Simple carbohydrates and obesity: Fact, Fiction and Future


The prevalence of overweight and obesity has risen dramatically over the past 3 decades and is threatening to become a global epidemic.1 A substantial proportion of the population is at increased risk of morbidity and mortality as a result of increased body weight. In affluent countries, excess body fat accounts for ≈30–40% of coronary heart disease;2 cancers of the colon, breast and endometrium; and most cases of non-insulin-dependent diabetes mellitus.3 Genetic susceptibility predisposes people to the development of body fatness but cannot account for the exponential increase in obesity in nearly all-Western countries.

Obesity is generally accepted as resulting from an imbalance between food intake and daily physical activity. Obesity is thus the largest nutrition-related problem in the developed world. Despite the overwhelming amount of research and statistical analysis, no clear explanation can be given for the relationship between changes in behavior and the rapid increase in obesity prevalence in the past 3 decades.

Health guidelines have been focused on three particular lifestyle factors: increased levels of daily physical activity and reduction of the intake of fat and sugars, particularly added sugars. The urgency to take public action regarding physical activity is generally accepted, but there is much debate about dietary factors such as total fat intake and intake of sugars and rapidly digested carbohydrates. In the 1970s, some nutritionists considered sucrose as perhaps the most important dietary factor predisposing to weight gain.4 Since then attention has shifted toward fat as the major nutritional component promoting excess energy intake and weight gain.5, 6 Evidence that the regulation of fat balance has a lower priority than that of carbohydrates, protein and alcohol has contributed to the general knowledge that fat intake increases the risk of excess energy intake and the promotion of fat storage.7, 8

Despite the controversy about the particular role of sugars, the message that fat in the diet is responsible for excess energy intake and weight gain became expanded rapidly in the 1990s.9 The actual intake of fat expressed as percent of energy (En%), based on subject's self-recordings, has decreased significantly over the past decade.10 The reduction in absolute fat intake was substantially less. Although a number of meta-analyses on the relationship between ad libitum low-fat diets and body weight control showed that dietary fat intake is directly associated with obesity,11, 12 the scientific evidence for the relationship between dietary fat content and the prevalence of obesity has been challenged. For example, Katan et al.13 questioned the importance of low fat, high-carbohydrate diets in the prevention and treatment of obesity. Reduction of fat intake resulted in only a very limited weight reduction of a few kilograms body weight. Another important argument concerns the so-called fat paradox.14 With the increasing popularity of lower-fat products, food intake statistics have shown a decrease in dietary fat intake although the prevalence of obesity is rising. A direct relationship between dietary fat and energy density was also questioned because of the observation that many lower-fat foods currently available are based on sugars, leading to energy density values similar to those of their high-fat counterparts.14 This has renewed the interest on sugars as being the primary nutritional factor behind the increase in obesity. Many refined carbohydrate foods produce a high-glycaemic response, thereby promoting postprandial carbohydrate oxidation at the expense of fat oxidation, thus altering fuel partitioning in a way that may be conducive to body fat gain.15 This is in contrast to foods that produce a low-glycaemic response and lower postprandial insulin secretion.

The glycaemic index (GI) of carbohydrates affects cardiovascular risk factors and glycaemic control in diabetics, and may play a role in appetite control.16 A number of studies have suggest that replacing high GI foods with similar low GI foods can reduce passive over-consumption of energy or lead to a greater loss of fat compare to lean body tissue during dieting.16, 17

However, there is a lot of debate about the use of GI. One of the major issues is whether it really is the glycaemic response to these foods that is important, or other characteristics of low GI foods, which tend to be higher in fiber and protein, or lower in sugar and energy density. Many studies suffer from lack of good dietary control, poor measures of dietary compliance, a lack of statistical power, or feeding of singular sugars as opposed to real multi-ingredient foods. A further problem is the reproducibility of the measurement of GI itself; GI is affected by, for example, fruit ripeness, food particle size, cooking methods.18

Few data are available about how much carbohydrate is ingested as a solid or a drink. This is important for two reasons, first, to validate the hypothesis that carbohydrates from fluids may promote excess energy intake and consequently weight gain. It is the physiological principle of the fast available energy from sports drinks to fuel the muscle during exercise. Second, but related, is the increase in the soft drink market in relation to the increase in prevalence of obesity. Third is the suggestion that the high intake of soft drinks is linked to higher BMI or weight gain in particular in children.

However, a substantial number of epidemiologic studies have found a clear inverse relationship between sucrose intake and body weight or BMI as well as sucrose intake and total fat intake. Most papers were reviewed in detail by Hill and Prentice19 and Astrup and Raben,20 and the suggestion is that a high intake of sucrose may help to prevent weight gain. However, one should be very cautious with the interpretation of this type of data because of the enormous bias in the food intake records of overweight and obese people.

The only large-scale, long-term, randomized control trial on the role of carbohydrate/fat ratio in the diet as well as the simple versus complex carbohydrate issue is the CARMEN multi-center trial, which involved 398 moderately overweight subjects in five different countries.21 This study investigated the effect on energy intake, body weight and blood lipids of over 6 months of ad libitum intake of low-fat diets (reduction of ≈10 En%) rich in either simple or complex carbohydrates. The results showed that both low-fat, high-carbohydrate diets reduced body weight significantly by 1.6 kg (for high simple carbohydrates) and 2.4 kg (for high complex) compared with a control normal-fat, normal-carbohydrate diet. Energy density of both carbohydrate diets was significantly reduced (−0.10 (high simple) and −0.18 (high complex) kcal/g, respectively) although a large number of the low-fat alternatives contained higher levels of carbohydrates, particularly sucrose.

The public debate got new input with the publication in The New England Journal of Medicine of two studies on the effects of the Atkins diet (high fat/low carbohydrate). Foster et al.22 followed 63 obese subjects in a randomized controlled diet for 12 months. One group was given a copy of the popular book ‘Dr Atkins New Diet revolution’ and the other group was asked to follow an energy restricted low fat diet. Although the initial weight loss was higher in the high fat diet, no significant difference could be observed after 12 months. However, dropout rate was high in both groups (40%). The study of Samaha et al.23 randomized 132 severely obese subjects to a low-carbohydrate diet (restriction to <30 g per day) or a low-fat and energy-restricted diet (minus 500 kcals and <30 En% from fat). Weight loss in the low-carbohydrate group was significantly less (1.8 kg) than in the high-fat group (5.7 kg) after 6 months. Interestingly macronutrient composition changes over the 6 months showed an increase in protein intake from 17 to 22 En% in addition to the increase in fat intake (33–41 En%). In the low-fat diet it turned out that the macronutrient composition of the diet did not change from habitual eating patterns (fat: 33 En%, Carbohydrate: 51 En% and protein: 16 En%).

What can we learn from all these studies? First of all that there are few other areas where the frontiers of science are so confused by such a multitude of conflicting opinions. Nevertheless, a better understanding of what is going on is direly needed since the epidemic of obesity is growing at a rate that urgently needs valid intervention strategies at a population level. However, our understanding of the mechanisms of hunger and food intake are still not at a comprehensive level despite the enormous research input in the last decades.

The present proceedings recapitulate the highlights of the workshop ‘Simple Carbohydrates and Obesity’ held on 5 and 6 April 2006 in Utrecht, The Netherlands. The workshop was set up to discuss in depth three major topics. For each topic speakers were invited to prepare in advance a paper. These papers were send to a first discussant to write a critical review. During the workshop the speakers presented their paper, followed by a reply of the first discussant and a plenary discussion with all experts. After the workshop, authors were able to update their papers based on the discussions.

The first session was aimed at presenting overviews on the selection of the macronutrients (carbohydrate, fat and protein) in the diet in relation to weight management control. The second session was focused on the role of sugar and in particular sugar in soft drinks in the development of obesity. The third and last session was dedicated to the GI and its role in body weight control.

In closing, our gratitude goes to all the invited experts, who not only presented authoritative and stimulating papers but also participated in a very lively discussion about this complex and conflicting topic in the nutritional science.

Finally, this workshop was supported by an unrestricted grant from the Dutch Sugar Foundation.


  1. 1

    World Health Organisation. Obesity: preventing and managing the global epidemic. WHO: Geneva, 1998. WHO/NUT/NCD/89.1.

  2. 2

    Grundy SM . Obesity, metabolic syndrome and cardiovascular disease. J Clin Endocrinol Metab 2004; 89: 2595–2600.

    CAS  Article  Google Scholar 

  3. 3

    Willett WC, Dietz WH, Colditz GA . Guidelines for healthy weight. N Engl J Med 1999; 341: 427–434.

    CAS  Article  Google Scholar 

  4. 4

    Yudkin J . Pure, White and Deadly. Viking: London, UK, 1986.

    Google Scholar 

  5. 5

    Astrup A . Macronutrient balances and obesity: the role of diet and physical activity. Public Health Nutr 1999; 2: 341–347.

    CAS  Article  Google Scholar 

  6. 6

    Flatt J . The difference in storage capacities for carbohydrate and for fat and its implications in the regulation of body weight. Ann NY Acad Sci 1987; 499: 104–123.

    CAS  Article  Google Scholar 

  7. 7

    Prentice AM, Poppitt SD . Importance of energy density and macronutrients in the regulation of energy intake. Int J Obes 1996; 20 (Suppl 2): S18–S23.

    CAS  Google Scholar 

  8. 8

    Prentice AM, Jebb SA . Obesity in Britain: gluttony or sloth? Br Med J 1995; 311: 437–439.

    CAS  Article  Google Scholar 

  9. 9

    Leveille M . Macronutrient substitutes: description and uses. Ann NY Acad Sci 1997; 499: 11–21.

    Article  Google Scholar 

  10. 10

    Kennedy ET, Bowman SA, Powell R . Dietary fat intake in the US population. Am Coll Nutr 1999; 18: 207–212.

    CAS  Article  Google Scholar 

  11. 11

    Lissner L, Heitmann BL . Dietary fat and obesity: evidence from epidemiology. Eur J Clin Nutr 1995; 49: 79–90.

    CAS  PubMed  Google Scholar 

  12. 12

    Astrup A, Grunwald GK, Melanson EL, Saris WHM, Hill JO . The role of low-fat diets in body weight control: a meta-analysis of ad-libitum dietary intervention studies. Int J Obes 2000; 24: 1545–1552.

    CAS  Article  Google Scholar 

  13. 13

    Katan MB, Grundy SM, Willet WC . Beyond low-fat diets. New Engl J Med 1997; 337: 563–566.

    CAS  PubMed  Google Scholar 

  14. 14

    Willet WC . Is dietary fat a major determinant of body fat? Am J Clin Nutr 1998; 67: S565–S625.

    Google Scholar 

  15. 15

    Brand-Miller JC, Holt SHA, Pawlak DB, McMillan J . Glycemic index and obesity. Am J Clin Nutr 2002; 76: 281S–285S.

    CAS  Article  Google Scholar 

  16. 16

    Pawlak DB, Ebbeling CB, Ludwig DS . Should obese patients be counselled to follow a low-glycaemic index diet. Yes Obes Rev 2002; 3: 235–243.

    CAS  Article  Google Scholar 

  17. 17

    Willet WC . Eat, Drink and be Healthy: The Havard Medical School Guide to Healthy Eating. Simon & Schuster: NY, 2002.

    Google Scholar 

  18. 18

    Pi-Sunyer FX . Glycaemic index and disease. Am J Clin Nutr 2002; 76: 290S–298S.

    CAS  Article  Google Scholar 

  19. 19

    Hill JO, Prentice AM . Sugar and body weight regulation. Am J Clin Nutr 1995; 62: 264S–274S.

    CAS  Article  Google Scholar 

  20. 20

    Astrup A, Raben A . Carbohydrate and obesity. Int J Obes 1995; 19: S27–S37.

    Google Scholar 

  21. 21

    Saris WHM, Astrup A, Prentice AM, Zunft HJ, Formiguera X, Verboeket-van der Venne W et al. Randomized controlled trial of changes in dietary carbohydrate/fat ratio and simple vs complex carbohydrates on body weight and blood lipids. The CARMEN study. Int J Obes 2000; 24: 1310–1318.

    CAS  Article  Google Scholar 

  22. 22

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

    CAS  Article  Google Scholar 

  23. 23

    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 

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Correspondence to W H M Saris.

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Saris, W., Foster, G. Simple carbohydrates and obesity: Fact, Fiction and Future. Int J Obes 30, S1–S3 (2006).

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