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Consequences of Diabetes

on Nutritional Status Topic 21

Module 21.1

Medical Nutrition in Diabetes Mellitus

Michela Zanetti, MD PhD

Coordinator Nutrition Team

Trieste University Hospital, Italy

Learning Objectives

1. Definition of diabetes mellitus

2. Criteria for the diagnosis of diabetes mellitus

3. Medical nutrition therapy for diabetes

3.1. Carbohydrate consistency

3.2. Meal/insulin timing

3.3. Physical activity/exercise

3.4. Weight management

3.5. Nutritional content

4. Nutritional issues during acute and chronic complications

5. Options for treatment

Contents

1. Definitions of diabetes mellitus type 1 (DMT1) and type 2 (DMT2)

2. Diagnosis of DM

3. Target of nutrition therapy in DM

3.1. Consistency of daily carbohydrate intake

3.2. Meal/insulin timing

3.3. Weight management and physical activity

3.4. Energy balance

3.5. Nutritional content

3.5.1. Carbohydrates

3.5.2. Glycaemic index and glycaemic load

3.5.3. Fibre

3.5.4. Sucrose, fructose and non-nutritive sweeteners

3.5.5. Protein

3.5.6. Fat

3.5.7. Micronutrients

3.5.8. Alcohol

3.6. Dietary patterns

4. Specific situations

4.1. Acute complications

4.1.1. Hypoglycaemia

4.1.2. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state

(HHS)

4.2. Chronic complications

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Copyright © by ESPEN LLL Programme 2017

4.2.1. Diabetic autonomic neuropathy

5. Summary

6. References

Key messages

Diabetes mellitus is a complex disease with metabolic and nutritional consequences;

The nutrition prescription for patients with diabetes should target glycaemic control,

blood pressure, and low-density lipoprotein cholesterol;

The nutritional prescription should be individualized to optimally manage pre-

existing diabetes-related complications, avoid those at which the patient is at risk,

and optimize other concomitant conditions;

The process by which nutrition is individualized, based on medical, lifestyle, and

personal factors, is known as medical nutrition therapy and is a cornerstone of

diabetes management and education;

Promoting dietary compliance is important to optimize glycaemic control and to

avoid acute and chronic complications.

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1. Definitions of Diabetes Mellitus Type 1 (DMT1) and 2 (Dmt2) The term diabetes mellitus (DM) describes several conditions associated with altered

carbohydrate metabolism characterized by hyperglycaemia. DM results from a relative or

absolute impairment in insulin secretion, along with varying degrees of peripheral

resistance to insulin action (1).

DMT1 is defined by autoimmune destruction of the pancreatic beta cells, leading to absolute

insulin deficiency. DMT2 is characterized by hyperglycaemia and variable degrees of insulin

resistance. In the long term, hyperglycaemia can impair pancreatic beta cell function and

lead to insulin deficiency. DMT2 is a common disorder strictly associated with obesity.

Patients suffering from DM are at increased risk of macro- and micro-vascular

complications, e.g. cardiovascular disease (CVD), cerebrovascular disease, peripheral

vascular disease, central and peripheral neuropathy, retinopathy, nephropathy and

gastrointestinal problems. These complications are of major importance, since they impair

function and quality of life as well as reducing life expectancy.

2. Diagnosis of DM The diagnosis of diabetes can be established with any of the following criteria (2):

Table 1

Criteria for the diagnosis of diabetes

1. HbA1C ≥6.5 %

OR

2. FPG ≥126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least

eight hours.*

OR

3. Two-hour plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT. The test should

be performed using a glucose load containing the equivalent of 75-gram anhydrous

glucose dissolved in water.*

OR

4. In a patient with classic symptoms of hyperglycaemia or hyperglycaemic crisis, a

random plasma glucose ≥ 200 mg/dL (11.1 mmol/L).

HbA1c: glycated haemoglobin; FPG: fasting plasma glucose; OGTT: oral glucose tolerance

test.

Criteria 2 and 3 were recommended by the American Diabetes Association (ADA) in 2003

for diagnosing diabetes (3). The use of an HbA1c value of ≥6.5 percent (≥48 mmol/mol)

was proposed in 2009 by an International Expert Committee to diagnose diabetes (4), the

ADA, EASD (European Association for the Study of Diabetes), and WHO confirmed the

decision (5, 6).

In the absence of overt hyperglycaemia, criteria 1 to 3 should be confirmed by repeating

the test. However, if two different tests (e.g., FPG and HbA1c) are available and are

concordant for the diagnosis of diabetes, additional testing is not needed. If two different

tests are discordant, the test that is diagnostic of diabetes should be repeated to confirm

the diagnosis (7). The importance of confirming the diagnosis by repeated measurements

is highlighted by the finding that the prevalence of diabetes decreased when the diagnosis

is based on two abnormal measurements rather than on one single abnormal test (8).

Since the different tests (FPG, two-hour plasma glucose and HbA1C) represent different

physiological phenomena, each test will identify different proportions of the population with

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diabetes. It has been suggested that the shift from using the FPG to using HbA1c to

diagnose diabetes may decrease the proportion of patients screening positive (7, 9).

However, in another study the use of HbA1c and FPG was concordant in the diagnosis of

DM in 98% of the population investigated (10). For this reason, in 2011 the WHO concluded

that an HbA1c value of <6.5 % (48 mmol/mol) does not exclude diabetes if diagnosed

using plasma glucose levels (6).

In addition to diabetes, four additional categories have been identified with respect to

glucose metabolism, as shown in Table 2 (3, 5, 7, 11, 12).

Table 2

Categories at normal or increased risk for diabetes

Normal glucose level

FPG <100 mg/dL (5.6 mmol/L).

Two-hour glucose during OGTT <140 mg/dL (7.8 mmol/L).

Increased risk for diabetes (prediabetes)

IFG – FPG 100-125 mg/dL (5.6-6.9 mmol/L).

IGT – Two-hour plasma glucose value during a 75 g OGTT 140-199 mg/dL (7.8-

11.0 mmol/L).

HbA1c 5.7-6.4% (39-46 mmol/mol) or 6.0-6.4% in (4) (42-46 mmol/mol).

FPG: fasting plasma glucose; OGTT: oral glucose tolerance test; IFG: impaired fasting

glucose; IGT: impaired glucose tolerance.

Impaired fasting glucose (IFG) is defined as a fasting plasma glucose of 110-125 mg/dL

(6.1 to 6.9 mmol/L) (2, 13).

Impaired glucose tolerance (IGT) is defined as a FPG <126 (7.0 mmol/L), and a two-hour,

post-OGTT glucose ≥140 mg/dL (7.8 mmol/L) but <200 mg/dL (11.05 mmol/L). HbA1c

levels in the range of 5.7-6.4% (39 to 46 mmol/mol) or 6.0-6.4% (42 to 46 mmol/mol)

according to the International Expert Committee report (4) are associated with the highest

risk of developing diabetes, although the risk increases progressively for hbA1c levels lower

than 6.5 percent (48 mmol/mol).

3. Target of Nutrition Therapy in DM

Diet is very important in the treatment of diabetes. In this setting nutrition should be

targeted at the control of glycated haemoglobin and of body weight by integrating with

diabetes therapy and physical activity, at the management of blood pressure and of low-

density lipoprotein (LDL)-cholesterol. Nutritional prescription should be individualized to

the individual’s needs in order to maintain optimal blood glucose levels, to manage risk

factors and to prevent/delay acute and chronic diabetic complications. In addition, personal

and cultural preferences should be considered and addressed in order to restrict food choice

only when strictly necessary. The relative impact of each nutritional goal varies in different

patients according to the individual’s characteristics.

The nutrition prescription for patients with diabetes is an integral component of diabetes

management and diabetes self-management education (14), and should be managed by a

registered dietitian from the time of diagnosis of DM, and based on medical, lifestyle, and

personal factors.

The effectiveness of nutrition therapy is demonstrated by randomized controlled trials

which have shown a decrease in HbA1c of approximately 0.3-1 % in patients with DMT1

(15, 16) and by 1-2% in DMT2 (17). Glycaemic control is tightly linked to the development

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and progression of neuropathy, nephropathy, retinopathy in both DMT1 and 2, and of

coronary artery disease in patients with DMT1 (18, 19). Diabetes nutrition therapy both

for DMT1 and 2 should be directed at increasing patients’ adherence to the meal plan, at

adjusting insulin dose for meal size and content, at regulating food and/or insulin in

response to hypo/hyperglycaemia and before physical activity, at managing weight

changes while achieving glycaemic control and at preventing acute and chronic

complications. To achieve these goals, the key points of diabetes nutrition therapy include

consistency in daily carbohydrate intake, meal/insulin timing, weight management and

physical activity, energy balance (caloric intake balanced with caloric expenditure) and

nutritional content (balance of selected protein, carbohydrates, and fats).

3.1. Consistency of Daily Carbohydrate Intake

Variations in daily carbohydrate intake can result in unstable glucose control and in

hypoglycaemia in DMT1. Basal-bolus insulin therapy allows for some flexibility in the

carbohydrate content of meals as well as short-acting insulin analogues or insulin pumps.

For patients receiving fixed doses of short- and intermediate-acting insulin, however, day-

to-day regularity in the amount and source and source of carbohydrate at meals and snacks

is important. Regularity in daily carbohydrate intake in these patients has been associated

with a lower HbA1c level, while variations in calorie, protein or fat intake did not affect it

(20).

Several approaches are known to plan meals in order to achieve carbohydrate consistency,

including basic and advanced carbohydrate counting and sample menus. The best approach

for each patient is determined depending on his/her lifestyle and learning capabilities.

Patients using carbohydrate counting consume a predetermined daily amount of

carbohydrate at meals and in snacks, calculated in grams of carbohydrate per food portion

(21). The calculated carbohydrate intake is derived from an optimal percentage of total

calories from carbohydrates, based on nutrition goals and the usual eating pattern.

Patients need to be comfortable with simple arithmetical computations and must be trained

by a dietician to set appropriate meal and snack targets and to measure or estimate portion

sizes and read food labels. Another basic approach to achieve carbohydrate consistency is

by using sample menus, which specify the time and amounts of food to be eaten at each

meal and snack. For type 1 diabetic patients, menus are developed to meet calorie needs,

to provide consistent carbohydrate intake at meals and snacks and to meet individual food

preferences and diabetes nutrition therapy goals. Advanced carbohydrate counting

approaches are based on a more detailed way of counting carbohydrates to maintain good

glucose control by matching mealtime insulin doses to the amount of carbohydrate

ingested.

3.2. Meal/Insulin Timing

Meal timing at regular intervals has traditionally been a cornerstone for diabetic patients

treated with fixed doses of short- and intermediate-acting insulin to achieve goals for

glycaemic control without hypoglycaemia (21). Newer rapidly-acting insulins, however,

allow for more flexibility in meal schedules and content.

Traditional insulin regimens were characterized by the injection of roughly the same

amount of insulin at the same time each day, without taking into account the amount and

timing of carbohydrate intake. This was associated with fluctuations in blood glucose

profiles, exposing the patients to the risk of hyper- and hypoglycaemia.

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The flexibility of intensive therapy regimens with newer insulins allows determination of

the amount of short- or rapid-acting insulin needed to cover an established amount of

carbohydrate. A significant inter- and intra-individual variability at different meals in the

carbohydrate-insulin ratio has however been described. Familiarity with carbohydrate

counting approaches becomes essential in making insulin therapy adjustments.

3.3. Weight Management and Physical Activity

The success of dietary intervention, which is strategic in achieving and maintaining an

appropriate body weight especially in DMT2, is associated with many patient related

factors. Self-monitoring for dietary intake and weight can be helpful in achieving and

maintaining weight loss. Self-monitoring for dietary intake include consciousness of eating

behaviour, refusal of food offered by others, stopping eating when appropriate and

provision of structured meal plans. Exercise is a significant component of diabetes

management. Benefits of exercise include improved glycaemic control, weight control,

reduction in co-morbidities (hypertension, dyslipidaemia, and cardiovascular disease),

improved mood, and quality of life (22, 23). These beneficial effects are more evident in

DMT2. Diabetic patients should perform 30-60 minutes of moderate-intensity aerobic

activity on most days of the week (to a minimum total of 150 minutes of moderate-intensity

aerobic exercise per week) (13, 24). Vigorous exercise should be avoided in the presence

of advanced microvascular complications and of established coronary heart disease. More

exercise may be beneficial for achieving and maintaining long-term weight loss. This should

be considered comprehensively when periodically adjusting the plan for dietary and

pharmacological interventions to optimize glucose control.

3.4. Energy Balance

The importance of caloric intake depends on several factors, including current weight,

weight history, fat distribution and waist circumference, lean muscle mass, genetics and

glycaemic control.

Lowering caloric intake and inducing weight loss are of major importance for overweight

and obese patients with DMT2. It is known also that modest weight loss is associated with

a reduction in clinical risk factors for cardiovascular disease (25).

3.5. Nutritional Content

The optimal mix of macronutrients for patients with DMT1 and 2 is so far controversial (16,

26) as the ideal percentage of calories from carbohydrate, protein, and fat may vary

depending on the individual’s eating patterns, preferences and targets for metabolic

control. In this view, several different eating patterns (low fat, low carbohydrate,

Mediterranean) can be accepted (16, 27).

3.5.1. Carbohydrates

Variations in carbohydrate intake can deeply impact glucose control, particularly in DMT1.

In this context, definitive evidence on the ideal amount of carbohydrates for diabetic

patients is lacking. However, monitoring carbohydrate intake (by basic or advanced

carbohydrate counting) is a very important strategy to improve and maintain glycaemic

control. Amongst the different carbohydrates, intake from fruits, vegetables, whole grains

and legumes should be encouraged (16).

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3.5.2. Glycaemic Index and Glycaemic Load

Foods containing the same amount of carbohydrate can differentially impact plasma

glucose levels because of different glycaemic index and/or glycaemic load:

Notably, glycaemic index is determined by the incremental rise in blood glucose after

ingestion of a portion of the test food containing 50 g of carbohydrate, compared with the

same amount of carbohydrate from a reference food, which is usually white bread or

glucose (28, 29). Some examples of low-glycaemic index foods include non-starchy

vegetables, nuts and legumes. High glycaemic index foods include white bread, and other

refined products made from grains.

In addition to the quality of carbohydrates ingested (i.e. the glycaemic index), the quantity

of carbohydrates also influences the blood glucose response. In this view, the glycaemic

load is the product of the glycaemic index value of a food and its total carbohydrate content

(30). Although glycaemic index and glycaemic load may have a deeper impact on metabolic

control than glycaemic control alone, a modest additional benefit for glycaemic control has

been shown in DM when substituting low-glycaemic load foods for higher glycaemic-load

foods (31). In subjects at increased risk for diabetes low glycaemic index diets have been

associated with improvement of cardiovascular risk factors (32).

The difficulty in defining the effects of glycaemic index and glycaemic load in clinical trials

lies on the fact that their effect is hardly dissectible from that of fibre.

3.5.3. Fibre

Fibre and whole grain intake should be at least equivalent to that recommended for the

general population (14 grams per 1000 calories daily or about 25 g/day for adult women

and 38 g/day for adult men) (13). Their effect on glycaemic control is modest, however

they may improve serum cholesterol and cardiovascular risk factors.

3.5.4. Sucrose, Fructose and Non-nutritive Sweeteners

Intake of sucrose, a disaccharide composed of glucose and fructose, does not significantly

impact glucose control at up to 35% of total daily calories, although care should be taken

to avoid excess calories (33); sucrose can be substituted for other carbohydrates (e.g.

starch) in the meal plan or, if added, covered with insulin. Intake of fructose from fruits

(“free fructose”) may improve glycaemic control as compared with sucrose or starch

without adversely affecting triglycerides as long as it does not exceed 12% of total caloric

content (16). Non-nutritive sweeteners may reduce calorie intake if used to replace caloric

sweeteners, although the evidence in terms of weight reduction is limited (34).

3.5.5. Protein

The ideal amount of dietary protein to be consumed in patients without kidney disease in

order to reach and maintain an optimal glucose control is uncertain (16). Furthermore, it

is unclear whether a low protein diet contributes with other measures (e.g. angiotensin-

converting enzyme (ACE) inhibition and aggressive control of blood pressure and blood

glucose) to reduce cardiovascular risk and to preserve renal function. Thus, protein intake

should be individualized. In the presence of kidney disease (e.g. macro- or

microalbuminuria) a reduction of dietary protein intake is not recommended. Patients

should be encouraged to substitute lean meats, fish, eggs, beans, peas, soy products, and

nuts and seeds for red meat (16). In DMT2 dietary proteins stimulate insulin secretion and

this should be taken into account in the presence of recurrent hypoglycaemia.

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3.5.6. Fat

As for proteins and carbohydrates, the ideal quantity of fat to be consumed in the diet in

DM is uncertain (16). In contrast, the type of fat consumed is more important than quantity

in terms of metabolic control and of cardiovascular risk management. Saturated fats and

trans fatty acids increase the risk of cardiovascular disease; in contrast, monounsaturated

and polyunsaturated fats show a protective effect. Saturated fats should be replaced with

monounsaturated and polyunsaturated fatty acids. An increased consumption of foods

containing omega-3 polyunsaturated fatty acids is recommended; the general suggestion

to assume at least two servings of fish per week applies also to diabetic patients. Trans

fatty acid consumption should be sharply limited.

3.5.7. Micronutrients

Specific deficits in selected vitamins and minerals have been associated with diabetes.

Vitamin D (cholecalciferol) is a lipid-soluble vitamin, which also acts as a hormone. The

major function of vitamin D is maintenance of calcium-phosphorus homeostasis and

promotion of bone mineralization. It has been suggested that low levels of vitamin D and

calcium may predispose to DMT1 and 2 by promoting inflammation and destruction of beta

cells (35). In addition, low vitamin D is associated with insulin resistance, development of

albuminuria, cardiovascular disease and higher HbA1c levels. Although several prospective

observational studies have shown an inverse relationship between circulating 25-

hydroxyvitamin D levels and risk of DMT2, intervention studies are scarce and mostly

inconclusive. Currently vitamin D supplementation is encouraged only in patients who show

evidence of reduced plasma concentrations. The intake of calcium in adults ≥50 years

should be 1200 mg/day and that of vitamin D 800-1000 IU, to maintain hydroxy-vitamin

D levels above 30 ng/ml.

Chromium and magnesium have been associated with insulin sensitivity and glucose

metabolism and their deficits could impact glucose control. However, in the absence of

documented deficiencies no clear benefits from routine vitamin or mineral supplementation

has been shown in diabetic patients (16). Currently, it is suggested that food choice is

optimized in order to satisfy recommended dietary allowance for all micronutrients and

vitamins.

3.5.8. Alcohol

Alcohol intake should be limited to no more than one drink (10g alcohol) per day for women

or two drinks per day for men; alcohol should be consumed with food. Because of an

increased risk of delayed hypoglycaemia particularly if associated with insulin therapy and

secretagogues, patients with DMT1 should closely monitor blood glucose to assess any

immediate or delayed effects of alcohol intake on blood glucose levels (16).

3.6. Dietary Patterns

In order to promote dietary compliance and to individualize the nutritional prescription a

variety of dietary patterns can be accepted to achieve glycaemic control and to target a

desirable body weight in DMT1 and 2, including Mediterranean, vegetarian, vegan, low fat,

and low carbohydrate diets (16). In DMT1 day-to-day carbohydrate consistency should be

emphasized if an intensive insulin therapy regimen is prescribed. In DMT2 monitoring

dietary intake and weight can be a helpful strategy to achieve weight loss.

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4. Specific Situations

4.1. Acute Complications

4.1.1. Hypoglycaemia

Hypoglycaemia can be a frequent event if the patient is not well trained to match

hypoglycaemic therapy with diet and physical activity. Overtreating hypoglycaemia can

result in undesired hyperglycaemia and increased calorie intake, resulting in weight gain;

therefore in case of frequent hypoglycaemic episodes, review and portential revision of any

hypoglycaemic therapy should be performed.

In case of hypoglycaemia (blood glucose <70 mg/dL), in the range of glucose levels

between 51 to 70 mg/dL, intake of 10 to 15 g of fast-acting carbohydrate is recommended,

and of 20 to 30 g of fast-acting carbohydrate if blood glucose levels fall ≤50 mg/dL.

Retesting 15 minutes after ingestion and repeating treatment as needed based on blood

sugar levels is recommended. Once blood glucose is >70 mg/dL, an appropriate insulin

dose to cover carbohydrate intake at the next meal should be administered (36).

4.1.2. Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycaemic State

(HHS)

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS) are two of the

most dangerous acute complications of DM. Each of them represents an extreme in the

spectrum of hyperglycaemia and there may be considerable diagnostic overlap between

them.

The main differences between DKA and HHS consist in the presence of ketoacidosis and,

usually, the degree of hyperglycaemia (37, 38). In DKA, metabolic acidosis is often the

major finding, while the serum glucose concentration is generally below 800 mg/dL (44.4

mmol/L). Serum glucose may be normal or minimally elevated in patients with euglycaemic

DKA. From a pathophysiologic perspective, DKA is a typical complication of DMT1 caused

by severe insulin deficiency. Its typical presentation includes hyperglycaemia, glycosuria,

polyuria and loss of fluids and electrolytes, including sodium and potassium, although their

serum levels are influenced by water balance. Phosphorus and magnesium deficiency also

develop. While the typical total body deficits of electrolytes are similar, total body water

deficit is much more marked in HHS than in DKA (9 vs. 6 litres).

HHS is typically a complication of DMT2. In HHS there is a relative insulin deficiency leading

to hyperglycaemia without ketoacidosis. It is usually precipitated by intercurrent illnesses

such as infection or acute myocardial infarction. Blood glucose levels are exceedingly high,

causing an osmotic diuresis and severe salt and water deficiency. The serum glucose

concentration frequently exceeds 1000 mg/dL (56 mmol/L), the plasma osmolality (Posm)

may reach 380 mOsmol/kg, and neurologic abnormalities are frequently present (including

coma in 25-50% of cases). The definitions and clinical features proposed by the American

Diabetes Association (ADA) for DKA and HHS are shown in Table 3 (39).

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Table 3

Typical laboratory and patient characteristics of DKA and HHS

DKA HHS

Mild Moderate Severe

Plasma glucose (mg/dL)

>250 >250 >250 >600

Plasma glucose (mmol/L)

>13.9 >13.9 >13.9 >33.3

Arterial pH 7.25 to 7.30 7.00 to 7.24 <7.00 >7.30

Serum bicarbonate (mEq/L)

15 to 18 10 to <15 <10 >18

Urine ketones Positive Positive Positive Small

Effective serum osmolality (mOsm/kg)◊

Variable Variable Variable >320

Anion gap >10 >12 >12 Variable

Alteration in sensoria or mental obtundation

Alert Alert/drowsy Stupor/coma Stupor/coma

Anion gap calculation: (Na+) – (Cl– + HCO3–) (mEq/L).

The treatment of DKA and HHS is similar, including fluids and potassium replacement and

intravenous administration of regular insulin or of insulin analogues according to

established algorithms. Frequent monitoring is essential, and underlying precipitating

events should be identified and corrected. Intravenous (IV) fluid replacement to correct

both hypovolaemia and hyperosmolality should be undertaken vigorously within the first

24 hours to correct estimated deficits, with care to avoid an exceedingly rapid reduction in

serum osmolality, which can precipitate cerebral oedema. Indications for sodium

bicarbonate administration to help correct the metabolic acidosis are controversial.

Monitoring involves hourly glucose measurement until stability, basic blood chemistry

profile and venous pH (for DKA) every two to four hours. The course of metabolic acidosis

can be assessed by direct measurement of the serum anion gap.

4.2. Chronic Complications

Both macrovascular (atherosclerosis) and microvascular complications (retinopathy,

nephropathy, and neuropathy) strongly contribute to the burden of diabetes morbidity.

Glucose control is highly related to the development and progression of microvascular

complications; in DMT2, both macrovascular and microvascular complications may be

present at the time of diagnosis (40) and altered glucose levels along with atherogenic

dyslipidaemia and hypertension together increase the risk of macrovascular disease.

Therefore, non-pharmacological interventions (medical nutrition therapy, exercise and

weight reduction) in combination with pharmacological interventions (aggressive

management of blood glucose, blood pressure, and lipids and use of the renin-angiotensin-

aldosterone system blockers) can prevent or delay the onset of complications.

The beneficial effects of strict glycaemic control on microvascular complications have been

demonstrated both in DMT1 and 2 by several prospective, randomized clinical trials, which

have shown that intensive therapy aimed at lowering HbA1c minimizes the risks for

retinopathy, nephropathy and neuropathy (18, 41) both in DMT1 and 2 and decreases the

risk for cardiovascular disease in DMT1 (19). These benefits have to be considered in front

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of the higher risk of severe hypoglycaemia associated with intensive therapy, particularly

in DMT1.

Prevention of cardiovascular disease is a priority in DM patients, especially type 2. To this

aim, aggressive reduction of modifiable risk factors, including comprehensive smoking

cessation, aggressive management of hypertension and cholesterol lowering (with a target

of low-density lipoprotein ≤100 mg/dL), should be undertaken (42). As a matter of fact,

intensive glycaemic alone control does not conclusively impact on cardiovascular outcomes

in DMT2.

Lifestyle interventions (medical nutrition therapy, weight loss, increased physical activity)

are the first steps to be undertaken in all patients affected by DM. Among complications

with nutritional impact gastrointestinal autonomic neuropathy is worth a special mention.

4.2.1. Diabetic Autonomic Neuropathy

Diabetic autonomic neuropathy describes a wide spectrum of symptoms affecting many

organs, including the cardiovascular, gastrointestinal, genitourinary, and neuroendocrine

systems. These abnormalities are most probably related to autonomic neuropathy of the

enteric nervous system.

Poor glucose control and cardiovascular risk factors are associated with the development

of diabetic neuropathy (43). In DMT1 intensive insulin therapy reduced cardiovascular

autonomic neuropathy incidence by 53% (44), this beneficial effect persisting for up to 14

years (45). In DMT2 intensive therapy consisting of lifestyle intervention (including diet,

exercise and smoking cessation) combined with pharmacological treatment (multiple

agents to achieve several therapeutic goals) has been shown to result in a delayed rate of

progression of autonomic neuropathy, a phenomenon with a metabolic memory of 13.3

years (46).

Gastrointestinal autonomic neuropathy is of particular interest as it may affect spontaneous

nutritional intake and nutritional status. The prevalence of gastrointestinal autonomic

neuropathy is unknown. Its clinical manifestations are shown in Table 4.

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Table 4

Abnormalities of gastrointestinal function in DM related to autonomic neuropathy

of the enteric nervous system

Complication Pathophysiology Clinical manifestations

Management

Gastro-

oesophageal reflux disease

-Decreased lower

oesophageal sphincter (LES) pressure -Increased number of transient LES relaxations due to hyperglycaemia -Impaired clearance function

of the tubular oesophagus -Delayed gastric emptying

Pyrosis

Regurgitation

Optimize glucose

control Lifestyle and dietary modifications Antacids Surface agents and alginates

Histamine 2 receptor antagonists Proton pump inhibitors

Gastroparesis -Impaired neural control of gastric function

Nausea Vomiting Abdominal pain

Early satiety Postprandial fullness Bloating

Optimize glucose control Lifestyle and dietary

modifications Antiemetic and prokinetic agents Discontinue incretin-based therapy

Diabetic

diarrhoea

-Disordered motility

- Increased intestinal secretion - Small intestinal bacterial overgrowth - Faecal incontinence - Medications (metformin,

artificial sweeteners)

Watery diarrhoea

Faecal incontinence Constipation

Hydration and

correction of electrolyte and nutrient deficiency Treatment of the underlying cause

Gastro-oesophageal reflux disease (GORD) is characterized by the retrograde passage of

gastric contents into the oesophagus. In DM, GORD may be caused by multiple

mechanisms as listed in Table 4. Its most common clinical manifestations include pyrosis

and regurgitation. The treatment of GORD in DM does not differ from that of GORD in the

general adult population and is summarized in Table 4.

Gastroparesis is characterized by anorexia, nausea, vomiting, early satiety, postprandial

fullness and, in severe cases, weight loss. A strong association between acute and chronic

elevations of blood glucose and delayed gastric emptying has been described (47). Dietary

modifications are the first step in treating gastroparesis; they consist of a limitation of fatty

foods and carbonated beverages, elimination of alcohol and fractionation of meals (small,

frequent meals, low in fat, containing only soluble fibre and of liquid/semiliquid

consistence). Concomitant measures include optimization of glucose control and adequate

hydration. In the case of failure of dietary modifications, pharmacological treatment with

prokinetics (metoclopramide, domperidone and erythromycin) to increase the rate of

gastric emptying can be prescribed (48).

In case of failure of pharmacotherapy in patients with abdominal pain and nausea a

gastrostomy tube for decompression can be considered. In the presence of unintentional

loss of 10% or more of the usual body weight during a period of three to six months,

and/or two or more hospitalizations for refractory symptoms in 6 months, then enteral

nutrition through a jejunostomy can be justified.

Clinical manifestations of diabetic enteropathy include chronic constipation, diarrhoea and

rarely steatorrhoea, or even incontinence. Diabetic diarrhoea may be secondary to a

variety of factors including intestinal dysmotility causing either delayed or accelerated

13


small bowel transit, intestinal oversecretion, bacterial overgrowth, pancreatic exocrine

insufficiency, faecal incontinence due to anorectal dysfunction and/or bile salt

malabsorption secondary to accelerated small bowel transit or bile acid deconjugation due

to bacterial overgrowth, medications (metformin and artificial sweeteners, sorbitol and

polyols). Both diarrhoea and gastroparesis can adversely affect glycaemic control

determining both hyper- and hypoglycaemia. Management of diabetic autonomic

enteropathy depends on the causal factors responsible for the diarrhoea (49). It should

begin with general measures such as hydration and correction of electrolyte and nutrient

deficiency and with symptomatic treatment of diarrhoea. Treatment of the underlying

cause should be directed at correcting aberrant motility and may include rotating antibiotics

for bacterial overgrowth.

5. Summary

Diabetes mellitus is a complex disease with various metabolic and nutritional

consequences. Diet and physical activity are crucial in the comprehensive treatment of

diabetes, especially of DMT1, and are two important components of the medical nutritional

therapy for a diabetic patient. The nutritional plan should be targeted not only at optimizing

glycated haemoglobin, but also at managing plasma lipids and blood pressure. The

prescription must be personalized to each individual’s needs and preferences in order to

minimize the incidence of acute and chronic diabetic complications.

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