http://www.ajcn.org/cgi/content/full/83/2/189
American Journal of Clinical Nutrition, Vol. 83, No. 2, 189-190,
February 2006
© 2006 American Society for Clinical Nutrition
EDITORIAL

Fast food and sedentary lifestyle: a combination that leads to
obesity1,2

David R Jacobs, Jr1

1 From the Division of Epidemiology, University of Minnesota,
Minneapolis, MN, and the Department of Nutrition, University of Oslo,
Oslo, Norway

2 Reprints not available. Address correspondence to DR Jacobs Jr,
Division of Epidemiology, School of Public Health, University of
Minnesota, 1300 South 2nd Street, Suite 300, Minneapolis, MN 55454.
E-mail: jacobs@epi.umn.edu.

See corresponding article on page 362.

Bes-Rastrollo et al (1) report in this issue of the Journal that the
consumption of sugar-sweetened soft drinks and fast-food intake—and,
to a lesser extent the consumption of sweetened fruit drinks and red
meat—predicts a weight gain of {approx}0.4 kg/y independent of energy
intake, physical activity, and television viewing. Their study was
conducted over 28.5 mo in a cohort of Spanish men and women with a
mean age of 41 y. For soft drinks, but not for the other foods, the
differential weight gain was most obvious in the subjects who had
gained weight in the 5 y before baseline. Although the authors spend
considerable effort showing this interaction, I suspect it is a chance
finding, perhaps associated with regression to the mean; the subjects
who gained weight in the 5 y before baseline gained less during the
follow-up than did those who had not gained weight. Thus, the authors
showed the first 28 mo of a trend similar to that recently reported
(2) over 15 y from the Coronary Artery Risk Development in Young
Adults (CARDIA) study: frequent fast-food consumption (soft drinks
could not be distinguished from other foods that are typical in
fast-food restaurants) was associated with a differential weight gain
of 0.3 kg/y and a worsening in insulin sensitivity compared with
infrequent fast-food consumption.

Bes-Rastrollo et al (1) opine that the energy obtained from soft
drinks does not fully displace that consumed from solid sources and
may encourage an increase in the consumption of other foods. However,
they concluded that higher total energy intake from other sources was
not the sole mechanism of weight gain after overconsumption of soft
drinks. They point out that soft drinks and other fast foods are low
in fiber, which, in their words, may exert adverse effects "on
satiety, glucose metabolism, energy density, and the rate of ingestion
and gastric emptying." The use of fructose rather than glucose may
have similar adverse metabolic implications (3). They also point to
the displacement of dairy products as one way in which soft drinks and
other fast foods could increase weight. Pereira et al (2) pointed out
that some fast-food meals approach the total daily energy intake
requirements and that the food is energy dense. They found that
increased fast-food intake led to insulin resistance.

Astrup (4), commenting on Pereira's CARDIA study finding, asked what
makes fast food fattening. Considering the convenience, low price, and
high-energy format of fast food, he said, "Human beings have only a
weak innate ability to recognize foods with high energy density and to
down-regulate the bulk eaten to meet energy requirements
appropriately." Animals gain weight if energy intake is greater than
energy expenditure, and they lose weight if energy intake is less than
energy expenditure. Cupples (5) stated that body weight is closely
regulated under most conditions; a failure in energy balance can have
severe consequences for the organism. In the long run, energy
consumption must be matched to energy expenditure. The situation is
remarkably subtle, however; the mean excess of 4.5 kg gained over 15 y
by fast-food eaters constituted only {approx}10 kcal/d, assuming that
1 kg fat corresponds to 7700 kcal. Clearly, it would not take much
disturbance in satiety and sensing of energy intake to throw energy
balance off by only a few kcal/d. Besides portion size, energy
density, and consequent changes in insulin action, small differences
in taste or rates of stomach emptying could make this a large
difference.

Individual susceptibility to weight gain varies (6); I suspect that a
sedentary lifestyle is important in this respect. Energy intake may be
determined, in part, by energy expenditure. The late Henry L Taylor
favored a model that linked energy intake to energy expenditure in a
J-shaped curve (personal communication, late 1970s). The first part of
his concept was that energy intake is in exact homeostasis with energy
expenditure under conditions of high energy expenditure. The second
part was that there is a failure of homeostasis in a sedentary
lifestyle because of its accompanying low energy expenditure. He
postulated that body signals go awry in sedentary lifestyles; when a
person does no physical work, the body will not recognize that it is
being overfed. Sedentary persons may lose the innate ability to
compensate for inactivity by reducing their eating. Neither
Bes-Rastrollo et al (1) nor Pereira et al (2) addressed whether the
weight gain associated with fast-food intake was enhanced by a
sedentary lifestyle.

Although this model is difficult to test, Stubbs et al have embarked
on a program to discover the conditions and timing under which humans
compensate for an energy deficit or surfeit. They asked whether
dietary intake is responsive to energy expenditure by studying the
effect of different levels of physical activity on ad libitum dietary
energy intake over a 7-d period. They found no compensatory increase
over this short time in lean men (7) and only a partial compensation
in lean women (8). In a follow-up study, they did detect some degree
of compensation of ad libitum intake both to a higher fat diet and to
an exercise program in men in a 7-d period (9); they projected that
energy balance would have been achieved over 2.4–4 wk. They felt that
the subjects compensated more readily to an increased energy deficit
(ie, more exercise) than to an energy surfeit (ie, offering more and
higher energy foods).

Many causes of the obesity epidemic exist. Fast food likely
contributes to overconsumption, and a sedentary lifestyle reduces
energy expenditure. Under the Taylor hypothesis (see above), a
sedentary lifestyle interacts with overconsumption to produce obesity.
Taylor believed that energy intake falls out of homeostasis with
energy expenditure when physical activity falls into the sedentary
range. Even if homeostasis could be maintained in sedentary people,
however, the low energy intake that may prevent obesity may at the
same time deplete micronutrient intake to such an extent that some
metabolic systems would not operate properly. Indeed, many of the
foods, including soft drinks and refined-wheat breads, are low in
micronutrients. Bes-Rastrollo et al (1) remind us of the need for
societal changes in diet; however, attention to physical activity is
also required.

ACKNOWLEDGMENTS

DR Jacobs has received grants from General Mills Inc and is a member
of the Scientific Advisory Board of the California Walnut Commission.

REFERENCES

  1. Bes-Rastrollo M, Sánchez-Villegas A, Gómez-Gracia E, Martínez
JA, Pajares RM, Martínez-González MA. Predictors of weight gain in a
Mediterranean cohort: the Seguimiento Universidad de Navarra Study. Am
J Clin Nutr 83;2:362-70.
  2. Pereira MA, Kartashov AI, Ebbeling CB, et al. Fast-food habits,
weight gain, and insulin resistance (the CARDIA study): 15-year
prospective analysis. Lancet 2005;365:36-42. (Published erratum
appears in Lancet 2005 16;365:1030.)[Medline]
  3. Elliott SS, Keim NL, Stern JS, Teff K, Havel PJ. Fructose,
weight gain, and the insulin resistance syndrome. Am J Clin Nutr
2002;76:911-22.[Abstract/Free Full Text]
  4. Astrup A. Super-sized and diabetic by frequent fast-food
consumption? Lancet 2005;365:4-5.[Medline]
  5. Cupples WA. Physiological regulation of food intake. Am J
Physiol Regul Integr Comp Physiol 2005;288:R1438-43.[Free Full Text]
  6. Blundell JE, Stubbs RJ, Golding C, et al. Resistance and
susceptibility to weight gain: individual variability in response to a
high-fat diet. Physiol Behav 2005; Oct 11 (Epub ahead of print;
DOI:10.1016/j.physbeh.2005.08.052).
  7. Stubbs RJ, Sepp A, Hughes DA, et al. The effect of graded levels
of exercise on energy intake and balance in free-living men, consuming
their normal diet. Eur J Clin Nutr 2002;56:129-40.[Medline]
  8. Stubbs RJ, Sepp A, Hughes DA, et al. The effect of graded levels
of exercise on energy intake and balance in free-living women. Int J
Obes Relat Metab Disord 2002;26:866-9.[Medline]
  9. Stubbs RJ, Hughes DA, Johnstone AM, et al. Rate and extent of
compensatory changes in energy intake and expenditure in response to
altered exercise and diet composition in humans. Am J Physiol Regul
Integr Comp Physiol 2004;286:R350-8.[Abstract/Free Full Text]

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http://www.ajcn.org/cgi/content/abstract/83/2/362
American Journal of Clinical Nutrition, Vol. 83, No. 2, 362-370,
February 2006
© 2006 American Society for Clinical Nutrition
ORIGINAL RESEARCH COMMUNICATION
Predictors of weight gain in a Mediterranean cohort: the Seguimiento
Universidad de Navarra Study 1 ,2 ,3
Maira Bes-Rastrollo1, Almudena Sánchez-Villegas1, Enrique
Gómez-Gracia1, J Alfredo Martínez1, Raquel M Pajares1 and Miguel A
Martínez-González1

1 From the Departments of Preventive Medicine and Public Health (MB-R,
AS-V, RM-P, and MAM-G) and Physiology and Nutrition (JAM), University
of Navarra, Pamplona, Spain; the Department of Clinical Sciences,
University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria,
Spain (AS-V); and the Department of Preventive Medicine and History of
Medicine, University of Málaga, Málaga, Spain (EG-G)

Background: High consumption of sugar-sweetened drinks has been
associated with weight gain and obesity in the United States. This
trend may also be affecting populations with different eating patterns
who increasingly are adopting typical US dietary patterns.

Objective: We assessed whether the consumption of sweetened drinks and
other food items increased the likelihood of weight gain in a
Mediterranean population.

Design: This was a prospective cohort analysis of 7194 men and women
with a mean age of 41 y who were followed-up for a median of 28.5 mo
with mailed questionnaires. Dietary exposure was assessed with a
previously validated semiquantitative food-frequency questionnaire.

Results: During follow-up, we observed that 49.5% of the participants
increased their weight (x weight gain: 0.64 kg; 95% CI: 0.55, 0.73
kg). In the participants who had gained ≥3 kg in the 5 y before
baseline, the adjusted odds ratio of subsequent weight gain for the
fifth quintile compared with the first quintile of sugar-sweetened
soft drink consumption was 1.6 (95% CI: 1.2, 2.1; P for trend = 0.02).
This association was absent in the participants who had not gained
weight in the 5-y period before baseline. The consumption of
hamburgers, pizza, and sausages (as a proxy for fast-food consumption)
was also independently associated with weight gain (adjusted odds
ratio for the fifth compared with the first quintile = 1.2; 95% CI:
1.0, 1.4; P for trend = 0.05). We also found a significant, but
weaker, association between weight gain and both red meat and
sweetened fruit juice consumption.

Conclusion: In a Mediterranean cohort, particularly in the
participants who had already gained weight, an increased consumption
of sugar-sweetened soft drinks and of hamburgers, pizza, and sausages
was associated with a higher risk of additional subsequent weight
gain.

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