Debate

International Journal of Obesity (2007) 31, 887–890; doi:10.1038/sj.ijo.0803616; published online 24 April 2007

Fast food: unfriendly and unhealthy

S Stender1, J Dyerberg1 and A Astrup2

  1. 1Department of Clinical Biochemistry, Gentofte Hospital University of Copenhagen, Copenhagen, Denmark
  2. 2Department of Human Nutrition, Centre for Advanced Food Studies, Faculty of Life Sciences, University of Copenhagen, Copenhagen, Denmark

Correspondence: A Astrup, Department of Human Nutrition, RVA University, 1958 Frederiksberg C, Denmark. E-mail: ast@kvl.dk

Top

Abstract

Although nutrition experts might be able to navigate the menus of fast-food restaurant chains, and based on the nutritional information, compose apparently 'healthy' meals, there are still many reasons why frequent fast-food consumption at most chains is unhealthy and contributes to weight gain, obesity, type 2 diabetes and coronary artery disease. Fast food generally has a high-energy density, which, together with large portion sizes, induces over consumption of calories. In addition, we have found it to be a myth that the typical fast-food meal is the same worldwide. Chemical analyses of 74 samples of fast-food menus consisting of French fries and fried chicken (nuggets/hot wings) bought in McDonalds and KFC outlets in 35 countries in 2005–2006 showed that the total fat content of the same menu varies from 41 to 65 g at McDonalds and from 42 to 74 g at KFC. In addition, fast food from major chains in most countries still contains unacceptably high levels of industrially produced trans-fatty acids (IP-TFA). IP-TFA have powerful biological effects and may contribute to increased weight gain, abdominal obesity, type 2 diabetes and coronary artery disease. The food quality and portion size need to be improved before it is safe to eat frequently at most fast-food chains.

Keywords:

trans-fatty acids, fast food, energy density

Top

Introduction

In the documentary film 'Super Size Me', the character Mr Spurlock ate McDonald's food three times a day for 30 days and gained 11 kg. It is quite obvious that one can purposely overeat on almost any diet, but the film raises the question of whether fast food poses a special health risk. To what extent this behaviour is a realistic trait in the general population, and to what extent fast-food consumption contributes to obesity and other morbidities such as type 2 diabetes and coronary artery disease, is still debatable.

Before drawing any conclusion as to whether there are causal links between intake of fast foods and disease, ideally randomised trials should be conducted to provide robust evidence on this issue. However, it is highly unlikely that such trials comparing frequent and infrequent fast-food consumption will ever be carried out. We therefore have to rely on observational epidemiology and on mechanistic studies.

Top

Epidemiological studies

A number of observational studies have assessed the association between frequent fast-food intake and weight gain. The American population study Cardia suggests that frequent fast-food consumption is positively associated with weight gain and risk of insulin resistance over 15 years. Individuals who had meals at fast-food restaurants more than two times a week gained 4.5 kg more weight and had a 104% greater increase in insulin resistance, at both baseline and follow-up, than individuals who ate less than one fast-food meal per week.1 This study was the first long-term project to find that people who frequently expose themselves to fast foods are at increased risk of weight gain over time and of developing type 2 diabetes. The study had several limitations such as the population size of only approx3000 individuals and the fact that self-reported information about diet, physical activity and other lifestyle factors has inherent measurement errors. These factors, however, would normally tend to underestimate the strength of the identified associations. Other observational studies have to some extent supported the existence of a causal link. However, observational studies cannot prove that the association between fast-food consumption and weight gain is causal. It remains possible that frequent fast-food consumption is simply a marker for a generally unhealthy lifestyle (e.g., less restrained eating behaviour, fatty and sweet food preferences, and a sedentary lifestyle), factors which are the real culprits in weight gain and in the increased risk of diabetes. Although every effort is made to adjust for potential confounders, one cannot adjust for unmeasured or unmeasurable lifestyle factors.

Top

Mechanisms by which fast food can be obesogenic

Portion size

Despite the above-mentioned limitations in epidemiological observational studies, most of us would accept that the link between intake of fast foods and weight gain is causal because there are several mechanisms whereby fast foods could produce weight gain. At least two important features of fast food could explain why fast food is fattening, namely, large portion sizes and high-energy density. It is well established that the bigger the portion size, the more we consume.2 Portion sizes of burgers, fried potatoes, pizzas, and soft drinks at fast-food outlets have all increased 2–5-fold over the last 50 years.3

Energy density

In addition to large portion sizes, fast food is also characterised by high-energy density, that is high energy-content/food-weight ratio. The energy density of the entire menu at fast-food outlets is typically approx1100 kJ/100 g.4 This is 65% higher than the average British diet (approx670 kJ/100 g) and more than twice the energy density of recommended healthy diets (approx525 kJ/100 g). Humans have only a weak innate ability to recognise foods with high-energy density and to downregulate the bulk eaten to meet energy requirements appropriately.4

Industrially produced trans fat

French fries and fried meat from fast-food outlets contain high amounts of industrially produced trans-fatty acids. Trans fats are fats in margarines, spreads, and frying oils, produced by industrial hardening of vegetable or marine oils, to make the product more stable and robust for handling and storage. The hardening results in the creation of a so-called trans double bonds in the fatty acids of the lipids, in contrast to the normally occurring cis double bonds. This increases the melting points of the fats, thereby increasing shelf-life. Trans-fatty acids are also found naturally in meat from ruminants and in dairy products, but not nearly to the same extent as in industrially produced trans fat (up to 5%, as compared to up to 60% in fats), and not of the same types as in IP-TFA. In a worldwide study of the content of IP-TFA in fast foods, biscuits, and snacks, we found contents of IP-TFA ranging up to 50% of the fat in the products, enabling consumers to ingest 36 g of IP-TFA in a single meal in the US.5 A daily intake of 5 g trans fat, corresponding to 2 energy percent, is associated with an approximately 30% increase in CHD risk.6

Observational studies have found that a high intake of IP-TFA is stronger associated to the risk of weight gain and gain in abdominal fatness than to the intake of other fat sources.7 Although unaccounted residual confounding cannot be ruled out, other sources of research support that the relationship is causal. First, IP-TFA serves as ligands for the PPAR-italic gamma system and can exert a biological effect that promotes abdominal obesity.6 Second, a recently reported long-term randomised trial in monkeys delivers robust evidence that IP-TFA induces weight gain and abdominal obesity. Kavanagh et al.8 reported their findings at the 66th ADA meeting in Washington, D.C. For over 6 years monkeys were fed two different isocaloric, western-style diets that contained either 8% of their calories from trans fat or the same amount of fat calories as cis-monounsaturated fat. After 6 years, the IP-TFA fed monkeys had gained 7.2% in body weight, compared to a 1.8% increase in body weight in monkeys fed with cis-monounsaturated fats. CT scans showed that the monkeys on the trans-fat diet had deposited 30% more abdominal fat than the monkeys on the cis-monounsaturated fat diet. Taken together these studies suggest that IP-TFA is obesity promoting, and that they particularly facilitate the deposition of the harmful abdominal fat associated with CHD. These findings can contribute to explaining why high intakes of IP-TFA may increase the risk of type 2 diabetes.9

Fat content in fast-food menus

To select more healthy choices at the fast-food restaurants, nutritional labelling must be both available and accurate. While most chains provide nutritional information about total calories, calories from macronutrients, and fibre content of their products, we do not think that the average consumer who eats at a fast-food chain has the time or ability to make a reasonable estimate of health consequences of such meals or their contribution to the day's caloric intake.

The results of our analyses of total fat and trans fat in 74 French fries and fried chicken (nuggets/hot wings) samples bought in McDonald's and KFC outlets in 35 countries during 2005–2006 are given in Figure 1. The figures represent the total fat and trans fat content in 160 g of chicken meat and 171 g of French fries, corresponding to a large serving at an American McDonald's outlet. In these meals the total fat content varies from 41 to 65 g at McDonald's and from 42 to 74 g at KFC; the trans fat content varies from 0.3 to 10.2 and 0.3 to 24 g, respectively. The differences in total fat content can – at least in part – be due to local taste preferences, but this is not the case for trans fat, which does not add a special flavour to the food. The results show that the same product, by the same provider, can vary in fat calorie content by more than 40%, and in trans fat content by several orders of magnitude. This demonstrates that the same product, unknown to the consumer, can vary substantially in its compliance with recommendations for healthy food.

Figure 1.
Figure 1 - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact help@nature.com or the author

The entire length of the bar (both colours included) indicates the amounts of total fat in a large fast-food meal consisting of 171 g French fries and 160 g chicken nuggets. The darker colour indicates the amounts of industrially produced trans fat. The values in parenthesis are the amounts of trans fat as a percentage of total fat.

Full figure and legend (305K)

Top

Conclusions

Fast-food restaurant chains may argue that the evidence linking their products to the super-sizing of their customers is too weak. But should not the customer be given the benefit of the doubt? Appropriate actions would include reducing portions to normal sizes, eliminating industrially produced trans fat, and selling burgers of lean meat, whole grain bread/buns, fat-reduced mayonnaise, more vegetables, lower-fat fried potatoes, reduced-sugar soft drinks, etc. Moreover, reliable nutritional information should be given by the chains, which requires better standardisation of the foods used.10 Although these measures may raise prices, such changes in fast-food meals would have no adverse health effects but quite the opposite!

Top

References

  1. Pereira MA, Kartashov AI, Ebbeling CB, Van Horn L, Slattery ML, Jacobs Jr DR et al. Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis. Lancet 2005; 365: 36–42. | Article | PubMed | ISI |
  2. Diliberti N, Bordi PL, Conklin MT, Roe LS, Rolls BJ. Increased portion size leads to increased energy intake in a restaurant meal. Obes Res 2004; 12: 562–568. | PubMed |
  3. Young LR, Nestle M. Expanding portion sizes in the US marketplace: implications for nutrition counseling. J Am Diet Assoc 2003; 103: 231–234. | Article | PubMed | ISI |
  4. Prentice AM, Jebb SA. Fast foods, energy density and obesity: a possible mechanistic link. Obes Rev 2003; 4: 187–194. | Article | PubMed | ChemPort |
  5. Stender S, Dyerberg J, Bysted A, Leth T, Astrup A. A trans world journey. Atheroscl Suppl 2006; 7: 47–52. | Article |
  6. Mozaffarian D, Katan MB, Ascherio A, Stampfer MJ, Willett WC. Trans fatty acids and cardiovascular disease. N Engl J Med 2006; 354: 1601–1613. | Article | PubMed | ChemPort |
  7. Koh-Banerjee P, Chu NF, Spiegelman D, Rosner B, Colditz G, Willett W et al. Prospective study of the association of changes in dietary intake, physical activity, alcohol consumption, and smoking with 9-y gain in waist circumference among 16 587 US men. Am J Clin Nutr 2003; 78: 719–727. | PubMed | ISI | ChemPort |
  8. Kavanagh K, Jones K, Sawyer J, Kelly K, Wagner JD, Rudel LL. Trans fat diet induces insulin resistance in monkeys. Diabetes Care 2006. Proceedings of 66th Scientific Sessions of the American Diabetes Association: Abstract 328-OR.
  9. Salmeron J, Hu FB, Manson JE, Stampfer MJ, Colditz GA, Rimm EB et al. Dietary fat intake and risk of type 2 diabetes in women. Am J Clin Nutr 2001; 73: 1019–1026. | PubMed | ChemPort |
  10. Astrup A. Super-sized and diabetic by frequent fast-food consumption? Lancet 2005; 365: 4–5. | Article | PubMed |
Top

Acknowledgements

SS and JD declare no conflict of interest. AA is medical advisor for Weight Watchers, and is member of several advisory boards for food producers. The Department of Human Nutrition receives/has received research funding from over 50 Danish and international food companies. Otherwise, I declare no conflict of interest.

Extra navigation

.

naturejobs

natureevents

ADVERTISEMENT