Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Proteins

Diets for body weight control and health: the potential of changing the macronutrient composition

Abstract

At the beginning of the last century obesity and type 2 diabetes were treated quite successfully using low-carbohydrate diets. Following the discovery of insulin, the carbohydrate content of the diabetic diet became more liberal, as glycaemia and glycosuria could be controlled, more or less well, with hypoglycaemic medication and insulin treatment. Later, saturated fats and high-plasma cholesterol concentrations were implicated in cardiovascular disease and since then high-carbohydrate diets have become synonymous with ‘health’ and have been conventional nutrition doctrine for the past 40 years. In spite of this, the prevalence of some non-communicable metabolic diseases have increased to epidemic proportions and have led an increasing number of researchers in the fields of medicine and nutrition to challenge the validity of present-day dietary guidelines. There is increasing evidence that diets with a lower, or even very-low, carbohydrate content can help overweight and obese individuals to lose and maintain lost weight, diabetics to control blood glucose with more ease and prevent the development of diabetic complications, while at the same time improving blood lipid profiles and biomarkers of cardiovascular risk. The present review considers the evolution of our diet and questions whether high-carbohydrate diets are indeed synonymous with health.

Introduction

At the beginning of the 19th century, the British economist Thomas Malthus1 developed the theory that human population growth would overwhelm and be controlled by the food supply; shrinking in times of war and famine and expanding in times of plenty. However, for many countries of the developed world that have experienced, and taken advantage of, the industrial, agricultural and technological revolutions; social, political and economic stability has led to food security providing a large and readily available food supply. This has not only resulted in population growth, as predicted by Malthus, but population girth and increased mortality and morbidities from non-communicable diseases, the antithesis of Malthusianism, where a plentiful food supply is associated with population decline.

Interestingly, Darwin used Malthusian theory to develop his concept of natural selection,1 and food supply has played a role in our own evolution since Palaeolithic times.2 It is generally accepted that Homo sapiens evolved as hunter-gatherers, and although there is debate about the macronutrient composition of our ancestral diet3, 4, 5, 6, 7 with carbohydrates contributing 3–50%,4 depending upon whether our ancestors were primarily hunters or gatherers, the distribution of macronutrient energy was of the order of 30% protein, 35% fat and 35% carbohydrate4, 5 supplied by animal flesh, tuberous vegetables, fruits and nuts.7 With the development of agrarian societies during the Neolithic period, and especially the advances in farming practices and technology over the past 200 years, the quantity and quality of our diet and our lifestyle has changed quite dramatically. While these changes have brought many advantages, they have also been accompanied by an increase in chronic non-infectious diseases, such as heart disease, cancer, stroke, diabetes, obesity and related morbidities that are the leading cause of death in present-day society.

Dietary recommendations

At the turn of the last century, the American diet was composed of 35% energy from fat, increasing to 40% in the 1950s and 1960s and was composed of 16% saturated, 17% monounsaturated and 4% polyunsaturated fatty acids,8 and it was about this time that Keys9 popularized the relationship between saturated fats, blood cholesterol and heart disease. Although, he demonstrated that the proportion of energy provided by dietary fat could explain 94% mortality from coronary heart disease using results from the six countries study, Yerushalmy and Hilleboe10 drew attention to the fact that when data from 21 countries were included, this relationship was reduced to 1%. Even though Keys9 admitted that large amounts of dietary cholesterol had very little effect on its blood concentration11 and there was little evidence to support reducing the fat content of the American diet,12 he and disciples of the ‘diet–heart hypothesis’ were able to convince the American Heart Association and other health organizations to decrease the fat content of the diet,13 which resulted in a corresponding increase in carbohydrate energy and the foundation of present-day dietary guidelines. Despite reports that there was a decline in mortality from coronary heart and cardiovascular diseases as a result of the recommended improvements in diet and exercise habits,14, 15 and incidentally the introduction of antihypertensive medication and improved therapies, they have been confounded by the increasing prevalence of obesity and diabetes that has occurred since then and for which heart disease is a related morbidity.

At the present time, high-carbohydrate, low-fat diets are recommended as ‘healthy’ for the population in general16 as well as for individuals susceptible to heart disease,15 cancer,17 hypertension15, 18 and diabetes.19 However, in spite of these recommendations, there is considerable evidence that high-carbohydrate, low-fat diets promote the insulin resistance syndrome20, 21, 22, 23 and that they are not favourable for patients with mild-to-moderately severe type 2 diabetes.24 In some individuals, high-carbohydrate diets promote the conversion of less atherogenic large low-density lipoproteins (LDL) into the more atherogenic small, dense LDL25 and fructose, once considered the ideal sweetener for diabetics, has now been shown to predict smaller LDL particle size in schoolchildren.26 These arguments, together with more recent evidence that low-carbohydrate diets have health benefits for weight management,27, 28, 29, 30 diabetes31, 32 and cardiovascular disease28, 33, 34, 35, 36 have led an increasing number of scientists to challenge present-day dietary guidelines,37, 38, 39, 40 whereas others question the relationship between dietary saturated fat and increased risk of cardiovascular disease41, 42 and the validity of reducing saturated fats to minimal levels.43

Dietary treatment of diabetes

A number of large cohort, long-term clinical trials have documented that tight glycaemic control has benefits not only in preventing the onset and progression of type 2 diabetes,44, 45, 46 but also in preventing or delaying the development of diabetic complications, such as retinopathy, nephropathy, neuropathy, foot ulcers and cardiovascular disease.44, 45, 46, 47, 48 In consequence, effective treatment of hyperglycaemia is the priority of diabetes associations worldwide49 to maintain blood glucose concentrations as near to normal as possible. Other studies have implicated high postprandial glucose concentrations as a risk factor for cardiovascular disease in both diabetic and non-diabetic individuals50, 51, 52, 53 as well as in the development of microvascular complications of diabetes50, 51, 53 and propose that targeting both chronic and acute glucose fluctuations is necessary51 to prevent their onset or progression. In spite of this, diabetic patients are still advised to consume a high-carbohydrate diet and to control glycaemia with hypoglycaemic agents and/or insulin, which even specialists in the field agree are associated with adverse side effects, such as reactive hypoglycaemia and weight gain.54, 55 It is perhaps surprising that when saturated fats were only weakly associated with cardiovascular disease in the 1950s, the recommendations were to decrease saturated fats and cholesterol in the diet. However, when studies provide irrefutable evidence that hyperglycaemia, in large part the result of consuming dietary carbohydrates, is associated with increased risk of cardiovascular diseases in apparently healthy individuals52 and is responsible for the progression of type 2 diabetes and the debilitating complications of both type 1 and type 2 diabetes,50, 51, 53 the recommendations are to consume a high-carbohydrate diet.

Before the discovery of insulin low-carbohydrate, low-energy diets were the treatment of choice for endocrinologists, such as Allen, Adlersberg,56 Joslin57 and Newburgh, however, 25 years after the use of insulin treatment Adlersberg56 lamented that its use had led to neglect of the dietary treatment of diabetes and emphasized that many mild and moderately severe cases of type 2 diabetes could be satisfactorily maintained without insulin by the proper application of ‘dietotherapy’. Indeed Joslin57 writing about the same time commented ‘insulin is so good that doctors and patients take advantage of it, disregarding diet and exercise’.

When describing the diet used by his patients at the George F Baker Clinic in 1941, Joslin57 indicated that the average carbohydrate intake for all patients and all ages was 156 g or 624 kcal/day, corresponding to 30–40% of their daily energy intake, and commented ‘with the carbohydrate in the diet as high as 150 g, the chances of a diabetic not being able to obtain enough calories in the form of protein and fat seem slight’.57 However, in the 70 years since this statement was made, the carbohydrate component of the diabetic diet has increased from 30% to as much as 65%58, 59 of daily energy requirements. Is this due to improvements in medical nutrition and pharmaceutical therapy for diabetics or is it as Joslin57 feared that ‘insulin is so good that it covers up a multitude of therapeutic sins.’?

Optimal diet

Most scientists agree that poor diet and physical inactivity are the major factors contributing not only to overweight and obesity but also to the increased prevalence of today’s metabolic diseases. In consequence, it should be possible to prevent or delay their onset by following an appropriate diet and increasing physical activity, rather than treating the consequences of an inappropriate diet by pharmaceutical means. The latest dietary guidelines for Americans16 propose a healthy eating pattern composed of nutrient rather than energy-dense foods with a macronutrient composition within the acceptable distribution ranges recommended by the Institute of Medicine.60 However, the Acceptable Macronutrient Distribution Ranges are quite large, especially for carbohydrate (45–65%) and protein (10–35%) and although it is indicated that reducing energy intake is more important for body weight control than the proportion of macronutrients in the diet; if changing the macronutrient composition of the diet can help some individuals to reduce energy intake, decrease body weight and improve biomarkers of cardiovascular disease, it is certainly worth trying.

Over the last decade, a number of clinical trials have demonstrated that reducing the carbohydrate content of the diet not only improves weight loss but also improves biomarkers associated with cardiovascular disease27, 28, 29 and often results in reduced medication for type 2 diabetics,29 independent of weight loss. Such observations are not new and have been demonstrated in obese type 2 diabetics consuming a Protein Sparing Modified Fast.61 More importantly, low-carbohydrate diets have often been consumed ad libitum and compared with reduced energy diets, indicating that by consciously avoiding or reducing added sugars, refined grains and their food products, an individual is able to unconsciously reduce his, or her, spontaneous energy intake. Whether this is due to a diet slightly higher in protein quantity and composition or that it is more structured and restrictive has not been determined. However, even when such diets are consumed to maintain body weight, improvements in disease-associated biomarkers have been observed.62, 63

With the exception of a few food groups, such as dairy and grains, which have become ubiquitous nutrient sources since the agricultural revolution, dietary recommendations appear to be evolving in the direction of diets consumed by our Palaeolithic ancestors, for whom some believe our present genome is most adapted.64 Indeed, the latest Dietary Guidelines for Americans propose the DASH (Dietary Approaches to Stop Hypertension) diet as a healthy diet. Although this diet only provides 15% daily energy intake from protein, with the remainder composed of 58% carbohydrate and 27% fat, results from the OmniHeart trial,63 in which the subjects maintained their body weight constant for periods of 6 weeks, indicate that further reductions in cardiovascular risk (lower blood pressure and improved blood lipid profiles) can be obtained when either protein or unsaturated fats (predominantly monounsaturated fatty acids) replace and reduce the carbohydrate content by 10% (Figure 1)

Figure 1
figure 1

Modification of the DASH (Dietary Approaches to Stop Hypertension) diet used in the OmniHeart trial.63

Although it is not possible to determine if the observed improvements were due to the decrease in carbohydrates alone, the increase in protein or unsaturated fats per se or their respective compositional changes, it would have been interesting to see whether a combination of these two diets (Figure 2 Modified OmniHeart) might have further improved cardiovascular risk factors, as the carbohydrate content would have been reduced further and the macronutrient composition is quite similar to that of the Palaeolithic diet. In the OmiHeart study, the carbohydrate content of the diet was reduced from 58% to 48%, however, others have demonstrated that if the carbohydrate content of the diet is reduced even further, as in very-low carbohydrate diets,65, 66 the quality of dietary fat, saturated or unsaturated, does not need to be controlled to improve biomarkers of cardiovascular disease and decrease those of inflammation.

Figure 2
figure 2

Combination of the high-protein and high-monounsaturated fatty acids (MUFA) components of the OmniHeart diets would have reduced the carbohydrate composition to 38%. Would further improvements in cardiovascular risk factors have been observed? DASH, Dietary Approaches to Stop Hypertension.

Reducing the carbohydrate content of the diet as in very-low carbohydrate diets, referred to as ketogenic diets, is not only of interest for controlling obesity and diabetes but neurological diseases as well. They have proved effective for decreasing epileptic seizures and more recently they have been proposed as therapy for a variety of neurological disorders that include Alzheimer’s and Parkinson’s disease67 as well as narcolepsy.68 Although the mechanisms by which ketogenic diets exert their effects are unclear, they do appear to normalize aberrant energy metabolism and have neuroprotective properties.67

Protein intake, how high should it be?

A recent analysis of the National Health and Nutrition Examination Survey data to determine trends in macronutrient composition of the diet, energy intake and body weight from 1971 to 2006, found that the increased prevalence of obesity in 2006 was associated with increases in energy and carbohydrate intakes and decreases in the proportions of fat and protein in the diet.69 It was further observed that a 1% increase in protein intake, replacing either carbohydrate or fat, decreases energy intake by 32 and 51 kcal, respectively. The authors conclude that while efforts should be focused on decreasing energy intake, this may be facilitated by increasing the protein composition of the diet.

A substantial decrease in the quantity of refined carbohydrates in the diet will be accompanied by increases in the composition of protein and fat, but this does not necessarily mean that the quantities of protein and fat in the diet will or should increase. Proteins are more satiating than carbohydrates70 and a number of studies have demonstrated spontaneous decreases in energy intake as the proportion of protein in the diet increases, or that subjects feel more satiated on higher protein diets. However, when energy intake is restricted, it is possible that protein requirements are greater than present-day dietary recommendations of 0.8–1 g/kg/day, to maintain nitrogen balance and ensure that lean body mass is not compromised during weight loss.71 One argument against increasing the protein content of the diet, especially with age, was the belief that due to its effect on acid/base balance and increased calcium excretion it exacerbates osteoporosis, but it is now understood that osteopenia and sarcopenia observed with ageing are interrelated and that optimal protein intakes to prevent bone and muscle degeneration are probably greater than current recommended dietary allowances72 and that higher protein diets are associated with greater bone mass and fewer fractures when calcium intake is sufficient. The acid-producing effects of high-protein intakes can be mitigated by the alkalinizing effects of fruits and vegetables or, in the case of very-low carbohydrate diets, potassium bicarbonate supplementation, which has been shown to reduce urinary nitrogen excretion and increase fractional calcium absorption.73

Different proteins different effects

Not only is an increase in the amount or proportion of dietary proteins thought to improve weight loss, heart health and prevent or retard the development of type 2 diabetes74 but protein quality also seems to offer health benefits.

Whey proteins are digested and absorbed more rapidly than casein, which influences postprandial plasma amino-acid profiles and increases muscle protein synthesis more than that of casein in older men.75 As a consequence, whey protein, together with resistance training, has been proposed to prevent age-related sarcopenia.75, 76 However, as casein has also been shown to increase muscle protein synthesis and whole-body protein retention in elderly men when administered during sleep,77 nutritional strategies combining rapidly digested whey protein supplementation during the day with a slowly digested casein meal immediately before sleep may be more effective in preventing sarcopenia than one based upon whey protein alone.

Whey protein supplementation at 60 g/day for 4 weeks, in obese non-diabetic women consuming their habitual diet was also shown to decrease liver lipids, fasting triglycerides and total cholesterol,78 however, whether these effects were specifically due to whey protein or the increased protein content of the diet cannot be determined.

Mikkelsen et al.79 observed that 24-h energy expenditure (24-h EE) increased after 4 days of replacing dietary carbohydrate isocalorically with either 17% animal or vegetable proteins but that animal proteins stimulated 24-h EE slightly but significantly more than vegetable proteins; and we have made similar observations using different protein sources, in which an isocaloric whey protein test meal increased EE more than those composed of casein or soy.80 Interestingly, the glucose responses to these test meals were lower than that of a meal containing the same amount of glucose alone. The lower glucose response after whey could be explained by a larger insulin response; however, the insulin responses following casein and soy were not significantly different from that after consuming the glucose meal alone. These results, together with those of other proteins, suggest that specific proteins can be incorporated into the diet to provide distinct and desired attributes tailored to take into account the health and metabolic conditions of the individual.

Conclusion

There is little doubt that much of the present pandemic of metabolic diseases is due to a combination of inappropriate diet(s) and lack of physical activity. Consequently, it should be possible to prevent or delay their development by appropriate ‘dietotherapy’ with little, or no, pharmaceutical intervention. In 2005, The Joslin Diabetes Centre issued ‘new’ dietary guidelines, reminiscent of those used by its founder at the George F Baker Clinic 70 years ago, in which they recommend 40% energy from carbohydrates, 20–30% from proteins, 30–35% from fats and containing at least 20–35 g of fibre. When incorporated into their 12-week ‘Why Wait’ diet and exercise programme,55 patients lost weight, composed of fat rather than lean mass, that was maintained for 1 year and although they did not increase their protein intake significantly, they were able to reduce or completely stop taking their diabetes medication. Dietary recommendations are reviewed at regular intervals and are updated according to evidence-based data published in the literature. With increasing evidence indicating the advantages of low-carbohydrate, higher protein diets having health benefits and proof-of-principle that the Joslin Centre’s ‘Why Wait’ programme can prevent and even reverse the progression of type 2 diabetes, is it not, conceivable, that such diets are more appropriate for optimal human health than the carbohydrate-rich diets that continue to be recommended?

References

  1. Thomas Robert Malthus http://en.wikipedia.org/wiki/Thomas_Robert_Malthus (accessed on 31 January 2012).

  2. Milton K . The critical role played by animal source foods in human (Homo) evolution. J Nutr 2003; 133 (Suppl 2), 3886S–3892S.

    CAS  Article  Google Scholar 

  3. Cordain L, Eaton SB, Miller JB, Mann N, Hill K . The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic. Eur J Clin Nutr 2002; 56 (Suppl 1), S42–S52.

    Article  Google Scholar 

  4. Strohle A, Hahn A . Diets of modern hunter-gatherers vary substantially in their carbohydrate content depending on ecoenvironments: results from an ethnographic analysis. Nutr Res 2011; 31: 429–435.

    Article  Google Scholar 

  5. Eaton SB . The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition? Proc Nutr Soc 2006; 65: 1–6.

    CAS  Article  Google Scholar 

  6. Garn SM, Leonard WR . What did our ancestors eat? Nutr Rev 1989; 47: 337–345.

    CAS  Article  Google Scholar 

  7. Konner M, Eaton SB . Paleolithic nutrition: twenty-five years later. Nutr Clin Pract 2010; 25: 594–602.

    Article  Google Scholar 

  8. Stephen AM, Wald NJ . Trends in individual consumption of dietary fat in the United States, 1920-1984. Am J Clin Nutr 1990; 52: 457–469.

    CAS  Article  Google Scholar 

  9. Keys A . Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp N Y 1953; 20: 118–139.

    CAS  PubMed  Google Scholar 

  10. Yerushalmy J, Hilleboe HE . Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med 1957; 57: 2343–2354.

    CAS  PubMed  Google Scholar 

  11. Keys A . Prediction and possible prevention of coronary disease. Am J Public Health Nations Health 1953; 43: 1399–1407.

    CAS  Article  Google Scholar 

  12. Kritchevsky D . History of recommendations to the public about dietary fat. J Nutr 1998; 128 (Suppl 2), 449S–452S.

    CAS  Article  Google Scholar 

  13. Report of Inter-Society Commission for Heart Disease Resources. Prevention of cardiovascular disease. Primary prevention of the atherosclerotic diseases. Circulation 1970; 42: A55–A95.

    Google Scholar 

  14. Stamler J . Diet and coronary heart disease. Biometrics 1982; 38 (Suppl), 95–118.

    Article  Google Scholar 

  15. Gidding SS, Lichtenstein AH, Faith MS, Karpyn A, Mennella JA, Popkin B et al. Implementing American Heart Association pediatric and adult nutrition guidelines: a scientific statement from the American Heart Association Nutrition Committee of the Council on Nutrition, Physical Activity and Metabolism, Council on Cardiovascular Disease in the Young, Council on Arteriosclerosis, Thrombosis and Vascular Biology, Council on Cardiovascular Nursing, Council on Epidemiology and Prevention, and Council for High Blood Pressure Research. Circulation 2009; 119: 1161–1175.

    Article  Google Scholar 

  16. US Department of Agriculture, US Department of Health and Human Services Report of the Dietary Guidelines Advisory Committee on the dietary guidelines for Americans, 2010.

  17. Kushi LH, Byers T, Doyle C, Bandera EV, McCullough M, McTiernan A et al. American Cancer Society Guidelines on Nutrition and Physical Activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA Cancer J Clin 2006; 56: 254–281.

    Article  Google Scholar 

  18. Appel LJ, Brands MW, Daniels SR, Karanja N, Elmer PJ, Sacks FM . Dietary approaches to prevent and treat hypertension: a scientific statement from the American Heart Association. Hypertension 2006; 47: 296–308.

    CAS  Article  Google Scholar 

  19. Bantle JP, Wylie-Rosett J, Albright AL, Apovian CM, Clark NG, Franz MJ et al. Nutrition recommendations and interventions for diabetes: a position statement of the American Diabetes Association. Diabetes Care 2008; 31: S61–S78.

    CAS  Article  Google Scholar 

  20. Abbasi F, McLaughlin T, Lamendola C, Kim HS, Tanaka A, Wang T et al. High carbohydrate diets, triglyceride-rich lipoproteins, and coronary heart disease risk. Am J Cardiol 2000; 85: 45–48.

    CAS  Article  Google Scholar 

  21. Jeppesen J, Hein HO, Suadicani P, Gyntelberg F . Relation of high TG-low HDL cholesterol and LDL cholesterol to the incidence of ischemic heart disease. An 8-year follow-up in the Copenhagen Male Study. Arterioscler Thromb Vasc Biol 1997; 17: 1114–1120.

    CAS  Article  Google Scholar 

  22. Jeppesen J, Schaaf P, Jones C, Zhou MY, Chen YD, Reaven GM . Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in postmenopausal women. Am J Clin Nutr 1997; 65: 1027–1033.

    CAS  Article  Google Scholar 

  23. Reaven GM . Diet and Syndrome X. Curr Atheroscler Rep 2000; 2: 503–507.

    CAS  Article  Google Scholar 

  24. Garg A, Grundy SM, Unger RH . Comparison of effects of high and low carbohydrate diets on plasma lipoproteins and insulin sensitivity in patients with mild NIDDM. Diabetes 1992; 41: 1278–1285.

    CAS  Article  Google Scholar 

  25. Krauss RM . Dietary and genetic effects on low-density lipoprotein heterogeneity. Annu Rev Nutr 2001; 21: 283–295.

    CAS  Article  Google Scholar 

  26. Aeberli I, Zimmermann MB, Molinari L, Lehmann R, l'Allemand D, Spinas GA et al. Fructose intake is a predictor of LDL particle size in overweight schoolchildren. Am J Clin Nutr 2007; 86: 1174–1178.

    CAS  Article  Google Scholar 

  27. Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA . A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab 2003; 88: 1617–1623.

    CAS  Article  Google Scholar 

  28. Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003; 348: 2082–2090.

    CAS  Article  Google Scholar 

  29. Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 2003; 348: 2074–2081.

    CAS  Article  Google Scholar 

  30. Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenberg I et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 2008; 359: 229–241.

    CAS  Article  Google Scholar 

  31. Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP . Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med 2005; 142: 403–411.

    CAS  Article  Google Scholar 

  32. Nielsen JV, Joensson EA . Low-carbohydrate diet in type 2 diabetes: stable improvement of bodyweight and glycemic control during 44 months follow-up. Nutr Metab (Lond) 2008; 5: 14.

    Article  Google Scholar 

  33. Foster GD, Wyatt HR, Hill JO, Makris AP, Rosenbaum DL, Brill C et al. Weight and metabolic outcomes after 2 years on a low-carbohydrate versus low-fat diet: a randomized trial. Ann Intern Med 2010; 153: 147–157.

    Article  Google Scholar 

  34. Layman DK, Evans EM, Erickson D, Seyler J, Weber J, Bagshaw D et al. A moderate-protein diet produces sustained weight loss and long-term changes in body composition and blood lipids in obese adults. J Nutr 2009; 139: 514–521.

    CAS  Article  Google Scholar 

  35. Samaha FF, Foster GD, Makris AP . Low-carbohydrate diets, obesity, and metabolic risk factors for cardiovascular disease. Curr Atheroscler Rep 2007; 9: 441–447.

    Article  Google Scholar 

  36. Stern L, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med 2004; 140: 778–785.

    Article  Google Scholar 

  37. Accurso A, Bernstein RK, Dahlqvist A, Draznin B, Feinman RD, Fine EJ et al. Dietary carbohydrate restriction in type 2 diabetes mellitus and metabolic syndrome: time for a critical appraisal. Nutr Metab (Lond) 2008; 5: 9.

    Article  Google Scholar 

  38. Hite AH, Meguid MM . Destined for greater obesity. Nutrition 2011; 27: 1078–1079.

    Article  Google Scholar 

  39. Hite AH, Feinman RD, Guzman GE, Satin M, Schoenfeld PA, Wood RJ . In the face of contradictory evidence: report of the Dietary Guidelines for Americans Committee. Nutrition 2010; 26: 915–924.

    Article  Google Scholar 

  40. Layman DK . Dietary Guidelines should reflect new understandings about adult protein needs. Nutr Metab (Lond) 2009; 6: 12.

    Article  Google Scholar 

  41. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM . Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr 2010; 91: 502–509.

    CAS  Article  Google Scholar 

  42. Winwood R . So you think you know the effects of dietary lipids on human health? - Fat chance!. J Inst Food Sci Tech 2011; 25: 26–28.

    Google Scholar 

  43. German JB, Dillard CJ . Saturated fats: what dietary intake? Am J Clin Nutr 2004; 80: 550–559.

    CAS  Article  Google Scholar 

  44. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2diabetes (UKPDS 33). Lancet 1998; 352: 837–853.

    Article  Google Scholar 

  45. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet 1998; 352: 854–865.

    Article  Google Scholar 

  46. Ohkubo Y, Kishikawa H, Araki E, Miyata T, Isami S, Motoyoshi S et al. Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with non-insulin-dependent diabetes mellitus: a randomized prospective 6-year study. Diabetes Res Clin Pract 1995; 28: 103–117.

    CAS  Article  Google Scholar 

  47. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 1993; 329: 977–986.

    Article  Google Scholar 

  48. Nathan DM, Cleary PA, Backlund JY, Genuth SM, Lachin JM, Orchard TJ et al. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. N Engl J Med 2005; 353: 2643–2653.

    Article  Google Scholar 

  49. Nathan DM, Buse JB, Davidson MB, Heine RJ, Holman RR, Sherwin R et al. Management of hyperglycemia in type 2 diabetes: A consensus algorithm for the initiation and adjustment of therapy: a consensus statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 2006; 29: 1963–1972.

    Article  Google Scholar 

  50. Ceriello A, Hanefeld M, Leiter L, Monnier L, Moses A, Owens D et al. Postprandial glucose regulation and diabetic complications. Arch Intern Med 2004; 164: 2090–2095.

    CAS  Article  Google Scholar 

  51. Heine RJ, Balkau B, Ceriello A, Del PS, Horton ES, Taskinen MR . What does postprandial hyperglycaemia mean? Diabet Med 2004; 21: 208–213.

    CAS  Article  Google Scholar 

  52. Levitan EB, Song Y, Ford ES, Liu S . Is nondiabetic hyperglycemia a risk factor for cardiovascular disease? A meta-analysis of prospective studies. Arch Intern Med 2004; 164: 2147–2155.

    Article  Google Scholar 

  53. Middelbeek RJ, Horton ES . The role of glucose as an independent cardiovascular risk factor. Curr Diab Rep 2007; 7: 43–49.

    CAS  Article  Google Scholar 

  54. Abdul-Ghani MA, Norton L, DeFronzo RA . Role of sodium-glucose cotransporter 2 (SGLT 2) inhibitors in the treatment of type 2 diabetes. Endocr Rev 2011; 32: 515–531.

    CAS  Article  Google Scholar 

  55. Hamdy O, Carver C . The Why WAIT program: improving clinical outcomes through weight management in type 2 diabetes. Curr Diab Rep 2008; 8: 413–420.

    Article  Google Scholar 

  56. Adlersberg D . The use of high protein diets in the treatment of diabetes mellitus. Am J Dig Dis 1948; 15: 109–115.

    CAS  Article  Google Scholar 

  57. Joslin EP . The Diabetic. Can Med Assoc J 1943; 48: 488–497.

    CAS  PubMed  PubMed Central  Google Scholar 

  58. Katsilambros N, Liatis S, Makrilakis K . Critical review of the international guidelines: what is agreed upon--what is not? Nestle Nutr Workshop Ser Clin Perform Programme 2006; 11: 207–218.

    CAS  Article  Google Scholar 

  59. Zivkovic AM, German JB, Sanyal AJ . Comparative review of diets for the metabolic syndrome: implications for nonalcoholic fatty liver disease. Am J Clin Nutr 2007; 86: 285–300.

    CAS  Article  Google Scholar 

  60. Dietary Reference Intakes For Energy. Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids. The National Academies Press: Washington DC, 2002.

  61. Bistrian BR, Blackburn GL, Flatt JP, Sizer J, Scrimshaw NS, Sherman M . Nitrogen metabolism and insulin requirements in obese diabetic adults on a protein-sparing modified fast. Diabetes 1976; 25: 494–504.

    CAS  Article  Google Scholar 

  62. Gannon MC, Nuttall FQ . Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition. Nutr Metab (Lond) 2006; 3: 16.

    Article  Google Scholar 

  63. Appel LJ, Sacks FM, Carey VJ, Obarzanek E, Swain JF, Miller ER et al. Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. JAMA 2005; 294: 2455–2464.

    CAS  Article  Google Scholar 

  64. Eaton SB . Evolution and cholesterol. World Rev Nutr Diet 2009; 100: 46–54.

    CAS  Article  Google Scholar 

  65. Forsythe CE, Phinney SD, Fernandez ML, Quann EE, Wood RJ, Bibus DM et al. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids 2008; 43: 65–77.

    CAS  Article  Google Scholar 

  66. Volek JS, Sharman MJ, Forsythe CE . Modification of lipoproteins by very low-carbohydrate diets. J Nutr 2005; 135: 1339–1342.

    CAS  Article  Google Scholar 

  67. Stafstrom CE, Rho JM . The ketogenic diet as a treatment paradigm for diverse neurological disorders. Front Pharmacol 2012; 3: 1–8.

    Article  Google Scholar 

  68. Husain AM, Yancy WS, Carwile ST, Miller PP, Westman EC . Diet therapy for narcolepsy. Neurology 2004; 62: 2300–2302.

    CAS  Article  Google Scholar 

  69. Austin GL, Ogden LG, Hill JO . Trends in carbohydrate, fat, and protein intakes and association with energy intake in normal-weight, overweight, and obese individuals: 1971-2006. Am J Clin Nutr 2011; 93: 836–843.

    CAS  Article  Google Scholar 

  70. Astrup A . The satiating power of protein--a key to obesity prevention? Am J Clin Nutr 2005; 82: 1–2.

    CAS  Article  Google Scholar 

  71. Hoffer LJ, Bistrian BR, Young VR, Blackburn GL, Matthews DE . Metabolic effects of very low calorie weight reduction diets. J Clin Invest 1984; 73: 750–758.

    CAS  Article  Google Scholar 

  72. Heaney RP, Layman DK . Amount and type of protein influences bone health. Am J Clin Nutr 2008; 87: 1567S–1570S.

    CAS  Article  Google Scholar 

  73. Ceglia L, Harris SS, Abrams SA, Rasmussen HM, Dallal GE, Dawson-Hughes B . Potassium bicarbonate attenuates the urinary nitrogen excretion that accompanies an increase in dietary protein and may promote calcium absorption. J Clin Endocrinol Metab 2009; 94: 645–653.

    CAS  Article  Google Scholar 

  74. Layman DK, Clifton P, Gannon MC, Krauss RM, Nuttall FQ . Protein in optimal health: heart disease and type 2 diabetes. Am J Clin Nutr 2008; 87: 1571S–1575S.

    CAS  Article  Google Scholar 

  75. Pennings B, Boirie Y, Senden JM, Gijsen AP, Kuipers H, van Loon LJ . Whey protein stimulates postprandial muscle protein accretion more effectively than do casein and casein hydrolysate in older men. Am J Clin Nutr 2011; 93: 997–1005.

    CAS  Article  Google Scholar 

  76. Tang JE, Phillips SM . Maximizing muscle protein anabolism: the role of protein quality. Curr Opin Clin Nutr Metab Care 2009; 12: 66–71.

    CAS  Article  Google Scholar 

  77. Groen BB, Res PT, Pennings B, Hertle E, Senden JM, Saris WH et al. Intragastric protein administration stimulates overnight muscle protein synthesis in elderly men. Am J Physiol Endocrinol Metab 2012; 302: E52–E60.

    CAS  Article  Google Scholar 

  78. Bortolotti M, Maiolo E, Corazza M, Van DE, Schneiter P, Boss A et al. Effects of a whey protein supplementation on intrahepatocellular lipids in obese female patients. Clin Nutr 2011; 30: 494–498.

    CAS  Article  Google Scholar 

  79. Mikkelsen PB, Toubro S, Astrup A . Effect of fat-reduced diets on 24-h energy expenditure: comparisons between animal protein, vegetable protein, and carbohydrate. Am J Clin Nutr 2000; 72: 1135–1141.

    CAS  Article  Google Scholar 

  80. Acheson KJ, Blondel-Lubrano A, Oguey-Araymon S, Beaumont M, Emady-Azar S, Ammon-Zufferey C et al. Protein choices targeting thermogenesis and metabolism. Am J Clin Nutr 2011; 93: 525–534.

    CAS  Article  Google Scholar 

Download references

Author information

Affiliations

Authors

Corresponding author

Correspondence to K J Acheson.

Ethics declarations

Competing interests

KJA is an employee of Nestec Ltd., a subsidiary of Nestlé Ltd, which provides professional assistance, research and consulting services for food, dietary, dietetic and pharmaceutical products of interest to Nestlé Ltd. There is no conflict of interest concerning opinions presented in this review.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Acheson, K. Diets for body weight control and health: the potential of changing the macronutrient composition. Eur J Clin Nutr 67, 462–466 (2013). https://doi.org/10.1038/ejcn.2012.194

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/ejcn.2012.194

Keywords

  • obesity
  • diabetes
  • dietary guidelines
  • optimal diet
  • low-carbohydrate diet

Further reading

Search

Quick links