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International Journal of Obesity (2007) 31, 887–890
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DEBATE
Fast food: unfriendly and unhealthy
S Stender1, J Dyerberg1 and A Astrup2
1
Department of Clinical Biochemistry, Gentofte Hospital University of Copenhagen, Copenhagen, Denmark and
Department of Human Nutrition, Centre for Advanced Food Studies, Faculty of Life Sciences, University of Copenhagen,
Copenhagen, Denmark
2
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.
International Journal of Obesity (2007) 31, 887–890; doi:10.1038/sj.ijo.0803616; published online 24 April 2007
Keywords: trans-fatty acids; fast food; energy density
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.
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 fastfood 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 B3000
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.
Fast food health consequences
S Stender et al
888
Although every effort is made to adjust for potential
confounders, one cannot adjust for unmeasured or unmeasurable lifestyle factors.
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 energycontent/food-weight ratio. The energy density of the entire
menu at fast-food outlets is typically B1100 kJ/100 g.4 This
is 65% higher than the average British diet (B670 kJ/100 g)
and more than twice the energy density of recommended
healthy diets (B525 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
International Journal of Obesity
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-g 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.
Fast food health consequences
S Stender et al
889
China, Hong Kong (15%)
China, Bejing (1%)
USA, NYC (16%)
USA, Philadelfia (11%)
USA, Chicago (16%)
USA, Boston 16%)
USA, Atlanta (14%)
S. Africa, Jo.berg (14%)
Denmark (1%)
Finland (10%)
Malaysia (1%)
Australia (2%)
Norway (10%)
Canada (4%)
Germany, Wiesbaden (9%)
The Netherlands (7%)
Turkey (12%)
Sweden, Malmø (9%)
Germany, Hamburg (9%)
Peru (17%)
Czech republic (6%)
UK, Glasgow (16%)
Thailand (0%)
Greece (4%)
Poland (14%)
Hungary (9%)
Italy (11%)
Ireland (10%)
UK, Aberdeen (15%)
Bulgaria (7%)
UK, London (15%)
Oman (20%)
France (13%)
Sweden, Visby (4%)
Austria (9%)
Romania (9%)
Germany, Berlin (4%)
Spain, Barcelona (11%)
Portugal (9%)
Switzerland (5%)
Iceland (12%)
Spain, Malaga (7%)
Russia (8%)
McDonald´s
0
20
40
60
Hungary (32%)
Iceland (20%)
USA, Boston (29%)
Bulgaria (34%)
The Netherlands (8%)
Malaysia (2%)
Spain, Malaga (4%)
Canada (20%)
Spain, Barcelona (4%)
Spain, Madrid (0%)
Romania (26%)
Thailand (7%)
Poland (34%)
China (6%)
USA, NYC (10%)
Portugal (4%)
Bahamas (19%)
Peru (31%)
Germany, Hamburg (9%)
Germany, Wiesbaden (1%)
Czech republic (29%)
UK, Glasgow (5%)
India (1%)
Russia (1%)
S. Africa, Jo.berg (15%)
Denmark (2%)
Oman (14%)
UK, Aberdeen (2%)
S. Africa, Durban (18%)
France (10%)
UK, London (9%)
80
100
KFC
0
20
40
60
80
100
Grams fat in a large meal
Figure 1 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.
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
International Journal of Obesity
Fast food health consequences
S Stender et al
890
used.10 Although these measures may raise prices, such
changes in fast-food meals would have no adverse health
effects but quite the opposite!
2
3
Acknowledgements
4
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.
A Astrup
Department of Human Nutrition, RVA University,
Frederiksberg C, Denmark. E-mail: [email protected]
1958
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
International Journal of Obesity
5
6
7
8
9
10
resistance (the CARDIA study): 15-year prospective analysis.
Lancet 2005; 365: 36–42.
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.
Young LR, Nestle M. Expanding portion sizes in the US marketplace: implications for nutrition counseling. J Am Diet Assoc 2003;
103: 231–234.
Prentice AM, Jebb SA. Fast foods, energy density and obesity: a
possible mechanistic link. Obes Rev 2003; 4: 187–194.
Stender S, Dyerberg J, Bysted A, Leth T, Astrup A. A trans world
journey. Atheroscl Suppl 2006; 7: 47–52.
Mozaffarian D, Katan MB, Ascherio A, Stampfer MJ, Willett WC.
Trans fatty acids and cardiovascular disease. N Engl J Med 2006;
354: 1601–1613.
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.
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.
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.
Astrup A. Super-sized and diabetic by frequent fast-food
consumption? Lancet 2005; 365: 4–5.