between screening and diagnostictesting. However, for diabetes, the sametests would be used for “screening” as fordiagnosis. Diabetes may be identified any-where along a spectrum of clinical scenar-ios ranging from a seemingly low-riskindividual who happens to have glucosetesting, to a higher-risk individual whomthe provider tests because of high suspicionof diabetes, to the symptomatic patient.The discussion herein is primarily framedas testing for diabetes in those withoutsymptoms. The same assays used for test-ing for diabetes will also detect individualswith prediabetes.A. Testing for type 2 diabetes andrisk of future diabetes in adultsPrediabetes and diabetes meet establishedcriteria for conditions in which early de-tection is appropriate. Both conditions arecommon, increasing in prevalence, andimpose significant public health burdens.There is a long presymptomatic phasebefore the diagnosis of type 2 diabetes isusually made. Relatively simple tests areavailable to detect preclinical disease. Ad-ditionally, the duration of glycemic burdenis a strong predictor of adverse outcomes,and effective interventions exist to preventprogression of prediabetes to diabetes (seeSection IV) and to reduce risk of compli-cations of diabetes (see Section VI).Type 2 diabetes is frequently not di-agnosed until complications appear, andapproximately one-fourth of all peoplewith diabetes in the U.S. may be undiag-nosed. The effectiveness of early identifica-tion of prediabetes and diabetes throughmass testing of asymptomatic individualshas not been proven definitively, andrigorous trials to provide such proof areunlikely to occur. In a large randomizedcontrolled trial (RCT) in Europe, generalpractice patients between the ages of 40–69 years were screened for diabetes andTable 2dCriteria for the diagnosis ofdiabetesA1C $6.5%. The test should be performed ina laboratory using a method that is NGSPcertified and standardized to the DCCTassay.*ORFPG $126 mg/dL (7.0 mmol/L). Fasting isdefined as no caloric intake for at least 8 h.*OR2-h plasma glucose $200 mg/dL (11.1 mmol/L)during an OGTT. The test should beperformed as described by the WHO, usinga glucose load containing the equivalent of75 g anhydrous glucose dissolved in water.*ORIn a patient with classic symptoms ofhyperglycemia or hyperglycemic crisis,a random plasma glucose $200 mg/dL(11.1 mmol/L).*In the absence of unequivocal hyperglycemia, re-sult should be confirmed by repeat testing.Table 3dCategories of increased risk fordiabetes (prediabetes)*FPG 100 mg/dL (5.6 mmol/L) to 125 mg/dL(6.9 mmol/L) (IFG)OR2-h plasmaglucoseinthe75-gOGTT140mg/dL(7.8 mmol/L) to 199 mg/dL (11.0 mmol/L)(IGT)ORA1C 5.7–6.4%*For all three tests, risk is continuous, extending be-low the lower limit of the range and becoming dis-proportionately greater at higher ends of the range.care.diabetesjournals.org DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 S13Position Statement
  4. 4. then randomly assigned by practice toroutine care of diabetes or intensive treat-ment of multiple risk factors. After 5.3years of follow-up, CVD risk factors weremodestly but significantly more improvedwith intensive treatment. Incidence of firstCVD event and mortality rates were notsignificantly different between groups(18). This study would seem to add sup-port for early treatment of screen-detecteddiabetes, as risk factor control was excel-lent even in the routine treatment armand both groups had lower event ratesthan predicted. The absence of a controlunscreened arm limits the ability to defi-nitely prove that screening impacts out-comes. Mathematical modeling studiessuggest that screening independent ofrisk factors beginning at age 30 yearsor age 45 years is highly cost-effective(,$11,000 per quality-adjusted life-year gained) (19).Recommendations for testing for di-abetes in asymptomatic, undiagnosedadults are listed in Table 4. Testing shouldbe considered in adults of any age withBMI $25 kg/m2and one or more of theknown risk factors for diabetes. In addi-tion to the listed risk factors, certain med-ications, such as glucocorticoids andantipsychotics (20), are known to in-crease the risk of type 2 diabetes. Thereis compelling evidence that lower BMI cutpoints suggest diabetes risk in some racialand ethnic groups. In a large multiethniccohort study, for an equivalent incidencerate of diabetes conferred by a BMI of 30kg/m2in whites, the BMI cutoff value was24 kg/m2in South Asians, 25 kg/m2inChinese, and 26 kg/m2in African Ameri-cans (21). Disparities in screening rates,not explainable by insurance status, arehighlighted by evidence that despitemuch higher prevalence of type 2 diabe-tes, non-Caucasians in an insured popu-lation are no more likely than Caucasiansto be screened for diabetes (22). Becauseage is a major risk factor for diabetes, test-ing of those without other risk factorsshould begin no later than age 45 years.The A1C, FPG, or the 2-h OGTT areappropriate for testing. It should be notedthat the tests do not necessarily detectdiabetes in the same individuals. Theefficacy of interventions for primary pre-vention of type 2 diabetes (23–29) hasprimarily been demonstrated among in-dividuals with IGT, not for individualswith isolated IFG or for individuals withspecific A1C levels.The appropriate interval betweentests is not known (30). The rationalefor the 3-year interval is that false nega-tives will be repeated before substantialtime elapses, and there is little likelihoodthat an individual will develop significantcomplications of diabetes within 3 yearsof a negative test result. In the modelingstudy, repeat screening every 3 or 5 yearswas cost-effective (19).Because of the need for follow-up anddiscussion of abnormal results, testingshould be carried out within the healthcare setting. Community screening outsidea health care setting is not recommendedbecause people with positive tests may notseek,orhaveaccessto,appropriatefollow-uptesting and care. Conversely, there may befailure to ensure appropriate repeat testingfor individuals who test negative. Commu-nity screening may also be poorly targeted; i.e., it may fail to reach the groups most at riskand inappropriately test those at low risk (theworried well) or even those already diag-nosed.B. Screening for type 2 diabetesin childrenRecommendationsc Testing to detect type 2 diabetes andprediabetes should be considered in chil-dren and adolescents who are overweightand who have two or more additionalrisk factors for diabetes (Table 5). (E)The incidence of type 2 diabetes inadolescents has increased dramatically inthe last decade, especially in minoritypopulations (31), although the diseaseremains rare in the general pediatric pop-ulation (32). Consistent with recom-mendations for adults, children andyouth at increased risk for the presenceor the development of type 2 diabetesshould be tested within the health caresetting (33). The recommendations ofthe ADA consensus statement “Type 2Diabetes in Children and Adolescents,”with some modifications, are summa-rized in Table 5.C. Screening for type 1 diabetesRecommendationsc Consider referring relatives of thosewith type 1 diabetes for antibody test-ing for risk assessment in the settingof a clinical research study. (E)Generally, people with type 1 diabetespresent with acute symptoms of diabetesand markedly elevated blood glucoselevels, and some cases are diagnosed withlife-threatening ketoacidosis. Evidencefrom several studies suggests that mea-surement of islet autoantibodies in rela-tives of those with type 1 diabetesidentifies individuals who are at risk fordeveloping type 1 diabetes. Such testing,coupled with education about symptomsof diabetes and follow-up in an observa-tional clinical study, may allow earlieridentification of onset of type 1 diabetesand lessen presentation with ketoacidosisat time of diagnosis. This testing may beappropriate in those who have relativeswith type 1 diabetes, in the context ofTable 4dCriteria for testing for diabetes in asymptomatic adult individuals1. Testing should be considered in all adults who are overweight (BMI $25 kg/m2*)and have additional risk factors:c physical inactivityc first-degree relative with diabetesc high-risk race/ethnicity (e.g., African American, Latino, Native American, AsianAmerican, Pacific Islander)c women who delivered a baby weighing .9 lb or were diagnosed with GDMc hypertension ($140/90 mmHg or on therapy for hypertension)c HDL cholesterol level ,35 mg/dL (0.90 mmol/L) and/or a triglyceridelevel .250 mg/dL (2.82 mmol/L)c women with polycystic ovary syndromec A1C $5.7%, IGT, or IFG on previous testingc other clinical conditions associated with insulin resistance (e.g., severe obesity,acanthosis nigricans)c history of CVD2. In the absence of the above criteria, testing for diabetes should begin at age 45 years.3. If results are normal, testing should be repeated at least at 3-year intervals, withconsideration of more frequent testing depending on initial results (e.g., those withprediabetes should be tested yearly) and risk status.*At-risk BMI may be lower in some ethnic groups.S14 DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 care.diabetesjournals.orgPosition Statement
  5. 5. clinical research studies (see, for example,http://www.diabetestrialnet.org). However,widespread clinical testing of asymptomaticlow-risk individuals cannot currently berecommended, as it would identify veryfew individuals in the general populationwho are at risk. Individuals who screenpositive should be counseled about theirrisk of developing diabetes and symptomsof diabetes, followed closely to prevent de-velopment of diabetic ketoacidosis, andinformed about clinical trials. Clinicalstudies are being conducted to test variousmethods of preventing type 1 diabetes inthose with evidence of autoimmunity.Some interventions have demonstratedmodest efficacy in slowing b-cell loss earlyin type 1 diabetes (34,35), and further re-search is needed to determine whetherthey may be effective in preventing type1 diabetes.III. DETECTION ANDDIAGNOSIS OF GDMRecommendationsc Screen for undiagnosed type 2 diabetesat the first prenatal visit in those withrisk factors, using standard diagnosticcriteria. (B)c In pregnant women not previouslyknown to have diabetes, screen forGDM at 24–28 weeks of gestation,using a 75-g 2-h OGTT and the di-agnostic cut points in Table 6. (B)c Screen women with GDM for persistentdiabetes at 6–12 weeks postpartum,using the OGTT and nonpregnancydiagnostic criteria. (E)c Women with a history of GDM shouldhave lifelong screening for the de-velopment of diabetes or prediabetes atleast every 3 years. (B)c Women with a history of GDM foundto have prediabetes should receivelifestyle interventions or metformin toprevent diabetes. (A)For many years, GDM was defined asany degree of glucose intolerance withonset or first recognition during preg-nancy (13), whether or not the conditionpersisted after pregnancy, and not ex-cluding the possibility that unrecognizedglucose intolerance may have antedatedor begun concomitantly with the preg-nancy. This definition facilitated a uniformstrategy for detection and classification ofGDM, but its limitations were recognizedfor many years. As the ongoing epidemicof obesity and diabetes has led to moretype 2 diabetes in women of childbearingage, the number of pregnant women withundiagnosed type 2 diabetes has increased(36). Because of this, it is reasonable toscreen women with risk factors for type2 diabetes (Table 4) for diabetes at theirinitial prenatal visit, using standard diag-nostic criteria (Table 2). Women with di-abetes found at this visit should receivea diagnosis of overt, not gestational,diabetes.GDM carries risks for the mother andneonate. The Hyperglycemia and Ad-verse Pregnancy Outcome (HAPO) study(37), a large-scale (;25,000 pregnantwomen) multinational epidemiologicalstudy, demonstrated that risk of adversematernal, fetal, and neonatal outcomescontinuously increased as a function ofmaternal glycemia at 24–28 weeks, evenwithin ranges previously considered nor-mal for pregnancy. For most complica-tions, there was no threshold for risk.These results have led to careful recon-sideration of the diagnostic criteria forGDM. After deliberations in 2008–2009, the International Association ofDiabetes and Pregnancy Study Groups(IADPSG), an international consensusgroup with representatives from multipleobstetrical and diabetes organizations,including ADA, developed revised rec-ommendations for diagnosing GDM.The group recommended that all womennot known to have prior diabetesundergo a 75-g OGTT at 24–28 weeksof gestation. Additionally, the group de-veloped diagnostic cut points for the fast-ing, 1-h, and 2-h plasma glucosemeasurements that conveyed an oddsratio for adverse outcomes of at least1.75 compared with women with themean glucose levels in the HAPO study.Current screening and diagnostic strate-gies, based on the IADPSG statement(38), are outlined in Table 6.These new criteria will significantlyincrease the prevalence of GDM, primar-ily because only one abnormal value, nottwo, is sufficient to make the diagnosis.The ADA recognizes the anticipated sig-nificant increase in the incidence of GDMdiagnosed by these criteria and is sensitiveto concerns about the “medicalization” ofpregnancies previously categorized as nor-mal. These diagnostic criteria changes arebeing made in the context of worrisomeworldwide increases in obesity and diabe-tes rates, with the intent of optimizing ges-tational outcomes for women and theirbabies.Admittedly, there are few data fromrandomized clinical trials regarding ther-apeutic interventions in women who willnow be diagnosed with GDM based ononly one blood glucose value above theTable 5dTesting for type 2 diabetes in asymptomatic children*Criteriac Overweight (BMI .85th percentile for age and sex, weight for height .85th percentile, orweight .120% of ideal for height)Plus any two of the following risk factors:c Family history of type 2 diabetes in first- or second-degree relativec Race/ethnicity (Native American, African American, Latino, Asian American, PacificIslander)c Signs of insulin resistance or conditions associated with insulin resistance (acanthosisnigricans, hypertension, dyslipidemia, polycystic ovary syndrome, or small-for-gestational-age birth weight)c Maternal history of diabetes or GDM during the child’s gestationAge of initiation: age 10 years or at onset of puberty, if puberty occurs at a younger ageFrequency: every 3 years*Persons aged 18 years and younger.Table 6dScreening for and diagnosis of GDMPerform a 75-g OGTT, with plasma glucose measurement fasting and at 1 and 2 h, at 24–28weeks of gestation in women not previously diagnosed with overt diabetes.The OGTT should be performed in the morning after an overnight fast of at least 8 h.The diagnosis of GDM is made when any of the following plasma glucose values are exceeded:c Fasting: $92 mg/dL (5.1 mmol/L)c 1 h: $180 mg/dL (10.0 mmol/L)c 2 h: $153 mg/dL (8.5 mmol/L)care.diabetesjournals.org DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 S15Position Statement
  6. 6. specified cut points (in contrast to the oldercriteria that stipulated at least two abnor-mal values). However, there is emergingobservational and retrospective evidencethat women diagnosed with the newcriteria (even if they would not havebeen diagnosed with older criteria) haveincreased rates of poor pregnancy out-comes similar to those of women withGDM by prior criteria (39,40). Expectedbenefits to these pregnancies and offspringare inferred from intervention trials thatfocused on women with more mild hyper-glycemia than identified using older GDMdiagnostic criteria and that found modestbenefits (41,42). The frequency of follow-up and blood glucose monitoring for thesewomen is not yet clear, but likely to be lessintensive than for women diagnosed by theolder criteria. It is important to note that80–90% of women in both of the mildGDM studies (whose glucose values over-lapped with the thresholds recommendedherein) could be managed with lifestyletherapy alone.The American College of Obstetri-cians and Gynecologists announced in2011 that they continue to recommenduse of prior diagnostic criteria for GDM(43). Several other countries haveadopted the new criteria, and a reportfrom the WHO on this topic is pendingat the time of publication of these stand-ards. The National Institutes of Health isplanning to hold a consensus develop-ment conference on this topic in 2013.Because some cases of GDM mayrepresent pre-existing undiagnosed type2 diabetes, women with a history ofGDM should be screened for diabetes6–12 weeks postpartum, using nonpreg-nant OGTT criteria. Because of their pre-partum treatment for hyperglycemia, useof the A1C for diagnosis of persistent di-abetes at the postpartum visit is not rec-ommended (44). Women with a historyof GDM have a greatly increased subse-quent risk for diabetes (45) and shouldbe followed up with subsequent screen-ing for the development of diabetes orprediabetes, as outlined in Section II.Lifestyle interventions or metforminshould be offered to women with a his-tory of GDM who develop prediabetes,as discussed in Section IV. In the pro-spective Nurses’ Health Study II, risk ofsubsequent diabetes after a history ofGDM was significantly lower in womenwho followed healthy eating patterns.Adjusting for BMI moderately, but notcompletely, attenuated this association(46).IV. PREVENTION/DELAYOF TYPE 2 DIABETESRecommendationsc Patientswith IGT (A),IFG (E),oran A1Cof 5.7–6.4% (E) should be referred to aneffective ongoing support program tar-geting weight loss of 7% of body weightand increasing physical activity to at least150 min/week of moderate activity suchas walking.c Follow-up counseling appears to beimportant for success. (B)c Based on the cost-effectiveness of diabetesprevention, such programs should becovered by third-party payers. (B)c Metformin therapy for prevention oftype 2 diabetes may be considered inthose withIGT (A),IFG (E),oranA1C of5.7–6.4% (E), especially for those withBMI .35 kg/m2, aged ,60 years, andwomen with prior GDM. (A)c At least annual monitoring for the de-velopment of diabetes in those withprediabetes is suggested. (E)c Screening for and treatment of modifi-ablerisk factors for CVD issuggested. (B)RCTs have shown that individuals athigh risk for developing type 2 diabetes(those with IFG, IGT, or both) can signif-icantly decreasethe rateofonset ofdiabeteswith particular interventions (23–29).These include intensive lifestyle modifica-tion programs that have been shown to bevery effective (;58% reduction after 3years) and use of the pharmacologicalagents metformin, a-glucosidase inhibi-tors, orlistat, and thiazolidinediones, eachof which has been shown to decrease inci-dentdiabetes to variousdegrees.Follow-upofall three large studiesof lifestyleinterven-tion has shown sustained reduction in therate of conversion to type 2 diabetes, with43% reduction at 20 years in the Da Qingstudy (47), 43% reduction at 7 years in theFinnish Diabetes Prevention Study (DPS)(48), and 34% reduction at 10 years inthe U.S. Diabetes Prevention ProgramOutcomes Study (DPPOS) (49). A cost-effectiveness model suggested that lifestyleinterventions as delivered in the DPP arecost-effective (50), and actual cost datafrom the DPP and DPPOS confirm that life-style interventions are highly cost-effective(51). Group delivery of the DPP interven-tion in community settings has the poten-tial to be significantly less expensive whilestill achieving similar weight loss (52).Based on the results of clinical trialsand the known risks of progression ofprediabetes to diabetes, persons with anA1C of 5.7–6.4%, IGT, or IFG should becounseled on lifestyle changes with goalssimilar to those of the DPP (7% weightloss and moderate physical activity of atleast 150 min/week). Regarding drugtherapy for diabetes prevention, metfor-min has a strong evidence base and dem-onstrated long-term safety (53). For otherdrugs, issues of cost, side effects, and lackof persistence of effect in some studies(54) require consideration. Metforminwas less effective than lifestyle modifica-tion in the DPP and DPPOS, but may becost-saving over a 10-year period (51). Itwas as effective as lifestyle modificationin participants with a BMI of at least 35kg/m2, but not significantly better thanplacebo than those over age 60 years(23). In women in the DPP with a historyof GDM, metformin and intensive lifestylemodification led to an equivalent 50% re-duction in the risk of diabetes (55). Met-formin therefore might reasonably berecommended for very high-risk individ-uals (those with a history of GDM, thevery obese, and/or those with more severeor progressive hyperglycemia).People with prediabetes often haveother cardiovascular risk factors, such asobesity, hypertension, and dyslipidemia.Assessing and treating these risk factors isan important aspect of reducing cardio-metabolic risk. In the DPP and DPPOS,cardiovascular event rates have been verylow, perhaps due to appropriate manage-ment of cardiovascular risk factors in allarms of the study (56).V. DIABETES CAREA. Initial evaluationA complete medical evaluation should beperformed to classify the diabetes, detectthe presence of diabetes complications,review previous treatment and risk factorcontrol in patients with established diabe-tes, assist in formulating a managementplan, and provide a basis for continuingcare. Laboratory tests appropriate to theevaluation of each patient’s medical condi-tion should be performed. A focus on thecomponents of comprehensive care (Table7) will assist the health care team to ensureoptimal management of the patient withdiabetes.B. ManagementPeople with diabetes should receive med-ical care from a team that may includephysicians, nurse practitioners, physician’sassistants, nurses, dietitians, pharmacists,and mental health professionals withS16 DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 care.diabetesjournals.orgPosition Statement
  7. 7. expertise and a special interest in diabetes.It is essential in this collaborative and in-tegrated team approach that individualswith diabetes assume an active role in theircare.The management plan should beformulated as a collaborative therapeuticalliance among the patient and family,the physician, and other members of thehealth care team. A variety of strategiesand techniques should be used to provideadequate education and developmentof problem-solving skills in the variousaspects of diabetes management. Imple-mentation of the management plan re-quires that the goals and treatment planare individualized and take patient pref-erences into account. The managementplan should recognize diabetes self-management education (DSME) and on-going diabetes support as an integralcomponent of care. In developing theplan, consideration should be given tothe patient’s age, school or work scheduleand conditions, physical activity, eatingpatterns, social situation and cultural fac-tors, and presence of complications of di-abetes or other medical conditions.C. Glycemic control1. Assessment of glycemic controlTwo primary techniques are available forhealth providers and patients to assess theeffectiveness of the management plan onglycemic control: patient self-monitoringof blood glucose (SMBG) or interstitialglucose, and A1C.a. Glucose monitoringRecommendationsc Patients on multiple-dose insulin (MDI)or insulin pump therapy should doSMBG at least prior to meals and snacks,occasionally postprandially, at bedtime,prior to exercise, when they suspect lowblood glucose, after treating low bloodglucose until they are normoglycemic,and prior to critical tasks such as driv-ing. (B)c When prescribed as part of a broadereducational context, SMBG results maybe helpful to guide treatment decisionsand/or patient self-management forpatients using less frequent insulin in-jections or noninsulin therapies. (E)c When prescribing SMBG, ensure thatpatients receive ongoing instructionand regular evaluation of SMBG tech-nique and SMBG results, as well as theirability to use SMBG data to adjust ther-apy. (E)c Continuous glucose monitoring (CGM)in conjunction with intensive insulinregimens can be a useful tool to lowerA1C in selected adults (aged $25 years)with type 1 diabetes. (A)c Although the evidence for A1C lower-ing is less strong in children, teens, andyounger adults, CGM may be helpfulin these groups. Success correlates withadherence to ongoing use of the device.(C)c CGM may be a supplemental tool toSMBG in those with hypoglycemiaunawareness and/or frequent hypogly-cemic episodes. (E)Major clinical trials of insulin-treatedpatients that demonstrated the benefits ofintensive glycemic control on diabetescomplications have included SMBG aspart of multifactorial interventions, sug-gesting that SMBG is a component ofeffective therapy. SMBG allows patientsto evaluate their individual response toTable 7dComponents of the comprehensive diabetes evaluationMedical historyc Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding)c Eating patterns, physical activity habits, nutritional status, and weight history; growth anddevelopment in children and adolescentsc Diabetes education historyc Review of previous treatment regimens and response to therapy (A1C records)c Current treatment of diabetes, including medications, medication adherence and barriersthereto, meal plan, physical activity patterns, and readiness for behavior changec Results of glucose monitoring and patient’s use of datac DKA frequency, severity, and causec Hypoglycemic episodesc Hypoglycemia awarenessc Any severe hypoglycemia: frequency and causec History of diabetes-related complicationsc Microvascular: retinopathy, nephropathy, neuropathy (sensory, including history of footlesions; autonomic, including sexual dysfunction and gastroparesis)c Macrovascular: CHD, cerebrovascular disease, and PADc Other: psychosocial problems*, dental disease*Physical examinationc Height, weight, BMIc Blood pressure determination, including orthostatic measurements when indicatedc Fundoscopic examination*c Thyroid palpationc Skin examination (for acanthosis nigricans and insulin injection sites)c Comprehensive foot examinationc Inspectionc Palpation of dorsalis pedis and posterior tibial pulsesc Presence/absence of patellar and Achilles reflexesc Determination of proprioception, vibration, and monofilament sensationLaboratory evaluationc A1C, if results not available within past 2–3 monthsIf not performed/available within past yearc Fasting lipid profile, including total, LDL and HDL cholesterol and triglyceridesc Liver function testsc Test for urine albumin excretion with spot urine albumin-to-creatinine ratioc Serum creatinine and calculated GFRc TSH in type 1 diabetes, dyslipidemia or women over age 50 yearsReferralsc Eye care professional for annual dilated eye examc Family planning for women of reproductive agec Registered dietitian for MNTc DSMEc Dentist for comprehensive periodontal examinationc Mental health professional, if needed*See appropriate referrals for these categories.care.diabetesjournals.org DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 S17Position Statement
  8. 8. therapy and assess whether glycemic tar-gets are being achieved. Results of SMBGcan be useful in preventing hypoglycemiaand adjusting medications (particularlyprandial insulin doses), medical nutritiontherapy (MNT), and physical activity.The frequency and timing of SMBGshould be dictated by the particular needsand goals of the patient. SMBG is espe-cially important for patients treated withinsulin to monitor for and prevent asymp-tomatic hypoglycemia and hyperglyce-mia. Most patients with type 1 diabetesand others on intensive insulin regimens(MDI or insulin pump therapy) should doSMBG at least prior to meals and snacks,occasionally postprandially, at bedtime,prior to exercise, when they suspect lowblood glucose, after treating low bloodglucose until they are normoglycemic,and prior to critical tasks such as driving.For many patients, this will require test-ing 6–8 times daily, although individualneeds may be greater. Although there arefew rigorous studies, a database study ofalmost 27,000 children and adolescentswith type 1 diabetes showed that, afteradjustment for multiple confounders, in-creased daily frequency of SMBG was sig-nificantly associated with lower A1C(20.2% per additional test per day, level-ing off at five tests per day) and with feweracute complications (57). The optimalfrequency of SMBG for patients on non-intensive regimens, such as those withtype 2 diabetes on basal insulin, is notknown, although a number of studieshave used fasting SMBG for patient or pro-vider titration of the basal insulin dose.TheevidencebaseforSMBGforpatientswith type 2 diabetes on noninsulin therapyis somewhat mixed. Several randomizedtrials have called into question the clinicalutility and cost-effectiveness of routineSMBG in non–insulin-treated patients(58–60). A recent meta-analysis suggestedthat SMBG reduced A1C by 0.25% at 6months (61), while a Cochrane review con-cluded that the overall effect of SMBG insuch patients is small up to 6 months afterinitiation and subsides after 12 months (62).Because the accuracy of SMBG isinstrument and user dependent (63), itis important to evaluate each patient’smonitoring technique, both initially andat regular intervals thereafter. Optimaluse of SMBG requires proper review andinterpretation of the data, both by the pa-tient and provider. Among patients whochecked their blood glucose at least oncedaily, many reported taking no actionwhen results were high or low (64). Inone study of insulin-naïve patients withsuboptimal initial glycemic control, useof structured SMBG (a paper tool to col-lect and interpret 7-point SMBG profilesover 3 days at least quarterly) reducedA1C by 0.3% more than in an active con-trol group (65). Patients should be taughthow to use SMBG data to adjust food in-take, exercise, or pharmacological therapyto achieve specific goals, and the ongoingneed for and frequency of SMBG should bere-evaluated at each routine visit.Real-time CGM through the measure-ment of interstitial glucose (which corre-lates well with plasma glucose) is available.These sensors require calibration withSMBG,andthe latter are stillrecommendedfor making acute treatment decisions.CGM devices have alarms for hypo- andhyperglycemic excursions. A 26-week ran-domized trial of 322 type 1 diabetic pa-tients showed that adults aged $25 yearsusing intensive insulin therapy and CGMexperienced a 0.5% reduction in A1C(from ;7.6 to 7.1%) compared with usualintensive insulin therapy with SMBG (66).Sensor use in children, teens, and adults toage 24 years did not result in significantA1C lowering, and there was no significantdifference in hypoglycemia in any group.Importantly, the greatest predictor of A1Clowering in this study for all age-groupswas frequency of sensor use, which waslower in younger age-groups. In a smallerRCT of 129 adults and children with base-line A1C ,7.0%, outcomes combiningA1C and hypoglycemia favored the grouputilizing CGM, suggesting that CGM is alsobeneficial for individuals with type 1 dia-betes who have already achieved excellentcontrol (67).A trial comparing CGM plus insulinpump to SMBG plus multiple injectionsof insulin in adults and children with type1 diabetes showed significantly greaterimprovements in A1C with “sensor-augmented pump” therapy (68,69), butthis trial did not isolate the effect of CGMitself. Overall, meta-analyses suggest thatcompared with SMBG, CGM lowers A1Cby ;0.26% (70). Altogether, these datasuggest that, in appropriately selected pa-tients who are motivated to wear it most ofthe time, CGM reduces A1C. The technol-ogy may be particularly useful in those withhypoglycemia unawareness and/or fre-quent episodes of hypoglycemia, althoughstudies as yet have not shown significantreductions in severe hypoglycemia (70).CGM forms the underpinning for the de-velopment of pumps that suspend insulindelivery when hypoglycemia is developingand for the burgeoning work on “artificialpancreas” systems.b. A1CRecommendationsc Perform the A1C test at least twotimes a year in patients who are meet-ing treatment goals (and who havestable glycemic control). (E)c Perform the A1C test quarterly in pa-tients whose therapy has changed orwho are not meeting glycemic goals. (E)c Use of POC testing for A1C providesthe opportunity for more timely treat-ment changes. (E)Because A1C is thought to reflect aver-age glycemia over several months (63) andhas strong predictive value for diabetescomplications (71,72), A1C testingshould be performed routinely in all pa-tients with diabetes, at initial assessmentand then as part of continuing care. Mea-surement approximately every 3 monthsdetermines whether patient’s glycemic tar-gets have been reached and maintained.For any individual patient, the frequencyof A1C testing should be dependent ontheclinicalsituation,the treatment regimenused, and the judgment of the clinician.Some patients with stable glycemia wellwithin target may do well with testingonly twice per year, while unstable orhighly intensively managed patients (e.g.,pregnant type 1 diabetic women) may betested more frequently than every 3months. The availability of the A1C resultat the time that the patient is seen (POCtesting) has been reported in small studiesto result in increased intensification of ther-apy and improvement in glycemic control(73,74). However, two recent systematicreviews and meta-analyses found no signif-icant difference in A1C between POC andlaboratory A1C usage (75,76).The A1C test is subject to certainlimitations. Conditions that affect eryth-rocyte turnover (hemolysis, blood loss)and hemoglobin variants must be consid-ered, particularly when the A1C resultdoes not correlate with the patient’s clin-ical situation (63). In addition, A1C doesnot provide a measure of glycemic vari-ability or hypoglycemia. For patientsprone to glycemic variability (especiallytype 1 diabetic patients or type 2 diabeticpatients with severe insulin deficiency),glycemic control is best judged by thecombination of results of self-monitoringand the A1C. The A1C may also serve as acheck on the accuracy of the patient’s me-ter (or the patient’s reported SMBGS18 DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 care.diabetesjournals.orgPosition Statement
  9. 9. results) and the adequacy of the SMBGtesting schedule.Table 8 contains the correlation be-tween A1C levels and mean plasma glu-cose levels based on data from theinternational A1C-Derived Average Glu-cose (ADAG) trial utilizing frequentSMBG and CGM in 507 adults (83% Cau-casian) with type 1, type 2, and no diabe-tes (77). The ADA and the AmericanAssociation for Clinical Chemistry havedetermined that the correlation (r 50.92) is strong enough to justify reportingboth an A1C result and an estimated av-erage glucose (eAG) result when a clini-cian orders the A1C test. The table in pre-2009 versions of the “Standards of Medi-cal Care in Diabetes” describing the cor-relation between A1C and mean glucosewas derived from relatively sparse data(one 7-point profile over 1 day per A1Creading) in the primarily Caucasian type 1diabetic participants in the DCCT (78).Clinicians should note that the numbersin the table are now different, as they arebased on ;2,800 readings per A1C in theADAG trial.In the ADAG trial, there were no sig-nificant differences among racial and eth-nic groups in the regression lines betweenA1C and mean glucose, although therewas a trend toward a difference betweenAfrican/African American participantsand Caucasian ones. A small study com-paring A1C to CGM data in type 1 di-abetic children found a highly statisticallysignificant correlation between A1C andmean blood glucose, although the corre-lation (r 5 0.7) was significantly lowerthan in the ADAG trial (79). Whetherthere are significant differences in howA1C relates to average glucose in childrenor in African American patients is an areafor further study. For the time being, thequestion has not led to different recom-mendations about testing A1C or to dif-ferent interpretations of the clinicalmeaning of given levels of A1C in thosepopulations.For patients in whom A1C/eAG andmeasured blood glucose appear discrep-ant, clinicians should consider the possi-bilities of hemoglobinopathy or alteredred cell turnover, and the options of morefrequent and/or different timing of SMBGor use of CGM. Other measures of chronicglycemia such as fructosamine are avail-able, but their linkage to average glucoseand their prognostic significance are notas clear as is the case for A1C.2. Glycemic goals in adultsRecommendationsc Lowering A1C to below or around 7%has been shown to reduce microvas-cular complications of diabetes and ifimplemented soon after the diagnosisof diabetes is associated with long-termreduction in macrovascular disease.Therefore, a reasonable A1C goal formany nonpregnant adults is ,7%. (B)c Providers might reasonably suggestmore stringent A1C goals (such as,6.5%) for selected individual pa-tients, if this can be achieved withoutsignificant hypoglycemia or other ad-verse effects of treatment. Appropriatepatients might include those with shortduration of diabetes, long life expec-tancy, and no significant CVD. (C)c Less stringent A1C goals (such as,8%) may be appropriate for patientswith a history of severe hypoglycemia,limited life expectancy, advanced mi-crovascular or macrovascular complica-tions, extensive comorbid conditions,and those with long-standing diabetes inwhom the general goal is difficult to at-tain despite DSME, appropriate glucosemonitoring, and effective doses of mul-tiple glucose-lowering agents includinginsulin. (B)Hyperglycemia defines diabetes, andglycemic control is fundamental to themanagement of diabetes. The DCCT(71), a prospective RCT of intensive ver-sus standard glycemic control in patientswith relatively recently diagnosed type 1diabetes, showed definitively thatimproved glycemic control is associ-ated with significantly decreased rates ofmicrovascular (retinopathy and nephro-pathy) and neuropathic complications.Follow-up of the DCCT cohorts in the Ep-idemiology of Diabetes Interventions andComplications (EDIC) study (80,81) dem-onstrated persistence of these microvascu-lar benefits in previously intensively treatedsubjects, even though their glycemic con-trol approximated that of previous stan-dard arm subjects during follow-up.The Kumamoto Study (82) and UKProspective Diabetes Study (UKPDS)(83,84) confirmed that intensive glycemiccontrol was associated with significantlydecreased rates of microvascular and neu-ropathic complications in patients withtype 2 diabetes. Long-term follow-up ofthe UKPDS cohorts showed persistence ofthe effect of early glycemic control onmost microvascular complications (85).Subsequent trials in patients withmore long-standing type 2 diabetes, de-signed primarily to look at the role ofintensive glycemic control on cardiovas-cular outcomes, also confirmed a benefit,although more modest, on onset or pro-gression of microvascular complications.The Veterans Affairs Diabetes Trial(VADT) showed significant reductionsin albuminuria with intensive (achievedmedian A1C 6.9%) compared with stan-dard glycemic control, but no differencein retinopathy and neuropathy (86,87).The Action in Diabetes and Vascular Dis-ease: Preterax and Diamicron MR Con-trolled Evaluation (ADVANCE) study ofintensive versus standard glycemic con-trol in type 2 diabetes found a statisticallysignificant reduction in albuminuria, butnot in neuropathy or retinopathy, with anA1C target of ,6.5% (achieved medianA1C 6.3%) compared with standard ther-apy achieving a median A1C of 7.0% (88).Analyses from the Action to Control Car-diovascular Risk in Diabetes (ACCORD)trial have shown lower rates of onset orprogression of early-stage microvascularcomplications in the intensive glycemiccontrol arm compared with the standardarm (89,90).Epidemiological analyses of the DCCTand UKPDS (71,72) demonstrate a curvi-linear relationship between A1C and mi-crovascular complications. Such analysessuggest that, on a population level, thegreatest number of complications will beaverted by taking patients from very poorcontrol to fair or good control. These anal-yses also suggest that further lowering ofA1C from7 to 6% isassociated with furtherreduction in the risk of microvascularcomplications, albeit the absolute riskTable 8dCorrelation of A1C with averageglucoseA1C (%)Mean plasma glucosemg/dL mmol/L6 126 7.07 154 8.68 183 10.29 212 11.810 240 13.411 269 14.912 298 16.5These estimates are based on ADAG data of ;2,700glucose measurements over 3 months per A1Cmeasurement in 507 adults with type 1, type 2, andno diabetes. The correlation between A1C and av-erage glucose was 0.92 (ref. 77). A calculator forconverting A1C results into eAG, in either mg/dL ormmol/L, is available at http://professional.diabetes.org/eAG.care.diabetesjournals.org DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 S19Position Statement
  10. 10. reductions become much smaller. Giventhe substantially increased risk of hypogly-cemia (particularly in those with type 1 di-abetes, but also in the recent type 2 diabetestrials), the concerning mortality findings inthe ACCORD trial (91), and the relativelymuch greater effort required to achievenear-normoglycemia, therisksoflower gly-cemic targets may outweigh the potentialbenefits on microvascular complicationson a population level. However, selectedindividual patients, especially those withlittle comorbidity and long life expectancy(who may reap the benefits of further low-ering of glycemia below 7%), may, basedon provider judgment and patient prefer-ences, adopt more intensive glycemic tar-gets (e.g., an A1C target ,6.5%) as long assignificant hypoglycemia does not becomea barrier.CVD, a more common cause of deathin populations with diabetes than micro-vascular complications, is less clearlyimpacted by levels of hyperglycemia orthe intensity of glycemic control. In theDCCT, there was a trend toward lowerrisk of CVD events with intensive control,and in 9-year post-DCCT follow-up of theEDIC cohort participants previously ran-domized to the intensive arm had a sig-nificant 57% reduction in the risk ofnonfatal myocardial infarction (MI), stroke,or CVD death compared with those pre-viously in the standard arm (92). The ben-efit of intensive glycemic control in thistype 1 diabetic cohort has recently beenshown to persist for several decades (93).In type 2 diabetes, there is evidencethat more intensive treatment of glycemiain newly diagnosed patients may reducelong-term CVD rates. During the UKPDStrial, there was a 16% reduction in car-diovascular events (combined fatal ornonfatal MI and sudden death) in theintensive glycemic control arm that didnot reach statistical significance (P 50.052), and there was no suggestion ofbenefit on other CVD outcomes such asstroke. However, after 10 years of follow-up, those originally randomized to inten-sive glycemic control had significantlong-term reductions in MI (15% withsulfonylurea or insulin as initial pharma-cotherapy, 33% with metformin as initialpharmacotherapy) and in all-cause mor-tality (13% and 27%, respectively) (85).Three more recent large trials(ACCORD, ADVANCE, and VADT) sug-gested no significant reduction in CVDoutcomes with intensive glycemic controlin participants who had more advancedtype 2 diabetes than UKPDS participants.All three of these trials were conducted inparticipants with more long-standing di-abetes (mean duration 8–11 years) andeither known CVD or multiple cardiovas-cular risk factors. Details of these threestudies are reviewed extensively in anADA position statement (94).The ACCORD study enrolled partici-pants with either known CVD or two ormore major cardiovascular risk factorsand randomized them to intensive glyce-mic control (goal A1C ,6%) or standardglycemic control (goal A1C 7–8%). Theglycemic control comparison was haltedearly due to the finding of an increasedrate of mortality in the intensive arm com-pared with the standard arm (1.41% vs.1.14% per year; HR 1.22; 95% CI 1.01–1.46), with a similar increase in cardiovas-cular deaths. This increase in mortality inthe intensive glycemic control arm wasseen in all prespecified patient subgroups.The primary outcome of ACCORD (non-fatal MI, nonfatal stroke, or cardiovascu-lar death) was nonsignificantly lower inthe intensive glycemic control groupdue to a reduction in nonfatal MI, bothwhen the glycemic control comparisonwas halted and all participants transi-tioned to the standard glycemic controlintervention (91), and at completion ofthe planned follow-up (95).Exploratory analyses of the mortalityfindings of ACCORD (evaluating vari-ables including weight gain, use of anyspecific drug or drug combination, andhypoglycemia) were reportedly unable toidentify a clear explanation for the excessmortality in the intensive arm (91). TheACCORD investigators subsequentlypublished additional epidemiologicalanalyses showing no increase in mortalityin the intensive arm participants whoachieved A1C levels below 7% nor inthose who lowered their A1C quickly af-ter trial enrollment. In fact, although therewas no A1C level at which intensive armparticipants had significantly lower mor-tality than standard arm participants, thehighest risk for mortality was observed inintensive arm participants with the high-est A1C levels (96).The role of hypoglycemia in the ex-cess mortality findings was also complex.Severe hypoglycemia was significantlymore likely in participants randomizedto the intensive glycemic control arm.However, excess mortality in the inten-sive versus standard arms was only sig-nificant for participants with no severehypoglycemia, and not for those with oneor more episodes. Severe hypoglycemiawas associated with excess mortality ineither arm, but the association was stron-ger in those randomized to the standardglycemic control arm (97). Unlike thecase with the DCCT trial, where lowerachieved A1C levels were related to sig-nificantly increased rates of severe hypo-glycemia, in ACCORD every 1% declinein A1C from baseline to 4 months into thetrial was associated with a significant de-crease in the rate of severe hypoglycemiain both arms (96).The primary outcome of ADVANCEwas a combination of microvascularevents (nephropathy and retinopathy)and major adverse cardiovascular events(MI, stroke, and cardiovascular death).Intensive glycemic control (to a goal A1C,6.5% vs. treatment to local standards)significantly reduced the primary endpoint. However, this was due to a significantreductioninthemicrovascularoutcome,pri-marily development of macroalbuminuria,with no significant reduction in the macro-vascular outcome. There was no differencein overall or cardiovascular mortality be-tween the intensive compared with thestandard glycemic control arms (88).The VADT randomized participantswith type 2 diabetes uncontrolled oninsulin or maximal-dose oral agents (me-dian entry A1C 9.4%) to a strategy ofintensive glycemic control (goal A1C,6.0%) or standard glycemic control,with a planned A1C separation of at least1.5%. The primary outcome of the VADTwas a composite of CVD events. The cu-mulative primary outcome was nonsig-nificantly lower in the intensive arm(86). An ancillary study of the VADTdemonstrated that intensive glycemiccontrol significantly reduced the primaryCVD outcome in individuals with lessatherosclerosis at baseline (assessed bycoronary calcium) but not in personswith more extensive baseline atheroscle-rosis (98). A post hoc analysis showed acomplex relationship between durationof diabetes before glycemic intensifica-tion and mortality: mortality in the inten-sive vs. standard glycemic control armwas inversely related to duration of dia-betes at the time of study enrollment.Those with diabetes duration less than15 years had a mortality benefit in the in-tensive arm, while those with duration of20 years or more had higher mortality inthe intensive arm (99).The evidence for a cardiovascular ben-efit of intensive glycemic control primarilyrests on long-term follow-up of studycohorts treated early in the course of typeS20 DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 care.diabetesjournals.orgPosition Statement
  11. 11. 1 and type 2 diabetes and subset analyses ofACCORD, ADVANCE, and VADT. Agroup-level meta-analysis of the latter threetrials suggests that glucose lowering has amodest (9%) but statistically significantreduction in major CVD outcomes, pri-marily nonfatal MI, with no significanteffecton mortality. However, heterogeneityof the mortality effects across studies wasnoted, precluding firm summary measuresof the mortality effects. A prespecified sub-group analysis suggested that major CVDoutcome reduction occurred in patientswithout known CVD at baseline (HR 0.84,95% CI 0.74–0.94) (100). Conversely, themortality findings in ACCORD and sub-group analyses of the VADT suggest thatthe potential risks of intensive glycemiccontrol may outweigh its benefits in somepatients, such as those with very long du-ration of diabetes, known history of severehypoglycemia, advanced atherosclerosis,and advanced age/frailty. Certainly, provid-ers should be vigilant in preventing severehypoglycemia in patients with advanceddisease and should not aggressively at-tempt to achieve near-normal A1C levelsin patients in whom such a target cannotbe safely and reasonably easily achieved.Severe or frequent hypoglycemia is an ab-solute indication for the modification oftreatment regimens, including settinghigher glycemic goals. Many factors, in-cluding patient preferences, should betaken into account when developing a pa-tient’s individualized goals (101).Recommended glycemic goals formany nonpregnant adults are shown inTable 9. The recommendations are basedon those for A1C values, with listed bloodglucose levels that appear to correlatewith achievement of an A1C of ,7%.The issue of pre- versus postprandialSMBG targets is complex (102). Elevatedpostchallenge (2-h OGTT) glucose valueshave been associated with increased car-diovascular risk independent of FPG insome epidemiological studies. In diabeticsubjects, some surrogate measures ofvascular pathology, such as endothelialdysfunction, are negatively affected bypostprandial hyperglycemia (103). It isclear that postprandial hyperglycemia,like preprandial hyperglycemia, contrib-utes to elevated A1C levels, with its rela-tive contribution being higher at A1Clevels that are closer to 7%. However,outcome studies have clearly shownA1C to be the primary predictor of com-plications, and landmark glycemic con-trol trials such as the DCCT and UKPDSrelied overwhelmingly on preprandialSMBG. Additionally, an RCT in patientswith known CVD found no CVD benefitof insulin regimens targeting postpran-dial glucose compared with thosetargeting preprandial glucose (104). Areasonable recommendation for post-prandial testing and targets is that for in-dividuals who have premeal glucosevalues within target but have A1C valuesabove target, monitoring postprandialplasma glucose (PPG) 1–2 h after the startof the meal and treatment aimed at reduc-ing PPG values to ,180 mg/dL may helplower A1C.Glycemic goals for children are pro-vided in Section VIII.A.1.a. As regards goalsfor glycemic control for women withGDM, recommendations from the FifthInternational Workshop-Conference onGestational Diabetes Mellitus (105) wereto target maternal capillary glucose con-centrations of:c preprandial: #95 mg/dL (5.3 mmol/L),and either:c 1-h postmeal: #140 mg/dL (7.8 mmol/L)orc 2-h postmeal:#120 mg/dL (6.7mmol/L)For women with pre-existing type 1or type 2 diabetes who become pregnant, arecent consensus statement (106) recom-mended the following as optimal glycemicgoals, if they can be achieved without ex-cessive hypoglycemia:c premeal, bedtime, and overnight glu-cose 60–99 mg/dL (3.3–5.4 mmol/L)c peak postprandial glucose 100–129mg/dL (5.4–7.1 mmol/L)c A1C ,6.0%D. Pharmacological and overallapproaches to treatment1. Insulin therapy for type 1 diabetesRecommendationsc Most people with type 1 diabetes shouldbe treated with MDI injections (threeto four injections per day of basal andprandial insulin) or continuous sub-cutaneous insulin infusion (CSII). (A)c Most people with type 1 diabetesshould be educated in how to matchprandial insulin dose to carbohydrateintake, premeal blood glucose, andanticipated activity. (E)c Most people with type 1 diabetesshould use insulin analogs to reducehypoglycemia risk. (A)c Consider screening those with type 1diabetes for other autoimmune dis-eases (thyroid, vitamin B12 deficiency,celiac) as appropriate. (B)The DCCT clearly showed that inten-sive insulin therapy (three or more in-jections per day of insulin, CSII, or insulinpump therapy) was a key part of im-proved glycemia and better outcomes(71,92). At the time of the study, therapywas carried out with short- and intermedi-ate-acting human insulins. Despite bettermicrovascular outcomes, intensive insulintherapy was associated with a high rate insevere hypoglycemia (62 episodes per 100patient-years of therapy). Since the time ofthe DCCT, a number of rapid-acting andlong-acting insulin analogs have been de-veloped. These analogs are associated withless hypoglycemia with equal A1C lower-ing in type 1 diabetes (107,108).Recommended therapy for type 1 di-abetesconsistsofthefollowingcomponents:Table 9dSummary of glycemic recommendations for many nonpregnant adults with diabetesA1C ,7.0%*Preprandial capillary plasma glucose 70–130 mg/dL* (3.9–7.2 mmol/L)Peak postprandial capillary plasma glucose† ,180 mg/dL* (,10.0 mmol/L)c *Goals should be individualized based on:c duration of diabetesc age/life expectancyc comorbid conditionsc known CVD or advanced microvascular complicationsc hypoglycemia unawarenessc individual patient considerationsc More or less stringent glycemic goals may be appropriatefor individual patientsc Postprandial glucose may be targeted if A1C goals arenot met despite reaching preprandial glucose goals†Postprandial glucose measurements should be made 1–2 h after the beginning of the meal, generally peaklevels in patients with diabetes.care.diabetesjournals.org DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 S21Position Statement
  12. 12. 1) use of MDI injections (three to four in-jections per day of basal and prandial in-sulin) or CSII therapy; 2) matching ofprandial insulin to carbohydrate intake,premeal blood glucose, and anticipatedactivity; and 3) for most patients (espe-cially if hypoglycemia is a problem), useof insulin analogs. There are excellent re-views available that guide the initiationand management of insulin therapyto achieve desired glycemic goals(107,109,110). Although most studies ofMDI versus pump therapy have been smalland of short duration, a systematic reviewand meta-analysis concluded that therewere no systematic differences in A1C orrates of severe hypoglycemia in childrenand adults between the two forms of inten-sive insulin therapy (70).Because of the increased frequencyof other autoimmune diseases in type 1diabetes, screening for thyroid dysfunc-tion, vitamin B12 deficiency, or celiacdisease should be considered based onsigns and symptoms. Periodic screeningin absence of symptoms has been recom-mended, but the effectiveness and opti-mal frequency are unclear.2. Pharmacological therapy for hyper-glycemia in type 2 diabetesRecommendationsc Metformin, if not contraindicated and iftolerated, is the preferred initial pharma-cological agent for type 2 diabetes. (A)c In newly diagnosed type 2 diabeticpatients with markedly symptomaticand/or elevated blood glucose levels orA1C, consider insulin therapy, with orwithout additional agents, from theoutset. (E)c If noninsulin monotherapy at maximaltolerated dose does not achieve or main-tain the A1C target over 3–6 months,add a second oral agent, a glucagon-likepeptide-1 (GLP-1) receptor agonist, orinsulin. (A)c A patient-centered approach should beused to guide choice of pharmacologicalagents. Considerations include efficacy,cost, potential side effects, effects onweight, comorbidities, hypoglycemiarisk, and patient preferences. (E)c Due to the progressive nature of type 2diabetes, insulin therapy is eventuallyindicated for many patients with type 2diabetes. (B)The ADA and EASD have recentlypartnered on guidance for individualiza-tion of use of medication classes andcombinations in patients with type 2diabetes (111). This 2012 position state-ment is less prescriptive than prior algo-rithms and discusses advantages anddisadvantages of the available medicationclasses and considerations for their use. Apatient-centered approach is stressed,taking into account patient preferences,cost and potential side effects of eachclass, effects on body weight, and hypo-glycemia risk. The position statement re-affirms metformin as the preferred initialagent, barring contraindication or intoler-ance, either in addition to lifestyle coun-seling and support for weight loss andexercise, or when lifestyle efforts alonehave not achieved or maintained glycemicgoals. Metformin has a long-standingevidence base for efficacy and safety, isinexpensive, and may reduce risk of car-diovascular events (85). When metforminfails to achieve or maintain glycemic goals,another agent should be added. Althoughthere are a number of trials comparingdual therapy to metformin alone, few di-rectly compare drugs as add-on therapy.Comparative effectiveness meta-analyses(112) suggest that overall each new classof noninsulin agents added to initial ther-apy lowers A1C around 0.9–1.1%.Many patients with type 2 diabeteseventually benefit from insulin therapy.The progressive nature of type 2 diabetesand its therapies should regularly beexplained in a matter-of-fact manner topatients, avoiding using insulin as a threator describing it as a failure or punishment.Providing patients with an algorithm forself-titration of insulin doses based onSMBG results improves glycemic controlin type 2 diabetic patients initiatinginsulin (113). For more details on phar-macotherapy for hyperglycemia in type2 diabetes, including a table of informa-tion about currently approved classesof medications for treating hyperglyce-mia in type 2 diabetes, readers are referredto the ADA-EASD position statement(111).E. MNTGeneral recommendationsc Individuals who have prediabetes ordiabetes should receive individualizedMNT as needed to achieve treatmentgoals, preferably provided by a regis-tered dietitian familiar with the com-ponents of diabetes MNT. (A)c Because MNT can result in cost-savingsand improved outcomes (B), MNTshould be adequately covered by in-surance and other payers. (E)Energy balance, overweight, and obesityc Weight loss is recommended for alloverweight or obese individuals whohave or are at risk for diabetes. (A)c For weight loss, either low-carbohydrate,low-fat calorie-restricted, or Mediterra-nean diets may be effective in the short-term (up to 2 years). (A)c For patients on low-carbohydrate diets,monitor lipid profiles, renal function,and protein intake (in those with ne-phropathy) and adjust hypoglycemictherapy as needed. (E)c Physical activity and behavior modifi-cation are important components ofweight loss programs and are mosthelpful in maintenance of weightloss. (B)Recommendations for primaryprevention of type 2 diabetesc Among individuals at high risk for de-veloping type 2 diabetes, structuredprograms that emphasize lifestylechanges that include moderate weightloss (7% body weight) and regularphysical activity (150 min/week), withdietary strategies including reducedcalories and reduced intake of dietaryfat, can reduce the risk for developingdiabetes and are therefore recom-mended. (A)c Individuals at risk for type 2 diabetesshould be encouraged to achieve theU.S. Department of Agriculture (USDA)recommendation for dietary fiber (14 gfiber/1,000 kcal) and foods containingwhole grains (one-half of grain intake).(B)c Individuals at risk for type 2 diabetesshould be encouraged to limit theirintake of sugar-sweetened beverages(SSBs). (B)Recommendations for managementof diabetesMacronutrients in diabetes managementc The mix of carbohydrate, protein, andfat may be adjusted to meet the meta-bolic goals and individual preferencesof the person with diabetes. (C)c Monitoring carbohydrate, whether bycarbohydrate counting, choices, or ex-perience-based estimation, remains a keystrategy in achieving glycemic control. (B)c Saturated fat intake should be ,7% oftotal calories. (B)c Reducing intake of trans fat lowers LDLcholesterol and increases HDL choles-terol (A); therefore, intake of trans fatshould be minimized. (E)S22 DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 care.diabetesjournals.orgPosition Statement
  13. 13. Other nutrition recommendationsc If adults with diabetes choose to usealcohol, they should limit intake to amoderate amount (one drink per day orless for adult women and two drinksper day or less for adult men) and shouldtake extra precautions to prevent hypo-glycemia. (E)c Routine supplementation with anti-oxidants, such as vitamins E and C andcarotene, is not advised because of lackof evidence of efficacy and concern re-lated to long-term safety. (A)c It is recommended that individualizedmeal planning include optimization offood choices to meet recommended di-etary allowance (RDA)/dietary referenceintake (DRI) for all micronutrients. (E)MNT is an integral component of di-abetes prevention, management, and self-management education. In addition to itsrole in preventing and controlling diabetes,the ADA recognizes the importance ofnutrition as an essential component of anoverall healthy lifestyle. A full review of theevidence regarding nutrition in preventingand controlling diabetes and its complica-tions and additional nutrition-related rec-ommendations can be found in the ADAposition statement “Nutrition Recommen-dations and Interventions for Diabetes”(114), which is being updated as of 2013.Achieving nutrition-related goals requires acoordinated team effort that includes the ac-tive involvement of the person with predia-betes or diabetes. Because of the complexityof nutrition issues, it is recommended that aregistered dietitian who is knowledgeableand skilled in implementing nutritiontherapy into diabetes management andeducation be the team member who pro-vides MNT.Clinical trials/outcome studies ofMNT have reported decreases in A1C at3–6 months ranging from 0.25 to 2.9%with higher reductions seen in type 2diabetes of shorter duration. Multiplestudies have demonstrated sustained im-provements in A1C at 12 months and lon-ger when a registered dietitian providedfollow-up visits ranging from monthly to3 sessions per year (115–122). Studies innondiabetic individuals suggest thatMNT reduces LDL cholesterol by 15–25mg/dL up to 16% (123) and support arole for lifestyle modification in treatinghypertension (123,124).Although the importance of weight lossfor overweight and obese individuals is welldocumented, an optimal macronutrientdistribution and dietary pattern of weightloss diets has not been established. Asystematic review of 80 weight loss studiesof $1-year duration demonstrated thatmoderate weight loss achieved throughdiet alone, diet and exercise, and meal re-placements can be achieved and main-tained (4.8–8% weight loss at 12 months)(125). Both low-fat low-carbohydrate andMediterranean style eating patterns havebeen shown to promote weight loss withsimilar results after 1 to 2 years of follow-up (126–129). A meta-analysis showedthat at 6 months, low-carbohydrate dietswere associated with greater improvementsintriglyceride and HDLcholesterolconcen-trations than low-fat diets; however, LDLcholesterol was significantly higher on thelow-carbohydrate diets (130).Because of the effects of obesity oninsulin resistance, weight loss is an im-portant therapeutic objective for over-weight or obese individuals who are atrisk for diabetes (131). The multifactorialintensive lifestyle intervention used in theDPP, which included reduced intake of fatand calories, led to weight loss averaging7% at 6 months and maintenance of 5%weight loss at 3 years, associated with a58% reduction in incidence of type 2 di-abetes (23). An RCT looking at high-riskindividuals in Spain showed that theMediterranean dietary pattern reducedthe incidence of diabetes in the absenceof weight loss by 52% compared with thelow-fat control group (132).Although our society abounds withexamples of high-calorie nutrient-poorfoods, large increases in the consumptionof SSBs have coincided with the epidemicsof obesity and type 2 diabetes. In a meta-analysis of eight prospective cohort stud-ies (n 5 310,819), a diet high in consump-tion of SSBs was associated with thedevelopment of type 2 diabetes (n 515,043). Individuals in the highest versuslowest quantile of SSB intake had a 26%greater risk of developing diabetes (133).For individuals with type 2 diabetes,studies have demonstrated that moderateweight loss (5% of body weight) is associ-ated with decreased insulin resistance, im-proved measures of glycemia and lipemia,and reduced blood pressure (134); longer-term studies ($52 weeks) showed mixedeffectsonA1C in adults with type 2diabetes(135–137), and in some studies resultswere confounded by pharmacologicalweight loss therapy. Look AHEAD (Actionfor Health in Diabetes) is a large clinical trialdesigned to determine whether long-termweight loss will improve glycemia and pre-vent cardiovascular events in subjects withtype 2 diabetes. One-year results of the in-tensive lifestyle intervention in this trialshow an average 8.6% weight loss, signifi-cant reduction of A1C, and reduction inseveral CVDrisk factors (138), with benefitssustained at 4 years (139). At the time thisarticle was going to press, the Look AHEADtrial was halted early, after 11 years of fol-low-up, because there was no significantdifference in the primary cardiovascularoutcome between the weight loss and stan-dard care group (http://www.nih.gov/news/health/oct2012/niddk-19.htm). Multiplecardiovascular risk factors were improvedwith weight loss, and those participantson average were on fewer medications toachieve these improvements.Although numerous studies have at-tempted to identify the optimal mix ofmacronutrients for meal plans of peoplewith diabetes, a recent systematic review(140) confirms that there is no most effec-tive mix that applies broadly, and thatmacronutrient proportions should be indi-vidualized. It must be clearly recognizedthat regardless of the macronutrient mix,total caloric intake must be appropriate toweight management goal. Further, individ-ualization of the macronutrient composi-tion will depend on the metabolic statusof the patient (e.g., lipid profile, renal func-tion) and/or food preferences. A variety ofdietary meal patterns are likely effective inmanaging diabetes including Mediterra-nean-style, plant-based (vegan or vegetar-ian), low-fat and lower-carbohydrate eatingpatterns (127,141–143).It should be noted that the RDA fordigestible carbohydrate is 130 g/day and isbased on providing adequate glucose as therequired fuel for the central nervous systemwithout reliance on glucose productionfrom ingested protein or fat. Althoughbrain fuel needs can be met on lowercarbohydrate diets, long-term metaboliceffects of very low-carbohydrate diets areunclear and such diets eliminate manyfoods that are important sources of energy,fiber, vitamins, and minerals and are im-portant in dietary palatability (144).Saturated and trans fatty acids are theprincipal dietary determinants of plasmaLDL cholesterol. There is a lack of evi-dence on the effects of specific fatty acidson people with diabetes, so the recom-mended goals are consistent with thosefor individuals with CVD (123,145).Reimbursement for MNTMNT, when delivered by a registereddietitian according to nutrition practiceguidelines, is reimbursed as part of thecare.diabetesjournals.org DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 S23Position Statement
  14. 14. Medicare program as overseen by theCenters for Medicare and Medicaid Serv-ices (CMS), as well as many health in-surance plans.F. Diabetes self-managementeducation and supportRecommendationsc People with diabetes should receiveDSME and diabetes self-managementsupport (DSMS) according to NationalStandards for Diabetes Self-Manage-ment Education and Support whentheir diabetes is diagnosed and asneeded thereafter. (B)c Effective self-management and qualityof life are the key outcomes of DSMEand DSMS and should be measuredand monitored as part of care. (C)c DSME and DSMS should addresspsychosocial issues, since emotionalwell-being is associated with positivediabetes outcomes. (C)c DSME and DSMS programs are appro-priate venues for people with prediabetesto receive education and support to de-velop and maintain behaviors that canprevent or delay the onset of diabetes. (C)c Because DSME and DSMS can result incost-savings and improved outcomes (B),DSME and DSMS should be adequatelyreimbursed by third-party payers. (E)DSME and DSMS are essential ele-ments of diabetes care (146–151), and re-cently updated National Standards forDiabetes Self-Management Education andSupport (152) are based on evidence for itsbenefits. Education helps people with dia-betes initiate effective self-management andcope with diabetes when they are first di-agnosed. Ongoing DSME and DSMS alsohelp people with diabetes maintain effec-tive self-management throughout a lifetimeof diabetes as they face new challenges andtreatment advances become available.DSME helps patients optimize metaboliccontrol, prevent and manage complica-tions, and maximize quality of life in acost-effective manner (153).DSME and DSMS are the ongoingprocesses of facilitating the knowledge,skill, and ability necessary for diabetesself-care. This process incorporates theneeds, goals, and life experiences of theperson with diabetes. The overall objec-tives of DSME and DSMS are to supportinformed decision making, self-care behav-iors, problem-solving, and active collabo-ration with the health care team to improveclinical outcomes, health status, and qual-ity of life in a cost-effective manner (152).Current best practice of DSME is askill-based approach that focuses onhelping those with diabetes make in-formed self-management choices. DSMEhas changed from a didactic approachfocusing on providing information tomore theoretically based empowermentmodels that focus on helping those withdiabetes make informed self-managementdecisions. Care of diabetes has shifted toan approach that is more patient centeredand places the person with diabetesand his or her family at the center of thecare model working in collaborationwith health care professionals. Patient-centered care is respectful of and respon-sive to individual patient preferences,needs, and values and ensures that patientvalues guide all decision making (154).Evidence for the benefits of DSME andDSMSMultiple studies have found that DSME isassociated with improved diabetes knowl-edge and improved self-care behavior(146), improved clinical outcomes suchas lower A1C (147,148,150,151,155–158), lower self-reported weight (146), im-proved quality of life (149,156,159),healthy coping (160), and lower costs(161). Better outcomes were reported forDSME interventions that were longer andincluded follow-up support (DSMS)(146,162–165), that were culturally(166,167) and age appropriate (168,169)and were tailored to individual needs andpreferences, and that addressed psychoso-cial issues and incorporated behavioralstrategies (146,150,170,171). Both indi-vidual and group approaches have beenfound effective (172,173). There isgrowingevidence for the role of community healthworkers and peer (174–180) and lay lead-ers (181) in delivering DSME and DSMS inconjunction with the core team (182).Diabetes education is associated withincreased use of primary and preventiveservices (161,183) and lower use of acute,inpatient hospital services (161). Patientswho participate in diabetes education aremore likely to follow best practice treat-ment recommendations, particularlyamong the Medicare population, andhave lower Medicare and commercialclaim costs (184,185).The National Standards for DiabetesSelf-Management Education andSupportThe National Standards for Diabetes Self-Management Education and Support aredesigned to define quality DSME andDSMS and to assist diabetes educatorsin a variety of settings to provide evidence-based education and self-managementsupport (152). The standards, recently up-dated, are reviewed and updated every 5years by a task force representing key or-ganizations involved in the field of diabeteseducation and care.DSME and DSMS providers and peo-ple with prediabetesThe new standards for DSME and DSMSalso apply to the education and support ofpeople with prediabetes. Currently, thereare significant barriers to the provision ofeducation and support to those with pre-diabetes. However, the strategies for sup-porting successful behavior change andthe healthy behaviors recommended forpeople with prediabetes are largely iden-tical to those for people with diabetes. Asbarriers to care are overcome, providers ofDSME and DSMS, given their training andexperience, are particularly well equippedto assist people with prediabetes in de-veloping and maintaining behaviors thatcan prevent or delay the onset of diabetes(152,186).Reimbursement for DSME and DSMSDSME, when provided by a program thatmeets national standards for DSME and isrecognized by the ADA or other approvalbodies,is reimbursed as partof the Medicareprogram as overseen by the CMS. DSMEis also covered by most health insuranceplans. Although DSMS has been shown tobe instrumental for improving outcomes, asdescribed in the “Evidence for the benefitsofDSME and DSMS,” and can be provided informats such as phone calls and via tele-health, it currently has limited reimburse-ment as face-to-face visits included asfollow-up to DSME.G. Physical activityRecommendationsc Adults with diabetes should be advisedto perform at least 150 min/week ofmoderate-intensity aerobic physicalactivity (50–70% of maximum heartrate), spread over at least 3 days/weekwith no more than two consecutivedays without exercise. (A)c In the absence of contraindications,adults with type 2 diabetes should beencouraged to perform resistance train-ing at least twice per week. (A)Exercise is an important part of thediabetes management plan. Regular exer-cise has been shown to improve bloodS24 DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 care.diabetesjournals.orgPosition Statement

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