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JDRF/ADA Type 1 Diabetes Sourcebook, Excerpt #7: Nutrition, Part 3

Anne Peters, MD, and Lori Laffel, MD, MPH, Editors
Jane Lee Chiang, MD, Managing Editor

ADA-JDRF-Type-1-Diabetes-Sourcebook-image

Marion J. Franz, MS, RD, CDE; Alison B. Evert, MS, RD, CDE; Gail Spiegel, MS, RD, CDE; Carol Brunzell, RD, CDE; Joyce Green Pastors, MS, RD, CDE; Joshua J. Neumiller, PharmD, CDE, CGP, FASCP; Laurie A. Higgins, MS, RD, LDN, CDE; and Mary Ziotas Zacharatos, RD, CDE, LD

MACRONUTRIENT CONSIDERATIONS (continued)

Carbohydrates

Sugars, starches, and fibers, rather than simple or complex carbohydrates, are the preferred names for carbohydrate categories, since these terms reflect the chemical composition of the carbohydrates.19

The DRIs set a recommended dietary allowance (RDA) of at least 130 g of carbohydrates/day for adults and children.26 This is based on the estimated average requirement for carbohydrate ingestion that will provide the brain with adequate glucose without drawing additional glucose from protein or triglycerides stored in the fat cells (100 g/day), and allows a 15% coefficient of variation for variable brain glucose utilization. The RDA is equal to the estimated average requirement plus twice the coefficient of variation to cover the needs of 97–98% of individuals. Thus, the RDA is at least 130% of the estimated average requirement, or at least 130 g/day of carbohydrate. The ADA notes: “Although brain fuel needs can be met on lower-carbohydrate diets, long-term metabolic effects of very-low-carbohydrate diets are unclear, and such diets eliminate many foods that are important sources of energy, fiber, vitamins, and minerals and that are important in dietary palatability.”11,27….

Carbohydrate intake. Many have thought that individuals with T1D should avoid sugars (especially sucrose and even naturally occurring sugars), assuming that sugars were rapidly absorbed and therefore aggravated hyperglycemia, and suggested replacement with starch. Starches or complex carbohydrates were thought to break down more slowly, thus producing a slower, steadier rise in blood glucose levels. This thinking began to change with research in 1977 that showed the glycemic response to potatoes was a little higher than that of dextrose.30

Recent research has consistently shown that sucrose and other sugars, when consumed separately or as a part of a meal or snack, do not have a greater impact on blood glucose levels as compared to other carbohydrates.31 Investigators replaced 45 g (~20% of calories) of starch with 45 g of sucrose for 6 weeks, with no significant differences in glycemic or lipid responses in T1D and T2D subjects.32 Fructose has a lower glycemic response than glucose if an individual is not insulin deficient.33 The lower response may be caused by its slow rate of absorption and its rapid removal by the liver and storage as glycogen rather than conversion to glucose.34 Sucrose-containing foods can be substituted for other carbohydrates in the meal plan or, if added to the meal plan, covered with insulin.13,31

In DCCT subjects receiving intensive treatment, a lower carbohydrate (37%) intake and higher total (45%) and saturated (17%) fat intakes were associated with worse glycemic control at year 5 compared to a higher carbohydrate (56%) intake (A1C values of 7.5 versus 7.0%, respectively). This finding was independent of exercise and BMI.35 The authors surmise that carbohydrate content is less critical than the total and saturated fat content, to which it is usually inversely related. It is suggested that high-fat meals may interfere with insulin signaling, resulting in a transient increase in insulin resistance,36 and that lower- fat diets reduce basal free-fatty acid concentrations and improve peripheral insulin sensitivity in T1D.27,37

A eucaloric diet higher in carbohydrate and lower in fat was compared to one lower in carbohydrate and higher in monounsaturated fatty acids (MUFAs) to determine dietary effects on CVD risk factors. After 6 months, other than decreased plasminogen activator inhibitor 1 and weight gain in the lower-carbohydrate/MUFA group, there was no significant difference between the groups. This suggests that if individuals choose to lower carbohydrate intake, the calories should be replaced with unsaturated fats (vs. saturated fats), with special attention to total energy intake.27,38

Carbohydrate types (recommendations for those with all types of diabetes). In studies where sucrose was substituted for isocaloric amounts of starch, the Acad Nutr Diet EBNPG concluded: “If persons with diabetes choose to eat foods containing sucrose, the sucrose-containing foods can be substituted for other carbohydrate foods. Sucrose intakes of 10–35% of total energy do not have a negative effect on glycemic or lipid level responses when substituted for isocaloric amounts of starch.”14,15 The ADA also concluded that: “Sucrose-containing foods can be substituted for other carbohydrates in the meal plan, or, if added to the food/meal plan, covered with insulin or other glucose-lowering medications.”13 However, in general, it is recommended that avoiding excess energy and sugar intake promotes a healthier eating pattern. The DGAC suggests limited adding sugar intake to ≤25% of total calories because consuming added sugars at or above this level is more likely to result in poor intakes of essential nutrients.19 For many, consuming this maximum limit can be a very high intake of sugar. For example, for a daily energy intake of ~2,000 kcal, this would be equal to ~31 tsp of added sugars (500 calories or 125 g of carbohydrate). The average daily intake in the U.S. is ~22 tsp sugar (~350 calories, 88 g of carbohydrate). (For comparison: one 12-oz can of cola contains ~9 tsp [~140–150 calories, 35–40 g of carbohydrate]). People with T1D are often made to feel guilt if they choose foods with added sugars. Knowing the total carbohydrate content, including sugars, can assist T1D individuals to make appropriate, enjoyable food choices while maintaining glycemic control. Some recommend that women eat or drink no more than 100 kcal/day from added sugars and men no more than 150 kcal/day.27,39

High fructose corn syrup. High fructose corn syrup is composed of either 42% or 55% fructose and has a similar composition to table sugar (sucrose). The above sucrose recommendations also apply to high fructose corn syrup and would be included in the overall sugar intake. High fructose corn syrup does not differ uniquely from sucrose and other nutritive sweeteners in metabolic effects (glucose, insulin, and triglycerides), subjective effects (hunger, satiety, and energy intake at subsequent meals), and adverse effects such as weight gain.27,40

Fiber and whole grains. The Acad Nutr Diet EBNPG evaluated the effect of fiber intake on glycemic and lipid outcomes in those with diabetes and concluded: “While diets containing 44 to 50 g fiber daily are reported to improve glycemia in persons with diabetes, more usual intakes (up to 24 g/day) have not shown beneficial effects on glycemia. Fiber intake recommendations are similar for patients with diabetes and for the general public (DRI: 14 g/1,000 kcal).”14,15,41 Guidelines recommend including foods containing 25–30 g fiber/day, emphasizing soluble fiber sources (7–13 g) due to fiber’s beneficial effect on lipids.27

The ADA also recommends that those with diabetes choose various soluble and insoluble fiber-containing foods such as legumes, fiber-rich cereals (≥5 g fiber/serving), fruits, vegetables, and whole-grain products due to the vitamins, minerals, and other substances important for good health. Of note, it is difficult to meet dietary fiber recommendations with a low-carbohydrate intake.19,27 Whole-grain foods are equally as important as fiber in reducing CVD risk.

Whole-grain foods contain fiber, minerals, vitamins, phenolic compounds, phytoestrogens, and other unmeasured constituents, which have been shown to lower blood pressure and serum lipids, improve glucose and insulin metabolism and endothelial function, and alleviate oxidative stress and inflammation in the general population.42 In a prospective study of 7,822 women with T2D, intake of cereal fiber, whole grain, and bran were inversely associated with all-cause and CVD mortality during a 26-year follow-up.42 Bran intake had the strongest association, but germ intake was not associated with all-cause or CVD mortality.27

Glycemic index or glycemic load. Glycemic index (GI) measures the relative area under the glucose curve after consuming 50 g digestible carbohydrate compared with 50 g of a standard food, either glucose or white bread. The GI index does not measure how rapidly blood glucose levels increase after eating different types of carbohydrate-containing foods, thus high-GI foods do not necessarily peak quicker compared to low-GI food. Studies comparing different types of low- and high-GI foods and glucose in people without diabetes showed that glucose peaks occurred consistently at ~30 min, regardless of whether the food had a low-, medium-, or high-GI, with a modest difference in glucose peak values between high- and low-GI foods.43 Contrary to popular belief, low-GI foods did not cause a slower rise in blood glucose, nor did they produce an extended, sustained glucose response. It is recommended that if individuals want to use the GI as a method of meal planning, they should be advised on the conflicting evidence of effectiveness and that research studies used various definitions of GI and different food components.14,15,27

The estimated glycemic load of foods, meals, and eating patterns is calculated by multiplying the GI by the carbohydrate amount in each food, and then adding all the individual food values in the meal. The glycemic load index is primarily used in epidemiological research since the extensive calculations make it impractical for meal-planning purposes or prandial insulin dosing.27

Nonnutritive sweeteners and sugar alcohols. Five nonnutritive sweeteners have been approved by the Food and Drug Administration (FDA): aspartame, saccharine, acesulfame K, neotame, and sucralose. Stevia is approved as Generally Recognized As Safe (GRAS). The FDA also sets a sweetener Acceptable Daily Intake (ADI), namely the level one may safely consume daily over a lifetime without incurring risk. The ADI is usually 1/100th of the amount shown to be safe in animal toxicology studies. All nonnutritive sweeteners undergo rigorous scrutiny in preliminary human studies (including people with diabetes and pregnant women), prior to wider public consumption.13 The Acad Nutr Diet EBNPG state that nonnutritive sweeteners alone do not affect glycemic responses, but some products contain energy and carbohydrate from other foods, which need to be accounted for.14,15,27

FDA-approved reduced-calorie sweeteners include sugar alcohols (polyols) such as erythritol, isomalt, lactitol, maltitol, mannitol, sorbitol, xylitol, tagatose, and hydrogenated starch hydrolysates. They have lower postprandial glucose responses than sucrose or glucose, and, on average, contain about 2 cal/g. There is no evidence that the sugar alcohol will reduce energy intake, glycemia, or weight. While safe, they may cause diarrhea, especially in children

Protein

The Acad Nutr Diet EBNPG and the ADA have insufficient evidence to recommend changing the usual protein intake of 15–20% of total daily energy intake for T1D or T2D individuals with normal renal function.13,15 Individuals who consume excessive amounts of protein-rich foods high in saturated fatty acids, those who have insufficient protein intake (less than the RDA of 0.8 g good-quality protein/kg body weight/day or on average ~10% of energy intake), or those with diabetic nephropathy need to consult with their health care provider and dietitian, as the recommendations may differ.27

Studies on protein intake in T1D individuals are limited. A standard lunch (450 kcal) was compared with a protein-added lunch (an additional 200 kcal). The early glucose response was similar, but the late glucose response (2–5 h) was slightly increased and required 3–4 units of additional insulin for those with higher protein intake. However, the total insulin requirement over the 5 h was not increased.44 Larger than usual amounts of protein may modestly increase postprandial glucose levels and may require slightly higher prandial insulin. If less protein than usual is consumed, insulin doses may also need to be decreased. Perhaps the best assumption is that prandial bolus insulin doses cover the carbohydrates and the basal insulin doses cover the protein consumed. Generally, an individual’s protein intake is fairly consistent, and extra insulin is only required when excessive protein is consumed. If lean proteins without fat (e.g., egg whites, skinless chicken) are consumed, additional insulin may not be needed, as protein alone does not necessarily delay glucose release into the blood stream. There is no evidence that suggests protein slows carbohydrate absorption, contributes to sustained glucose elevations, or aids in hypoglycemia treatment.27,45

Dietary Fat

There is no evidence that dietary fats slow glucose absorption and delay peak glycemic response after carbohydrate consumption. A study of T2D subjects showed that adding varying amounts of fat (5, 15, 30, or 50 g butter) to a 50 g carbohydrate meal (potato) resulted in similar postprandial mean glucose area response.46 In another study, 50 g potato alone or with 100 g butter or 80 g olive oil was compared (discrepancy in amounts of fats was due to the 20% water content of the butter), and the addition of both fats had no effect on glucose or insulin postprandial responses.47 In T1D subjects, adding 200 kcal (22 g fat) to a standard meal did not affect glucose response or insulin requirements.44 Therefore, these limited studies show that the addition of fat appears to have minimal effect on postprandial glucose.27

The effects of trans fatty acids on CVD risk are due to their positive association with LDL cholesterol, the effect on inflammatory processes, and their interference with fat metabolism. The reverse association is seen with HDL cholesterol. The majority of trans fatty acids come from commercial hydrogenation of unsaturated fats, 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, while leaving small amounts of ruminant trans fats in the diet.19,27

The DGAC studied the effects of dietary cholesterol. From a review of 16 studies published since 1991, the committee concluded that consumption of one egg/day is not associated with CVD risk or stroke in healthy adults, but eating seven or more eggs/week was associated with increased risk. Omega-3 fatty acids (ω-3) from fish or from supplements have been shown to reduce adverse CVD outcomes in people with and without diabetes. A Cochrane Systematic Review and a second systematic review and meta-analysis concluded that ω-3 supplementation in T2D subjects lowers triglyceride levels but may raise LDL cholesterol and have no effect on glycemic control or fasting insulin.27,48,49 In the ORIGIN Trial, an RCT performed in over 12,000 T2D individuals, supplementation with 1 g of ω-3 fatty acids daily did not reduce CVD events compared to placebo.50

The Acad Nutr Diet EBNPG reviews research on CVD prevention and treatment in people with diabetes. Its guidelines recommend that cardioprotective nutrition interventions start in the initial nutrition therapy encounters, since both glycemic control and cardioprotective nutrition interventions improve the lipid profile, reduce CVD risk, and improve CVD outcomes.14,15 Nutrition interventions include reducing saturated and trans fatty acids and dietary cholesterol and improving blood pressure.27

REFERENCES
  1. Pastors JG, Franz MJ: Effectiveness of medical nutrition therapy in diabetes. In American Diabetes Association Guide to Nutrition Therapy for Diabetes. 2nd ed. Franz MJ, Evert AB, Eds. Alexandria, VA, American Diabetes Association, 2012, p. 1–18
  2. American Diabetes Association. Clinical Practice Recommendations 2012. Diabetes Care 35 (Suppl. 1):S1–S110, 2012
  3. DAFNE Study Group: Training in flexible, intensive insulin management to enable dietary freedom in people with type 1 diabetes: Dose Adjustment for Normal Eating (DAFNE) randomised controlled trial. BMJ 325:746, 2002
  4. Speight J, Amiel SA, Bradley C, Heller S, Oliver L, Roberts S, Rogers H, Taylor C, Thompson G: Long-term biomedical and psychosocial outcomes following DAFNE (Dose Adjustment For Normal Eating) structured education to promote intensive insulin therapy in adults with sub-optimally controlled type 1 diabetes. Diabetes Res Clin Pract 89:22–29, 2010. Epub 18 April 2010
  5. Lawton J, Rankin D, Cooke DD, Clark M, Elliot J, Heller S: UK NIHR DAFNE Study Group: Dose Adjustment for Normal Eating: a qualitative longitudinal exploration of the food and eating practices of type 1 diabetes patients converted to flexible intensive insulin therapy in the UK. Diabetes Res Clin Pract 91:87–93, 2011. Epub 3 December 2010
  6. Pieber TR, Brunner GA, Schnedl WJ, Schattenberg S, Kaufmann P, Krejs GJ: Evaluation of a structured outpatient group education program for intensive insulin therapy. Diabetes Care 18:625–630, 1995
  7. Sämann A, Mühlhauser I, Bender R, Kloos Ch, Müller UA: Glycaemic control and severe hypoglycaemia following training in flexible, intensive insulin therapy to enable dietary freedom in people with type 1 diabetes: a prospective implementation study. Diabetologia 48:1965–1970, 2005. Epub 18 August 2005
  8. Lowe J, Linjawi S, Mensch M, James K, Attia J: Flexible eating and flexible insulin dosing in patients with diabetes: results of an intensive self-management course. Diabetes Res Clin Pract 80:439–443, 2008. Epub 18 March 2008
  9. Delahanty LM, Halford BN: The role of diet behaviors in achieving improved glycemic control in intensively treated patients in the Diabetes Control and Complications Trial. Diabetes Care 16:1453–1458, 1993
  10. Spiegel G: Nutrition therapy for youth with diabetes. In American Diabetes Association Guide to Nutrition Therapy for Diabetes. 2nd ed. Franz MJ, Evert AB, Eds. Alexandria, VA, American Diabetes Association, 2012, p. 143–168
  11. American Diabetes Association: Standards of medical care in diabetes—2012. Diabetes Care 35 (Suppl. 1):S11–S63, 2012; doi:10.2337/dc12-s011
  12. Evert AB: Nutrition therapy for adults with type 1 and insulin-requiring type 2 diabetes. In American Diabetes Association Guide to Nutrition Therapy for Diabetes. 2nd ed. Franz MJ, Evert AB, Eds. Alexandria, VA, American Diabetes Association, 2012, p. 95–116
  13. American Diabetes Association: Nutrition recommendations and interventions for diabetes. Diabetes Care 31 (Suppl. 1):S61–S78, 2008; doi: 10.2337/ dc08-S061
  14. Franz MJ, Powers MA, Leontos C, Holzmeister LA, Kulkarni K, Monk A, Wedel N, Gradwell E: The evidence for medical nutrition therapy for type 1 and type 2 diabetes in adults. J Am Diet Assoc 110:1852–1889, 2010
  15. Academy of Nutrition and Dietetics: Diabetes Mellitus Type 1 & 2 Evidence-Based Nutrition Practice Guideline, 2008. Available at http:// andevidencelibrary.com/topic.cfm?cat=3252. Accessed 30 October 2012
  16. Casey D, Murphy K, Lawton J, White FF, Dineen S: A longitudinal qualitative study examining the factors impacting on the ability of persons with T1DM to assimilate the Dose Adjustment for Normal Eating (DAFNE) principles into daily living and how these factors change over time. BMC Public Health 11:672, 2011
  17. Centers for Disease Control and Prevention: Growth Charts, 2010.
  18. Silverstein J, Klingensmith G, Copeland K, Plotnick L, Kaufman F, Laffel L, Deeb L, Grey M, Anderson B, Holzmeister LA, Clark N: American Diabetes Association: Care of children and adolescents with type 1 diabetes: a statement of the American Diabetes Association. Diabetes Care 28:186–212, 2005
  19. Dietary Guidelines Advisory Committee: Report of the Dietary Guide-lines Advisory Committee on the Dietary Guidelines for Americans, 2010, to the Secretary of Agriculture and the Secretary of Health and Human Services. Washington, DC, U.S. Department of Agriculture, Agricultural Research Service, 2010
  20. Helgeson VS, Viccaro L, Becker D, Escobar O, Siminerio L: Diet of adolescents with and without diabetes: trading candy for potato chips? Diabetes Care 29:982–987, 2006
  21. Mayer-Davis EJ, Nichols M, Liese AD, Bell RA, Dabelea DM, Johansen JM, Pihoker C, Rodriguez BL, Thomas J, Williams D: SEARCH for Diabetes in Youth Study Group: Dietary intake among youth with diabetes: the SEARCH for Diabetes in Youth Study. J Am Diet Assoc 106:689–697, 2006
  22. Patton SR, Dolan LM, Powers SW: Dietary adherence and associated glycemic control in families of young children with type 1 diabetes. J Am Diet Assoc 107:46–52, 2007
  23. Overby NC, Flaaten V, Veierød MB, Bergstad I, Margeirsdottir HD, Dahl- Jørgensen K, Andersen LF: Children and adolescents with type 1 diabetes eat a more atherosclerosis-prone diet than healthy control subjects. Diabetologia 50:307–316, 2007. Epub 29 November 2006
  24. Overby NC, Margeirsdottir HD, Brunborg C, Andersen LF, Dahl-Jør-gensen K: The influence of dietary intake and meal pattern on blood glucose control in children and adolescents using intensive insulin treatment. Diabetologia 50:2044–2051, 2007. Epub 9 August 2007
  25. McLaughlin S: Considerations in caring for older persons with diabetes. In Handbook of Diabetes Medical Nutrition Therapy. Powers MA, Ed. Gaithersburg, MD, Aspen Publishers, Inc., 1996, p. 527–546
  26. Institute of Medicine: Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Washington, DC, National Academies Press, 2002
  27. Franz MJ: Macronutrients and nutrition therapy for diabetes. In American Diabetes Association Guide to Nutrition Therapy for Diabetes. 2nd ed. Franz MJ, Evert AB, Eds. Alexandria, VA, American Diabetes Association, 2012, p. 19–40
  28. Wheeler ML, Dunbar SA, Jaacks LM, Karmally W, Mayer-Davis EJ, Wylie- Rosett J, Yancy WS Jr: Macronutrients, food groups, and eating patterns in the management of diabetes: a systematic review of the literature, 2010. Diabetes Care 35:434–445, 2012
  29. U.S. Department of Agriculture, U.S. Department of Health and Human Services: Dietary Guidelines for Americans, 2010. 7th ed. Washington, DC, U.S. Government Printing Office, 2010
  30. Crapo PA, Reaven G, Olefsky J: Postprandial plasma-glucose and insulin responses to different complex carbohydrates. Diabetes 26:1178, 1977
  31. Academy of Nutrition and Dietetics: Diabetes mellitus type 1 & 2 evidence-based nutrition practice guideline, 2008. Available at http://andevidenceli-brary.com/topic.cfm?cat=3252. Accessed 30 October 2012
  32. Peterson DB, Lambert J, Gerring S, Darling P, Carter RD, Jelfs R, Mann JL: Sucrose in the diet of diabetic patients–just another carbohydrate? Diabetologia 29:216–220, 1986
  33. Uusitupa MI: Fructose in the diabetic diet. Am J Clin Nutr 59 (Suppl.):753S– 757S, 1994
  34. Rumessen JJ, Gudmand-Høyer E: Absorption capacity of fructose in healthy adults. Comparison with sucrose and its constituent monosaccharides. Gut 27:1161–1168, 1986
  35. Delahanty LM, Nathan DM, Lachin JM, Hu FB, Cleary PA, Ziegler GK, Wylie-Rosett J, Wexler DJ: Diabetes Control and Complications Trial/ Epidemiology of Diabetes: Association of diet with glycated hemoglobin during intensive treatment of type 1 diabetes in the Diabetes Control and Com-plications Trial. Am J Clin Nutr 89:518–524, 2009. Epub 23 December 2008
  36. Savage DB, Petersen KF, Shulman GI: Disordered lipid metabolism and the pathogenesis of insulin resistance. Physiol Rev 87:507–520, 2007
  37. Rosenfalck AM, Almdal T, Viggers L, Madsbad S, Hilsted J: A low-fat diet improves peripheral insulin sensitivity in patients with type 1 diabetes. Diabet Med 23:384–392, 2006
  38. Strychar I, Cohn JS, Renier G, Rivard M, Aris-Jilwan N, Beauregard H, Meltzer S, Bélanger A, Dumas R, Ishac A, Radwan F, Yale JF: Effects of a diet higher in carbohydrate/lower in fat versus lower in carbohydrate/higher in monounsaturated fat on postmeal triglyceride concentrations and other cardiovascular risk factors in type 1 diabetes. Diabetes Care 32:1597–1599, 2009. Epub 18 June 2009
  39. Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig RH, Sacks F, Steffen LM, Wylie-Rosett J: on behalf of the American Heart Association Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism and the Council on Epidemiology and Prevention: AHA Scientific Statement: Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association. Circulation 120:1011–1020, 2009
  40. Fitch C, Keim KS; Academy of Nutrition and Dietetics: Position of the Academy of Nutrition and Dietetics: use of nutritive and nonnutritive sweeteners. J Acad Nutr Diet 112:739–758, 2012. Epub 25 April 2012
  41. Franz MJ, Powers MA, Leontos C, Holzmeister LA, Kulkarni K, Monk A, Wedel N, Gradwell E: The evidence for medical nutrition therapy for type 1 and type 2 diabetes in adults. J Am Diet Assoc 110:1852–1889, 2010
  42. He M, van Dam RM, Rimm E, Hu FB, Qi L: Whole-grain, cereal fiber, bran, and germ intake and the risks of all-cause and cardiovascular disease- specific mortality among women with type 2 diabetes mellitus. Circulation 121:2162–2168, 2010. Epub 10 May 2010
  43. Brand-Miller JC, Stockmann K, Atkinson F, Petocz P, Denyer G: Glycemic index, postprandial glycemia, and the shape of the curve in healthy subjects: analysis of a database of more than 1,000 foods. Am J Clin Nutr 89:97–105, 2009. Epub 3 December 2008
  44. Peters AL, Davidson MB: Protein and fat effects on glucose responses and insulin requirements in subjects with insulin-dependent diabetes mellitus. Am J Clin Nutr 58:555–560, 1993
  45. Franz MJ: Protein and diabetes: much advice, little research. Curr Diab Rep 2:457–464, 2002
  46. Gannon MC, Ercan N, Westphal SA, Nuttall FQ: Effect of added fat on plasma glucose and insulin response to ingested potato in individuals with NIDDM. Diabetes Care 16:874–880, 1993
  47. Thomsen C, Storm H, Holst JJ, Hermansen K: Differential effects of satu-rated and monounsaturated fats on postprandial lipemia and glucagon-like peptide 1 responses in patients with type 2 diabetes. Am J Clin Nutr 77:605– 611, 2003
  48. Hartweg J, Perera R, Montori V, Dinneen S, Neil HA, Farmer A: Omega-3 polyunsaturated fatty acids (PUFA) for type 2 diabetes mellitus. Cochrane Database Syst Rev CD003205, 2008
  49. Hartweg J, Farmer AJ, Holman RR, Neil A: Potential impact of omega-3 treatment on cardiovascular disease in type 2 diabetes. Curr Opin Lipidol 20:30–38, 2009
  50. Bosch J, Gerstein HC, Dagenais GR, Díaz R, Dyal L, Jung H, Maggiono AP, Probstfield J, Ramachandran A, Riddle MC, Rydén LE, Yusuf S: ORIGIN Trial Investigators: n-3 fatty acids and cardiovascular outcomes in patients with dysglycemia. N Engl J Med 367:309–318, 2012. Epub 11 June 2012

Used with permission by the American Diabetes Association. Copyright © 2013 American Diabetes Association.

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