Recent research has focused on higher-protein diets and lower-carbohydrate diets for beneficial effects on glycemia and CVD risk factors. In a small crossover study, a high-protein, low-fat (30% protein, 50% carbohydrate, 20% fat) diet was compared to a low-protein, high-fat (15% protein, 50% carbohydrate, 35% fat) diet, each for 4 weeks. Both diets had beneficial effects on weight loss, fasting glucose, and total and LDL cholesterol, with no differences in postprandial glucose and insulin responses. However, the high-protein, low-fat diet improved both triglyceride levels and blood pressure (Papakonstantinou 2010b). In two small 5-week and 10-week studies of men with untreated diabetes, weight-maintaining diets containing 30% protein, 30% carbohydrate, and 40% fat decreased glycated hemoglobin (% GHb) by 13% at 5 weeks and 25% at 10 weeks with no changes in insulin, glucagon, and blood pressure and without the addition of glucose-lowering medications (Gannon 2010).
Studies thus far on high-protein diets for people with type 2 diabetes have been of short duration and with small numbers of subjects with diabetes. Although beneficial outcomes have been reported, studies on higher protein intakes are usually conducted in research centers or food is provided to subjects, and the ability of individuals to increase protein intake long term is unknown (Brinkworth 2004).
DIETARY FAT AND DIABETES NUTRITION THERAPY
Dietary fats are said to slow glucose absorption and delay the peak glycemic response after consuming carbohydrate foods. However, evidence to support this statement is difficult to find. In an early study in subjects with type 2 diabetes, 5, 15, 30, or 50 g fat (butter) were added to 50 g carbohydrate (potato), resulting in a mean glucose area response that was similar after ingestion of the potato with or without the differing amounts of butter (Gentilcore 2006). In another study, 50 g potato alone or with 100 g butter or 80 g olive oil were compared, and the addition of both fats had no effect on glucose or insulin postprandial responses (Thomsen 2003). In subjects with type 1 diabetes, the addition of 200 kcal (22 g fat) to a standard meal also did not affect the glucose response or insulin requirements (Peters 1993). Therefore, in acute studies, with a limited number of subjects, the addition of fat to meals appears to have minimal effects on postprandial glucose.
Epidemiological data and controlled clinical trials have reported that long-term higher levels of total fat intake results in greater whole-body insulin resistance. However, obesity may complicate the relationship (Lovejoy 2002). The data further support an adverse effect of saturated fatty acids on insulin sensitivity. The DGAC reviewed the evidence for the effect of saturated fatty acid intake on type 2 diabetes or increased risk of CVD and concluded that intake of saturated fatty acids increases total and LDL cholesterol, increases risk of CVD, and increases markers of insulin resistance and risk of type 2 diabetes. The committee concluded from 12 studies published since 2000 and reviewed in the nutrition evidence library that a 5% energy decrease in saturated fatty acids, replaced by MUFAs or polyunsaturated fatty acids, decreases risk of CVD and type 2 diabetes in healthy adults and improves insulin responsiveness in insulin-resistant individuals and individuals with type 2 diabetes (DGAC 2010).
The risk of CVD associated with trans fatty acids is due to their positive association with LDL cholesterol and the reverse association with HDL cholesterol, the effect on inflammatory processes, and their interference with fat metabolism. The majority of trans fatty acids come from hydrogenation of unsaturated fats industrially, but ~1–2% (<2% of total energy intake) is found naturally in the gastrointestinal tracts of ruminant animals, ending up in meats and dairy products. The DGAC concluded that avoiding industrial trans fats is important, but small amounts of ruminant trans fats in the diet is acceptable (DGAC 2010).
The DGAC also reviewed the evidence for the effect of dietary cholesterol. From a review of 16 studies published since 1991, the committee concluded that consumption of one egg per day is not associated with risk of CVD or stroke in healthy adults, although consumption of more than seven eggs per week has been associated with increased risk. They note, however, that in three methodologically strong prospective cohort studies, in individuals with type 2 diabetes, egg consumption (one egg/day) does have negative effects on serum lipids and lipoproteins and does increase risk of CVD. Therefore, it is recommended that dietary cholesterol be limited to <200 mg/day for people with type 2 diabetes (DGAC 2010). Conflicting evidence comes from a study in 65 adults with type 2 diabetes or impaired glucose tolerance comparing a hypoenergetic high-protein, high-cholesterol diet (two eggs/day) to a high-protein, low-cholesterol diet (100 g lean animal protein). At 12 weeks, weight loss was similar and LDL cholesterol was unchanged. All the subjects experienced a reduction in total cholesterol, A1C, and blood pressure (Pearce 2011).
Consumption of n-3 fatty acids (omega-3 fatty acids) from fish or from supplements has been shown to reduce adverse CVD outcomes in persons with and without diabetes. A Cochrane Systematic Review and a second systematic review and meta-analysis concluded that omega-3 supplementation in persons with type 2 diabetes lowers triglyceride levels, but may raise LDL cholesterol and have no effect on glycemic control or fasting insulin (Hartweg 2008; Hartweg 2009) (see Chapter 13).
Endothelial dysfunction precedes the onset of atherosclerosis and the occurrence of CVD risk. The correction of fasting endothelial dysfunction with n-3 fatty acids is reported, but in people with type 2 diabetes, postprandial vascular dysfunction is also of concern. Supplementation with 2 g n-3 fatty acids or olive oil in people with type 2 diabetes revealed that n-3 fatty acids also improved postprandial vascular function (Stirban 2010). The DGAC concluded that two servings of fatty seafood per week (4-oz servings) providing an average of 250 mg/day of n-3 fatty acids decreases risk of CVD (DGAC 2010). The ADA also recommends two or more servings of fatty fish per week (with the exception of commercially fried fish filets) (ADA 2008).
The Acad Nutr Diet EBNPG reviewed a total of 43 studies related to the prevention and treatment of CVD in people with diabetes. It is recommended that cardioprotective nutrition interventions be implemented in the initial series of nutrition therapy encounters, since both glycemic control and cardioprotective nutrition interventions improve the lipid profile, reduce CVD risk, and improve CVD outcomes (Acad Nutr Diet 2008; Franz 2010). Nutrition interventions include reduction in saturated and trans fatty acids and dietary cholesterol and interventions to improve blood pressure. Chapter 13 reviews nutrition therapy for lipid disorders.
SUMMARY OF RECOMMENDATIONS FOR MACRONUTRIENTS
Since no ideal percentages of macronutrients—carbohydrate, protein, and fat—appear to exist, it would seem prudent to base the nutrition prescription for individuals with diabetes on an appropriate energy intake and a healthy eating pattern. Individuals with both type 1 and type 2 diabetes report eating a moderate carbohydrate eating pattern (~45–50% of total kcal), which would appear to be of less importance than total energy intake. However, nutrition interventions must always be based on changes that the individual with diabetes is willing and able to make. Even small changes in food/nutrient intake can result in beneficial outcomes.
Although total carbohydrate intake appears to determine glycemic responses more than the type of carbohydrate (i.e., starch vs. sugar or high- vs. low-GI foods) and because of similarities and conflicting metabolic outcomes from differing amounts