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Capillary whole-blood samples contain a mixture of arterial and venous blood. Fasting levels are equivalent to

whole-blood venous samples.

A1C, glycosylated hemoglobin; FPG, fasting plasma glucose; OGTT, oral glucose tolerance test.

Individuals with A1C, FPG, or OGTT values that are intermediate between normal

and those considered diagnostic of diabetes are considered to have prediabetes. The

terms IFG and IGT should not be used interchangeably because each results from

somewhat different physiologic processes. It is important to interpret the categories

listed in Table 53-3 as a continuum of increased risk for diabetes, rather than focus

on the absolute cutoff points for prediabetes or diabetes.

Many factors can impair glucose tolerance or increase plasma glucose. These must

be excluded before a definitive diagnosis is made. For example, an individual who

has not fasted for a minimum of 8 hours may have an elevated FPG. Patients who are

tested for glucose tolerance during, or very soon after, an acute illness (e.g., a

myocardial infarction [MI]) or who are on corticosteroids (e.g., prednisone,

dexamethasone) may be misdiagnosed because of the presence of high concentrations

of counter-regulatory hormones that increase glucose concentrations. Glucose

tolerance often returns to normal in these individuals.

LONG-TERM COMPLICATIONS

Although acute hyperglycemic crises can occur in patients with diabetes, the longterm sequelae of diabetes account for most of the morbidity and mortality in the

diabetic population. Complications are typically designated as microvascular or

macrovascular in nature. Glucose toxicity contributes most to the development and

progression of microvascular complications (retinopathy, nephropathy, and

neuropathy) owing to the particular susceptibility of these cell systems to elevated

glucose.

22 Diabetes is the

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p. 1078

leading cause of new cases of adult blindness and kidney failure in the United States.

1

About 60% to 70% of people with diabetes also have some manifestation of

peripheral or autonomic neuropathy. Severe peripheral neuropathy coupled with

abnormalities in immune function likely contributes to the high rate of lowerextremity amputations among patients with diabetes.

1,23 Finally, poor glucose control

promotes development of dental and oral complications and increases the risk of

complications during pregnancy for both mother and fetus.

24,25 Macrovascular

complications are multifactorial in their etiology and less dependent on

hyperglycemia. Diabetes mellitus itself is a well-known risk factor for

macrovascular disease (peripheral vascular disease, CVD, stroke). Patients with

diabetes have a threefold-to-fourfold elevated risk for MI and cardiovascular death

compared with nondiabetic subjects.

26

Insulin resistance and the resultant

hyperinsulinemia in Type 2 diabetes mellitus contribute to the development of

hypertension, dyslipidemia, and platelet hypersensitivity, all of which then contribute

to the increased CVD risk in patients with diabetes.

27 Thus, although tight glycemic

control (A1C <7.0%) will dramatically reduce the risk for microvascular disease, its

relationship to macrovascular disease is still under intense debate.

RELATIONSHIP OF GLYCEMIC CONTROL TO

MICROVASCULAR AND MACROVASCULAR

DISEASE

Although epidemiologic studies have shown a general relationship between glucose

control and cardiovascular events, recent randomized trials have failed to confirm a

benefit of tight glucose control compared with standard control, which highlights the

multifactorial nature of macrovascular disease.

28 However, the clear relationship

between microvascular events and glycemic control is well established from

randomized, clinical trials. The Diabetes Control and Complications Trial (DCCT),

and the open-label follow-up trial, DCCT-EDIC (Epidemiology of Diabetes

Interventions and Complications), established the benefits of intensive glycemic

control on microvascular end points.

29,30

In the DCCT, intensive treatment (A1C

7.1% vs. 9.0%) reduced the risk of clinically meaningful retinopathy, nephropathy,

and neuropathy by approximately 60%. The EDIC study was followed as an openlabel extension of the DCCT cohorts. Patients originally assigned to the intensive

treatment group were shown to have a persistently lower incidence of microvascular

complications even after the glucose control reached parity between the two study

groups after the end of the randomized portion of the trial.

30,31 The EDIC study also

showed a significant reduction in cardiovascular complications among patients

previously assigned to the intensive therapy DCCT arm.

32 See Table 53-4 for the

glycemic goals of intensive insulin therapy (herein called physiologic or basal-bolus

therapy). This persistence of the microvascular benefits of glycemic control has also

been demonstrated in patients with Type 2 diabetes in the United Kingdom

Prospective Diabetes Study (UKPDS) (see Case 53-11, Question 2).

33

The relationship between glycemic control and macrovascular disease has always

been less clear. Evidence of early atherosclerosis in patients with Type 1 diabetes in

whom dyslipidemia and hypertension are typically absent argues strongly for a role

of hyperglycemia itself in the development or progression of macrovascular

disease.

34 The UKPDS trial was the first to report the benefit of tight BG control on

cardiovascular complications in Type 2 diabetes.

35 Although the microvascular

benefits were clear, the 21% relative risk reduction for fatal and nonfatal MI and

sudden cardiac death failed to reach statistical significance (p = 0.052). However, in

a planned 10-year follow-up of patients enrolled in the trial, a significant 15%

reduction was seen in the risk of MI (p = 0.01).

33 A similar finding for macrovascular

benefit was reported in a 17-year follow-up of the DCCT-EDIC study.

32 Thus,

although glycemic control benefited macrovascular disease, it took more than a

decade to see the benefit. Reducing macrovascular risk in patients with diabetes thus

takes a more comprehensive approach than just glycemic control. In a trial of

multiple risk factor control in Type 2 diabetes, the STENO-2 trial found a significant

53% reduction in macrovascular events with modest control of hypertension,

dyslipidemia, and glycemia simultaneously.

36 Control of all major CVD risk factors

is highlighted by the ADA for its importance in reducing macrovascular disease

risk.

37 See Table 53-5 for the metabolic goals for adults with diabetes.

38,39

Table 53-4

Goals of Physiologic (Basal-Bolus) Insulin Therapy

Monitoring Parameter

Adults

(mg/dL)

School Age (6–

12 years)

(mg/dL)

Adolescents and Young

Adults (13–29 years)

(mg/dL)

Pregnancy

(mg/dL)

Premeals 80–130 90–130 90–130 60–99

2-hour postprandial plasma

glucose

<180 Not routinely

recommended

Not routinely

recommended

100–129

Bedtime/overnight (2–4

AM) plasma glucose

>70 90–150 90–150 60–99

A1C

a <7.0%b <7.5%c <7.5%c <6%

Urine ketones

d Absent to

rare

Absent to rare Absent to rare Rare

See Case 53-2, Question 2, and Case 53-4, Question 2, for discussion. Basal-bolus insulin therapy is a complete

therapeutic program of diabetes management and requires a team approach.

aA1C, glycosylated hemoglobin, referenced to a nondiabetic range of 4% to 6% using a Diabetes Control and

Complications Trial (DCCT)-based assay.

bAcceptable values should be individualized to levels that are attainable without creating undue risk for

hypoglycemia. These results are similar to the results achieved in the DCCT trial. The American Diabetes

Association recommends consideration for a lower goal (e.g., <6%) in individuals with a short duration of diabetes,

long life expectancy, and no significant cardiovascular disease. Less stringent goals may be appropriate for patients

with hypoglycemic unawareness, history of severe hypoglycemia, counter-regulatory insufficiency, advanced

microvascular or macrovascular complications, or other complicating features (Table 53-10).

cA lower goal (<7%) is reasonable if it can be achieved without creating excessive risk for hypoglycemia.

dDoes not apply to type 2 diabetes patients.

Modified and extrapolated from American Diabetes Association. Standards of medical care in diabetes—2015.

Diabetes Care. 2015;38(Suppl 1):S5; American Diabetes Association. Preconception care of women with diabetes.

Diabetes Care. 2004;27(Suppl 1):S76; Kitzmiller JL et al. Managing preexisting diabetes for pregnancy: summary

of evidence and consensus recommendations for care. Diabetes Care. 2008;31:1060; The Diabetes Control and

Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and

progression of long-term complications in insulin-dependent diabetes mellitus. N EnglJ Med. 1993;329:977.

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p. 1079

Three trials published in 2008 and 2009 have raised new questions about tight

glycemic control in patients with Type 2 diabetes. In the Action to Control

Cardiovascular Risk in Diabetes (ACCORD) trial, a higher rate of mortality was

seen in the intensive treatment arm, which achieved an A1C of 6.4% compared with

the standard arm, which achieved 7.5%.

40 The ACCORD study was a National Heart,

Lung, and Blood Institute study of more than 10,000 patients with Type 2 diabetes

with known heart disease or multiple cardiovascular risk factors. The intensively

treated group had an excess of 3 deaths per 1,000 participants per year compared

with the standard group during an average of 4 years on treatment (257 vs. 203

deaths). The higher mortality rate was not attributable to a specific drug therapy or to

severe hypoglycemia.

41 A second trial, the Action in Diabetes and Vascular Disease

a Controlled Evaluation (ADVANCE), was an even larger study of more than 11,000

patients, which had different findings from ACCORD. In ADVANCE, there was an

insignificant trend for reduced cardiovascular mortality and reduced overall

mortality with tight glycemic control (A1C of 6.3% compared with 7.0%).

42 Lastly,

in the smaller Veterans Affairs Diabetes Trial (VADT), nearly 2,000 patients were

studied and found to have an insignificant 12% relative risk reduction in

macrovascular end points but a 7% relative increase in overall mortality (95 vs. 102

deaths). Neither finding was statistically significant.

43 After approximately 10-year

follow-up to the VADT trial, the study found 1 fewer cardiovascular event/116

person-years without a reduction in mortality. The intensive arm of this study had a

mean A1C of 6.9%, not <6.5%.

44

In the face of these new data, the ADA, along with the American Heart Association

(AHA) and the American College of Cardiology (ACC), issued a position statement

in 2009.

45 Although acknowledging the findings of the ACCORD trial, the persistent

trend for reductions in macrovascular events in all three trials was found to be

reassuring. The position of the committee (which continues to be the official position

of the ADA in the 2015 guidelines) is that although intensive glycemic control did not

improve macrovascular outcomes, a goal of less than 7% is still reasonable based on

microvascular benefits and a clear lack of harm across the trials of intensive versus

standard glycemic control.

38 However, the ADA does acknowledge that there is room

to individualize the A1C goal and that achieving an A1C of less than 7% has limited

macrovascular benefit compared with A1C values of 7% to 8%. Patients with Type 2

diabetes and CVD or multiple risk factors for CVD should discuss their treatment

goals with their providers. In these patients, a less intensive goal may be appropriate,

particularly for patients who have difficulty achieving the goal of less than 7%.

38

Table 53-5

American Diabetes Association Metabolic Goals for Adults with Diabetes

Mellitus

7

Glycemic goals

A1C <7.0% (normal, 4%–6%)

a

Preprandial plasma glucose 80–130 mg/dL (3.9–7.2 mmol/L)

b

Postprandial plasma glucose <180 mg/dL (<10.0 mmol/L)

c

Blood pressure <140/90 mm Hg (Refer to Essential Hypertension

Chapter 11)

Lipids Refer to Lipid Chapter 8

Goals must be individualized to the patient. See Case 53-2, Question 2, Case 53-14, Question 2, and Case 53-24,

Questions 1–4, for broader discussion.

7

aMore stringent goals (i.e., <6%) can be considered for select individuals. American Association of Clinical

Endocrinologists/American College of Endocrinology recommends A1C goal of ≤6.5%.

39

bAmerican Association of Clinical Endocrinologists recommends a fasting blood glucose goal of <110 mg/dL (6.1

mmol/L).

39

cAmerican Association of Clinical Endocrinologists/American College of Endocrinology recommends goal of <140

mg/L (7.8 mmol/L).

39

A1C, glycosylated hemoglobin.

PREVENTION OF TYPE 1 AND TYPE 2 DIABETES

MELLITUS

Because the clinical symptoms of Type 1 diabetes mellitus are the overt expression

of an insidious pathogenic process that begins years earlier, investigators are

focusing attention on strategies that alter the natural history of the disease (Fig. 53-1).

First-degree relatives of individuals with Type 1 diabetes mellitus have an increased

risk for developing the diabetes and can be identified by the presence of immune

markers that may herald the disease by many years.

11 This has led to attempts at

immune intervention at the prediabetes stage (primary prevention) or after the

development of islet antibodies (secondary prevention). Most immunotherapy trials

are tertiary prevention after diagnosis of Type 1 diabetes. Results have not been

extraordinary, but will areas of future study. For primary prevention, vaccines, and

secondary prevention, immunomodulatory agents will continue to be an area of

research.

46 The Diabetes Prevention Program Research Group studied a diverse

group of 3,234 individuals at high risk for developing diabetes to determine whether

lifestyle interventions or metformin (850 mg by mouth [PO] twice a day [BID])

would prevent or delay the onset of Type 2 diabetes.

47 After 3 years, the incidence of

diabetes was reduced by 58% and 31% in the intensive lifestyle and metformin

groups, respectively, compared with the control group. Diabetes incidence during 10

years of follow-up was persistently lower in the groups originally treated with

lifestyle (34% reduction) and metformin (18% reduction) interventions compared

with the control group.

48 Other studies have confirmed the value of lifestyle

intervention and other drugs (acarbose, orlistat, and various thiazolidinediones

(TZDs)) in the prevention of Type 2 diabetes, but the strongest evidence is with

metformin.

49 Lifelong medication therapy, however, is not without its own risks and

complications. Current recommendations regarding the treatment for individuals with

prediabetes include lifestyle modification (5%–10% weight loss and 150

minutes/week of moderately intense physical activity).

50 Metformin, although less

effective than lifestyle changes, can be considered for very high-risk individuals.

49

CASE 53-1

QUESTION 1: R.P. is a 43-year-old African-American woman visiting a primary-care clinic to obtain a

routine physical examination for her new job. Her past medical history is significant for GDM. She was told

during her two pregnancies (last child born 3 years ago) that she had “borderline diabetes,” which resolved each

time after giving birth. Her family history is significant for Type 2 diabetes (mother, maternal grandmother, older

first cousin), hypertension, and CVD. She denies tobacco or alcohol use. She states that she tries to walk 15

minutes twice a week. Physical examination is significant for moderate central obesity (5 feet 4 inches; 160

pounds; BMI, 30.2 kg/m

2

) and blood pressure (BP) 145/85 mm Hg. R.P. denies any symptoms of polyphagia,

polyuria, or lethargy. On checking her electronic medical record, she has documented hypertension and an FPG

value of 119 mg/dL, measured 2 months prior. What features of R.P.’s history and examination are consistent

with an increased risk of developing Type 2 diabetes?

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p. 1080

The features of R.P.’s history that are consistent with an increased risk of

developing Type 2 diabetes include her age, ethnicity, weight, family history of

diabetes, history of GDM, and a documented IFG. In addition, Type 2 diabetes is

also often associated with other disorders such as hypertension. The fact that R.P. has

hypertension that is not well controlled and has a family history of hypertension and

CVD may indicate that she is predisposed to insulin resistance, further putting her at

risk for developing Type 2 diabetes.

CASE 53-1, QUESTION 2: The physician orders an A1C for R.P., which comes back at 6.1%. How should

R.P. be managed at this time?

Both the A1C and FPG values are in the prediabetes range. R.P. should be

educated about her risk for developing Type 2 diabetes. Working with her healthcare

providers, R.P. should be encouraged and educated on how to institute lifestyle

modifications (MNT, physical activity) that will help her to lose weight, improve her

cardiovascular health, and decrease her risk for developing Type 2 diabetes. A

weight-loss goal of 5% to 10% during the next 6 to 12 months should be

recommended, and she should increase her level of moderate physical activity to at

least 150 minutes/week. Her hypertension should be managed. At this time, the use of

pharmacologic agents (i.e., metformin) to prevent the development of Type 2

diabetes is not recommended.

TREATMENT

There are three major components to the treatment of diabetes: diet, drugs (insulin

and antidiabetic agents [oral and injectable]), and exercise. Each of these

components interacts with the others to the extent that no assessment and modification

of one can be made without knowledge of the other two.

Medical Nutrition Therapy

PRINCIPLES

MNT plays a crucial role in the therapy of all individuals with diabetes.

50,51

Unfortunately, patient acceptance and adherence to diet and meal planning are often

poor, but revised evidence-based recommendations that are more flexible than

previous approaches offer new opportunities to increase the effectiveness of nutrition

therapy.

Nutrition therapy is designed to help patients achieve appropriate metabolic and

physiologic goals (e.g., glucose, lipids, BP, proteinuria, weight), select healthy

foods, and take into consideration personal and cultural preferences. Appropriate

levels and types of physical activity to achieve a healthier status are incorporated

into the nutrition plan.

NUTRITION THERAPY AND TYPE 1 DIABETES MELLITUS

For patients with Type 1 diabetes taking fixed doses of insulin, a meal plan is

designed to provide adequate carbohydrates timed to match the peak action of

exogenously administered mealtime insulin. Regularly scheduled meals and snacks

should contain consistent carbohydrate amounts, which are required to prevent

hypoglycemic reactions. Fortunately, newer insulins and insulin regimens provide

much more flexibility in the amount and timing of food intake. Patients who are taught

to count carbohydrates can inject rapid- or short-acting insulin doses designed to

match their anticipated intake. Integration of food intake, physical activity, and

insulin dose is critical and discussed extensively in the cases that follow.

NUTRITION THERAPY AND TYPE 2 DIABETES MELLITUS

For patients with Type 2 diabetes, meal plans emphasize normalizing plasma glucose

and lipid levels as well as maintaining a normal BP to prevent or mitigate

cardiovascular morbidity. Although weight loss reduces insulin resistance and

improves glycemic control, traditional dietary strategies incorporating hypocaloric

diets have not been effective in achieving long-term weight loss. A sustainable

weight loss can be achieved within structured programs that emphasize lifestyle

changes, physical activity, and food intake that modestly reduces caloric and fat

intake.

50,51

SPECIFIC NUTRITION COMPONENTS

MNT is an integral and critical component of diabetes care. For a more extensive

discussion of the principles underlying nutrition therapy, the reader is directed to

other sources.

51–53 A few key principles are briefly noted below because they are

common sources of misunderstanding.

Carbohydrates and Artificial Sweeteners

Carbohydrates include sugar (sucrose), starch, and fiber and are liberally

incorporated into the diet of a person with diabetes. In fact, the amount of dietary

carbohydrate is the main determinant of insulin demand and is commonly used to

determine the premeal insulin dose. Furthermore, patients using fixed doses of insulin

or antihyperglycemic medications (e.g., sulfonylureas) must eat meals containing

consistent amounts of carbohydrate to avoid hypoglycemia. Because isocaloric

amounts of sucrose and starch produce the same degree of glycemia, sucrose can be

substituted for a portion of the total carbohydrate intake and should be incorporated

into an otherwise healthful diet.

Whole grains, fruits, and vegetables high in fiber are recommended for people

with diabetes, because they are for the general population. There is no evidence that

larger amounts produce a differential metabolic benefit with regard to plasma

glucose and lipid levels. Nonnutritive sweeteners (saccharin, aspartame, neotame,

acesulfame potassium, sucralose) and sugar alcohols have been rigorously tested by

the US Food and Drug Administration (FDA) for safety in people with diabetes and

are safe at approved daily intakes. Fructose and the reduced-calorie sweeteners

called sugar alcohols produce lower postprandial glucose responses than sucrose,

glucose, and starch. When sugar alcohols (e.g., sorbitol, mannitol, lactitol, xylitol,

and maltitol) are consumed, it is recommended to subtract half of their grams from

the total carbohydrate amount because their effect on BG is less. Patients should be

advised that when these sweeteners are used in foods labeled “dietetic” or “sugar

free,” they still add to the carbohydrate content and provide substantial calories (2

cal/g). Furthermore, excessive intake of sorbitol-sweetened foods (e.g., 30–50 g/day)

can induce an osmotic diarrhea, and excessive amounts of fructose can increase total

and LDL cholesterol (LDL-C).

Counting Carbohydrates

When patients are taught to estimate the grams of carbohydrate in a meal, they are

given the following guideline: One carbohydrate serving = 1 starch or 1 fruit or 1 cup

milk = 15 g carbohydrate. Patients vary with regard to their insulin-to-carbohydrate

ratio throughout time and throughout the day; however, a typical starting point is 1

unit/15 g carbohydrate.

Fat

CVD is a major cause of morbidity and mortality in patients with diabetes.

Therefore, saturated fats should be limited to less than 7% of calories. The intake of

trans fat should also be minimized. The recommended cholesterol intake is less than

200 mg/day for patients with diabetes. Two or more servings/week of fish to provide

n-3 polyunsaturated fatty acids and omega-3 fatty acids are advised.

50,51

p. 1080

p. 1081

Protein

Data are insufficient to support special dietary protein recommendations for persons

with diabetes if kidney function is normal. Generally, 15% to 20% of the daily

caloric intake comes from animal and vegetable protein sources in the US diet. This

amount may be liberalized in pregnant and lactating women or in elderly people.

With the onset of nephropathy, a lower protein intake of 0.8 to 1.0 g/kg/day is

considered sufficiently restrictive. For patients in later stages of nephropathy,

reduction of protein intake to 0.8 g/kg/day is recommended. High-protein diets are

not recommended as a long-term method for weight loss, because the effects on

kidney function are not known.

50,51

Sodium

The ADA recommends a reduced sodium intake of less than 2,300 mg/day in

normotensive and hypertensive individuals. For patients with diabetes and

symptomatic heart failure (HF), sodium should be further restricted to less than 2,000

mg/day to help reduce symptoms. For all other patients, the ADA has no particular

restrictions on sodium intake, but recommends individualizing amounts based on the

patient’s sensitivity to salt and concurrent conditions such as hypertension or

nephropathy.

50,51

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