WHAT IS DIABETES?
Diabetes is a heterogeneous disease. Traditionally, one distinguishes two major types of diabetes: type 1 diabetes (insulinopenic), which is usually secondary to the autoimmune destruction of the insulin-secreting β cells in the pancreas (insulitis) and usually begins at a young age. These patients require insulin treatment within the first year after the onset of diabetes. Type 2 diabetes is usually seen in elderly individuals. Increasingly, however, it is also seen in the obese young. Type 2 diabetes is characterized by insulin resistance that is, to a large extent, genetically determined. After years or decades, the secretory capacity of the pancreatic islets is exhausted. The patients respond initially to weight reduction, oral hypoglycemic agents, or both. As the disease progresses, these patients usually require insulin.
Matters are much more complex than this simple scheme suggests; up to 10% of elderly patients with diabetes have an autoimmune illness (Late Autoimmune Diabetes in Adults [LADA]). Conversely, 10% to 15% of patients with type 2 diabetes develop diabetes at a relatively young age as a result of genetic abnormalities of insulin secretion (Maturity Onset Diabetes of the Young [MODY]) or premature obesity for reasons of lifestyle. The major health problem in Western populations is currently type 2 diabetes of the adult. It affects approximately up to 10% of the general population. In some populations, the prevalence is much higher. For instance, in Saudi women aged 50 years, the prevalence is no less than 50%. The prevalence increases with advancing age. Currently, the prevalence of type 2 diabetes is increasing throughout the Western world and particularly also in rapidly Westernizing countries, e.g., India and China.
Both type 1 and type 2 diabetes cause similar long-term complications, namely macrovascular disease (coronary heart disease [CHD], cerebrovascular disease, and peripheral arterial disease) and microvascular disease (retinopathy and nephropathy).
THE EPIDEMIOLOGY OF NEPHROPATHY AND END-STAGE RENAL DISEASE IN DIABETES
Diabetic nephropathy, usually in patients with type 2 diabetes, recently has become the single most common cause of end-stage renal disease (ESRD). Currently, more than 50% of patients admitted to start renal replacement therapy at the University of
Heidelberg have type 2 diabetes. Comparable figures have been reported from the United States, where the incidence of ESRD with diabetes as primary diagnosis has stabilized in recent years at 150 new cases per million population per year according to the United States Renal Data System (USRDS) report 2007 (http://www.USRDS.org). These high rates of diabetic nephropathy not only impose a burden on the health budget but are also associated with immense human suffering as a result of amputation, blindness, heart disease, and kidney disease.
WHY IS THE PREVALENCE OF TYPE 2 DIABETES RISING?
Undoubtedly, a strong genetic predisposition plays an important role, as illustrated by family studies and, more specifically, by twin studies, although the genes that are responsible have not been identified. Despite the strong genetic determination, the risk for developing type 2 diabetes is considerably influenced by intrauterine programming (reflected by birth weight) as well as by lifestyle factors. That lifestyle, particularly the diet, plays an important role as illustrated by observations that indicate that the prevalence of type 2 diabetes is very low in periods of nutritional deprivation, for example, during and after World War II in Europe. Conversely, type 2 diabetes becomes extremely prevalent when indigenous populations adopt a Western lifestyle, for example, Pima Indians, inhabitants of the Pacific island of Nauru, or Australian Aboriginals and particularly the increase in South-East Asia.
The current epidemic of obesity throughout the Western world, particularly in the United States, is certainly a major predisposing factor for type 2 diabetes. Why did the predisposition for such an adverse condition as diabetes not disappear during evolution by natural selection? One very persuasive explanation is provided by the so-called thrifty gene hypothesis. According to this theory, survival in our ancestors was often limited by frequent periods of nutritional deprivation. In that case, insulin resistance and the consecutive storage of energy available in visceral adipose tissue from periods of adequate nutrition provided a survival advantage. Consequently, when individuals whose ancestors had been genetically programmed for survival in a lean environment are today exposed to an environment with excessive calorie supply and physical inactivity, this persisting metabolic program causes insulin resistance, central obesity, dyslipidemia, and hypertension. This constellation has been called metabolic syndrome or syndrome X and is thought to be the forerunner of type 2 diabetes. This subject is covered in more detail in Chapter 16.
Several observations suggest that lifestyle modification still provides major benefit even once type 2 diabetes has developed. Australian investigators sent diabetic Australian aborigines back into the desert to adopt the lifestyle of their ancestors as hunters and gatherers. Within several weeks, glycemia and dyslipidemia were reversed. The salutary effects of dietary restriction and physical exercise have been known for several millennia. Wise ancient Indians advised individuals whose (glycosuric) urine attracted flies to visit on foot at least 100 villages—a therapy that involved physical exercise and weight reduction.
THE ROLE OF NUTRITION THERAPY IN THE MANAGEMENT OF DIABETES MELLITUS
Nutrition therapy is not only one of the most challenging aspects of diabetes care but is also an essential component of successful diabetes management. Current thinking about nutrition and diabetes is reviewed in the recent statements of Franz et al. and Sheard in the nutrition recommendations of the American Diabetes Association (ADA). The interested reader is referred to these excellent in-depth reviews.
The goals of nutrition therapy in terms of optimal glycemic control are summarized in
Table 7-1. One major goal is to achieve and maintain near-normal glucose concentrations. A second goal is to manage dyslipidemia, particularly in view of the excessive cardiovascular risk of the patient with diabetes, a risk comparable to that of the survivor of an acute myocardial infarction. Recognition of this risk has prompted a marked downward revision of acceptable low-density lipoprotein (LDL) cholesterol concentrations in the Third Report of the National Cholesterol Education Program.
Table 7-2 summarizes the recommended lipid concentrations for a patient with diabetes.
Another goal is to control or even reverse obesity in type 2 diabetics through lifestyle modifications that include caloric restriction and physical exercise. Clinical data strongly support the potential for moderate weight loss to reduce the risk for developing diabetes. The benefit from loss of weight is improved control of glycemia, of dyslipidemia, and of blood pressure; these interventions often become less effective, however, as the disease progresses.
The dietary recommendations regarding the relative proportions of carbohydrates, protein, and fat have changed with greater insights into the pathologic mechanisms.
Table 7-3 shows that the recommended relative contribution of calories from carbohydrates has progressively increased, whereas the recommended proportion of fat has progressively decreased. The currently accepted recommendations can be summarized as follows. There has been a recent trend, however, to reduce carbohydrate intake compared with previous recommendations and to increase the proportion of unsaturated fat.
CARBOHYDRATE
In contrast to previous opinion, the total amount of carbohydrate in a diet rather than the type of carbohydrate is what is important in controlling postprandial glucose levels. Individuals with diabetes should reduce their intake of low molecular weight sugars (mono- and disaccharides) to the same extent as, but no more than, individuals without diabetes. The general philosophy is that patients with diabetes should eat the same prudent diet that is recommended for the general population. The problem is to adjust the insulin dose, or oral hypoglycemic agents, to dietary carbohydrates, taking into account the effectiveness of insulin (i.e., insulin sensitivity). Although carbohydrates provoke differing glycemic responses, evidence of a long-term benefit is still insufficient to recommend the use of low glycemic index diets as a primary strategy in dietary advice.
FAT
In patients with type 1 diabetes, hyperlipidemia and, to a major extent, hypertriglyceridemia can be reversed by tight glycemic
control. In contrast, in patient with type 2 diabetes dyslipidemia had usually been present even before the onset of diabetes. Although somewhat improved by adequate glycemic control, it usually persists despite dietetic measures. The difficulties with lipid control are aggravated with the onset of renal disease and proteinuria, particularly at nephrotic levels of proteinuria. Specifically in individuals with diabetes and elevated LDL cholesterol, decreasing saturated fat intake to less than 7% of total calories is recommended. In individuals with pronounced hyperglycemia, weight reduction and decreasing intake of sucrose, total carbohydrates, and alcohol are recommended; carbohydrates should be exchanged for more monounsaturated fat (olive oil or canola oil) in the diet. Specific recommendations have been made for patients with chronic kidney disease. Apart from dietary measures, administration of statins is strongly advocated by all recent guidelines.
PROTEIN
The recommended dietary allowance (RDA) for protein in the general population is 0.8 g/kg b.w., or approximately 10% of total calories. The usual protein intake in Europe and in the United States is far greater than RDA. The nutritional requirement for protein in the patient with well-controlled diabetes is not different from that recommended for the general population. However, in hyperglycemic individuals, protein synthesis is decreased and protein breakdown is increased, thus leading to a negative nitrogen balance. During periods of hyperglycemia or weight loss, somewhat higher protein intakes may improve nitrogen balance, but this theory is not proved. The influence of reduced dietary protein intake on the progression of chronic kidney disease (CKD), especially diabetic nephropathy, is discussed in detail in
Chapter 9.
The impressive changes of dietary recommendations to diabetic patients with time and today’s more liberal approach have been nicely summarized by Sheard and Nathaniel (
Table 7-3).
SODIUM CHLORIDE
Blood pressure in diabetic individuals tends to be sodium sensitive. It is wise to follow the recommendation of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure for individuals with hypertension and lower the sodium chloride intake to 6 g per day; the importance of reducing dietary sodium intake has been illustrated by recent studies, which show that reduced sodium intake lowers blood pressure and that sodium intake even predicts cardiovascular mortality. Whether the interesting experimental results showing that in diabetic rats high salt intake reduced proximal tubular reabsorption thus reducing glomerular hyperfiltration via the tubulo-glomerular feedback have clinical implications is not clear. The salient features of the nutritional recommendations by theADAfor individuals with diabetes mellitus are summarized in
Table 7-4.
Alcohol
Several studies documented that moderate alcohol consumption reduced the incidence of type 2 diabetes, and a recent observational study found even less risk of end-stage kidney disease with moderate use of alcohol. Moderate use of alcohol should not be completely discouraged, but an eye must be kept on the sugar content of the beverages and the risk of hypoglycemia in patients on glucose-lowering agents must be considered.
Vitamin D
Vitamin D deficiency increases the risk of onset of type 1 and type 2 diabetes, and there is some evidence that vitamin D and calcium insufficiency negatively influences glycemic control and that supplementation with both nutrients may be beneficial in optimizing glucose control. The pleiotropic effect of Vitamin D on insulin sensitivity is a subject of further studies.
WHAT ARE THE NUTRITIONAL REQUIREMENTS OF PATIENTS WITH DIABETES AND NEPHROPATHY?
To answer this question one has to address several different issues:
Do dietary factors contribute to the development or progression of diabetic nephropathy?
Does the presence of advanced diabetic nephropathy necessitate changes in the management of patients with diabetes?
Does renal replacement therapy have an effect on the management of patients with diabetes?
Management of Lipid Abnormalities in the Patient with Kidney Disease
Nutritional Support in Acute Renal Failure
Nutritional Requirements in Hemodialysis Patients
Exercise and Physical Function in Kidney Disease
