Diabetes is a chronic illness that requires continuing medical care and ongoing patient
self-management education and support to prevent acute complications and to reduce
the risk of long-term complications. Diabetes care is complex and requires that many
issues, beyond glycemic control, be addressed. A large body of evidence exists that
supports a range of interventions to improve diabetes outcomes.
These standards of care are intended to provide clinicians, patients, researchers,
payors, and other interested individuals with the components of diabetes care, general
treatment goals, and tools to evaluate the quality of care. While individual preferences,
comorbidities, and other patient factors may require modification of goals, targets
that are desirable for most patients with diabetes are provided. These standards are
not intended to preclude clinical judgment or more extensive evaluation and management
of the patient by other specialists as needed. For more detailed information about
management of diabetes, refer to references 1
The recommendations included are screening, diagnostic, and therapeutic actions that
are known or believed to favorably affect health outcomes of patients with diabetes.
A grading system (Table 1), developed by the American Diabetes Association (ADA) and
modeled after existing methods, was used to clarify and codify the evidence that forms
the basis for the recommendations. The level of evidence that supports each recommendation
is listed after each recommendation using the letters A, B, C, or E.
ADA evidence grading system for clinical practice recommendations
Level of evidence
Clear evidence from well-conducted, generalizable, randomized controlled trials that
are adequately powered, including:
Evidence from a well-conducted multicenter trial
Evidence from a meta-analysis that incorporated quality ratings in the analysis
Compelling nonexperimental evidence, i.e., “all or none” rule developed by Center
for Evidence Based Medicine at Oxford
Supportive evidence from well-conducted randomized controlled trials that are adequately
Evidence from a well-conducted trial at one or more institutions
Evidence from a meta-analysis that incorporated quality ratings in the analysis
Supportive evidence from well-conducted cohort studies:
Evidence from a well-conducted prospective cohort study or registry
Evidence from a well-conducted meta-analysis of cohort studies
Supportive evidence from a well-conducted case-control study
Supportive evidence from poorly controlled or uncontrolled studies
Evidence from randomized clinical trials with one or more major or three or more minor
methodological flaws that could invalidate the results
Evidence from observational studies with high potential for bias (such as case series
with comparison to historical controls)
Evidence from case series or case reports
Conflicting evidence with the weight of evidence supporting the recommendation
Expert consensus or clinical experience
These standards of care are revised annually by the ADA multidisciplinary Professional
Practice Committee, and new evidence is incorporated. Members of the Professional
Practice Committee and their disclosed conflicts of interest are listed in the Introduction.
Subsequently, as with all position statements, the standards of care are reviewed
and approved by the Executive Committee of ADA's Board of Directors.
I. CLASSIFICATION AND DIAGNOSIS
The classification of diabetes includes four clinical classes:
type 1 diabetes (results from β-cell destruction, usually leading to absolute insulin
type 2 diabetes (results from a progressive insulin secretory defect on the background
of insulin resistance)
other specific types of diabetes due to other causes, e.g., genetic defects in β-cell
function, genetic defects in insulin action, diseases of the exocrine pancreas (such
as cystic fibrosis), and drug- or chemical-induced diabetes (such as in the treatment
of AIDS or after organ transplantation)
gestational diabetes mellitus (GDM) (diabetes diagnosed during pregnancy)
Some patients cannot be clearly classified as having type 1 or type 2 diabetes. Clinical
presentation and disease progression vary considerably in both types of diabetes.
Occasionally, patients who otherwise have type 2 diabetes may present with ketoacidosis.
Similarly, patients with type 1 diabetes may have a late onset and slow (but relentless)
progression despite having features of autoimmune disease. Such difficulties in diagnosis
may occur in children, adolescents, and adults. The true diagnosis may become more
obvious over time.
B. Diagnosis of diabetes
For decades, the diagnosis of diabetes has been based on plasma glucose (PG) criteria,
either fasting PG (FPG) or 2-h 75-g oral glucose tolerance test (OGTT) values. In
1997, the first Expert Committee on the Diagnosis and Classification of Diabetes Mellitus
revised the diagnostic criteria using the observed association between glucose levels
and presence of retinopathy as the key factor with which to identify threshold FPG
and 2-h PG levels. The committee examined data from three cross-sectional epidemiologic
studies that assessed retinopathy with fundus photography or direct ophthalmoscopy
and measured glycemia as FPG, 2-h PG, and HbA1c (A1C). The studies demonstrated glycemic
levels below which there was little prevalent retinopathy and above which the prevalence
of retinopathy increased in an apparently linear fashion. The deciles of FPG, 2-h
PG, and A1C at which retinopathy began to increase were the same for each measure
within each population. The analyses helped to inform a then-new diagnostic cut point
of ≥126 mg/dl (7.0 mmol/l) for FPG and confirmed the long-standing diagnostic 2-h
PG value of ≥200 mg/dl (11.1 mmol/l) (4).
ADA has not previously recommended the use of A1C for diagnosing diabetes, in part
due to lack of standardization of the assay. However, A1C assays are now highly standardized,
and their results can be uniformly applied both temporally and across populations.
In a recent report (5), after an extensive review of both established and emerging
epidemiological evidence, an international expert committee recommended the use of
the A1C test to diagnose diabetes with a threshold of ≥6.5%, and ADA affirms this
decision (6). The diagnostic test should be performed using a method certified by
the National Glycohemoglobin Standardization Program (NGSP) and standardized or traceable
to the Diabetes Control and Complications Trial (DCCT) reference assay. Point-of-care
A1C assays are not sufficiently accurate at this time to use for diagnostic purposes.
Epidemiologic datasets show a relationship between A1C and the risk of retinopathy
similar to that which has been shown for corresponding FPG and 2-h PG thresholds.
The A1C has several advantages to the FPG, including greater convenience, since fasting
is not required; evidence to suggest greater preanalytical stability; and less day-to-day
perturbations during periods of stress and illness. These advantages must be balanced
by greater cost, limited availability of A1C testing in certain regions of the developing
world, and incomplete correlation between A1C and average glucose in certain individuals.
In addition, the A1C can be misleading in patients with certain forms of anemia and
hemoglobinopathies. For patients with a hemoglobinopathy but normal red cell turnover,
such as sickle cell trait, an A1C assay without interference from abnormal hemoglobins
should be used (an updated list of A1C assays and whether abnormal hemoglobins impact
them is available at www.ngsp.org/prog/index3.html). For conditions with abnormal
red cell turnover, such as pregnancy or anemias from hemolysis and iron deficiency,
the diagnosis of diabetes must use glucose criteria exclusively.
The established glucose criteria for the diagnosis of diabetes (FPG and 2-h PG) remain
valid. Patients with severe hyperglycemia such as those who present with severe classic
hyperglycemic symptoms or hyperglycemic crisis can continue to be diagnosed when a
random (or casual) PG of ≥200 mg/dl (11.1 mmol/l) is found. It is likely that in such
cases the health care professional would also conduct an A1C test as part of the initial
assessment of the severity of the diabetes and that it would be above the diagnostic
cut point. However, in rapidly evolving diabetes such as the development of type 1
in some children, the A1C may not be significantly elevated despite frank diabetes.
Just as there is <100% concordance between the FPG and 2-h PG tests, there is not
perfect concordance between A1C and either glucose-based test. Analyses of National
Health and Nutrition Examination Survey (NHANES) data indicate that, assuming universal
screening of the undiagnosed, the A1C cut point of ≥6.5% identifies one-third fewer
cases of undiagnosed diabetes than a fasting glucose cut point of ≥126 mg/dl (7.0
mmol/l) (E. Gregg, personal communication). However, in practice, a large portion
of the diabetic population remains unaware of their condition. Thus, the lower sensitivity
of A1C at the designated cut point may well be offset by the test's greater practicality,
and wider application of a more convenient test (A1C) may actually increase the number
of diagnoses made.
As with most diagnostic tests, a test result diagnostic of diabetes should be repeated
to rule out laboratory error, unless the diagnosis is clear on clinical grounds, such
as a patient with classic symptoms of hyperglycemia or hyperglycemic crisis. It is
preferable that the same test be repeated for confirmation, since there will be a
greater likelihood of concurrence in this case. For example, if the A1C is 7.0% and
a repeat result is 6.8%, the diagnosis of diabetes is confirmed. However, there are
scenarios in which results of two different tests (e.g., FPG and A1C) are available
for the same patient. In this situation, if the two different tests are both above
the diagnostic threshold, the diagnosis of diabetes is confirmed.
On the other hand, if two different tests are available in an individual and the results
are discordant, the test whose result is above the diagnostic cut point should be
repeated, and the diagnosis is made on the basis of the confirmed test. That is, if
a patient meets the diabetes criterion of the A1C (two results ≥6.5%) but not the
FPG (<126 mg/dl or 7.0 mmol/l), or vice versa, that person should be considered to
have diabetes. Admittedly, in most circumstance the “nondiabetic” test is likely to
be in a range very close to the threshold that defines diabetes.
Since there is preanalytic and analytic variability of all the tests, it is also possible
that when a test whose result was above the diagnostic threshold is repeated, the
second value will be below the diagnostic cut point. This is least likely for A1C,
somewhat more likely for FPG, and most likely for the 2-h PG. Barring a laboratory
error, such patients are likely to have test results near the margins of the threshold
for a diagnosis. The healthcare professional might opt to follow the patient closely
and repeat the testing in 3–6 months.
The current diagnostic criteria for diabetes are summarized in Table 2.
Criteria for the diagnosis of diabetes
A1C ≥6.5%. The test should be performed in a laboratory using a method that is NGSP
certified and standardized to the DCCT assay.*
FPG ≥126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least
Two-hour plasma glucose ≥200 mg/dl (11.1 mmol/l) during an OGTT. The test should be
performed as described by the World Health Organization, using a glucose load containing
the equivalent of 75 g anhydrous glucose dissolved in water.*
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random
plasma glucose ≥200 mg/dl (11.1 mmol/l).
*In the absence of unequivocal hyperglycemia, criteria 1–3 should be confirmed by
C. Categories of increased risk for diabetes
In 1997 and 2003, The Expert Committee on the Diagnosis and Classification of Diabetes
Mellitus (4,7) recognized an intermediate group of individuals whose glucose levels,
although not meeting criteria for diabetes, are nevertheless too high to be considered
normal. This group was defined as having impaired fasting glucose (IFG) (FPG levels
of 100 mg/dl [5.6 mmol/l] to 125 mg/dl [6.9 mmol/l]) or impaired glucose tolerance
(IGT) (2-h OGTT values of 140 mg/dl [7.8 mmol/l] to 199 mg/dl [11.0 mmol/l]).
Individuals with IFG and/or IGT have been referred to as having pre-diabetes, indicating
the relatively high risk for the future development of diabetes. IFG and IGT should
not be viewed as clinical entities in their own right but rather risk factors for
diabetes as well as cardiovascular disease (CVD). IFG and IGT are associated with
obesity (especially abdominal or visceral obesity), dyslipidemia with high triglycerides
and/or low HDL cholesterol, and hypertension. Structured lifestyle intervention, aimed
at increasing physical activity and producing 5–10% loss of body weight, and certain
pharmacological agents have been demonstrated to prevent or delay the development
of diabetes in people with IGT (see Table 7). It should be noted that the 2003 ADA
Expert Committee report reduced the lower FPG cut point to define IFG from 110 mg/dl
(6.1 mmol/l) to 100 mg/dl (5.6 mmol/l), in part to make the prevalence of IFG more
similar to that of IGT. However, the World Health Organization (WHO) and many other
diabetes organizations did not adopt this change.
As the A1C becomes increasingly used to diagnose diabetes in individuals with risk
factors, it will also identify those at high risk for developing diabetes in the future.
As was the case with the glucose measures, defining a lower limit of an intermediate
category of A1C is somewhat arbitrary, since risk of diabetes with any measure or
surrogate of glycemia is a continuum extending well into the normal ranges. To maximize
equity and efficiency of preventive interventions, such an A1C cut point, should balance
the costs of false negatives (failing to identify those who are going to develop diabetes)
against the costs of false positives (falsely identifying and then spending intervention
resources on those who were not going to develop diabetes anyway).
Linear regression analyses of nationally representative U.S. data (NHANES 2005–2006)
indicate that among the nondiabetic adult population, an FPG of 110 mg/dl corresponds
to an A1C of 5.6%, while an FPG of 100 mg/dl corresponds to an A1C of 5.4%. Receiver
operating curve analyses of these data indicate that an A1C value of 5.7%, compared
with other cut points, has the best combination of sensitivity (39%) and specificity
(91%) to identify cases of IFG (FPG ≥100 mg/dl [5.6 mmol/l]) (R.T. Ackerman, Personal
Communication). Other analyses suggest that an A1C of 5.7% is associated with diabetes
risk similar to that of the high-risk participants in the Diabetes Prevention Program
(DPP) (R.T. Ackerman, personal communication). Hence, it is reasonable to consider
an A1C range of 5.7–6.4% as identifying individuals with high risk for future diabetes
and to whom the term pre-diabetes may be applied (6).
As is the case for individuals found to have IFG and IGT, individuals with an A1C
of 5.7–6.4% should be informed of their increased risk for diabetes as well as CVD
and counseled about effective strategies to lower their risks (see IV. PREVENTION/DELAY
OF TYPE 2 DIABETES). As with glucose measurements, the continuum of risk is curvilinear,
so that as A1C rises, the risk of diabetes rises disproportionately. Accordingly,
interventions should be most intensive and follow-up should be particularly vigilant
for those with an A1C >6.0%, who should be considered to be at very high risk. However,
just as an individual with a fasting glucose of 98 mg/dl (5.4 mmol/l) may not be at
negligible risk for diabetes, individuals with an A1C <5.7% may still be at risk,
depending on the level of A1C and presence of other risk factors, such as obesity
and family history.
Table 3 summarizes the categories of increased risk for diabetes.
Categories of increased risk for diabetes*
FPG 100–125 mg/dl (5.6–6.9 mmol/l) [IFG]
2-h PG on the 75-g OGTT 140–199 mg/dl (7.8–11.0 mmol/l) [IGT]
*For all three tests, risk is continuous, extending below the lower limit of the range
and becoming disproportionately greater at higher ends of the range.
II. TESTING FOR DIABETES IN ASYMPTOMATIC PATIENTS
Testing to detect type 2 diabetes and assess risk for future diabetes in asymptomatic
people should be considered in adults of any age who are overweight or obese (BMI
≥25 kg/m2) and who have one or more additional risk factors for diabetes (Table 4).
In those without these risk factors, testing should begin at age 45 years. (B)
If tests are normal, repeat testing should be carried out at least at 3-year intervals.
To test for diabetes or to assess risk of future diabetes, either A1C, FPG, or 2-h
75-g OGTT are appropriate. (B)
In those identified with increased risk for future diabetes, identify and, if appropriate,
treat other CVD risk factors. (B)
Criteria for testing for diabetes in asymptomatic adult individuals
Testing should be considered in all adults who are overweight (BMI ≥25 kg/m2
*) and have additional risk factors:
first-degree relative with diabetes
members of a high-risk ethnic population (e.g., African American, Latino, Native American,
Asian American, Pacific Islander)
women who delivered a baby weighing >9 lb or were diagnosed with GDM
hypertension (≥140/90 mmHg or on therapy for hypertension)
HDL cholesterol level <35 mg/dl (0.90 mmol/l) and/or a triglyceride level >250 mg/dl
women with polycystic ovary syndrome
A1C ≥5.7%, IGT, or IFG on previous testing
other clinical conditions associated with insulin resistance (e.g., severe obesity,
history of CVD
In the absence of the above criteria, testing diabetes should begin at age 45 years
If results are normal, testing should be repeated at least at 3-year intervals, with
consideration of more frequent testing depending on initial results and risk status.
*At-risk BMI may be lower in some ethnic groups.
For many illnesses there is a major distinction between screening and diagnostic testing.
However, for diabetes the same tests would be used for “screening” as for diagnosis.
Type 2 diabetes has a long asymptomatic phase and significant clinical risk markers.
Diabetes may be identified anywhere along a spectrum of clinical scenarios ranging
from a seemingly low-risk individual who happens to have glucose testing, to a higher-risk
individual who the provider tests because of high suspicion of diabetes, to the symptomatic
patient. The discussion herein is primarily framed as testing for diabetes in individuals
without symptoms. Testing for diabetes will also detect individuals at increased future
risk for diabetes, herein referred to as pre-diabetic.
A. Testing for type 2 diabetes and risk of future diabetes in adults
Type 2 diabetes is frequently not diagnosed until complications appear, and approximately
one-fourth of all people with diabetes in the U.S. may be undiagnosed. Although the
effectiveness of early identification of pre-diabetes and diabetes through mass testing
of asymptomatic individuals has not been proven definitively (and rigorous trials
to provide such proof are unlikely to occur), pre-diabetes and diabetes meet established
criteria for conditions in which early detection is appropriate. Both conditions are
common, are increasing in prevalence, and impose significant public health burdens.
There is a long presymptomatic phase before the diagnosis of type 2 diabetes is usually
made. Relatively simple tests are available to detect preclinical disease (9). Additionally,
the duration of glycemic burden is a strong predictor of adverse outcomes, and effective
interventions exist to prevent progression of pre-diabetes to diabetes (see IV. PREVENTION/DELAY
OF TYPE 2 DIABETES) and to reduce risk of complications of diabetes (see VI. PREVENTION
AND MANAGEMENT OF DIABETES COMPLICATIONS).
Recommendations for testing for diabetes in asymptomatic undiagnosed adults are listed
in Table 4. Testing should be considered in adults of any age with BMI ≥25 kg/m2 and
one or more risk factors for diabetes. Because age is a major risk factor for diabetes,
testing of those without other risk factors should begin no later than at age 45 years.
Either A1C, FPG, or 2-h OGTT is appropriate for testing. The 2-h OGTT identifies people
with either IFG or IGT and thus more people at increased risk for the development
of diabetes and CVD. It should be noted that the two tests do not necessarily detect
the same individuals (10). The efficacy of interventions for primary prevention of
type 2 diabetes (11
–17) has primarily been demonstrated among individuals with IGT, but not for individuals
with IFG (who do not also have IGT) or those with specific A1C levels.
The appropriate interval between tests is not known (18). The rationale for the 3-year
interval is that false negatives will be repeated before substantial time elapses,
and there is little likelihood that an individual will develop significant complications
of diabetes within 3 years of a negative test result.
Because of the need for follow-up and discussion of abnormal results, testing should
be carried out within the health care setting. Community screening outside a health
care setting is not recommended because people with positive tests may not seek, or
have access to, appropriate follow-up testing and care. Conversely, there may be failure
to ensure appropriate repeat testing for individuals who test negative. Community
screening may also be poorly targeted, i.e., it may fail to reach the groups most
at risk and inappropriately test those at low risk (the worried well) or even those
already diagnosed (19,20).
B. Testing for type 2 diabetes in children
The incidence of type 2 diabetes in adolescents has increased dramatically in the
last decade, especially in minority populations (21), although the disease remains
rare in the general pediatric population (22). Consistent with recommendations for
adults, children and youth at increased risk for the presence or the development of
type 2 diabetes should be tested within the health care setting (23). The recommendations
of the ADA consensus statement on type 2 diabetes in children and youth, with some
modifications, are summarized in Table 5.
Testing for type 2 diabetes in asymptomatic children
Overweight (BMI >85th percentile for age and sex, weight for height >85th percentile,
or weight >120% of ideal for height)
Plus any two of the following risk factors:
Family history of type 2 diabetes in first- or second-degree relative
Race/ethnicity (Native American, African American, Latino, Asian American, Pacific
Signs of insulin resistance or conditions associated with insulin resistance (acanthosis
nigricans, hypertension, dyslipidemia, polycystic ovary syndrome, or small for gestational
Maternal history of diabetes or GDM during the child's gestation
Age of initiation:
Age 10 years or at onset of puberty, if puberty occurs at a younger age
Every 3 years
C. Screening for type 1 diabetes
Generally, people with type 1 diabetes present with acute symptoms of diabetes and
markedly elevated blood glucose levels, and most cases are diagnosed soon after the
onset of hyperglycemia. However, evidence from type 1 diabetes prevention studies
suggests that measurement of islet autoantibodies identifies individuals who are at
risk for developing type 1 diabetes. Such testing may be appropriate in high-risk
individuals, such as those with prior transient hyperglycemia or those who have relatives
with type 1 diabetes, in the context of clinical research studies (see, for example,
http://www2.diabetestrialnet.org). Widespread clinical testing of asymptomatic low-risk
individuals cannot currently be recommended, as it would identify very few individuals
in the general population who are at risk. Individuals who screen positive should
be counseled about their risk of developing diabetes. Clinical studies are being conducted
to test various methods of preventing type 1 diabetes or reversing early type 1 diabetes
in those with evidence of autoimmunity.
III. DETECTION AND DIAGNOSIS OF GDM
Screen for GDM using risk factor analysis and, if appropriate, an OGTT. (C)
Women with GDM should be screened for diabetes 6–12 weeks postpartum and should be
followed up with subsequent screening for the development of diabetes or pre-diabetes.
For many years, GDM has been defined as any degree of glucose intolerance with onset
or first recognition during pregnancy (4). Although most cases resolve with delivery,
the definition applied whether the condition persisted after pregnancy and did not
exclude the possibility that unrecognized glucose intolerance may have antedated or
begun concomitantly with the pregnancy. This definition facilitated a uniform strategy
for detection and classification of GDM, but its limitations were recognized for many
years. As the ongoing epidemic of obesity and diabetes has led to more type 2 diabetes
in women of childbearing age, the number of pregnant women with undiagnosed type 2
diabetes has increased (24). After deliberations in 2008–2009, the International Association
of Diabetes and Pregnancy Study Groups (IADPSG), an international consensus group
with representatives from multiple obstetrical and diabetes organizations, including
ADA, recommended that high-risk women found to have diabetes at their initial prenatal
visit using standard criteria (Table 2) receive a diagnosis of overt, not gestational,
Approximately 7% of all pregnancies (ranging from 1 to 14% depending on the population
studied and the diagnostic tests used) are complicated by GDM, resulting in more than
200,000 cases annually.
Because of the risks of GDM to the mother and neonate, screening and diagnosis are
warranted. Current screening and diagnostic strategies, based on the 2004 ADA position
statement on GDM (25), are outlined in Table 6.
Screening for and diagnosis of GDM
Carry out diabetes risk assessment at the first prenatal visit.
Women at very high risk should be screened for diabetes as soon as possible after
the confirmation of pregnancy. Criteria for very high risk are:
Prior history of GDM or delivery of large-for-gestational-age infant
Presence of glycosuria
Diagnosis of PCOS
Strong family history of type 2 diabetes
Screening/diagnosis at this stage of pregnancy should use standard diagnostic testing
All women of greater than low risk of GDM, including those above not found to have
diabetes early in pregnancy, should undergo GDM testing at 24–28 weeks of gestation.
Low-risk status, which does not require GDM screening, is defined as women with ALL
of the following characteristics:
Age <25 years
Weight normal before pregnancy
Member of an ethnic group with a low prevalence of diabetes
No known diabetes in first-degree relatives
No history of abnormal glucose tolerance
No history of poor obstetrical outcome
Two approaches may be followed for GDM screening at 24–28 weeks:
Perform initial screening by measuring plasma or serum glucose 1 h after a 50-g load
of ≥140 mg/dl identifies ∼80% of women with GDM, while the sensitivity is further
increased to ∼90% by a threshold of ≥130 mg/dl.
Perform a diagnostic 100-g OGTT on a separate day in women who exceed the chosen threshold
on 50-g screening.
One-step approach (may be preferred in clinics with high prevalence of GDM): Perform
a diagnostic 100-g OGTT in all women to be tested at 24–28 weeks.
The 100-g OGTT should be performed in the morning after an overnight fast of at least
To make a diagnosis of GDM, at least two of the following plasma glucose values must
Fasting ≥95 mg/dl
1-h ≥180 mg/dl
2-h ≥155 mg/dl
3-h ≥140 mg/dl
Results of the Hyperglycemia and Adverse Pregnancy Outcomes (HAPO) study (26), a large-scale
(∼25,000 pregnant women) multinational epidemiologic study, demonstrated that risk
of adverse maternal, fetal, and neonatal outcomes continuously increased as a function
of maternal glycemia at 24–28 weeks, even within ranges previously considered normal
for pregnancy. For most complications there was no threshold for risk. These results
have led to careful reconsideration of the diagnostic criteria for GDM. The IADPSG
recommended that all women not known to have prior diabetes undergo a 75-g OGTT at
24–28 weeks of gestation. The group developed diagnostic cut points for the fasting,
1-h, and 2-h PG measurements that conveyed an odds ratio for adverse outcomes of at
least 1.75 compared with women with the mean glucose levels in the HAPO study.
At the time of this update to the Standards of Medical Care in Diabetes, ADA is planning
to work with U.S. obstetrical organizations to consider adoption of the IADPSG diagnostic
criteria and to discuss the implications of this change. While this change will significantly
increase the prevalence of GDM, there is mounting evidence that treating even mild
GDM reduces morbidity for both mother and baby (27).
Because women with a history of GDM have a greatly increased subsequent risk for diabetes
(28), they should be screened for diabetes 6–12 weeks postpartum, using nonpregnant
OGTT criteria, and should be followed up with subsequent screening for the development
of diabetes or pre-diabetes, as outlined in II. TESTING FOR DIABETES IN ASYMPTOMATIC
PATIENTS. Information on the National Diabetes Education Program (NDEP) campaign to
prevent type 2 diabetes in women with GDM can be found at http://ndep.nih.gov/media/NeverTooEarly_Tipsheet.pdf.
IV. PREVENTION/DELAY OF TYPE 2 DIABETES
Patients with IGT (A), IFG (E), or an A1C of 5.7–6.4% (E) should be referred to an
effective ongoing support program for weight loss of 5–10% of body weight and an increase
in physical activity of at least 150 min/week of moderate activity such as walking.
Follow-up counseling appears to be important for success. (B)
Based on potential cost savings of diabetes prevention, such counseling should be
covered by third-party payors. (E)
In addition to lifestyle counseling, metformin may be considered in those who are
at very high risk for developing diabetes (combined IFG and IGT plus other risk factors
such as A1C >6%, hypertension, low HDL cholesterol, elevated triglycerides, or family
history of diabetes in a first-degree relative) and who are obese and under 60 years
of age. (E)
Monitoring for the development of diabetes in those with pre-diabetes should be performed
every year. (E)
Randomized controlled trials have shown that individuals at high risk for developing
diabetes (those with IFG, IGT, or both) can be given interventions that significantly
decrease the rate of onset of diabetes (11
–17). These interventions include intensive lifestyle modification programs that have
been shown to be very effective (58% reduction after 3 years) and use of the pharmacologic
agents metformin, α-glucosidase inhibitors, orlistat, and thiazolidinediones, each
of which has been shown to decrease incident diabetes to various degrees. A summary
of major diabetes prevention trials is shown in Table 7.
Therapies proven effective in diabetes prevention trials
Mean age (years)
Intervention (daily dose)
Incidence in control subjects (%/year)
Relative risk reduction (%) (95% CI)
3-Year number needed to treat*
Finnish DPS (12)
IGT, BMI ≥25 kg/m2
IGT, BMI ≥24 kg/m2, FPG >5.3 mmol/l
Da Qing (13)
IGT (randomized groups)
Toranomon Study (31)
IGT (men), BMI = 24 kg/m2
67 (P < 0.043)‡
Indian DPP (17)
IGT, BMI >24 kg/m2, FPG >5.3 mmol/l
Metformin (1,700 mg)
Indian DPP (17)
Metformin (500 mg)
STOP NIDDM (15)
IGT, FPG >5.6 mmol/l
Acarbose (300 mg)
BMI >30 kg/m2
Orlistat (360 mg)
IGT or IFG
Rosiglitazone (8 mg)
Voglibose Ph-3 (33)
3.0 (1-year Rx)
Vogliobose (0.2 mg)
21 (1-year Rx)
IGT or IFG
Pioglitizone (45 mg)
Modified and reprinted with permission (35). Percentage points:
*Number needed to treat to prevent 1 case of diabetes, standardized for a 3-year period
to improve comparisons across studies.
†Number of participants in the indicated comparisons, not necessarily in entire study.
‡Calculated from information in the article. ACT-NOW, ACTos Now Study for the Prevention
of Diabetes; DPP, Diabetes Prevention Program; DPS, Diabetes Prevention Study; DREAM,
Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication; STOP NIDDM,
Study to Prevent Non-Insulin Dependent Diabetes; XENDOS, Xenical in the prevention
of Diabetes in Obese Subjects. I, individual; G, group; D&E, diet and exercise.
Two studies of lifestyle intervention have shown persistent reduction in the role
of conversion to type 2 diabetes with 3 years (29) to 14 years (30) of postintervention
Based on the results of clinical trials and the known risks of progression of pre-diabetes
to diabetes, an ADA Consensus Development Panel (36) concluded that people with IGT
and/or IFG should be counseled on lifestyle changes with goals similar to those of
the DPP (5–10% weight loss and moderate physical activity of ∼30 min/day). Regarding
the more difficult issue of drug therapy for diabetes prevention, the consensus panel
felt that metformin should be the only drug considered for use in diabetes prevention.
For other drugs, the issues of cost, side effects, and lack of persistence of effect
in some studies led the panel to not recommend use for diabetes prevention. Metformin
use was recommended only for very-high-risk individuals (those with combined IGT and
IFG who are obese and have at least one other risk factor for diabetes) who are under
60 years of age. In addition, the panel highlighted the evidence that in the DPP,
metformin was most effective compared with lifestyle in individuals with BMI ≥35 kg/m2
and those under age 60 years.
V. DIABETES CARE
A. Initial evaluation
A complete medical evaluation should be performed to classify the diabetes, detect
the presence of diabetes complications, review previous treatment and glycemic control
in patients with established diabetes, assist in formulating a management plan, and
provide a basis for continuing care. Laboratory tests appropriate to the evaluation
of each patient's medical condition should be performed. A focus on the components
of comprehensive care (Table 8) will assist the health care team to ensure optimal
management of the patient with diabetes.
Components of the comprehensive diabetes evaluation
Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding)
Eating patterns, physical activity habits, nutritional status, and weight history;
growth and development in children and adolescents
Diabetes education history
Review of previous treatment regimens and response to therapy (A1C records)
Current treatment of diabetes, including medications, meal plan, physical activity
patterns, and results of glucose monitoring and patient's use of data
DKA frequency, severity, and cause
Any severe hypoglycemia: frequency and cause
History of diabetes-related complications
Microvascular: retinopathy, nephropathy, neuropathy (sensory, including history of
foot lesions; autonomic, including sexual dysfunction and gastroparesis)
Macrovascular: CHD, cerebrovascular disease, PAD
Other: psychosocial problems*, dental disease*
Height, weight, BMI
Blood pressure determination, including orthostatic measurements when indicated
Skin examination (for acanthosis nigricans and insulin injection sites)
Comprehensive foot examination:
Palpation of dorsalis pedis and posterior tibial pulses
Presence/absence of patellar and Achilles reflexes
Determination of proprioception, vibration, and monofilament sensation
A1C, if results not available within past 2–3 months
If not performed/available within past year:
Fasting lipid profile, including total, LDL- and HDL cholesterol and triglycerides
Liver function tests
Test for urine albumin excretion with spot urine albumin/creatinine ratio
Serum creatinine and calculated GFR
TSH in type 1 diabetes, dyslipidemia, or women over age 50 years
Annual dilated eye exam
Family planning for women of reproductive age
Registered dietitian for MNT
Mental health professional, if needed
* See appropriate referrals for these categories.
People with diabetes should receive medical care from a physician-coordinated team.
Such teams may include, but are not limited to, physicians, nurse practitioners, physician's
assistants, nurses, dietitians, pharmacists, and mental health professionals with
expertise and a special interest in diabetes. It is essential in this collaborative
and integrated team approach that individuals with diabetes assume an active role
in their care.
The management plan should be formulated as a collaborative therapeutic alliance among
the patient and family, the physician, and other members of the health care team.
A variety of strategies and techniques should be used to provide adequate education
and development of problem-solving skills in the various aspects of diabetes management.
Implementation of the management plan requires that each aspect is understood and
agreed to by the patient and the care providers and that the goals and treatment plan
are reasonable. Any plan should recognize diabetes self-management education (DSME)
and on-going diabetes support as an integral component of care. In developing the
plan, consideration should be given to the patient's age, school or work schedule
and conditions, physical activity, eating patterns, social situation and cultural
factors, and presence of complications of diabetes or other medical conditions.
C. Glycemic control
1. Assessment of glycemic control
Two primary techniques are available for health providers and patients to assess the
effectiveness of the management plan on glycemic control: patient self-monitoring
of blood glucose (SMBG) or interstitial glucose and A1C.
a. Glucose monitoring
SMBG should be carried out three or more times daily for patients using multiple insulin
injections or insulin pump therapy. (A)
For patients using less frequent insulin injections, noninsulin therapies, or medical
nutrition therapy (MNT) alone, SMBG may be useful as a guide to the success of therapy.
To achieve postprandial glucose targets, postprandial SMBG may be appropriate. (E)
When prescribing SMBG, ensure that patients receive initial instruction in, and routine
follow-up evaluation of, SMBG technique and using data to adjust therapy. (E)
Continuous glucose monitoring (CGM) in conjunction with intensive insulin regimens
can be a useful tool to lower A1C in selected adults (age ≥25 years) with type 1 diabetes
Although the evidence for A1C lowering is less strong in children, teens, and younger
adults, CGM may be helpful in these groups. Success correlates with adherence to ongoing
use of the device. (C)
CGM may be a supplemental tool to SMBG in those with hypoglycemia unawareness and/or
frequent hypoglycemic episodes. (E)
The ADA consensus and position statements on SMBG provide a comprehensive review of
the subject (37,38). Major clinical trials of insulin-treated patients that demonstrated
the benefits of intensive glycemic control on diabetes complications have included
SMBG as part of multifactorial interventions, suggesting that SMBG is a component
of effective therapy. SMBG allows patients to evaluate their individual response to
therapy and assess whether glycemic targets are being achieved. Results of SMBG can
be useful in preventing hypoglycemia and adjusting medications (particularly prandial
insulin doses), MNT, and physical activity.
The frequency and timing of SMBG should be dictated by the particular needs and goals
of the patient. SMBG is especially important for patients treated with insulin in
order to monitor for and prevent asymptomatic hypoglycemia and hyperglycemia. For
most patients with type 1 diabetes and pregnant women taking insulin, SMBG is recommended
three or more times daily. For these populations, significantly more frequent testing
may be required to reach A1C targets safely without hypoglycemia. The optimal frequency
and timing of SMBG for patients with type 2 diabetes on noninsulin therapy is unclear.
A meta-analysis of SMBG in non–insulin-treated patients with type 2 diabetes concluded
that some regimen of SMBG was associated with a reduction in A1C of 0.4%. However,
many of the studies in this analysis also included patient education with diet and
exercise counseling and, in some cases, pharmacologic intervention, making it difficult
to assess the contribution of SMBG alone to improved control (39). Several recent
trials have called into question the clinical utility and cost-effectiveness of routine
SMBG in non–insulin-treated patients (40
Because the accuracy of SMBG is instrument and user dependent (43), it is important
to evaluate each patient's monitoring technique, both initially and at regular intervals
thereafter. In addition, optimal use of SMBG requires proper interpretation of the
data. Patients should be taught how to use the data to adjust food intake, exercise,
or pharmacological therapy to achieve specific glycemic goals, and these skills should
be reevaluated periodically.
CGM through the measurement of interstitial glucose (which correlates well with PG)
is available. These sensors require calibration with SMBG, and the latter are still
recommended for making acute treatment decisions. CGM devices also have alarms for
hypo- and hyperglycemic excursions. Small studies in selected patients with type 1
diabetes have suggested that CGM use reduces the time spent in hypo- and hyperglycemic
ranges and may modestly improve glycemic control. A larger 26-week randomized trial
of 322 type 1 diabetic patients showed that adults age 25 years and older using intensive
insulin therapy and CGM experienced a 0.5% reduction in A1C (from ∼7.6 to 7.1%) compared
with usual intensive insulin therapy with SMBG (44). Sensor use in children, teens,
and adults to age 24 years did not result in significant A1C lowering, and there was
no significant difference in hypoglycemia in any group. Importantly, the greatest
predictor of A1C lowering in this study for all age-groups was frequency of sensor
use, which was lower in younger age-groups. In a smaller randomized controlled trial
of 129 adults and children with baseline A1C <7.0%, outcomes combining A1C and hypoglycemia
favored the group using CGM, suggesting that CGM is also beneficial for individuals
with type 1 diabetes who have already achieved excellent control with A1C <7.0% (45).
Although CGM is an evolving technology, emerging data suggest that it may offer benefit
in appropriately selected patients who are motivated to wear it most of the time.
CGM may be particularly useful in those with hypoglycemia unawareness and/or frequent
episodes of hypoglycemia, and studies in this area are ongoing.
Perform the A1C test at least two times a year in patients who are meeting treatment
goals (and who have stable glycemic control). (E)
Perform the A1C test quarterly in patients whose therapy has changed or who are not
meeting glycemic goals. (E)
Use of point-of-care testing for A1C allows for timely decisions on therapy changes,
when needed. (E)
Because A1C is thought to reflect average glycemia over several months (43) and has
strong predictive value for diabetes complications (11,46), A1C testing should be
performed routinely in all patients with diabetes, at initial assessment and then
as part of continuing care. Measurement approximately every 3 months determines whether
a patient's glycemic targets have been reached and maintained. For any individual
patient, the frequency of A1C testing should be dependent on the clinical situation,
the treatment regimen used, and the judgment of the clinician. Some patients with
stable glycemia well within target may do well with testing only twice per year, while
unstable or highly intensively managed patients (e.g., pregnant type 1 diabetic women)
may be tested more frequently than every 3 months. The availability of the A1C result
at the time that the patient is seen (point-of-care testing) has been reported to
result in increased intensification of therapy and improvement in glycemic control
The A1C test is subject to certain limitations. Conditions that affect erythrocyte
turnover (hemolysis, blood loss) and hemoglobin variants must be considered, particularly
when the A1C result does not correlate with the patient's clinical situation (43).
In addition, A1C does not provide a measure of glycemic variability or hypoglycemia.
For patients prone to glycemic variability (especially type 1 diabetic patients, or
type 2 diabetic patients with severe insulin deficiency), glycemic control is best
judged by the combination of results of SMBG testing and the A1C. The A1C may also
serve as a check on the accuracy of the patient's meter (or the patient's reported
SMBG results) and the adequacy of the SMBG testing schedule.
Table 9 contains the correlation between A1C levels and mean PG levels based on data
from the international A1C-Derived Average Glucose (ADAG) trial using frequent SMBG
and CGM in 507 adults (83% Caucasian) with type 1, type 2, and no diabetes (49). ADA
and the American Association of Clinical Chemists have determined that the correlation
(r = 0.92) is strong enough to justify reporting both an A1C result and an estimated
average glucose (eAG) result when a clinician orders the A1C test. In previous versions
of the Standards of Medical Care in Diabetes, the table describing the correlation
between A1C and mean glucose was derived from relatively sparse data (one seven-point
profile over 1 day per A1C reading) in the primarily Caucasian type 1 participants
in the DCCT (50). Clinicians should note that the numbers in the table are now different,
as they are based on ∼2,800 readings per A1C in the ADAG trial.
Correlation of A1C with average glucose
Mean plasma glucose
These estimates are based on ADAG data of ∼2,700 glucose measurements over 3 months
per A1C measurement in 507 adults with type 1, type 2, and no diabetes. The correlation
between A1C and average glucose was 0.92 (49). A calculator for converting A1C results
into estimated average glucose (eAG), in either mg/dl or mmol/l, is available at http://professional.diabetes.org/eAG.
In the ADAG trial, there were no significant differences among racial and ethnic groups
in the regression lines between A1C and mean glucose, although there was a trend toward
a difference between Africans/African Americans participants and Caucasians that might
have been significant had more Africans/African Americans been studied. A recent study
comparing A1C to CGM data in 48 type 1 diabetic children found a highly statistically
significant correlation between A1C and mean blood glucose, although the correlation
(r = 0.7) was significantly lower than in the ADAG trial (51). Whether there are significant
differences in how A1C relates to average glucose in children or in African American
patients is an area for further study. For the time being, the question has not led
to different recommendations about testing A1C or different interpretations of the
clinical meaning of given levels of A1C in those populations.
For patients in whom A1C/eAG and measured blood glucose appear discrepant, clinicians
should consider the possibilities of hemoglobinopathy or altered red cell turnover
and the options of more frequent and/or different timing of SMBG or use of CGM. Other
measures of chronic glycemia such as fructosamine are available, but their linkage
to average glucose and their prognostic significance are not as clear as is the case
2. Glycemic goals in adults
Lowering A1C to below or around 7% has been shown to reduce microvascular and neuropathic
complications of type 1 and type 2 diabetes. Therefore, for microvascular disease
prevention, the A1C goal for nonpregnant adults in general is <7%. (A)
In type 1 and type 2 diabetes, randomized controlled trials of intensive versus standard
glycemic control have not shown a significant reduction in CVD outcomes during the
randomized portion of the trials. Long-term follow-up of the DCCT and UK Prospective
Diabetes Study (UKPDS) cohorts suggests that treatment to A1C targets below or around
7% in the years soon after the diagnosis of diabetes is associated with long-term
reduction in risk of macrovascular disease. Until more evidence becomes available,
the general goal of <7% appears reasonable for many adults for macrovascular risk
Subgroup analyses of clinical trials such as the DCCT and UKPDS, and evidence for
reduced proteinuria in the Action in Diabetes and Vascular Disease: Preterax and Diamicron
Modified Release Controlled Evaluation (ADVANCE) trial suggest a small but incremental
benefit in microvascular outcomes with A1C values closer to normal. Therefore, for
selected individual patients, providers might reasonably suggest even lower A1C goals
than the general goal of <7%, if this can be achieved without significant hypoglycemia
or other adverse effects of treatment. Such patients might include those with short
duration of diabetes, long life expectancy, and no significant CVD. (B)
Conversely, less-stringent A1C goals than the general goal of <7% may be appropriate
for patients with a history of severe hypoglycemia, limited life expectancy, advanced
microvascular or macrovascular complications, and extensive comorbid conditions and
those with longstanding diabetes in whom the general goal is difficult to attain despite
diabetes self-management education, appropriate glucose monitoring, and effective
doses of multiple glucose-lowering agents including insulin. (C)
Glycemic control is fundamental to the management of diabetes. The DCCT, a prospective,
randomized, controlled trial of intensive versus standard glycemic control in patients
with relatively recently diagnosed type 1 diabetes, showed definitively that improved
glycemic control is associated with significantly decreased rates of microvascular
(retinopathy and nephropathy) as well as neuropathic complications (53). Follow-up
of the DCCT cohorts in the Epidemiology of Diabetes Interventions and Complications
(EDIC) study has shown persistence of this effect in previously intensively treated
subjects, even though their glycemic control has been equivalent to that of previous
standard arm subjects during follow-up (54,55).
In type 2 diabetes, the Kumamoto study (56) and the UKPDS (57,58) demonstrated significant
reductions in microvascular and neuropathic complications with intensive therapy.
Similar to the DCCT-EDIC findings, long-term follow-up of the UKPDS cohort has recently
demonstrated a “legacy effect” of early intensive glycemic control on long-term rates
of microvascular complications, even with loss of glycemic separation between the
intensive and standard cohorts after the end of the randomized controlled trial (59).
The more recent Veterans Affairs Diabetes Trial (VADT) in type 2 diabetes also showed
significant reductions in albuminuria with intensive (achieved median A1C 6.9%) compared
with standard glycemic control but no difference in retinopathy and neuropathy (60,61).
In each of these large randomized prospective clinical trials, treatment regimens
that reduced average A1C to 7% (1% above the upper limits of normal) were associated
with fewer markers of long-term microvascular complications; however, intensive control
was found to increase the risk of severe hypoglycemia and led to weight gain (46,60,62).
Epidemiological analyses of the DCCT and UKPDS (46,53) demonstrate a curvilinear relationship
between A1C and microvascular complications. Such analyses suggest that, on a population
level, the greatest number of complications will be averted by taking patients from
very poor control to fair or good control. These analyses also suggest that further
lowering of A1C from 7 to 6% is associated with further reduction in the risk of microvascular
complications, albeit the absolute risk reductions become much smaller. The ADVANCE
study of intensive versus standard glycemic control in type 2 diabetes found a statistically
significant reduction in albuminuria with an A1C target of <6.5% (achieved median
A1C 6.3%) compared with standard therapy achieving a median A1C of 7.0% (63). Given
the substantially increased risk of hypoglycemia (particularly in those with type
1 diabetes, but also in the recent type 2 diabetes trials described below), the concerning
mortality findings in the Action to Control Cardiovascular Risk in Diabetes (ACCORD)
trial described below and the relatively much greater effort required to achieve near-normoglycemia,
the risks of lower targets may outweigh the potential benefits on microvascular complications
on a population level. However, selected individual patients, especially those with
little comorbidity and long life expectancy (who may reap the benefits of further
lowering glycemia below 7%) may, at patient and provider judgment, adopt glycemic
targets as close to normal as possible as long as significant hypoglycemia does not
become a barrier.
Whereas many epidemiologic studies and meta-analyses (64,65) have clearly shown a
direct relationship between A1C and CVD, the potential of intensive glycemic control
to reduce CVD has been less clearly defined. In the DCCT, there was a trend toward
lower risk of CVD events with intensive control (risk reduction 41%, 95% CI 10–68%),
but the number of events was small. However, 9-year post-DCCT follow-up of the cohort
has shown that participants previously randomized to the intensive arm had a 42% reduction
(P = 0.02) in CVD outcomes and a 57% reduction (P = 0.02) in the risk of nonfatal
myocardial infarction (MI), stroke, or CVD death compared with participants previously
in the standard arm (66). The benefit of intensive glycemic control in this type 1
diabetic cohort has recently been shown to persist for up to 30 years (67).
The UKPDS trial of type 2 diabetes observed a 16% reduction in cardiovascular complications
(combined fatal or nonfatal MI and sudden death) in the intensive glycemic control
arm, although this difference was not statistically significant (P = 0.052), and there
was no suggestion of benefit on other CVD outcomes such as stroke. In an epidemiologic
analysis of the study cohort, a continuous association was observed such that for
every percentage point lower median on-study A1C (e.g., 8–7%), there was a statistically
significant 18% reduction in CVD events, again with no glycemic threshold. A recent
report of 10 years of follow-up of the UKPDS cohort described, for the participants
originally randomized to intensive glycemic control compared with those randomized
to conventional glycemic control, long-term reductions in MI (15% with sulfonylurea
or insulin as initial pharmacotherapy, 33% with metformin as initial pharmacotherapy,
both statistically significant) and in all-cause mortality (13 and 27%, respectively,
both statistically significant) (59).
Because of ongoing uncertainty regarding whether intensive glycemic control can reduce
the increased risk of CVD events in people with type 2 diabetes, several large long-term
trials were launched in the past decade to compare the effects of intensive versus
standard glycemic control on CVD outcomes in relatively high-risk participants with
established type 2 diabetes. In 2008, results of three large trials (ACCORD, ADVANCE,
and VADT) suggested no significant reduction in CVD outcomes with intensive glycemic
control in these populations. Details of these three studies are shown in Table 10,
and their results and implications are reviewed more extensively in a recent ADA position