Nutrition Recommendations and Interventions for Diabetes-2008 American Diabetes Association Diabetes Care 2008 31 Suppl 1 S61 S78 10.2337/dc08-S061 18165339

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DOI: 10.2337/dc08-S061 · Source: PubMed
Evidence-Based Nutrition Principles and
Recommendations for the Treatment and
Prevention of Diabetes and Related
Complications
MARION J. FRANZ,
RD
,
CDE
,
C
O
-C
HAIR
1
JOHN P. BANTLE,
MD
,
C
O
-C
HAIR
2
CHRISTINE A. BEEBE,
RD
,
CDE
3
JOHN D. BRUNZELL,
MD
4
JEAN-LOUIS CHIASSON,
MD
5
ABHIMANYU GARG,
MD
6
LEA ANN HOLZMEISTER,
RD
,
CDE
7
BYRON HOOGWERF,
MD
8
ELIZABETH MAYER-DAVIS,
P
H
D
,
RD
9
ARSHAG D. MOORADIAN,
MD
10
JONATHAN Q. PURNELL,
MD
11
MADELYN WHEELER,
RD
,
CDE
12
H
istorically, nutrition principles and
recommendations for diabetes and
related complications have been
based on scientific evidence and diabetes
knowledge when available and, when ev-
idence was not available, on clinical expe-
rience and expert consensus. Often it has
been difficult to discern the level of evi-
dence used to construct the nutrition
principles and recommendations. Fur-
thermore, in clinical practice, many nutri-
tion recommendations that have no
scientific supporting evidence have been
and are still being given to individuals
with diabetes. To address these problems
and to incorporate the research done in
the past 8 years, this 2002 technical re-
view provides principles and recommen-
dations classified according to the level of
evidence available. It reviews the evi-
dence from randomized, controlled trials;
cohort and case-controlled studies; and
observational studies, which can also pro-
vide valuable evidence (1,2), and takes
into account the number of studies that
have provided consistent outcomes of
support. In this review, nutrition princi-
ples are graded into four categories based
on the available evidence: those with
strong supporting evidence, those with
some supporting evidence, those with
limited supporting evidence and those
based on expert consensus.
Evidence-based nutrition recommen-
dations attempt to translate research data
and clinically applicable evidence into
nutrition care. However, the best avail-
able evidence must still be moderated by
individual circumstances and prefer-
ences. The goal of evidence-based recom-
mendations is to improve the quality of
clinical judgments and facilitate cost-
effective care by increasing the awareness
of clinicians and patients with diabetes of
the evidence supporting nutrition ser-
vices and the strength of that evidence,
both in quality and quantity.
Before 1994, the American Diabetes
Association’s (ADA’s) nutrition principles
and recommendations attempted to de-
fine an “ideal” nutrition prescription that
would apply to everyone with diabetes
(3–5). Although individualization was a
major principle of all recommendations,
it was usually done within defined limits
for recommended energy intake and ma-
cronutrient composition. The 1994 nutri-
tion recommendations shifted this focus
to one that emphasized effects of nutrition
therapy on metabolic control (6,7). The
nutrition prescription is determined con-
sidering treatment goals and lifestyle
changes the diabetic patient is willing and
able to make, rather than predetermined
energy levels and percentages of carbohy-
drate, protein, and fat. The goal of nutri-
tion intervention is to assist and facilitate
individual lifestyle and behavior changes
that will lead to improved metabolic con-
trol. This focus continues with the 2002
nutrition principles and recommenda-
tions.
Medical nutrition therapy (MNT) is
an integral component of diabetes man-
agement (8,9) and diabetes self-
management education (10). (Medical
nutrition therapy is the preferred term
and should replace other terms, such as
diet, diet therapy, and dietary manage-
ment.) MNT for diabetes includes the
process and the system by which nutri-
tion care is provided for diabetic individ-
uals and the specific lifestyle recommen-
dations for that care. However, recom-
mendations should not only be based on
scientific evidence but should also take
into consideration lifestyle changes the
●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●
From
1
Nutrition Concepts by Franz, Inc., Minneapolis, Minnesota;
2
Division of Endocrinology and Diabetes,
Department of Medicine, University of Minnesota, Minneapolis, Minnesota;
3
University of Illinois, Chicago,
Illinois;
4
Department of Medicine, University of Washington, Seattle, Washington;
5
Research Center, Centre
Hospitalier de l’Universite´ de Montre´al, Campus Ho¯tel-Dieu and Department of Medicine, University of
Montreal, Montreal, Ontario, Canada;
6
Department of Internal Medicine and Center for Human Nutrition,
University of Texas Southwestern Medical Center, Dallas, Texas;
7
Holzmeister Nutrition Consulting, Tempe,
Arizona;
8
Department of Endocrinology, Cleveland Clinic Foundation, Cleveland, Ohio;
9
Department of
Epidemiology and Biostatistics, School of Public Health, University of South Carolina, Columbia, South
Carolina;
10
Division of Endocrinology, St. Louis University Medical Center, St. Louis, Missouri;
11
Division
of Endocrinology, Diabetes, and Clinical Nutrition, Oregon Health and Science University, Portland, Ore-
gon; and
12
Diabetes Research and Training Center, Indiana University School of Medicine, Indianapolis,
Indiana.
Address correspondence and reprint requests to Marion J. Franz, MS, RD, CDE, Nutrition Concepts by
Franz, Inc., 6635 Limerick Dr., Minneapolis, MN 55439. E-mail: marionfranz@aol.com.
This paper was peer-reviewed, modified, and approved by the Professional Practice Committee, October
2001.
Abbreviations: ADA, American Diabetes Association; ADI, acceptable daily intake; DASH, Dietary Ap-
proaches to Stop Hypertension; DCCT, Diabetes Control and Complications Trial; DPP, Diabetes Prevention
Program; DRI, Dietary Reference Intake; FDA, U.S. Food and Drug Administration; FPG, fasting plasma
glucose; GFR, glomerular filtration rate; GRAS, Generally Recognized as Safe; MNT, medical nutrition
therapy; NCEP, National Cholesterol Education Program; NHANES, National Health and Nutrition Exam-
ination Survey; RD, registered dietitian; RDA, recommended dietary allowance; UKPDS, U.K. Prospective
Diabetes Study; VLCD, very-low-calorie diet.
A table elsewhere in this issue shows conventional and Syste`me International (SI) units and conversion
factors for many substances.
Reviews/Commentaries/Position Statements
TECHNICAL REVIEW
148 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002
individual can make and maintain. Cul-
tural and ethnic preferences should be
taken into account, and the person with
diabetes should be involved in the deci-
sion-making process.
Results from the Diabetes Control
and Complications Trial (DCCT) and the
U.K. Prospective Diabetes Study (UK-
PDS) convincingly demonstrated the im-
portance of glycemic control in
preventing the microvascular complica-
tions of diabetes (11,12). In both trials,
MNT was important in achieving treat-
ment goals (13,14). MNT in diabetes ad-
dresses not only glycemic control but
other aspects of metabolic status as well,
including dyslipidemia and hyperten-
sionmajor risk factors for cardiovascu-
lar disease. This is important, as
macrovascular complications are the ma-
jor contributors to the morbidity and
mortality associated with diabetes (15).
The current nutrition principles and
recommendations for diabetes focus on
lifestyle goals and strategies for the treat-
ment of diabetes. Now, for the rst time,
the 2002 recommendations specically
address lifestyle approaches to diabetes
prevention; they distinguish MNT for
treating and managing diabetes from
MNT for preventing or delaying the onset
of diabetes, as the two may not necessarily
be the same.
Whether for management or preven-
tion of diabetes and its complications, ba-
sic to the nutrition recommendations is
the underlying concern for optimal nutri-
tion through healthy food choices and an
active lifestyle. The ADA supports and in-
corporates the nutrition recommenda-
tions from major organizations, such as
the U.S. Department of Agriculture (Di-
etary Guidelines for Americans) (16),
American Heart Association (17), Na-
tional Cholesterol Education Program
(18), American Institute for Cancer Re-
search (19), and Joint National Commit-
tee on Prevention, Detection, Evaluation,
and Treatment of High Blood Pressure
(20).
Although many studies have focused
on the role of single nutrients, food, or
food groups in disease prevention or pro-
motion, emerging research suggests there
are health benets from food patterns that
include mixtures of food containing mul-
tiple nutrients and nonnutrients (2127).
Although this approach makes it difcult
to elucidate mechanisms through which
the diet composition affects a particular
health outcome, it does represent a prac-
tical approach to making realistic nutri-
tion recommendations for improving
health.
The health professional with the
greatest expertise in providing MNT for
diabetes is the registered dietitian (RD)
knowledgeable and skilled in diabetes
management (810,28). Outcome stud-
ies (13,2934) have demonstrated that
MNT provided by RDs results in a 1.0%
decrease in HbA
1c
in patients with newly
diagnosed type 1 diabetes (29), a 2.0%
decrease in HbA
1c
in patients with newly
diagnosed type 2 diabetes (14), and a
1.0% decrease in HbA
1c
in patients with
an average 4-year duration of type 2 dia-
betes (30). The effectiveness of dietitian-
delivered MNT in improving
dyslipidemia has also been demonstrated
(3541). However, it is essential that all
team members involved in diabetes treat-
ment and management be knowledgeable
about MNT and supportive of the pa-
tients need to make lifestyle changes (42
45).
GOALS OF MEDICAL
NUTRITION THERAPY FOR
DIABETES Goals of MNT that ap-
ply to all persons with diabetes are as fol-
lows:
1. To attain and maintain optimal meta-
bolic outcomes, including
a. blood glucose levels in the normal
range or as close to normal as is
safely possible to prevent or reduce
the risk for complications of diabe-
tes
b. a lipid and lipoprotein prole that
reduces the risk for macrovascular
disease
c. blood pressure levels that reduce
the risk for vascular disease
2. To prevent and treat the chronic com-
plications of diabetes; modify nutrient
intake and lifestyle as appropriate for
prevention and treatment of obesity,
dyslipidemia, cardiovascular disease,
hypertension, and nephropathy
3. To improve health through healthy
food choices and physical activity
4. To address individual nutritional
needs, taking into consideration per-
sonal and cultural preferences and life-
style while respecting the individuals
wishes and willingness to change
The goals of MNT that apply to spe-
cic situations include the following:
1. For youth with type 1 diabetes, to pro-
vide adequate energy to ensure normal
growth and development, and to inte-
grate insulin regimens into usual eat-
ing and physical activity habits
2. For youth with type 2 diabetes, to fa-
cilitate changes in eating and physical
activity habits that reduce insulin re-
sistance and improve metabolic status
3. For pregnant or lactating women, to
provide adequate energy and nutrients
needed for optimal outcomes
4. For older adults, to provide for the nu-
tritional and psychosocial needs of an
aging individual
5. For individuals being treated with in-
sulin or insulin secretagogues, to pro-
vide self-management education for
treatment (and prevention) of hypo-
glycemia, acute illnesses, and exercise-
related blood glucose problems
6. For individuals at risk for diabetes, to
decrease the risk by encouraging phys-
ical activity and promoting food
choices that facilitate moderate weight
loss or at least prevent weight gain
The next sections of this technical review
paper focus on MNT for the management
of diabetes. The rst section includes nu-
trition recommendations for type 1 and
type 2 diabetesintake of carbohydrate,
sweeteners, protein, fat, micronutrients,
and alcohol; energy balance and obesity;
and special considerations. The second
section reviews MNT for special popula-
tionschildren and adolescents, preg-
nant and lactating women, and older
adults. The third section reviews MNT for
acute complicationshypoglycemia and
acute illnessand comorbid condi-
tionshypertension, dyslipidemia, ne-
phropathy, and catabolic illness. The last
section reviews lifestyle recommenda-
tions for the prevention or delay of diabe-
tes.
MEDICAL NUTRITION
THERAPY FOR TYPE 1 AND
TYPE 2 DIABETES
Carbohydrate and diabetes
When referring to common food carbo-
hydrates, the following terms are pre-
ferred: sugars, starch, and ber (Table 1).
This classication is based on the recom-
mendations of the Food and Agriculture
Franz and Associates
DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002 149
Organization of the United Nations and
the World Health Organization in which
carbohydrates are classied according to
their degree of polymerization and are ini-
tially divided into three principal
groupssugars, oligosaccharides, and
polysaccharides (46). Terms such as sim-
ple sugars, complex carbohydrates, and
fast-acting carbohydrates are not well de-
ned; use of these terms should be aban-
doned.
A number of factors inuence glyce-
mic response to food, including the
amount of carbohydrate (47), type of
sugar (glucose, fructose, sucrose, lactose)
(48), nature of the starch (amylose, amy-
lopectin, resistant starch) (49), cooking
and food processing (degree of starch ge-
latinization, particle size, cellular form)
(50), and food structure (51), as well as
other food components (fat and natural
substances that slow digestionlectins,
phytates, tannins, and starch-protein and
starch-lipid combinations) (52). Fasting
and preprandial glucose concentrations
(5356), the severity of glucose intoler-
ance (57), and the second meal or lente
effect (58) are other factors affecting the
glycemic response to food.
Carbohydrate and type 1 diabetes
In trying to establish nutrition recom-
mendations for the prescription of carbo-
hydrate for patients with type 1 diabetes,
there are several problems: the paucity of
studies, the small number of subjects
studied, and the lack of long-term studies.
Although several studies in subjects with
type 1 diabetes have been done compar-
ing differing amounts or percentages of
calories from carbohydrate (59 61),
there is no body of evidence to suggest
changing the 1994 recommendation that
6070% of total energy be distributed be-
tween carbohydrate and monounsatu-
rated fat based on nutrition assessment
and treatment goals (6). A basis for choos-
ing between carbohydrate and monoun-
saturated fat, other than ethnic or cultural
preferences, is not readily available. In
some studies (59,60), a high-carbohy-
drate diet compared to a highmono-
unsaturated fat diet resulted in a higher
glycemic prole, with no differences in
the lipid prole; however, insulin may not
have been adjusted appropriately to cover
the amount of carbohydrate ingested. In
another study (61) comparing a high-
carbohydrate diet to a highmonoun-
saturated fat diet, there were no
differences in glycemia, but there was an
increase in postprandial triglycerides with
the highmonounsaturated fat diet.
More information is available regard-
ing the effects of different types of carbo-
hydrate on postprandial glycemia. In type
1 patients with diabetes, the ingestion of a
variety of starches or sucrose, both
acutely (6268) and for up to 6 weeks
(6972), was shown to produce no sig-
nicant differences in glycemic response
if the total amount of carbohydrate is sim-
ilar. Studies in controlled settings (62
69) and in free-living subjects (70 72)
have demonstrated similar results.
Studies show a strong relationship
between the premeal insulin dosage and
the postprandial response to the carbohy-
drate content of the meal (7376). In in-
dividuals receiving intensive insulin
therapy, the total amount of carbohydrate
in the meal did not inuence glycemic
response if the premeal insulin was ad-
justed for the carbohydrate content of the
meal (73). The premeal insulin dosage re-
quired was not affected by the glycemic
index, ber, fat, or caloric content of the
meal. Furthermore, wide variations in
meal carbohydrate content did not mod-
ify the basal (long-acting) insulin require-
ment. The concept of total meal
carbohydrate determining the premeal
insulin dosage is further supported by the
DCCT, in which it was shown that indi-
viduals who adjusted their premeal insu-
lin dosages based on the carbohydrate
content of meals had 0.5% (P 0.03)
lower HbA
1c
levels than those who did
not adjust premeal insulin (13).
For individuals receiving xed dos-
ages of short- and intermediate-acting in-
sulin, day-to-day consistency in the
amount and source of carbohydrate has
been associated with lower HbA
1c
levels
(77). Day-to-day variations in energy and
protein or fat intakes were not signi-
cantly related to HbA
1c
.
Glycemic index. The usefulness of
lowglycemic index diets in individuals
with type 1 diabetes is controversial. Five
studies (n 48; range 12 days to 6 weeks)
(78 82) have compared lowglycemic
index diets to highglycemic index diets
for longer than 1 day. The results from
these studies did not provide convincing
evidence of benet. Four studies (78,80
82) measured HbA
1c
, and none reported
differences in HbA
1c
between low and
highglycemic index diets. Four studies
(78 81) measured glycated albumin or
Table 1 —Carbohydrate classification and terminology
Major dietary carbohydrate classes based on
degree of polymerization and subgroups Components
U.S. food labeling
designation
Sugars* (12 molecules)
Monosaccharides Glucose, galactose, fructose Sugars
Disaccharides Sucrose, lactose Sugars
Polyols (sugar alcohols) Sorbitol, mannitol, xylitol, isomalt, malitol, lactitol,
hydrogenated starch hydrolysates
Sugar alcohol
Oligosaccharides (39 molecules)
Malto-oligosaccharides Maltodextrins Other carbohydrate
Other oligosaccharides Rafnose, stachyose, fructo-oligosaccharides Other carbohydrate
Polysaccharides (9 molecules)
Starch* Amylose, amylopectin, modied starches Other carbohydrate
Fiber* (non-starch polysaccharides) Cellulose, hemicellulose, pectins, hydrocolloids Dietary ber
All U.S. food labeling designations are in total grams of carbohydrate. *Preferred terminology. Adapted from World Health Organization and Food and Agriculture
Organization of the United Nations: Carbohydrates in Human Nutrition. Food and Agriculture Organization of the United Nations, Rome, 1998.
Technical Review
150 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002
fructosamine; three of those (7880) re-
ported decreases in glycated albumin or
serum fructosamine after the incorpora-
tion of lowglycemic index food in the
diet, and one reported no differences in
serum fructosamine (81). Three studies
(78 80) measured fasting plasma glu-
cose (FPG) concentrations, and none re-
ported differences in FPG between low
and highglycemic index diets. Insulin
requirements were measured in four
studies (7982); one (79) reported lower
insulin requirements from low com-
pared to highglycemic index diets,
whereas three (80 82) reported no dif-
ferences in insulin dosages. Therefore, al-
though the use of lowglycemic index
food may reduce postprandial glucose
levels, there is not sufcient evidence of
long-term benet to recommend general
use of lowglycemic index diets in indi-
viduals with type 1 diabetes.
In a cross-sectional study of 2,810
people with type 1 diabetes from the EU-
RODIAB IDDM Complications Study
(83), the glycemic index calculated from
3-day food records was examined for its
relation to HbA
1c
and serum lipid con
-
centrations. HbA
1c
levels were lower in
the lowest glycemic index quartile com-
pared with the highest quartile. Of the
serum lipids, only HDL cholesterol was
independently related to the glycemic in-
dex. Interestingly, the consumption of
bread and pasta had the biggest effect on
the overall glycemic index.
The effects on lipids after low com-
pared to highglycemic index diets ap-
pear to be minimal. Two studies (79,80)
measured cholesterol concentrations and
three studies (78 80) measured HDL
cholesterol concentrations, but none re-
ported differences in the low compared
to the highglycemic index diets. One
study (80) reported lower triglyceride lev-
els, but one (78) did not.
Although it is clear that carbohy-
drates do have differing glycemic re-
sponses, the data reveal no clear trend in
outcome benets. If there are long-term
effects on glycemia and lipids, these ef-
fects appear to be modest. Moreover, the
number of studies is limited, and the de-
sign and implementation of several of
these studies is subject to criticism.
Fiber. Early short-term studies using
large amounts of ber (30 g/day) in
small numbers of suboptimally controlled
type 1 subjects (8487) suggested a pos-
itive effect of ber on glycemia. However,
in a study of type 1 diabetes subjects on
intensive insulin therapy, 56 g of ber had
no benecial effect on glycemic control
(81). A recent study (88) randomized
subjects being treated with two or more
injections of insulin per day and HbA
1c
levels of 710% to either a high-ber (50
g/day), lowglycemic index diet or a low-
ber (15 g/day), highglycemic index
diet for 24 weeks. The high-ber diet sig-
nicantly reduced mean daily blood glu-
cose concentration (P 0.05), the
number of hypoglycemic events (P
0.01), and, in the subgroup of patients
compliant to diet, HbA
1c
(P 0.05), but
had no benecial effect on cholesterol,
HDL cholesterol, or triglyceride concen-
trations. Conversely, a cross-sectional
analysis of dietary ber in type 1 diabetes
patients enrolled in the EURODIAB
IDDM Complications Study revealed that
a higher intake of total ber (grams per
day) was independently associated with
higher levels of HDL cholesterol in both
men and women, and lower LDL choles-
terol levels in men but not women (89).
No substantial differences were observed
between soluble and insoluble ber in-
takes. Mean total ber intake was 18.5
g/day in men and 16.2 g/day in women.
The Dietary Guidelines for Americans
(16) recommends that all Americans
choose a variety of ber-containing food,
such as whole grains, fruits, and vegeta-
bles, because they provide vitamins, min-
erals, ber, and other substances
important for good health. This is an ap-
propriate recommendation for people
with type 1 diabetes as well.
There is strong evidence for the fol-
lowing statements:
Studies in healthy subjects support the
importance of including food contain-
ing carbohydrate from whole grains,
fruits, vegetables, and low-fat milk in
the diet.
With regard to the glycemic effects of
carbohydrates, the total amount of car-
bohydrate in meals and snacks is more
important than the source or type.
Individuals receiving intensive insulin
therapy should adjust their premeal in-
sulin dosages based on the carbohy-
drate content of meals.
There is some evidence for the follow-
ing statements:
Individuals receiving xed daily insulin
dosages should try to be consistent in
day-to-day carbohydrate intake.
Although the use of lowglycemic in-
dex food may reduce postprandial hy-
perglycemia, there is not sufcient
evidence of long-term benet to recom-
mend use of lowglycemic index diets
as a primary strategy in food/meal plan-
ning for individuals with type 1 diabe-
tes.
As for the general public, consumption
of ber is to be encouraged; however,
there is no reason to recommend that
people with type 1 diabetes consume a
greater amount of ber than other
Americans.
Percentages of carbohydrate should be
based on individual nutrition assess-
ment.
The following statement is based on
expert consensus:
Carbohydrate and monounsaturated
fat together should provide 6070% of
energy intake.
Carbohydrate and type 2 diabetes
As is the case for type 1 diabetes, there is
no body of evidence relating to people
with type 2 diabetes to suggest changing
the 1994 recommendation that 60 70%
of total energy be divided between carbo-
hydrate and monounsaturated fat. In
weight-maintaining diets for type 2 pa-
tients with diabetes, replacing carbohy-
drate with monounsaturated fat reduces
postprandial glycemia and triglyceride-
mia (90,91), but there is concern that in-
creased fat intake in ad libitum diets may
promote weight gain and potentially con-
tribute to insulin resistance (92100).
Thus the contributions of carbohydrate
and monounsaturated fat to energy intake
should be individualized based on nutri-
tion assessment, metabolic proles, and
weight and treatment goals.
In individuals with type 2 diabetes,
postprandial glucose levels and insulin re-
sponses to a variety of starches and su-
crose are similar if the amount of
carbohydrate is constant (69,71,101
106). This has been demonstrated in both
controlled (69,101104) and in free-
living subjects (71,105,106). When stud-
ied, the effects of starches and sucrose on
plasma lipids were similar and no adverse
effects were observed (103106).
Franz and Associates
DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002 151
Glycemic index. There have been nine
studies (80,82,107113) involving type 2
diabetes subjects (n 129) that have
compared lowglycemic index and
highglycemic index diets for longer
than 1 day. One study (107) reported
lower HbA
1c
levels in low compared to
highglycemic index diets, whereas four
studies (80,82,108,109) reported no dif-
ferences in HbA
1c
levels. Three studies
(110112) reported signicantly lower
fructosamine levels in low compared to
highglycemic index diets, whereas
three other studies (108,109,113) re-
ported no signicant differences in fruc-
tosamine. No differences in fasting
plasma glucose concentrations were re-
ported in eight studies (80,107113), and
no differences in insulin levels were found
in two studies (107,109).
In studies that also assessed the effects
of low and highglycemic index diets
on plasma lipids, there were no consistent
results. One study (112) reported positive
differences on cholesterol levels, whereas
four (80,107,108,113) reported no differ-
ences. One study reported positive differ-
ences in HDL cholesterol levels (109),
whereas ve (80,108,110,112,113) re-
ported no differences. Four studies (108
110,112) reported no differences in LDL
cholesterol levels. One study (80) re-
ported positive differences in triglyceride
levels; ve studies (107,108,110112)
reported no differences.
Although studies in type 2 diabetes
subjects have not consistently reported a
relation between glycemic index and in-
sulin and lipid levels, studies in other
populations have reported an association
between either lower glycemic index diets
or lower glycemic loads with lipids, in
particular HDL cholesterol, and insulin
levels. In a cross-sectional study of mid-
dle-aged adults, the glycemic index of the
diet was the only dietary variable signi-
cantly related to serum HDL cholesterol
concentration (114), and a recent analysis
(115) of the Third National Health and
Nutrition Examination Survey (NHANES
III) reported a change in HDL concentra-
tion of 2.3 mg/dl per 15-unit increase in
glycemic index. In a study of 32 patients
with advanced coronary heart disease, 4
weeks of a lowglycemic index diet im-
proved glucose tolerance and insulin sen-
sitivity compared to a highglycemic
index diet over the same period (116).
The same group reported that a low
compared to a highglycemic index diet
improved adipocyte insulin sensitivity in
women at risk for coronary heart disease
(117).
The glycemic load, denedasthe
product of the glycemic index value of a
food and its carbohydrate content, has
been reported to be positively associated
with the risk of developing type 2 diabetes
in men and women (118,119) and coro-
nary heart disease in women (120). In a
cross-sectional study of healthy post-
menopausal women, dietary glycemic
load was inversely related to plasma HDL
cholesterol and positively related to fast-
ing triglycerides (121). In the analysis of
the NHANES III results, a high glycemic
load was associated with a lower concen-
tration of plasma HDL cholesterol (115).
Fiber. Early studies of the effects of ber
on glycemia showed promising results,
but may have suffered from methodolog-
ical errors (i.e., poor control of confound-
ing variables such as weight loss,
differences in energy consumed, different
food sources with potential differences in
starch digestibility, and differences in di-
etary fat content) (122). In a study in
which dietary variables were controlled
for, increasing the ber content of the diet
from 11 to 27 g/1,000 kcal did not lead to
improvements in glycemia, insulinemia,
or lipemia (123).
In contrast, a diet supplemented with
large amounts of water-soluble, gel-
forming ber, such as guar gum, reduced
postprandial glycemia (124). In support
of this nding, another study comparing a
diet containing 24 g ber per day (high
usual intake) to a diet containing 50 g
ber per day found that the intake of food
high in dietary ber improved glycemic
control, reduced hyperinsulinemia, and
decreased plasma lipids (125). It thus ap-
pears that ingestion of large amounts of
ber is necessary to confer metabolic ben-
et. It is not clear whether the palatability
and gastrointestinal side effects of ber in
this amount would be acceptable to most
people.
A meta-analysis of 67 controlled clin-
ical trials indicated that diets high in sol-
uble ber decrease total and LDL
cholesterol, but had a small HDL-
lowering effect and did not affect triglyc-
eride concentrations (126). Patients with
hypercholesterolemia were not more re-
sponsive to dietary ber than healthy in-
dividuals. However, the authors concluded
that the effect of soluble ber within prac-
tical ranges on cholesterol was modest
(daily intake of 3 g soluble ber, e.g.,
3 apples or 3 bowls [29-g servings] oat-
meal can decrease total cholesterol by 5
mg/dl, an 2% reduction), and on risk of
heart disease may be only small.
Newer ber supplements such as
psyllium (127) and -glucan (128,129)
have mixed short-term effects on glyce-
mia and lipemia and require further
study.
There is strong evidence for the fol-
lowing statements:
Studies in healthy subjects and those at
risk for type 2 diabetes support the im-
portance of including food containing
carbohydrate from whole grains, fruits,
vegetables, and low-fat milk in the diet.
With regard to the glycemic effect of
carbohydrates, the total amount of car-
bohydrate in meals or snacks is more
important than the source or type.
There is some evidence for the follow-
ing statements:
Although the use of lowglycemic in-
dex food may reduce postprandial hy-
perglycemia, there is not sufcient
evidence of long-term benet to recom-
mend general use of lowglycemic in-
dex diets in type 2 diabetes patients.
As for the general population, con-
sumption of ber is to be encouraged.
Although large amounts of dietary ber
(50 g per day) may have benecial
effects on glycemia, insulinemia, and li-
pemia, it is not known if such high lev-
els of ber intake can be maintained
long-term.
The following statement is based on
expert consensus:
Carbohydrate and monounsaturated
fat should together provide 6070% of
energy intake. However, the individu-
als metabolic prole and need for
weight loss should be considered when
determining the monounsaturated fat
content of the diet. Increasing fat intake
may result in increased energy intake.
Nutritive sweeteners
Sucrose. Sucrose is a common, naturally
occurring disaccharide composed of a
glucose and a fructose molecule. Average
per capita consumption of sucrose and
other sugars in the U.S. is estimated to be
94 g/day, accounting for 22% of energy
Technical Review
152 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002
intake (130). Historically, the most
widely held belief about nutrition and di-
abetes was that added sugars should be
avoided and naturally occurring sugars
restricted. This belief was based on the
assumption that sucrose and other sugars
were more rapidly digested and absorbed
then starch-containing food and thereby
aggravated hyperglycemia. However, sci-
entic evidence does not support this as-
sumption.
The available evidence from clinical
studies demonstrates that dietary sucrose
does not increase glycemia more than iso-
caloric amounts of starch (67,69,101,103,
104,106,131,132). Thus the intake of
sucrose and sucrose-containing food in
diabetic individuals need not be restricted
because of a concern about aggravating
hyperglycemia. If sucrose is part of the
food/meal plan, it should be substituted
for other carbohydrate sources or, if
added, should be adequately covered
with insulin or other glucose-lowering
medication. In addition, the intake of
other nutrients (such as fat) often ingested
with sucrose-containing food should be
taken into account. In one study, when
individuals with type 2 diabetes included
sucrose in their daily meal plan, no nega-
tive impact on dietary habits or metabolic
control was observed (133).
Fructose. Fructose is a common, natu-
rally occurring monosaccharide that ac-
counts for 9% of average energy intake
in the U.S. (134). Fructose is somewhat
sweeter than sucrose. It has been reported
that 33% of dietary fructose comes from
fruits, vegetables, and other natural
sources in the diet and 67% comes from
food and beverages to which fructose has
been added (135).
In several studies in diabetic subjects,
fructose produced a reduction in post-
prandial glycemia when it replaced su-
crose or starch as a carbohydrate source
(69,106,136,137). Thus fructose might
be a good sweetening agent in the diabetic
diet. However, this potential benetis
tempered by the concern that fructose
may have adverse effects on plasma lipids.
Consumption of large amounts of fruc-
tose (1520% of daily energy intake [90
th
percentile of usual intake]) has been
shown to increase fasting total and LDL
cholesterol in subjects with diabetes
(137) and fasting total and LDL choles-
terol and triglycerides in nondiabetic sub-
jects (138141).
Sugar alcohols (polyols). Sugar alco-
hols are classied as hydrogenated
monosaccharides (e.g., sorbitol, manni-
tol, xylitol), hydrogenated disaccharides
(e.g., isomalt, maltitol, lactitol), and mix-
tures of hydrogenated mono- (sorbitol),
di- (maltitol), and oligosaccharides (e.g.,
hydrogenated starch hydrolysates) (46).
They are used in food as sweeteners and
bulking agents. Sugar alcohols have been
designated by the U.S. Food and Drug
Administration (FDA) as safe for use as
food additives or as Generally Recognized
as Safe (GRAS) by afrmation petitions
accepted for ling by the FDA (Table 2).
The FDA has not indicated a need to des-
ignate an acceptable daily intake. Food
prepared with sugar alcohols may claim
on the label that there is an association
between sugar alcohols and reduced risk
of dental caries. Because sugar alcohols
are only partially absorbed from the small
intestine, the claim of reduced energy val-
ues per gram is allowed. However, if cer-
tain polyols are used in food, a warning
concerning excess consumption and lax-
ative effects of polyols is required on the
food label (Table 2).
In some studies, ingestion of sugar al-
cohols (50 g) by healthy and diabetic
individuals has produced lower post-
prandial glucose responses than after in-
gestion of fructose, sucrose, or glucose
(142147). Because of the reduced avail-
able energy of sugar alcohols, the possi-
bility exists that they could be used to
reduce energy intake (as with fat replacers
and nonnutritive sweeteners). However,
no studies have been published showing
this to be the case, and the small energy
savings do not appear to result in a signif-
icant reduction in total daily energy in-
take. Intake of food containing sugar
alcohols such as sorbitol has been re-
ported to cause diarrhea in children with
diabetes (148) and adults (149).
There is strong evidence for the fol-
lowing statements:
Sucrose does not increase glycemia to a
greater extent than isocaloric amounts
of starch.
Sucrose and sucrose-containing food
do not need to be restricted by people
with diabetes based on a concern about
aggravating hyperglycemia. However,
if sucrose is included in the food/meal
plan, it should be substituted for other
carbohydrate sources or, if added, be
adequately covered with insulin or
other glucose-lowering medication.
There is some evidence for the follow-
ing statements:
Fructose reduces postprandial glyce-
mia when it replaces sucrose or starch
in the diabetic diet.
Consumption of fructose in large
amounts may have adverse effects on
plasma lipids.
The use of sugar alcohols as sweetening
agents appears to be safe.
Sugar alcohols may cause diarrhea, es-
pecially in children.
Table 2 Sugar alcohols: caloric content and regulatory status
Sugar alcohol
Caloric content
(kcal/g) FDA designation
Erythritol 0.2 GRAS afrmation petition accepted for ling
Hydrogenated starch
hydrolysates
3.0 GRAS afrmation petitions accepted for ling
Isomalt 2.0 GRAS afrmation petition accepted for ling
Lactitol 2.0 GRAS afrmation petition accepted for ling
Maltitol 3.0 GRAS afrmation petition accepted for ling
Mannitol* 1.6 Food additive permitted in food or in contact with
food on an interim basis pending additional study
Sorbitol* 2.6 Afrmed as GRAS
Xylitol 2.4 Food additive permitted for direct addition to food
for human consumption
Caloric content based on Federation of American Societies for Experimental Biology, The evaluation of the
energy of certain polyols used as food ingredients,June 1994, (unpublished), and Life Sciences Research
Ofce: Evaluation of the net energy value of maltitol, April 1999 (unpublished). *Excess consumption
may have a laxative effect must be on label for foods whose reasonably foreseeable consumption may result
in the daily ingestion of 20 g mannitol or 50 g sorbitol.
Franz and Associates
DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002 153
There is limited evidence for the fol-
lowing statement:
The use of added fructose as a sweeten-
ing agent is not recommended.
The following statements are based
on expert consensus:
Sucrose and sucrose-containing food
should be eaten in the context of a
healthy diet, and the intake of other nu-
trients ingested with sucrose, such as
fat, should be taken into account.
There is no reason to recommend that
diabetic individuals avoid naturally oc-
curring fructose in fruits, vegetables,
and other food.
It is unlikely that sugar alcohols in the
amounts likely to be ingested in indi-
vidual food servings or meals will con-
tribute to a signicant reduction in total
energy or carbohydrate intake, al-
though no studies have been conducted
to support this.
Resistant starch. Resistant starch (non-
digestible oligosaccharides and the starch
amylose) (Table 1) is not digested and
therefore not absorbed as glucose in the
small intestine. It is, however, almost
completely fermented in the colon and
produces about 2 kcal/g of energy (46). It
is estimated that resistant starch and un-
absorbed starch represent 25% (usu-
ally 10 g/day) of the total starch
ingested in the average Western diet
(150). Legumes are the major food source
of resistant starch in the diet, containing
23 g resistant starch per 100 g cooked
legumes. Uncooked cornstarch contains
about 6 g resistant starch per 100 g dry
weight (151). It has been suggested that
ingestion of resistant starch produces a
lesser increase in postprandial glucose
than digestible starch and correspond-
ingly lower insulin levels. As a result, it
has been proposed that food containing
naturally occurring resistant starch (corn-
starch) or food modied to contain more
resistant starch (high amylose cornstarch)
may modify postprandial glycemic re-
sponse, prevent hypoglycemia, and re-
duce hyperglycemia; these effects may
explain differences in the glycemic in-
dexes of some food.
There have been several one-meal
(152154) and second-meal studies
(155157) in nondiabetic subjects, com-
paring subjects physical response to food
high in resistant starch and their response
to food with an equivalent amount of di-
gestible starch. All studies found some re-
duction in postprandial glucose and
insulin responses to the rst meal, but ob-
served mixed results after the second
meal. Long-term studies have not consis-
tently conrmed these results (155,158
161).
Published studies involving people
with diabetes have focused on uncooked
cornstarch and its potential to prevent
nighttime hypoglycemia (162165). In
uncontrolled studies, evening cornstarch
in specic dosages or dosages based on
g/kg body weight resulted in less hypogly-
cemia around 0200 h in all groups (166,
167). Longer term studies of evening
cornstarch snacks in adults with type 1
diabetes reported less hypoglycemia at
0300 h (168). In subjects with type 2 di-
abetes, evening cornstarch snacks in-
creased nocturnal glucose and insulin
(165). It has not been established that
bedtime cornstarch snacks are more effec-
tive in preventing nocturnal hypoglyce-
mia than other types of carbohydrate.
The is limited evidence for the follow-
ing statement:
Resistant starches have no established
benet for people with diabetes.
Nonnutritive sweeteners. There are
presently four nonnutritive sweeteners
(also referred to as high-intensity sugar
alternatives, low calorie, or alternative
sweeteners) approved for use in the U.S.:
saccharin, aspartame, acesulfame potas-
sium (acesulfame K), and sucralose. Sac-
charin, originally linked to human cancer
based on a study in rats more than two
decades ago, has now been dropped from
the FDA list of cancer-causing chemicals
(169).
The newest product approved by the
FDA is sucralose (made from sucrose
through a multistep process in which
three hydrogen-oxygen groups are re-
placed with three chlorine atoms). Sucra-
lose has been shown to have no effect on
glucose homeostasis in diabetic subjects
(170,171). FDA approval is being sought
for three other nonnutritive sweeteners:
alitame (formed from the amino acids as-
partic acid and alanine), cyclamates (re-
moved from the market in 1970), and
neotame (similar to aspartame but 3060
times sweeter and will not require special
labeling for phenylketonuria) (172). A re-
cent trend in the food industry is to blend
high-intensity sweeteners. This decreases
the total amount of individual sweeteners
used and may improve taste.
Nonnutritive sweeteners approved by
the FDA must undergo rigorous scrutiny
and are not allowed on the market unless
they are demonstrated to be safe for the
public, including people with diabetes, to
consume. For all food additives, includ-
ing nonnutritive sweeteners, the FDA de-
termines an acceptable daily intake (ADI),
dened as the amount of a food additive
that can be safely consumed on a daily
basis over a persons lifetime without risk.
Actual intake is much less than the ADI.
Although the daily ADI for aspartame is
50 mg/kg body wt, the range of actual
daily aspartame intake at the 90
th
percen
-
tile is 23 mg/kg body wt (173). Table 3
lists ADIs of nonnutritive sweeteners
(174).
Studies to determine the effects of
nonnutritive sweeteners during preg-
Table 3ADI of nonnutritive sweeteners
ADI
(mg/kg
body wt)
Average
amount in
12-oz can of
soda* (mg)
Cans of soda to
reach ADI for
60-kg (132-lb)
person (n)
Amount in
packet of
sweetener
(mg)
Packets to
reach ADI for
60-kg (132-lb)
person (n)
Acesulfame K 15 40 25 50 18
Aspartame 50 200 15 35 86
Saccharin 5 140 2 40 7.5
Sucralose 5 70 4.5 5 60
*Fountain drinks may have different amounts and may contain a sweetener blend. based on most typical
blend with 90 mg aspartame. ADIs are independent. With this sweetener blend, it takes 35 cans to reach the
ADI of aspartame. set by Joint Expert Committee of Food Additives of World Health Organization (175).
Adapted from Powers M: Sugar alternatives and fat replacers. In American Diabetes Association Guide to
Medical Nutrition Therapy for Diabetes. Franz MJ, Bantle JP, Eds. Alexandria, VA, American Diabetes Associ-
ation, 1999.
Technical Review
154 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002
nancy and lactation have been conducted
in animals. No adverse effects have been
reported (175).
There is strong evidence for the fol-
lowing statement:
Nonnutritive sweeteners are safe for
people with diabetes when consumed
within the ADI levels established by the
FDA.
The following statement is based on
expert consensus:
It is unknown if use of nonnutritive
sweeteners improves long-term glyce-
mic control or assists in weight loss.
Protein and diabetes
In the U.S., protein intake accounts for
1520% of average adult energy intake, a
statistic that has varied little from 1909 to
the present. Protein intake is also fairly
consistent across all ages, from infancy to
older age (176, 177), and appears to be
similar in individuals with diabetes. Pro-
tein intake in subjects with type 2 diabe-
tes in the U.K. Prospective Diabetes Study
was 21% of daily energy (32); protein in-
take in children with type 1 diabetes has
been reported to be 17% of daily energy
(178).
Protein needs. It has been assumed that
in people with diabetes, abnormalities of
protein metabolism are less affected by
insulin deciency and insulin resistance
than abnormalities of glucose metabolism
(179). However, moderate hyperglyce-
mia may contribute to increased turnover
of protein in type 2 diabetic subjects. Dur-
ing moderate hyperglycemia, obese sub-
jects with type 2 diabetes, compared to
nondiabetic obese subjects, had an in-
crease in whole-body nitrogen ux and a
higher rate of protein synthesis and
breakdown (180,181).
A high-quality protein (95 g protein/
day), very-low-energy diet capable of
maintaining nitrogen balance in obese
subjects without diabetes did not prevent
negative nitrogen balance in diabetic sub-
jects, despite weight loss and improved
glycemic control (181). This increased
protein turnover was restored to normal
only with oral glucose-lowering agents or
exogenous insulin sufcient to achieve
euglycemia and with increased protein in-
take (182,183). These study results sug-
gest that people with type 2 diabetes have
an increased need for protein during
moderate hyperglycemia and an altered
adaptive mechanism for protein sparing
during weight loss. Thus with energy re-
striction, the protein requirements of peo-
ple with diabetes may be greater than the
recommended dietary allowance (RDA)
of 0.8 g protein/kg body wt, although not
greater than usual intake, which is 1.0 g
protein/kg body wt or 100 g protein/
day (32). However, individuals consum-
ing very low energy intakes may have a
deciency in protein intake and require
an assessment of protein adequacy.
Protein degradation and conversion
of endogenous and exogenous protein to
glucose in type 1 diabetes depends on the
state of insulinization and corresponding
glycemic control. Insulin deciency in-
creases whole-body protein synthesis,
protein breakdown, oxidation of essential
amino acids (184), and gluconeogenesis
(185). Conversion of excess dietary pro-
tein or endogenous protein to glucose
may occur and, in turn, adversely inu-
ence glycemia.
Short-term kinetic studies have dem-
onstrated increased protein catabolism in
type 1 diabetic subjects treated with con-
ventional insulin therapy (186188). In
one study, to protect against increased
protein catabolism, type 1 subjects re-
quired near-normal glycemia and an ade-
quate protein intake (188). Because most
adults eat at least 50% more protein than
required, people with diabetes appear to
be protected against protein malnutrition
when consuming a usual diet.
Protein and development of nephropa-
thy. An association between dietary pro-
tein intake and the development of renal
disease has been suggested. In seven stud-
ies, dietary protein intake was reported to
be similar in patients with diabetes with
and without nephropathy (189195). In
all studies, protein intake was in the range
of usual intake and rarely exceeded 20%
of the energy intake. In a cross-sectional
study of 2,500 type 1 diabetic subjects,
those who reported protein consumption
20% of total energy had average albu-
min excretion rates 20 mcg/min (196).
Those in whom protein intake was 20%
of daily energy (22% of patients) had av-
erage albumin excretion rates 20 mcg/
min (in the range of microalbuminuria).
In individuals with macroalbuminuria,
32% consumed 20% of total energy
from protein versus 23% for those with
microalbuminuria and 20% for those
with normal albumin excretion. This sug-
gests that a high-protein intake may have
a detrimental effect on renal function.
The long-term effects of consuming
20% of energy as protein on the devel-
opment of nephropathy has not been de-
termined. However, intake of protein in
the usual range does not appear to be as-
sociated with the development of diabetic
nephropathy.
Glucose responses to protein. A num-
ber of studies in healthy, normal-weight
subjects (197) and subjects with con-
trolled type 2 diabetes (blood glucose
200 mg/dl) (198200) have demon-
strated that ingested protein does not in-
crease plasma glucose concentration.
Gannon et al. (200) reported that during
the 8-h period after subjects with type 2
diabetes ingested 50 g protein in the form
of very lean beef, 2023 g of protein
were deaminated, which in theory could
yield 1113 g glucose. However, the
amount of glucose appearing in the circu-
lation was only 2 g, conrming that in-
gested protein does not result in a
signicant increase in glucose concentra-
tion. This raises the question that if glu-
coneogenesis from protein is occurring,
why does the glucose produced not ap-
pear in the general circulation after the
ingestion of protein?
In type 2 diabetic subjects, the peak
plasma glucose response to carbohydrate
is similar to the response to carbohydrate
plus protein (197199), suggesting that
protein does not slow the postprandial
absorption of carbohydrate.
In individuals capable of secreting in-
sulin, protein ingestion is just as potent as
glucose ingestion in stimulating insulin
secretion (197200). The net effect on
glucose output by the liver depends on
the ratio of insulin to glucagon. In type 1
or type 2 diabetic subjects, the glucagon
response to protein is considerably
greater than in nondiabetic subjects
(201).
In one study of subjects with well-
controlled type 1 diabetes, the addition of
protein to a meal did not slow the absorp-
tion of carbohydrate or change either the
postprandial peak glucose response to the
meal or glucose levels at 5 h (202). Fur-
thermore, in type 1 diabetic subjects, the
rate of restoration to euglycemia after hy-
poglycemia did not differ when treatment
was given with carbohydrate or carbohy-
drate plus protein (203). Glucose levels,
the time to peak plasma glucose levels,
Franz and Associates
DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002 155
and subsequent rate of glucose fall were
similar after both treatments.
Proteins effect on satiety and/or en-
ergy balance. It has been claimed that
high-protein, low-carbohydrate diets
produce weight loss and improvements in
glycemia. It should be noted that most of
these diets tend to be high in fat. In one
study of high-protein diets, there was a
signicant decrease in weight and plasma
triglycerides at 12 weeks (204). However,
plasma LDL cholesterol levels were in-
creased. There is no research available to
document that high-protein diets main-
tain long-term weight reduction any bet-
ter than traditional weight-loss diets and
that they are safe for long-term use.
The Continuing Survey of Food In-
take by Individuals 19941996 (177)
was used to examine the relationship
among prototype popular diets (205). In a
comparison of low-carbohydrate diets
(30% of energy from carbohydrate
[high protein diets]) and high-
carbohydrate diets (55% of energy from
carbohydrate), diet quality was lower and
total and saturated fat intake was higher
on the lower carbohydrate diet, whereas
energy intake and BMI were approxi-
mately similar between the two.
The effects of dietary protein on the
regulation of energy intake and satiety
have not been adequately studied
(206,207). Short-term meal studies sug-
gest that protein does exert a positive ef-
fect on satiety (208 211). However,
results from one study demonstrated that
although hunger was suppressed to a
greater extent after a high-protein than a
high-fat or high-carbohydrate breakfast,
the changes in hunger were not of suf-
cient magnitude to change ad libitum
lunchtime energy intake 5 h later or en-
ergy intake for the rest of the day, which
were similar after all three breakfast types
(210).
There is strong evidence for the fol-
lowing statement:
In individuals with controlled type 2
diabetes, ingested protein does not in-
crease plasma glucose concentrations,
although ingested protein is just as po-
tent a stimulant of insulin secretion as
carbohydrate.
There is some evidence for the follow-
ing statements:
For diabetic individuals, there is no ev-
idence to suggest that usual protein in-
take (1520% of total daily energy)
should be modied if renal function is
normal.
For diabetic individuals, especially
those with less-than-optimal glycemic
control, the protein requirement may
be greater than the RDA, but not greater
than usual intake.
Contrary to advice often given to pa-
tients with diabetes, the available evi-
dence suggests the following: 1) dietary
protein does not slow the absorption of
carbohydrate and 2) dietary protein
and carbohydrate do not raise plasma
glucose later than carbohydrate alone
and thus do not prevent late-onset hy-
poglycemia.
There is limited evidence for the fol-
lowing statement:
It may be prudent to avoid protein in-
take 20% of total daily energy.
The following statement is based on
expert consensus:
The long-term effects of diets high in
protein and low in carbohydrate are un-
known. Although such diets may pro-
duce short-term weight loss and
improved glycemia, it has not been es-
tablished that weight loss is main-
tained. The long-term effect of such
diets on plasma LDL cholesterol is also
a concern.
Dietary fat and diabetes
Saturated fats and dietary cholesterol.
The primary goal regarding dietary fat in
patients with diabetes is to decrease in-
take of saturated fat and cholesterol (212
214). Saturated fat is the principal dietary
determinant of LDL cholesterol (213).
Compared to nondiabetic subjects, dia-
betic subjects have an increased risk of
coronary heart disease with higher in-
takes of dietary cholesterol (215). The
ADA (8,212) and the National Choles-
terol Education Programs Adult Treat-
ment Panel III (18) have recommended
that the serum LDL cholesterol goal be
100 mg/dl. To assist in achieving this
goal, it is recommended that food with a
high content of saturated fatty acids and
cholesterol be limited (17,18).
In a meta-analysis (216) of 37 dietary
intervention studies in free-living sub-
jects, plasma total cholesterol decreased
from baseline by 24 mg/dl (10%), LDL
cholesterol by 19 mg/dl (12%), and trig-
lycerides by 15 mg/dl (8%) in Step I (10%
saturated fat and 300 mg cholesterol) in-
terventions (P 0.01 for all). In Step II
interventions (7% saturated fat and 200
mg cholesterol), total cholesterol de-
creased by from baseline by 32 mg/dl
(13%), LDL cholesterol by 25 mg/dl
(16%), and triglycerides by 17 mg/dl
(8%) (P 0.01 for all). HDL cholesterol
decreased by 7% (P 0.05) in response
to Step II but not Step I dietary interven-
tions. Positive correlations between
changes in dietary total and saturated
fatty acids and changes in total, LDL, and
HDL cholesterol were observed. Adding
exercise resulted in greater decreases in
total and LDL cholesterol and triglycer-
ides and prevented the decrease in HDL
cholesterol associated with low-fat diets.
However, studies in diabetic subjects
demonstrating the effects of specic per-
centages of saturated fatty acids (e.g., 10
vs. 7% of energy) and specic amounts of
dietary cholesterol (e.g., 300 vs. 200 mg)
are not available. Therefore, the goal for
patients with diabetes remains the same
as for the general population: to reduce
saturated fat intake to 10% of energy
intake. Some individuals (i.e., those with
LDL cholesterol 100 mg/dl) may benet
by reducing saturated fat to 7% of en-
ergy intake. The goal for dietary choles-
terol intake is 300 mg/day and for
individuals with LDL cholesterol 100
mg/dl, 200 mg/day.
For patients with diabetes, the debate
has focused not on the extent to which
saturated fatty acids and cholesterol in-
take should be limited, but rather on what
is the best alternative energy source.
Plasma cholesterol reductions of 929%
have been reported in four studies in
which saturated fat was replaced with car-
bohydrate in diabetic diets (217220).
Two of these studies also measured
plasma LDL and HDL cholesterol and re-
ported that substituting a low-fat (30%
of total daily calories), high-carbohydrate
diet for a highsaturated fat diet resulted
in reductions in LDL, but not HDL, cho-
lesterol. (217,218) Glycemic control was
improved or unchanged as a result of re-
stricting dietary saturated fat and replac-
ing it with carbohydrate (217,219,221
224). See Table 4 for classication of fatty
acids (225).
Technical Review
156 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002
Monounsaturated fats. Diets high in
cis-monounsaturated fatty acids (hereaf-
ter referred to simply as monounsaturated
fat) (90,226 229) or low in fat and high
in carbohydrate (216223) result in im-
provements in glucose tolerance and lip-
ids compared with diets high in saturated
fat. Diets enriched with monounsaturated
fat may also reduce insulin resistance
(227); however, some studies have re-
ported total dietary fat to be associated
with insulin resistance (96100). Meta-
bolic study diets in which energy intake is
maintained and that are high in either car-
bohydrate or monounsaturated fat lower
plasma LDL cholesterol equivalently (90).
Lowsaturated fat (i.e., 10% of energy),
high-carbohydrate diets increase post-
prandial levels of plasma glucose and in-
sulin, increase plasma triglycerides (90),
and, in some studies, were shown to de-
crease plasma HDL cholesterol when
compared in metabolic studies to isoca-
loric highmonounsaturated fat diets
(91,230). However, highmonoun-
saturated fat diets have not been shown to
improve fasting plasma glucose or HbA
1c
values. Therefore, if saturated fat calories
need to be replaced, they can be replaced
with carbohydrate or monounsaturated
fat, either of which can contribute to a
reduction in plasma LDL cholesterol.
There is, however, concern that when
highmonounsaturated fat diets are
eaten ad libitum outside of a controlled
setting, they may result in increased en-
ergy intake and weight gain (216). Studies
comparing diets high in monounsatu-
rated fat with diets high in carbohydrate
with ad libitum energy intake are needed
to evaluate the efcacy of these diets and
determine which dietary intervention is
superior for reducing cardiovascular risk.
Each individuals metabolic prole and
need to lose weight will determine the
MNT recommendations. For example, a
diet in which 6070% of energy is to be
derived from carbohydrate and monoun-
saturated fat may emphasize carbohy-
drate intake for the patient to achieve
weight loss and monounsaturated fat for
the patient to improve plasma triglyceride
levels or postprandial glycemia. Further-
more, an Asian patient may be more com-
fortable with a high-carbohydrate diet,
whereas a patient of Mediterranean de-
scent may prefer a monounsaturated
fatcontaining diet. Monounsaturated
fats can also be considered for food prep-
aration and substituted for saturated fats
in fat spreads and snacks.
Polyunsaturated fats. Only a few stud-
ies have evaluated the effects of polyun-
saturated fat on plasma lipid levels and
glycemic control in subjects with diabe-
tes. In one study of type 2 subjects with
diabetes, a diet high in total and polyun-
saturated fat resulted in lower plasma to-
tal and LDL cholesterol than a diet high in
Table 4 Composition of some common dietary fatty acids and typical food sources
Fatty acid (common name) Chemical notation
Amount found in U.S.
diet (g/day)
Food sourcesMen Women
Polyunsaturated fatty acids
Linoleic acids 18:2, n-6 14.7 10.4 Vegetable oil, nuts, seeds
-linolenic acid 18:3, n-3 1.6 1.1 Flaxseed oil (linseed oil), canola
oil, soybean oil, walnuts
Eicosapentaenoic acid (EPA)* 20:5, n-3 0.1 (based on EPA
and DHA together)
Fish and sh oil, plankton
Docosahexaenoic acid (DHA)* 22:6, n-3 Fish and sh oil, oceanic algae,
plankton
Monounsaturated fatty acids
Oleic acid 18:1, n-9 (cis form) 31.0 20.8 Olive oil, soybean oil, canola oil,
safower oil, peanut oil,
almonds, cashews, pecans,
avocado, peanuts, peanut butter
Elaidic acid 18:1 n-9 (trans form) 4.2 1.8 Solid margarines, shortenings,
salad dressing, processed food
containing partially
hydrogenated oil
Saturated fatty acids
Lauric acid 12:0 0.9 0.7 Meats, poultry, butterfat in butter,
nonskim milk or yogurt,
cheese, ice cream, egg yolks
Myristic acid 14:0 2.7 1.9 Dairy products, food made with
coconut oil
Palmitic acid 16:0 1.7 11.6 Dairy products, meat, processed
grain products
Stearic acid 18:0 8.1 5.4 Dairy products, meat, processed
grain products, chocolate
*Both DHA and EPA can be synthesized from -linolenic acid. Adapted from Sega-Isaacson CJ, Carello E, Wylie-Rosett J: Dietary fats and diabetes mellitus. Is there
a food fat? Current Diabetes Reports 1:161169, 2001
Franz and Associates
DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002 157
total and saturated fat, but produced no
difference in other plasma lipid levels
(231). Another study in type 2 diabetic
subjects compared a diet high in polyun-
saturated fat with one high in monounsat-
urated fat and reported higher plasma
total and LDL cholesterol, fasting glucose,
and insulin levels with the polyunsatu-
rated fat diet (232).
N-3 polyunsaturated fat (omega-3 fatty
acids). Food sources of n-3 polyunsatu-
rated fatty acids include sh, especially
fatty sh, as well as plant sources such as
axseed and axseed oil, canola oil, soy-
bean oil, and nuts. N-3 fatty acid supple-
ments have been shown to reduce plasma
triglyceride levels, especially in hypertri-
glyceridemic individuals (233), and to
have benecial effects on platelet aggrega-
tion and thrombogenicity (234). Increas-
ing the intake of n-3 polyunsaturated fatty
acids has been shown to be benecial in
subjects with diabetes (235237). Al-
though sh oil supplementation may be
benecial in lowering plasma triglyceride
levels in type 2 diabetic subjects, the ac-
companying rise in plasma LDL choles-
terol is of concern (238,239). Therefore, if
n-3 fatty acid supplements are used, the
effects on plasma LDL cholesterol should
be monitored. Glucose metabolism is not
likely to be adversely affected with the use
of n-3 supplements (236,237,240). N-3
supplements may be most benecial in
the treatment of severe hypertriglyceride-
mia (236,241). Although studies of the
effects of n-3 fatty acids in patients with
diabetes have primarily used supple-
ments, there is evidence from the general
population that food containing n-3 fatty
acids, specically eicosapentaenoic acid
and docosahexaenoic acid, has cardiopro-
tective benets (242246).
Transunsaturated fatty acids. Trans
fats unsaturated fatty acids formed
when vegetable oils are processed and
made more solid (hydrogenation)are
found in some margarines and in food
prepared or fried in hydrogenated vegeta-
ble oils. Trans fats also occur naturally in
small amounts in meats and dairy prod-
ucts. The mean intake of trans fatty acids
in the U.S. has been estimated at 2.6% of
total caloric intake and 7.4% of total fat
intake (247). When studied indepen-
dently of other fatty acids, the effect of
trans fatty acids is similar to that of satu-
rated fats in raising plasma LDL choles-
terol. Trans fatty acids also lower plasma
HDL cholesterol (248250). Studies in
nondiabetic subjects support limiting the
intake of trans fatty acids.
Stanols/sterols. Plant stanols are found
in very small amounts in food from plants
such as corn and soy and in other vegeta-
ble or plant oils. Within plant tissue they
are derived from plant phytosterols. They
differ from plant sterols in that their ring
structure is saturated. Plant stanols are es-
teried to other vegetable oil fatty acids to
enhance their lipid solubility and make
them easier to use as an ingredient in
food. Plant sterol and stanol esters block
the intestinal absorption of dietary and
biliary cholesterol (251) by competing
with cholesterol for entry into the mixed
micelles that must form during digestion
for dietary fatty acids, cholesterol, and fat-
soluble vitamins to be absorbed. Plant
stanols/sterols in the amount of 2 g/day
have been shown to lower serum total
cholesterol by up to 10% and LDL cho-
lesterol by up to 14% (251255).
Low-fat diets. There are potential bene-
ts from low-fat diets. Low-fat diets are
usually associated with modest loss of
weight, which can be maintained as long
as the diet is continued (230,256) and if
combined with aerobic exercise
(216,257,258). In studies evaluating the
effect of ad libitum energy intake as a
function of dietary fat content, low-fat,
high-carbohydrate intake is associated
with a transient decrease in caloric intake
and modest weight loss, leading to a new
equilibrium body weight (221,259268).
With this modest weight loss, a decrease
in total cholesterol and plasma triglycer-
ides and an increase in HDL cholesterol
occur. Consistent with this, low-fat, high-
carbohydrate diets over long periods of
time have been shown to not increase
plasma triglycerides and, when reported,
have led to modest weight loss (230,269,
270). Although the signicance of the ef-
fects of reduced dietary fat intake are
controversial (256,271279), reduced-
fat diets have been shown to maintain
weight loss better than other types of re-
duced energy diets (216,257,280283).
In type 2 diabetic subjects, restrained
eating behaviors combined with dietary
fat restriction have been shown to have
benecial effects on glycemia, plasma lip-
ids, and/or weight (284286). A higher
intake of total dietary fat is associated with
higher levels of plasma LDL cholesterol,
and the adverse effect of a higher carbo-
hydrate intake on triglycerides has been
found in individuals who have undiag-
nosed diabetes or have gained weight dur-
ing the previous year (287).
Fat replacers/substitutes. Dietary fat
intake can be decreased by reducing the
amount of high-fat food in the diet. An-
other option is to provide lower fat or fat-
free versions of food and beverages. This
can be accomplished by removing some
fat or by using fat replacers (ingredients
that mimic the properties of fat with sig-
nicantly fewer calories than fat) in food
formulations. The FDA has approved the
majority of the fat replacers as GRAS be-
cause the substances ingredients have a
long history of safe use in food. A few
replacers (notably olestra) have been ap-
proved as food additives; approval of
these requires both demonstration of
safety and premarket approval (288
290). Although olestra has no effect on
water-soluble nutrients, it can lead to a
loss of fat-soluble vitamins.
Two recent studies involving diabetic
subjects and food made with fat replacers
have been reported (291,292). One of
these, a short-term study (292), provided
correctly labeled regular or fat-free food
to free-living subjects with and without
diabetes. Use of fat substitutes/replacers
in reasonable amounts (ve low-fat or no-
fat products per day) produced a small
decrease in dietary fat, saturated fat, and
cholesterol intake with little or no de-
crease in total energy intake or weight.
When fat replacers are used in larger
amounts (293,294), there can be a signif-
icant decrease in energy intake. Long-
term studies are needed to assess the
effect of food containing fat replacers/
substitutes on the macronutrient content
of the diets patients with diabetes and
their utility in achieving treatment goals.
Studies in nondiabetic subjects pro-
vide strong evidence for the following
statements:
In all, 10% of energy intake should be
derived from saturated fats. Some indi-
viduals (i.e., those with LDL cholesterol
100 mg/dl) may benet from lower-
ing saturated fat intake to 7% of en-
ergy intake.
Dietary cholesterol intake should be
300 mg/day. Some individuals (i.e.,
those with LDL cholesterol 100 mg/
dl) may benet from lowering dietary
cholesterol to 200 mg/day.
Intake of transunsaturated fatty acids
should be minimized.
Current fat replacers/substitutes ap-
Technical Review
158 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002
proved by the FDA are safe for use in
food.
Studies in diabetic subjects provide
strong evidence for the following state-
ment:
To lower plasma LDL cholesterol, en-
ergy derived from saturated fat can be
reduced if concurrent weight loss is de-
sirable or replaced with carbohydrate
or monounsaturated fat if weight loss is
not a goal.
There is some evidence for the follow-
ing statements:
Polyunsaturated fat intake should be
10% of energy intake.
In weight-maintaining diets, when
monounsaturated fat replaces carbohy-
drate, it may benecially affect post-
prandial glycemia and plasma tri-
glycerides but not necessarily fasting
plasma glucose or HbA
1c
.
Incorporation of two to three servings
of plant stanols/sterols (2 g) food per
day, substituted for similar food, will
lower total and LDL cholesterol.
Reduced-fat diets when maintained
long term contribute to modest loss of
weight and improvement in dyslipide-
mia.
There is limited evidence for the fol-
lowing statement:
Two or more servings of sh per week
provide dietary n-3 polyunsaturated fat
and can be recommended.
The following statements are based
on expert consensus:
Monounsaturated fat and carbohydrate
together should provide 6070% of
energy intake. However, increasing fat
intake may result in increased energy
intake.
Fat intake should be individualized and
designed to t ethnic and cultural back-
grounds.
Use of low fat food and fat replacers/
substitutes by patients with diabetes
may reduce total fat and energy intake
and thereby facilitate weight loss.
Energy balance and obesity
Many individuals with type 2 diabetes are
overweight, with 36% having a BMI
30 kg/m
2
, which would classify them as
obese (295). The prevalence of obesity is
higher in women and members of minor-
ity populations with type 2 diabetes
(295). As body adiposity increases, so
does insulin resistance (296298). Obe-
sity may also aggravate hyperlipidemia
and hypertension in type 2 patients with
diabetes (299).
Because of the effects of obesity on
insulin resistance, weight loss is an im-
portant therapeutic objective for obese in-
dividuals with type 2 diabetes. Short-term
studies lasting 6 months or less have dem-
onstrated that weight loss in type 2 dia-
betic subjects is associated with decreased
insulin resistance, improved measures of
glycemia, reduced serum lipids, and re-
duced blood pressure (300302). Long-
term data assessing the extent to which
these improvements can be maintained in
people with type 2 diabetes are not avail-
able.
Data from the general public suggest
that long-term maintenance of weight loss
is challenging. In two observational stud-
ies on weight maintenance after weight
loss in nondiabetic subjects, one study
(303) reported that only 6% in the nal
study group maintained a 5% weight loss
over 915 years, while in a random tele-
phone survey (304), 21% of 228 over-
weight subjects reported that they had
intentionally lost weight and maintained a
weight loss of 10% for at least 5 years.
However, long-term data assessing the ex-
tent to which weight loss is maintained in
patients with diabetes are not available. In
studies of weight loss in type 2 diabetic
subjects (305307), the most successful
long-term weight loss from diet was re-
ported in the Diabetes Treatment Study
(307), with weight loss of 9 kg maintained
over the 6-year study period. To accom-
plish this required long-term access to
therapeutic contact.
The reason that long-term weight loss
is difcult for most people to accomplish
is probably because energy intake and en-
ergy expenditure, and thereby body
weight, are controlled and regulated by
the central nervous system (308310).
Although our understanding of central
nervous system regulation of energy bal-
ance is incomplete, it is thought that the
hypothalamus may be the center of con-
trol. Neuropeptide Y, leptin, insulin, and
a variety of other neural, endocrine, and
gastrointestinal signals also appear to be
involved. Individual characteristics of
central nervous system control of energy
balance may be genetically determined.
For example, in a study of Danish adopt-
ees, there was a strong relation between
BMI of the adoptees and their biological
parents, and no relation whatsoever be-
tween the BMI of the adoptees and their
adoptive parents (311). These study re-
sults suggest that genetic factors have an
important role in determining body
weight. Other data support this conclu-
sion (312,313). Furthermore, environ-
mental factors often make losing weight
difcult for those genetically predisposed
to obesity.
The National Weight Control Regis-
try has enrolled over 3,000 subjects suc-
cessful at long-term maintenance of
weight loss (314). A group of 800 peo-
ple who lost an average of 30 kg and
maintained a minimum weight loss of
13.6 kg (30 lb) for 5 years were identied
from the registry (315). Slightly more
than half lost weight through formal pro-
grams, and the remainder lost weight
with a program of their own. Average en-
ergy consumption was 1,400 kcal/day,
with 24% of energy derived from fat. Av-
erage energy expenditure through added
physical activity was 2,800 kcal/week.
Importantly, nearly 77% of this sample of
people who were successful in achieving
and maintaining weight loss reported a
triggering event that preceded the weight
loss. The most common triggering events
were acute medical conditions and emo-
tional problems. Thus a new diagnosis of
type 2 diabetes could trigger lifestyle
changes that result in reduced fat and en-
ergy intake, increased physical activity,
and associated weight loss.
Structured programs to produce life-
style change. The recently completed
Diabetes Prevention Program (DPP) dem-
onstrated long-term benet in people
with glucose intolerance from structured,
intensive lifestyle programs (316,317). In
the DPP, participants randomly assigned
to an intensive lifestyle intervention that
included a low-fat diet, increased physical
activity, educational sessions, and fre-
quent follow-up were able to lose 7% of
body weight in the rst year and sustain a
5% weight loss over an average follow-up
period of 3 years. DPP program partici-
pants received training in diet, exercise,
and behavior modication from case
managers who met with them for at least
16 sessions in the rst 24 weeks and
monthly thereafter. With intensive life-
Franz and Associates
DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002 159
style intervention, the risk of developing
diabetes was reduced by 58% relative to
standard care. Wing et al. (318) demon-
strated a 2.5-kg weight loss and Tuo-
milehto et al. (319) documented a 3.5-kg
weight loss at 2 years with such programs,
and also demonstrated that lifestyle
changes reduce the risk of developing di-
abetes. A recently initiated clinical trial
called Look AHEAD (Action for Health in
Diabetes) will assess the long-term effects
of diet and exercise in type 2 patients with
diabetes.
For weight loss, dietary fat is probably
the most important nutrient to be re-
stricted. Spontaneous food consumption
and total energy intake are increased
when the diet is high in fat and decreased
when the diet is low in fat (259,260).
Moreover, epidemiological studies have
demonstrated that dietary fat intake is
positively associated with adiposity and
BMI (320,321). In healthy individuals,
simply reducing the fat content of the diet
can result in reduced energy intake and
weight loss of 23 kg (260,322,323).
Toubro and Astrup (283) compared the
efcacy of an ad libitum, low-fat, high-
carbohydrate diet with that of a
xedenergy intake diet for long-term
maintenance of weight loss. Both treat-
ment groups attended reinforcement ses-
sions 23 times weekly. At 1-year follow
up, the ad libitum group had maintained
a greater weight loss than the xed
energy intake group.
Exercise improves insulin sensitivity,
can acutely lower blood glucose in pa-
tients with diabetes, and may also im-
prove cardiovascular status. Exercise by
itself has only a modest effect on weight
(324). Exercise is to be encouraged, but
like behavioral therapies, may be most
useful as an adjunct to other weight-loss
strategies, such as dietary fat reduction.
Exercise is, however, important in long-
term maintenance of weight loss
(325,326).
Behavioral approaches to weight loss
include strategies such as self-monitoring
of food intake and exercise, nutrition ed-
ucation, stimulus control, preplanning of
food intake, and self-reinforcement.
Weight loss with behavioral therapy alone
has been modest (327,328); behavioral
approaches may be most useful as an ad-
junct to other weight-loss strategies.
Other nutrition interventions. Stan-
dard weight-reduction diets, meal re-
placements, and very-low-calorie diets
(VLCDs) are other nutrition options.
Standard weight-reduction diets provide
5001,000 fewer calories than are esti-
mated to be necessary for weight mainte-
nance. An ADA technical review paper on
the prevention and treatment of obesity
(326) concluded when such diets are
used alone in patients with type 2 diabetes
as well as in the general population, par-
ticipants generally lose 10% of initial
body weight (329). However, an average
of 33% of the lost weight is usually re-
gained in the year after treatment, and al-
most all of the lost weight may be
regained within 5 years (330). Neverthe-
less, standard weight-reduction diets may
still be recommended for overweight pa-
tients with type 2 diabetes as some people
can lose weight with them and maintain
the weight loss, particularly if they in-
crease their physical activity.
Structured meal replacements pro-
vide a dened amount of energy (usually
200300 calories), often as a prepack-
aged meal, snack bar, or formula product.
Most of the energy is derived from protein
and carbohydrate. Vitamins, minerals,
and ber may also be included. Use of
meal replacements once or twice daily to
replace a usual meal can result in signi-
cant weight loss (331335). Presumably
the meal replacement causes a reduction
in energy intake by eliminating the choice
of type and amount of food. Weight loss
can be as much as 11% of starting weight
at 2 years, but meal replacement therapy
must be continued if weight loss is to be
maintained; attrition may occur in about
33% of patients (331).
VLCDs provide 800 or fewer calories
daily, primarily from protein and carbo-
hydrate, with mineral and vitamin sup-
plementation. These diets can produce
substantial weight loss and rapid im-
provements in glycemia and lipemia in
patients with type 2 diabetes (301,336).
Of note, reductions in glycemia occur be-
fore signicant weight loss, suggesting
that caloric restriction plays an important
role in correcting hyperglycemia. Unfor-
tunately, when VLCDs are stopped and
self-selected meals are reintroduced,
weight gain is common (337,338). Most
people treated with VLCDs are not able to
maintain long-term weight loss. Thus
VLCDs appear to have limited utility in
the treatment of type 2 diabetes and
should be considered only in conjunction
with a structured weight-maintenance
program.
Pharmacological therapy. If energy bal-
ance is regulated by a hypothalamic con-
trol center that produces and responds to
biochemical signals, it might be possible
to inuence the control center pharmaco-
logically. This possibility rst received at-
tention with the publication of a
landmark study by Weintraub, who de-
scribed the effects of fenuramine and
phentermine to induce weight loss (339).
When the study was published in 1992, it
initiated widespread increased use of fen-
uramine and phentermine (fen-phen)
for weight loss and maintenance (340).
Before the withdrawal of fenuramine be-
cause of cardiac effects, the combination
of fenuramine and phentermine was
demonstrated to have benecial weight-
loss effects in type 2 diabetic subjects
(341).
Since the withdrawal of fenuramine
and its dextroenantiomer dexfenura-
mine, only a limited number of weight-
loss medications remain available in the
U.S. Some are listed in Table 5. Phenter-
mine continues to be available, but ap-
pears to have limited efcacy when used
as a single agent. Sibutramine suppresses
the appetite by inhibiting reuptake of se-
rotonin and norepinephrine in the central
nervous system. A 24-week, placebo-
controlled study compared sibutramine
Table 5 Selected weight-loss drugs available in the U.S.
Drug Mechanism of action FA Labeling
Phentermine Nonadrenergic; appetite
suppression and/or
stimulation of metabolic rate
Short-term usage
Sibutramine Serotonin and norepinephrine
reuptake inhibition; appetite
suppression
Safety and effectiveness beyond
1 year not determined
Orlistat Inhibition of pancreatic lipase;
partial malabsorption of fat
Safety and effectiveness beyond
2 years not determined
Technical Review
160 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002
and diet to placebo and diet in type 2 di-
abetic subjects (342). Subjects treated
with sibutramine lost 4.0 kg more weight,
but did not have a signicant improve-
ment in HbA
1c
levels when compared to
subjects treated with placebo. Orlistat is a
medication that inhibits pancreatic lipase
and causes malabsorption of a portion of
ingested fat. In a 1-year, placebo-
controlled study comparing orlistat and
diet to placebo and diet in type 2 diabetic
subjects, the orlistat group lost 6.2% of
initial body weight as compared to 4.3%
weight loss in the placebo group (343). In
the orlistat group, HbA
1c
decreased by
0.2%, whereas in the placebo group it in-
creased by 0.3%. In a second 1-year, pla-
cebo-controlled study of orlistat, a
diabetic subgroup experienced a reduc-
tion in HbA
1c
that was 0.5% more with
orlistat than with placebo (344).
The available data suggest that weight
loss medications may be useful in the
treatment of overweight patients with
type 2 diabetes. However, the effect of
these medications is modest. The data
also suggest that these drugs work best in
conjunction with lifestyle strategies. In
addition, like antihypertensive and anti-
hyperlipidemic medications, these medi-
cations must be continued to maintain
any benecial effect. As more is learned
about the regulation of energy balance,
new weight-loss drugs should become
available.
Gastric reduction surgery. Gastric re-
duction surgery can be an effective weight
loss treatment for severely obese patients
(including those with type 2 diabetes)
(345347). A National Institute of Health
Consensus Development Panel has rec-
ommended that such surgery be consid-
ered in patients with type 2 diabetes and
with a BMI 35 kg/m
2
(348). The two
surgical procedures most widely used are
vertical banded gastroplasty and gastric
bypass. Both procedures involve creation
of a small (2550 ml) gastric pouch to
receive food. This small pouch permits
consumption of small meals without epi-
gastric pain or vomiting. Larger meals or
large uid intakes cause pain and vomit-
ing.
In a series of 70 obese patients treated
with vertical banded gastroplasty, median
weight losses 1 and 3 years after surgery
were 37 and 32 kg, respectively (345). In
a large series of 515 obese patients treated
with gastric bypass, mean weight losses at
1 and 3 years were 50 and 45 kg, respec-
tively, and weight loss was well main-
tained in 44 patients who achieved 10
years of follow-up (346). Within the sub-
group of 137 patients in this study who
had type 2 diabetes, 107 (78%) experi-
enced clinical remission of diabetes. From
a group of 500 patients consecutively
treated with laparoscopic adjustable gas-
tric band surgery, 50 patients with type 2
diabetes were studied preoperatively and
again 1 year after surgery (347). Their
postoperative mean weight loss was 27
kg, with signicant improvement in all
measures of glucose metabolism and re-
mission of diabetes in 32 (64%) patients,
major improvement in control of diabetes
in 13 (26%), and no change in 5 (10%).
Potential adverse effects of gastric re-
duction surgery include perioperative
mortality in 12% of patients, wound de-
hiscence, vitamin and mineral decien-
cies, cholelithiasis, inability to eat certain
types of food (particularly meat, un-
toasted bread, and raw fruit), and persis-
tent vomiting (345348). Prophylactic
treatment with ursodiol may prevent gall-
stone formation (349).
It is unfortunate that there are no data
comparing medical and surgical ap-
proaches to weight loss in obese patients
with type 2 diabetes; thus the relative
benets and risks of surgical approaches
are uncertain. In the absence of data de-
ning benets and risks, gastric reduction
surgery probably should be considered
unproven in treating diabetes.
There is strong evidence for the fol-
lowing statements:
In insulin-resistant individuals, re-
duced energy intake and modest
weight loss improve insulin resistance
and glycemia in the short term.
Structured programs that emphasize
lifestyle changes, including education,
reduced fat (30% of daily energy) and
energy intake, regular physical activity,
and regular participant contact can pro-
duce long-term weight loss of 57% of
starting weight.
Exercise and behavior modication are
most useful as adjuncts to other weight-
loss strategies. Exercise is helpful in
maintaining weight loss.
Nutrition interventions, such as stan-
dard weight-reduction diets, when
used alone are unlikely to produce
long-term weight loss. Structured, in-
tensive lifestyle programs are neces-
sary.
Optimal strategies for preventing and
treating obesity long-term have yet to
be dened.
There is some evidence for the follow-
ing statement:
Currently available weight-loss drugs
have modest benecial effects in pa-
tients with diabetes. These drugs
should be used only in people with BMI
27.0 kg/m
2
.
There is limited evidence for the fol-
lowing statement:
Gastric reduction surgery can be con-
sidered for patients with diabetes and a
BMI 35.0 kg/m
2
. Long-term data
comparing the benets and risks of gas-
tric reduction surgery to those of med-
ical therapy are not available.
Micronutrients and diabetes
Adequate intake of micronutrients within
the range of Dietary Reference Intake
(DRI) prevents deciency diseases and is
important in maintaining the health and
well-being of patients with diabetes. Nu-
trient recommendations for adults, ado-
lescents, and children with type 1 or type
2 diabetes and for women with diabetes
during pregnancy and lactation are simi-
lar for people with or without diabetes
(350355). However, uncontrolled dia-
betes is often associated with micronutri-
ent deciencies (356,357).
Individuals with diabetes should be
educated about the importance of acquir-
ing daily vitamin and mineral require-
ments from natural food sources, and
about the potential toxicity of megadoses
of vitamin and mineral supplements. In
select groups, such as elderly individuals,
pregnant or lactating women, strict vege-
tarians, or individuals on calorie-
restricted diets, supplementation with a
multivitamin preparation is advisable
(16). However, vitamin and mineral sup-
plementation in pharmacological dosages
should be viewed as a therapeutic inter-
vention and, as with medications, be sub-
jected to placebo-controlled trials to
demonstrate its safety and efcacy.
To determine how much of a specic
micronutrient an individual needs on a
daily basis, four estimates of DRIs have
been made by the Institute of Medicines
Food and Nutrition Board: Estimated Av-
erage Requirement (EAR), the Recom-
Franz and Associates
DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002 161
mended Dietary Allowance (RDA), the
Adequate Intake (AI), and the Tolerable
Upper Intake Level (UL). The RDA is a
daily intake level that is sufcient to meet
the nutrient requirement of nearly all
(9798%) healthy individuals within a
specic age, sex, life stage, and physiolog-
ical state; the UL is the largest amount of a
nutrient that is likely to pose no risk of
adverse health effects for almost all the
general population (350353). Table 6
provides RDAs for certain vitamins and
minerals and upper limits for those
deemed harmful at high dosages.
Evaluation of the micronutrient sta-
tus of patients with diabetes begins with a
careful clinical history and should include
a food/nutrition history to document use
of health food; over-the-counter vita-
min, mineral, and herbal supplements;
food supplements; and methods of pre-
paring food. Laboratory evaluation of mi-
cronutrient status is confounded by
methodological problems and, as a result,
does not always dene micronutrient de-
ciencies. For example, wide seasonal
variations for vitamin D occur in some
parts of the country, and serum mea-
surements of intracellular cat ions poorly
reect body stores. However, measure-
ments of serum folate, vitamin B
12
, vita-
min D, calcium, potassium, magnesium,
and iron concentrations may be clinically
useful.
Antioxidants and vitamins. An Insti-
tute of Medicine report concluded that
consuming megadoses of dietary antioxi-
dantsvitamin C, vitamin E, selenium,
beta carotene, and other carotenoids
has not been demonstrated to protect
against cardiovascular disease, diabetes,
or various forms of cancer, nor does
megavitamin use necessarily prevent ba-
sic nutritional deciencies. In fact, the op-
posite may be true. High dosages of
antioxidants may lead to health problems,
including diarrhea, bleeding, and toxic
reactions (350). Although results from a
large number of population-based studies
have suggested a link between antioxi-
dants and a lower incidence of certain
Table 6 Adult DRIs for select vitamins and minerals
RDA Tolerable upper intake level
Adverse effects upon which
upper intake level is based
Vitamin A 700 g/day for women 900 g/day
for men
3,000 g/day
Vitamin B
6
1.3 mg/day 100 mg/day Sensory neuropathy
Vitamin B
12
2.4 g/day Insufcient data to set upper intake level
Folic acid 400 g/day of dietary folate
equivalents
1,000 g/day from fortied food and
supplement intake (exclusive of food
intake)
Niacin 14 mg/day niacin equivalents for
women, 16 mg/day niacin
equivalents for men
35 mg/day niacin equivalents Flushing
Riboavin 1.1 mg/day for women, 1.3 mg/day
for men
Insufcient data to set upper intake level
Thiamin 1.1 mg/day for women, 1.3 mg/day
for men
Insufcient data to set upper intake level
Vitamin C 75 mg/day for women, 90 mg/day
for men
2,000 mg/day Diarrhea and other
gastrointestinal disturbances
Vitamin E 15 mg/day -tocopherol 1,000 mg/day Hemorrhage
Calcium 1,000 mg/day for adults age 50
years, 1,200 mg/day for adults
age 50 years
2,500 mg/day
Chromium Insufcient data to set RDA; adequate
intake is 25 g/day for women and
35 g/day for men
Not established
Iron 8 mg/day for men and postmeno-
pausal women, 18 mg/day for
premenopausal women
45 mg/day Gastrointestinal disturbances
Magnesium 320 mg/day for women, 420 mg/day
for men
350 mg/day from supplements
(exclusive of intake from food and
water)
Selenium 55 g/day 400 g/day Selenosis
Vanadium Insufcient data to set RDA or
adequate intake
1.8 mg/day
Zinc 8 mg/day for women, 11 mg/day
for men
40 mg/day Interference with the
absorption of copper
From the Institute of Medicine Food and Nutrition Board.
Technical Review
162 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002
chronic diseases, the Institute of Medi-
cines comprehensive review of the scien-
tic evidence concluded it was not certain
that antioxidants were responsible for any
benet.
Antioxidants. Because diabetes may be a
state of increased oxidative stress, there
has been interest in prescribing antioxi-
dant vitamins to patients with diabetes.
Large observational studies have shown a
correlation between dietary or supple-
mental consumption of antioxidants and
a variety of clinical outcomes, such as pre-
vention of disease states (358377).
However, large, placebo-controlled clini-
cal trials have failed to show a benet
from antioxidants and, in some instances,
have suggested adverse effects (378
383). Of particular interest is the Heart
Outcomes Prevention Evaluation Trial,
which included 9,541 subjects, 38% of
whom had diabetes (378). Supplementa-
tion with vitamin E (400 IU/day) for 4.5
years did not result in any signicant ben-
et.
Several placebo-controlled studies of
small numbers of subjects have found
benecial effects of antioxidants on phys-
iological and biochemical end points
(384388). However, most of these nd-
ings have not been conrmed. In addi-
tion, concern remains about potential
long-term toxicity of antioxidants. Two
trials with beta carotene found an unex-
pected increase in the incidence of lung
cancer in those randomized to beta caro-
tene (380,382).
Folate. The role of folate in preventing
birth defects is widely accepted and has
been the impetus for folate fortication of
wheat and grain products in the U.S.
(351). Because of the association between
elevated serum homocysteine levels and
cardiovascular disease, there has been in-
creasing interest in folate supplementa-
tion to lower homocysteine (389).
However, the role of folate supplementa-
tion in reducing cardiovascular events is
far from settled. It is noteworthy that
there are no health concerns with folate
supplementation, except for aggravating
vitamin B
12
deciency and occasionally
causing seizures in people with epilepsy
and marginal folate status who are receiv-
ing anticonvulsants. Folate supplementa-
tion trials are currently ongoing and are
likely to yield important information.
B vitamins. The role of vitamins B
1
,B
6
,
and B
12
in the treatment of diabetic neu
-
ropathy has not been established; there-
fore, supplementing diet with B vitamins
cannot be recommended as a standard or
routine therapeutic option (356,357). It
has been suggested from some studies
that nicotinamide might preserve -cell
mass in newly diagnosed type 1 diabetic
subjects, but the number of subjects en-
rolled in these studies has not been large
enough and the treatment effect was not
clear enough to warrant application of the
ndings (390,391).
Minerals. Deciencies of certain miner-
als, such as potassium and magnesium,
and possibly zinc and chromium, may
predispose a person to carbohydrate in-
tolerance. Whereas the need for potas-
sium or magnesium replacement is
relatively easy to detect based on low se-
rum levels of these minerals, the need for
zinc or chromium supplementation is
more difcult to detect (356,357).
Chromium. There have been two ran-
domized, placebo-controlled studies in
Chinese diabetic subjects where chro-
mium supplementation has had bene-
cial effects on glycemia (392,393).
However, the study populations may
have had marginal baseline chromium
status. In the rst study (392), the chro-
mium status was not evaluated either at
baseline or after supplementation. Other
smaller studies have also suggested a role
for chromium supplementation in the
management of diabetes (394), glucose
intolerance (395), gestational diabetes
(396), and corticosteroid-induced diabe-
tes (397). Results from these studies indi-
cate that the dosage and formulation of
chromium used signicantly inuences
the outcome. In one study of patients with
diabetes (392), 1,000 g/day of chro-
mium picolinate was more effective than
200 g/day. Similarly, in gestational dia-
betes, 8 g kg
1
day
1
of chromium
was more effective than 4 g kg
1
day
1
(396). In contrast, two well-
designed studies in the U.S. (398,399)
and two in Finland (400,401) failed to
demonstrate any signicant benetof
chromium supplementation in patients
with diabetes. The latter studies used
chromium chloride, which may not be as
bioavailable as chromium picolinate. At
the present time, benet from chromium
supplementation in diabetic individuals
has not been conclusively demonstrated.
The Institute of Medicine Food and
Nutrition Boards DRIs found insufcient
evidence to set an estimated average re-
quirement for chromium. An adequate
intake was determined based on esti-
mated mean intakes. The adequate intake
for adult men 51 years is 30 g/day and
for women 51 years is 20 g/day. How-
ever, few serious adverse effects have been
associated with excess intake of chro-
mium from food, and therefore a tolerable
upper intake level has not been estab-
lished (352).
Zinc. Another area of current interest in
micronutrient supplementation is the role
of zinc in diabetic individuals. Small stud-
ies in older subjects with diabetes have
suggested some benet from zinc supple-
mentation in healing skin ulcerations
(356,357). A more recent placebo-
controlled trial with a formulation of zinc
and rabbit prostatic extracts found a sig-
nicant reduction in HbA
1c
in subjects
randomized to the active treatment arm
(402). However, in that study, those ran-
domized to the active treatment had
higher baseline HbA
1c
levels than those
randomized to placebo.
Calcium. The rationale for recommend-
ing daily intakes of 1,0001,500 mg of
calcium, especially in older subjects with
diabetes (403), is based on the recom-
mendations of the Institute of Medicine
Food and Nutrition Board (353) and the
National Institutes of Health Consensus
Development Panel on Osteoporosis Pre-
vention, Diagnosis, and Therapy (404).
This recommendation appears to be safe
and likely to reduce the incidence of os-
teoporosis in older individuals. Vitamin D
is also required for optimal calcium ab-
sorption, and a recommended vitamin D
intake of 400600 IU/day has been estab-
lished for adults (353,404). The uncer-
tainty of the value of calcium
supplementation in younger individuals
and potential long-term benets have
been discussed in a critical review by Ka-
nis (405).
Vanadium. The role of vanadium salts in
diabetes has been explored in several
small studies. There is no clear evidence
of efcacy and there is a potential for tox-
icity (406 409).
Herbal preparations. A full review of
herbal preparations and issues is outside
the scope of this technical review paper. A
variety of herbal preparations have been
shown to have modest short-term bene-
cial effects on glycemia. Of these, the best
studied is American ginseng (410,411).
Many herbal supplements used to treat
obesity also have caffeine and ephedrine-
containing herbs in them. Commercially
Franz and Associates
DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002 163
available products are not well standard-
ized, varying greatly in content of active
ingredients. In addition, some herbal
preparations have been found to surrep-
titiously include pharmaceutical agents
that produce hypoglycemia. Herbal prep-
arations also have the potential to interact
with other medications. Therefore, it is
important that health care providers
know when their patients with diabetes
are using these products.
There is some evidence for the follow-
ing statements:
There is no clear evidence of benet
from vitamin or mineral supplementa-
tion in patients with diabetes who do
not have underlying deciencies. Ex-
ceptions include folate for prevention
of birth defects (strong evidence) and
calcium for prevention of bone disease
(some evidence).
Although difcult to ascertain, if de-
ciencies of vitamins and minerals are
identied, supplementation can be
benecial.
Routine supplementation of the diet
with antioxidants is not advised be-
cause of uncertainties related to long-
term efcacy and safety.
The following statements are based
on expert consensus:
Select populations, such as elderly in-
dividuals, pregnant or lactating
women, strict vegetarians, and people
on calorie-restricted diets, may benet
from supplementation with a multivita-
min preparation.
In individuals with diabetes, there is no
evidence to suggest long-term benet
from herbal preparations.
Alcohol and diabetes
According to data for the period 1989
1991, alcohol accounts for 2.5% of en-
ergy intake in U.S. adults (412) compared
with the previous 5% based on
NHANES II data (19761980) (413). It is
not clear whether this change is attribut-
able to decreased intake or to method-
ological differences in the measurement
of alcohol intake. Nearly 67% of the adult
U.S. population are reported to drink al-
coholic beverages, whereas 33% claim to
abstain from them (414). People with di-
abetes undoubtedly fall into both catego-
ries.
The alcohol in distilled spirits (hard
liquor), wine, and beer is ethanol (ethyl
alcohol, C
2
H
5
OH). It is the by-product of
the oxidation of sugars by yeast enzymes
(fermentation). One drink or alcoholic
beverage is commonly dened as 12-oz
beer, 5-oz glass of wine, or 1.5-oz glass of
distilled spirits, each of which contains
15 g of alcohol. The cardioprotective
effects of alcohol are not determined by
the type of alcoholic beverage (415,416).
A summary of ecological, case-control,
and cohort studies concluded that all al-
coholic drinks are linked with lower risk
of coronary heart disease, so that much of
the benet is from the alcohol itself rather
than other components of each type of
drink (415).
The same precautions that apply to
the general population regarding the use
of alcohol apply to individuals with dia-
betes. Abstention from alcohol should be
advised for women during pregnancy and
for people with medical problems such as
pancreatitis, advanced neuropathy, se-
vere hypertriglyceridemia (417), or alco-
hol abuse. The Dietary Guidelines for
Americans (16) recommends no more
than two drinks per day for adult men and
no more than one drink per day for adult
women. After consuming comparable
amounts of alcohol, women have higher
blood ethanol concentrations than men,
even with allowances for size differences.
Women, compared to men, have an in-
creased bioavailability of alcohol resulting
from decreased gastric rst-pass metabo-
lism and decreased gastric alcohol dehy-
drogenase activity; this may contribute to
the enhanced susceptibility of women to
the effects of alcohol (418).
Alcohol and blood glucose levels. Al-
coholic beverages can have both hypo-
and hyperglycemic effects in patients with
diabetes, depending on the amount of al-
cohol acutely ingested, if alcohol is con-
sumed with or without food, and if
alcohol use is chronic or excessive. Mod-
erate (419) or severe hypoglycemia (420),
no hypoglycemia (421,422), and hyper-
glycemia (423,424) have all been re-
ported in patients with diabetes after
alcohol ingestion. Ingestion of moderate
amounts of alcohol has also been shown
to blunt the awareness of hypoglycemia in
type 1 diabetic subjects (425).
Moderate amounts of alcohol can en-
hance the glucose-lowering action of ex-
ogenous insulin and certain oral glucose-
lowering agents. Although alcohol does
not affect the rate and degree of decline in
plasma glucose, it appears to alter the
phase of glucose recovery by interfering
with hepatic gluconeogenesis. The hypo-
glycemia induced by alcohol is not ame-
liorated by glucagon because it is caused
by indirect impairment of gluconeogene-
sis and is not associated with excessive
insulin secretion (420).
In type 1 and type 2 diabetic subjects,
it has been shown that ingesting moderate
amounts of alcohol with food has no acute
effect on blood glucose or insulin levels
(419,421,422,426 434). The risk of al-
cohol-induced hypoglycemia during fast-
ing is modest for type 2 diabetic
individuals, and is probably present only
if they are being treated with insulin or
insulin secretagogues.
Relationship of alcohol to other health
risks. Heavy or excessive alcohol con-
sumption is a leading, avoidable cause of
death in the U.S. There may be additional
specic adverse effects of chronic alcohol
consumption for patients with diabetes.
In people with type 2 diabetes, chronic
alcohol ingestion (customary intake of
45 g/day) causes deterioration in long-
and short-term glucose metabolism
(423). Therefore metabolic control
should be carefully monitored if alcohol is
an important component of a patients
diet. The effects induced by excess alco-
hol are reversed after abstinence from al-
cohol for 3 days (423,424).
Epidemiological evidence in nondia-
betic individuals suggests that light-to-
moderate alcohol ingestion in adults is
associated with decreased risk of type 2
diabetes (435437) and stroke (438) and
increased insulin sensitivity (439441),
although insulin sensitivity may be atten-
uated by central adiposity (441). In adults
with diabetes, chronic intake of light-to-
moderate amounts of alcohol (515
g/day) is associated with a decreased risk
for coronary heart disease, perhaps be-
cause of the concomitant increase in HDL
cholesterol (442 444). Prospective,
long-term studies are needed to conrm
these observations.
Alcohol ingestion increases the ca-
pacity for lipoprotein synthesis, especially
of VLDL particles. This increase in syn-
thesis is enhanced by a genetic predispo-
sition, high-fat diet, and diabetes (445).
Increased lipoprotein synthesis may be
more an effect of chronic or excessive al-
cohol intake, as nondiabetic subjects with
fasting hypertriglyceridemia who, in one
Technical Review
164 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002
study, consumed the equivalent of two
alcoholic beverages did not demonstrate
an acute increase in triglycerides (417).
This suggests that even people with hy-
pertriglyceridemia may occasionally use
alcohol in moderation.
There appears to be a U- or J-shaped
relationship between alcohol intake and
blood pressure. Light-to-moderate
amounts of alcohol do not raise blood
pressure (446451). However, a strong
association exists between chronic, exces-
sive intake of alcohol (3060 g/day)
and blood pressure elevation in men and
women. Each additional 10-g increment
of alcohol intake above 30 g/day increases
systolic blood pressure by an average of
12 mmHg and diastolic blood pressure
by 1 mmHg (452). In addition to being a
risk factor for hypertension, alcohol may
interfere with antihypertensive therapy
and may be a risk factor for stroke
(446,452).
There is strong evidence for the fol-
lowing statements:
If individuals choose to drink alcohol,
daily intake should be limited to one
drink for adult women and two drinks
for adult men. One drink is dened as a
12-oz beer, 5-oz glass of wine, or 1.5-oz
glass of distilled spirits.
The type of alcoholic beverage con-
sumed does not make a difference.
When moderate amounts of alcohol are
consumed with food, blood glucose
levels are not affected.
To reduce risk of hypoglycemia, alco-
hol should be consumed with food.
Ingestion of light-to-moderate amounts
of alcohol does not raise blood pres-
sure; excessive, chronic ingestion of al-
cohol raises blood pressure and may be
a risk factor for stroke.
Pregnant women and people with med-
ical problems such as pancreatitis, ad-
vanced neuropathy, severe hypertri-
glyceridemia, or alcohol abuse should
be advised to not ingest alcohol.
There is some evidence for the follow-
ing statement:
There are potential benets from the in-
gestion of moderate amounts of alco-
hol, such as decreased risk of type 2
diabetes, coronary heart disease, and
stroke.
The following statement is based on
expert consensus:
Alcoholic beverages should be consid-
ered an addition to the regular food/
meal plan for all patients with diabetes.
No food should be omitted.
Special considerations
Type 1 diabetes. Nutrition recommen-
dations for a healthy lifestyle for the gen-
eral public are also appropriate for
individuals with type 1 diabetes. What
differs for individuals requiring insulin is
the integration of an insulin regimen into
their lifestyle. With the many insulin op-
tions available, if an individuals preferred
meal routine and food choices are known,
an appropriate insulin regimen can usu-
ally be developed. The food/meal plan
should be based on an assessment of the
individuals appetite, preferred types of
food, and usual eating and exercise sched-
ule, and should reect cultural and ethnic
preferences. The food/meal plan should
be shared with the entire health profes-
sional team so that insulin therapy can be
integrated into the individuals preferred
food and physical activity patterns (46).
As discussed in the CARBOHYDRATE AND
DIABETES section, above, for individuals re-
quiring insulin, the total carbohydrate
content of meals and snacks is the rst
priority and determines the premeal insu-
lin dosage and postprandial glucose re-
sponse (6276,81). Glycemic index and
usual ber content of meals and snacks do
not affect the premeal insulin dosage
(73,81). Subjects in the DCCT who re-
ported following their meal plan at least
90% of the time and adjusted their pre-
meal insulin based on changes in usual
carbohydrate intake had HbA
1c
levels
1.0% lower than those who reported fol-
lowing their meal plan less often (13). For
individuals who are on xed insulin reg-
imens and do not adjust premeal insulin
dosages, consistency of carbohydrate in-
take is the rst priority (77).
Improved glycemic control with in-
tensive insulin therapy is often associated
with an increase in body weight (453
455). In DCCT subjects, a BMI 30
kg/m
2
has been associated with increases
in lipids and blood pressure (456). In the
Pittsburgh Epidemiology of Diabetes
Complications study, moderate weight
gain did not adversely affect lipid proles
if glycemic control was improved (457).
Given the potential for weight gain to ad-
versely affect glycemia, lipemia, blood
pressure, and general health, the preven-
tion of weight gain is desirable. Because
strategies effective in preventing weight
gain have not been dened, treatment of
the adverse metabolic effects of weight
gain is indicated (456).
For individuals with type 1 diabetes,
attention also must be paid to nutrition
therapy for improving lipids and blood
pressure control, and, if present, reducing
microalbuminuria. (See
MEDICAL NUTRITION
THERAPY FOR THE
TREATMENT/PREVENTION OF
ACUTE COMPLICATIONS OF DIABETES AND CO-
MORBID COMPLICATIONS, below, for the con-
ditions comorbid with diabetes).
Hypoglycemia is more frequent in in-
dividuals with type 1 diabetes as blood
glucose levels and HbA
1c
are reduced
(458), and needs to be treated appropri-
ately to prevent cognitive changes, re-
bound hyperglycemia, and weight gain.
With hypoglycemia, 10 g of oral glucose
can raise blood glucose levels by 40
mg/dl (2.2 mmol/l) over 30 min, and 20 g
of oral glucose can raise blood glucose
levels by 60 mg/dl (3.3 mmol/) over 45
min (459). With both treatments, how-
ever, glucose levels begin to fall 60 min
after glucose ingestion. Although glucose
may be the preferred treatment choice,
any form of carbohydrate will raise blood
glucose (460). In one study, adding pro-
tein to the treatment of hypoglycemia did
not affect the response to carbohydrate
treatment or prevent later-onset hypogly-
cemia (203). (See
MEDICAL NUTRITION THER-
APY FOR THE TREATMENT/PREVENTION OF
ACUTE COMPLICATIONS OF DIABETES AND CO-
MORBID COMPLICATIONS, below, for more de-
tails on the treatment/prevention of acute
complications of diabetes.)
Additional carbohydrate may be
needed for unplanned exercise. Carbohy-
drate supplementation is based on the
blood glucose level before exercise, previ-
ous experience with the particular form of
exercise, and the individuals insulin reg-
imen (461). Exercise of moderate inten-
sity increases glucose uptake by 23mg
kg
1
min
1
above usual requirements
(e.g., a 70-kg person would need 8.412.6
g of carbohydrate per hour of exercise)
(1015 g). During high-intensity exercise,
glucose uptake increases by 56mg kg
1
min
1
; however, exercise of this inten
-
sity usually cannot be sustained for long
intervals (462). For planned exercise, re-
duction in the insulin dosage may be the
Franz and Associates
DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002 165
preferred choice to prevent hypoglycemia
(463). Regardless, carbohydrate-
containing food should be readily avail-
able during and after exercise (461,464).
Carbohydrate is needed during exer-
cise lasting longer than 6090 min
(465,466) as well as after such exercise to
replenish muscle glycogen stores (467).
Fluid intake is also essential. It has been
found that 68% carbohydrate solutions
are absorbed better and cause less gastric
upset than regular soft drinks and fruit
juices, which are 1314% carbohydrate
solutions (464).
Type 2 diabetes. Nutrition recommen-
dations for a healthy lifestyle for the gen-
eral public are also appropriate for
individuals with type 2 diabetes. Because
most type 2 patients with diabetes are
overweight and resistant to insulin, MNT
should emphasize lifestyle strategies that
result in reduced energy intake (468
470), usually through reducing the fat
content of the diet, and increased energy
expenditure through exercise (471). Most
patients with diabetes also have dyslipi-
demia and hypertension, making reduc-
tions in dietary intake of saturated fat,
cholesterol, and sodium desirable. There-
fore, the emphasis of nutrition therapy for
type 2 diabetes is on lifestyle strategies to
reduce glycemia, dyslipidemia, and blood
pressure. These strategies should be im-
plemented as soon as the diagnosis of di-
abetes is made (472).
Moderate amounts of short-term
weight loss improve metabolic abnormal-
ities in many individuals with type 2 dia-
betes (473), but not in all (474). Moderate
amounts of weight loss, especially of in-
tra-abdominal fat, reduce insulin resis-
tance and help correct dyslipidemia
(475,476). Intentional weight loss is also
associated with reductions in mortality in
overweight individuals with diabetes
(477). However, the best strategy for ac-
complishing and maintaining weight loss
is unclear and may vary from person to
person.
In the UKPDS, before being random-
ized into study groups, subjects received
3 months of intensive nutrition therapy,
which resulted in an 2% reduction in
HbA
1c
and a mean 5% weight loss (14).
The initial glucose response was reported
to be more related to the decreased energy
intake, with the decrease in body weight
being a secondary response. Fasting
plasma glucose levels of 100 mg/dl (5.6
mmol/l) were maintained only in indi-
viduals who continued a restricted ener-
gy intake; once caloric intake was in-
creased, fasting plasma glucose levels in-
creased, even when weight loss was
maintained.
Increased physical activity is impor-
tant for the maintenance of weight loss.
Furthermore, increased physical activity
can improve glycemia (478), decrease in-
sulin resistance (479,480), and reduce
cardiovascular risk factors in women with
diabetes (481) and may independently re-
duce the risk of mortality in men with
type 2 diabetes (482). A minimum cumu-
lative total of 1,000 kcal/week from phys-
ical activities is recommended (471).
Food intake frequencythree meals
or smaller meals and snacksis not asso-
ciated with long-term differences in glu-
cose, lipid, or insulin responses
(483,484). Therefore, division of food in-
take should be based on individual pref-
erences.
Food containing carbohydrate is an
important component of a healthy diet.
Individuals with type 2 diabetes may ben-
et by knowing what types of food con-
tain carbohydrate (starches, fruits,
starchy vegetables, milk, sweets), portion
sizes, and the number of servings for
meals and, if desired, for snacks. The ef-
fect of carbohydrate on blood glucose and
plasma lipids may depend on the severity
of glucose intolerance (57). With the use
of pre- and postmeal blood glucose mon-
itoring data, it can be determined if ad-
justments in food/meal planning will be
helpful or if medication(s) need to be
combined with nutrition therapy.
When individuals with type 2 diabe-
tes require insulin, consistency in the tim-
ing of meals and carbohydrate content
becomes important. As with type 1 diabe-
tes, exible insulin dosing regimens allow
for variations in food intake and a more
exible lifestyle. Treatment with sulfonyl-
ureas and other insulin secretagogues also
requires consistency in timing and carbo-
hydrate content of meals. Short-acting in-
sulin secretagogues may allow for greater
exibility in mealtimes. People with type
2 diabetes are more resistant to hypogly-
cemia than people with type 1 diabetes;
nevertheless, when type 2 patients with
diabetes being treated with insulin or in-
sulin secretagogues may need to reduce
medication dosages if they are not able to
eat.
MEDICAL NUTRITION
THERAPY FOR SPECIAL
POPULATIONS
Children and adolescents with
diabetes
Most diabetes cases diagnosed in children
are type 1 diabetes, although the preva-
lence of type 2 diabetes in youth is in-
creasing (485 488). Nutrition recom-
mendations for children and adolescents
with type 1 diabetes should focus on achiev-
ing blood glucose goals without excessive
hypoglycemia (489 492). This can be ac-
complished through individualized food
and meal planning, exible insulin regi-
mens and algorithms, self-blood glucose
monitoring, and education promoting deci-
sion making based on outcomes (493). Nu-
trition recommendations for youth with
type 2 diabetes focus on a healthy lifestyle
and treatment goals to normalize glycemia
(494).
There is no research on the nutrient
requirements for children and adoles-
cents with diabetes; therefore, nutrient
recommendations are based on require-
ments for all healthy children and adoles-
cents (350353,495). Children and
adolescents should achieve healthful eat-
ing habits to ensure adequate intake of
essential vitamins and minerals. In gen-
eral, U.S. children are not eating the rec-
ommended amounts of fruits and
vegetables (496), although children with
diabetes may be doing somewhat better
than the general population in some ar-
eas. A 1996 report (178) on dietary intake
of children with type 1 diabetes, ages 49
years, found that their energy, vitamin,
and mineral intakes were adequate,
whereas ber intake was less than recom-
mended. Of concern was a reported mean
saturated fat intake that exceeded the Na-
tional Cholesterol Education Program
(NCEP) recommendations (497). Many
children consumed levels of saturated fat
well above recommendations. The Food
Guide Pyramid, which is a broad tool en-
compassing food preferences and differ-
ences in food choices among various
segments of the population, can be used
to increase selection of fruits, vegetables,
whole grains, and nuts and reduce intake
of total and saturated fat (498).
Energy. Many children with type 1 dia-
betes present at diagnosis with weight loss
that must be restored through insulin ini-
tiation, hydration, and adequate energy
intake. The best method for estimating a
Technical Review
166 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002
child or adolescents energy needs is a
food/nutrition history of a typical daily
intake as obtained from a 24-h recall or
3-day food record, provided that growth
and development are within normal lim-
its. The typical daily energy intake can be
compared to reference intakes for normal
growth and development. An evaluation
of weight gain and growth begins at diag-
nosis by recording height and weight on
the Centers for Disease Control pediatric
growth charts (499). Adequacy of energy
intake can be evaluated by following
weight gain and growth patterns on a reg-
ular basis.
Consideration of a childs appetite
must be given when determining energy
requirements and the nutrition prescrip-
tion. Because energy requirements
change with age, physical activity, and
growth rate, an evaluation of height,
weight, and energy intake is recom-
mended every 36 months (29). Achiev-
ing good metabolic control is essential to
normal growth and development (489).
However, the practice of withholding
food or having the child eat consistently
without an appetite for food in an effort to
control blood glucose is discouraged.
Macronutrients. Macronutrient com-
position of the nutrition prescription is
individualized according to blood glucose
and plasma lipid goals and requirements
for growth and development. Children
and adolescents with type 1 diabetes are
not at high risk for developing lipid ab-
normalities, but should be screened and
monitored according to guidelines issued
by the NCEP in the report of its Expert
Panel on Blood Cholesterol Levels in Chil-
dren and Adolescents (497) and by the
American Academy of Pediatrics (500).
The stepwise approach to dietary man-
agement of lipid abnormalities suggested
by the NCEP recommends a reduction in
total fat, saturated fat, and cholesterol for
children over age 2 years.
Fiber. Dietary ber recommendations
for children with diabetes are the same as
for nondiabetic children. It has been rec-
ommended that children older than age 2
years increase their intake of dietary ber
to an amount equal to or greater than their
age plus 5 g/day (501).
Physical activity. Physical inactivity is
associated with adverse health effects
(502). Intervention strategies for the en-
tire family that promote lifelong physical
activity may help children overcome
these adverse effects. Physical activity
may also provide a lipid-lowering effect in
adolescents with diabetes (503).
Type 2 diabetes in youth. Successful
treatment of type 2 diabetes in children
and adolescents with nutrition therapy
and exercise is comprised of the cessation
of excessive weight gain with normal lin-
ear growth and the achievement of blood
glucose and HbA
1c
goals (494). Nutrition
recommendations for children and ado-
lescents with type 2 diabetes should also
address comorbidities, such as hyperten-
sion and dyslipidemia (494). Behavior
modication strategies to decrease intake
of high-calorie, high-fat food while en-
couraging healthy eating habits and regu-
lar physical activity for the entire family
should be considered. Regular exercise in
obese children, without dietary interven-
tion, has been shown to lead to favorable
changes in plasma triglycerides, serum in-
sulin concentrations, and percent body
fat (504). However, the benets of exer-
cise were lost when the children became
less active. Intervention strategies should
be culturally appropriate, sensitive to
family resources, provided to all caregiv-
ers, and followed consistently by all
health care providers.
Adolescents whose parents have type
2 diabetes have more risk factorshigher
BMI, plasma cholesterol, plasma triglyc-
erides, serum insulin, plasma glucose,
and insulin-resistance index and lower
plasma HDL cholesterol compared
with adolescents whose parents do not
have diabetes (505). These risk factors
can be detected early and provide incen-
tive for interventions, such as control of
weight gain and increased exercise.
There is some evidence for the follow-
ing statements:
Individualized food/meal plans, insulin
regimens using basal and bolus insu-
lins, and insulin algorithms can provide
exibility for children with type 1 dia-
betes and their families to accommo-
date irregular meal times and
schedules, varying appetite, and vary-
ing activity levels.
Blood glucose monitoring data can be
used to integrate an insulin regimen
into the meal/snack and exercise sched-
ules.
Nutrient requirements for children and
adolescents with type 1 or type 2 dia-
betes appear to be similar to those for
same-age nondiabetic children and ad-
olescents.
In obese children, increased physical
activity improves plasma lipids and in-
sulin sensitivity.
The following statement is based on
expert consensus:
Successful lifestyle treatment regimens
for youth with type 2 diabetes have not
been dened.
Pregnant and lactating women
During pregnancy, the goals of nutrition
are similar for women with and without
diabetes. MNT goals are to provide ade-
quate maternal and fetal nutrition, energy
intake for appropriate maternal weight
gain (506), and any necessary vitamin and
mineral supplements. For pregnancy
complicated by diabetes, nutrition ther-
apy should also attempt to achieve and
sustain optimal maternal blood glucose
control. A favorable pregnancy outcome
is dened as gestational duration of
39 41 weeks and live birth of an infant
weighing 6.6 8.8 lb. (34 kg) (355).
Weight gain/energy requirements. In-
fant birth weight is related to maternal
size and weight gain during pregnancy.
Recommended weight gain goals are
based on pregravid BMI and should be
steady and progressive (355). For obese
women (BMI 30 kg/m
2
), a relatively
small weight gain of 7 kg is recom-
mended during pregnancy (507). For un-
derweight women (BMI 19.8 kg/m
2
),
greater weight gain (up to 18 kg) is rec-
ommended. A normal-weight woman
should gain 1.4 2.3 kg/month during the
rst trimester and 0.50.9 kg/week dur-
ing the rest of her pregnancy. Overweight
women should gain weight at 50% of
these rates (355).
Energy intake should be sufcient to
promote appropriate weight gain. Unless
a woman begins pregnancy with depleted
body reserves, energy needs do not in-
crease in the rst trimester. An additional
300 kcal/day are suggested during the
second and third trimesters for increases
in maternal blood volume and breast,
uterus, and adipose tissue; placental
growth; fetal growth; and amniotic uids
(508). Obese women with ample body fat
stores may require fewer calories. Studies
have reported successful pregnancy out-
comes for women with energy intake of
only 100 kcal/day above prepregnancy
intake during the