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Acta Cardiol 2010; 65(4): 377-386
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doi: 10.2143/AC.65.4.2053895
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TUTORIAL
Dietary determinants of obesity
Huaidong DU1,2,3, PhD; Edith FESKENS4, PhD
1Clinical
Trial Service Unit (CTSU), University of Oxford, UK; 2National Institute for Public Health
and the Environment (RIVM), Bilthoven, The Netherlands; 3Dept. of Human Biology, Nutrition and
Toxicology Research Institute of Maastricht (NUTRIM), Maastricht, The Netherlands; 4Division of
Human Nutrition, Wageningen University, The Netherlands.
Obesity has become a serious public health problem worldwide, and dietary composition can play
a role in its prevention and treatment. However, available literature on the impacts of different
dietary factors on weight change is inconsistent, or even conflicting. In this review, we briefly summarized the mechanisms and influences of several major dietary determinants of weight change,
with a focus on their potential in the prevention of weight gain or regain. We discussed the intake
of fat, protein, total carbohydrates, fruits and vegetables, fibre, free sugars, fructose and sugar sweetened beverages, dietary energy density, portion size, eating outside home, glycaemic index and glycaemic load. Popular weight loss diets, including the Atkins diet, Weight Watchers, Ornish diet and
Zone diet, are also briefly discussed for their safety and efficacy in the maintenance of weight loss.
Keywords: Obesity – weight management – diet – determinants.
Introduction
Obesity (body mass index (BMI) higher or equal
to 30∞∞kg/m2), and to a lesser extent overweight (BMI
higher or equal to 25∞∞kg/m2), is characterized as an
excessive accumulation of energy in the form of body
fat. It has reached an epidemic proportion globally
and the most recent estimate indicates that more than
1 billion adults worldwide are overweight, of whom at
least 300∞∞million are obese1. This poses serious health
problems and a huge economic burden on society
because overweight and obesity lead to adverse metabolic effects on blood pressure, blood lipids, and insulin
resistance, consequently increase the risk of chronic
diseases such as type 2 diabetes, cardiovascular disease
(CVD), hypertension, stroke, certain forms of cancer
and premature death1.
One of the few non-controversial facts about obesity is that weight is only gained when energy intake
exceeds energy expenditure for a prolonged time
period. A high total energy intake is the main driver
of higher body weights in modern populations2. During the past several decades, a large number of studies have investigated the effects of different dietary
Address for correspondence: Huaidong Du, PhD, Clinical Trial Service
Unit (CTSU), University of Oxford, OX3 7LF, UK. E-mail:
[email protected]
Received 18 May 2010; accepted for publication 21 May 2010.
composition factors and eating behaviours on energy
intake, weight gain and obesity. This review addresses
some of these factors and summarizes the mechanisms
underlying their potential associations with weight
change or obesity. Several associated popular weight
loss diets are also discussed in terms of their effectiveness and safety. Before reviewing the data, we
briefly introduce the process of food intake regulation.
Physiological regulation of food intake
Food intake is under-sophisticated regulation which
involves many psychological, hormonal and nutrientrelated factors. In general, it can be divided into two
phases: satiation and satiety. Satiation develops during a meal, ends eating, and determines the meal sizes.
Satiety develops after foods have been ingested, delays
the onset of the next meal and controls the inter-meal
intervals. The regulation of energy intake by satiation
and satiety is conducted by the hypothalamic signalling
pathway3. This pathway integrates three main sets of
signals.
The first set comprises gut hormones such as cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1)
and ghrelin. Ghrelin is the only gut hormone stimulating meal initiation (reducing satiety). CCK and
GLP-1 are released from the gut following food consumption to terminate meals (satiation) and their
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Fig.∞∞1. – Schematic overview of energy intake regulation.
effects depend on gastric distention4. In addition,
metabolites in blood after absorption could influence
people’s feeling of fullness (satiety). For example, the
transient and dynamic declines in blood glucose concentrations could promote eating (glucostatic hypothesis)4.
Signals secreted by adipose tissue and pancreas,
including leptin and insulin, represent the second set
of signals. They monitor the nutritional status of the
body, mediate the effects of gut hormones on the hypothalamus, and influence the sensitivity of the hypothalamus to satiety hormones such as CCK. For example, leptin deficiency induced by fasting limits the
satiating effect of CCK, which, in turn, leads to an
increased food intake during a meal, thereby restoring
energy balance5.
Signals released by the central nerve system, especially the hypothalamus, are the third set of signals
and include alpha-melanocyte-stimulating hormone
(a-MSH) and its precursor pro-opiomelanocortin
(POMC) (inhibits food intake) and neuropeptide Y
(NPY) (increases food intake)3. A simplistic overview
of the physiological regulation of energy intake is
depicted in figure 1.
Weight loss, weight maintenance and
the prevention of weight gain
Obesity is a preventable condition and the prevention is easier, less expensive and more effective as compared to the treatment. However, given the current obesogenic environment, which is characterized by an
essentially cheap and unlimited supply of convenient,
highly palatable, energy-dense foods, coupled with a
lifestyle prohibiting a sufficient level of physical activity, the incidence and prevalence of obesity is escalating. Weight reduction, even in a modest amount,
among those who are obese could significantly improve
obesity-related conditions, such as CVD and diabetes6.
However, initial weight loss is very difficult to sustain
due to the compensatory physiological processes which
seem to stimulate a weight regain7. The amount of
quick weight loss is less important if the weight is eventually regained. In other words, the real challenge of
weight loss regimes is to maintain weight loss and prevent weight regain. The main determinant of the
amount and rate of weight loss is the extent of energy
deficit, while the effects of dietary composition are
likely to be very small6-8. For weight loss maintenance,
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however, dietary composition might play a role through
influencing the insulin secretion and leptin production,
thus energy intake and energy balance9. More importantly, dietary composition could significantly influence cardiovascular risk through its impact on factors
other than body composition, such as blood pressure,
blood lipid profile, and insulin sensitivity10.
In the following section of the current tutorial, we
summarize the mechanisms of several major dietary
determinants of weight change, with a focus on the
prevention of weight gain or regain. Popular weight
loss diets are briefly discussed for their safety and efficacy in the maintenance of weight loss.
Dietary determinants of weight change
I. DIETARY
FACTORS IN RELATION TO OVERALL
ENERGY INTAKE
Energy density (ED)
Energy density (ED) is defined as the amount of
available energy per unit weight of foods or meals (kJ/g
or kcal/g). Experimental data convincingly show that
people tend to eat a constant volume/weight of food
to feel satiated4, and, accordingly, energy-dense foods
could cause passive over-eating in terms of energy. Furthermore, energy-dense foods, usually high in fat and
sugar but low in fibre and water, tend to be less satiating and highly palatable, thus could stimulate overeating11. It is believed that the generally accepted harmful impact of high fat diets on obesity is primarily
mediated by dietary ED. Several intervention studies
consistently demonstrate that ED reduction is associated with weight loss12,13. Results from most, but not
all, of the long-term observational studies also support
a positive association between ED and weight gain14-17.
Fruits and vegetables
Fruits and vegetables are fibre rich, low in ED and
high in vitamins and antioxidants therefore are of potential benefit for weight control. Although not completely
consistent, findings in general support the beneficial role
of fruit- and vegetable-rich diets in preventing weight
gain18-20. Therefore, fruits and vegetables are usually
included in dietary guidelines to combat obesity.
Portion size
Larger portion size is often accompanied by a higher
total energy content, and thus could contribute to
weight gain21. Large portion sizes served at restaurants
and produced by manufactures may be an important
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cause for the rising prevalence of obesity22. However,
the influence of portion size on food intake may vary
by age23 and weight status, and may also depend on the
ED of the foods, because it is possible that consumption
of a larger portion of lower energy dense foods, such as
fruits and vegetables, is protective against weight gain21.
Eating outside home
Eating outside home may be a risk factor of obesity because foods prepared at restaurants, especially
fast food restaurants, are often of lower nutritional
quality and have higher fat and energy contents than
foods eaten at home24. Individuals who eat more fast
foods tend to have a higher intake of energy, fat, and
soft drinks, and a lower intake of dietary fibre, fruits
and vegetables25. In addition, portion sizes served at
restaurants are often larger and the palatability and
variety of restaurant-prepared foods are often increased22. These factors may contribute to an increased
energy intake subsequently leading to obesity22.
II. FAT
INTAKE
Dietary fat has long been blamed as the main cause
for the current obesity epidemic because its higher ED
and palatability and lower satiety power could promote energy intake26. Moreover, its metabolic efficiency
is higher (i.e. lower thermogenesis) as compared to carbohydrates and protein. Therefore, the high-fat diet
would lead to a more efficient energy storage in the
adipose tissue27. In a meta-analysis of 16 trials comparing ad libitum low-fat diets with control diets, the
low-fat intervention group lost on average 3.2∞∞kg more
weight than the control group during the 2-12∞∞months
intervention periods28. In a recent analysis of data
from the US Nurses’ Health Study, total fat intake was
weakly but positively associated with weight gain over
8∞∞years29. In the Women’s Health Initiative Dietary
Modification Trial, weight loss in the first year was
more pronounced among women who had the greatest decrease in percentage of energy from fat30. However, most of the lost weight was regained and the difference in weight loss between the two groups was
negligible at the end of the follow-up period30. Similarly, there is no association between fat intake and
long-term weight and waist change observed in a large
prospective cohort study in Europe31.
Not all fats are alike. The harmful effects of saturated fatty acids (SFAs) and the potential health benefits of n-3 polyunsaturated fatty acids (PUFAs) and
monounsaturated fatty acids (MUFAs) have been well
established in the past two decades32. These fatty acids
may also have different impacts on body fat accumulation, due to their diverse metabolic fate in humans29,33.
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Therefore, encouraging a low SFA, high MUFA and n-3
PUFA diet may favourably influence the metabolic and
CVD risk, which is important for those who are overweight or obese.
III. CARBOHYDRATE-RELATED
DIETARY FACTORS
As carbohydrates are stored less efficiently than fat,
high carbohydrate foods are thought to reduce weight
gain in the long term as compared to high fat diets.28
However, in spite of the reported cutting down of fat
consumption in the western world since decades, the
prevalence of obesity has continued to rise. This secular trend data tends to implicate carbohydrate intake
as a contributor to the current obesity epidemic. However, there is no clear evidence that altering the energy
percentage of total carbohydrate is an important determinant of energy intake, thus weight change7,34.
Carbohydrates are composed of various nutrients
which have diverse effects on energy intake and general
health. Of particular interest are dietary fibre, free sugars, particularly fructose, sugar-sweetened beverages
(SSB), and glycaemic index and load.
Dietary fibre
Dietary fibre is defined as the edible parts of plant
foods that are resistant to digestion and absorption in
the human small intestine with complete or partial fermentation in the large intestine. It can facilitate body
weight control through different physiological mechanisms35. Firstly, fibre-rich foods tend to be more satiating due to their relatively low energy density and
palatability as compared to low fibre foods. Secondly,
dietary fibre, especially soluble fibre, could increase the
viscosity of diets and slow down the gastric emptying
and digestion, thus stimulating the release of gut hormones and promote satiety. In addition, dietary fibre
could provide a mechanical barrier to the enzymatic
digestion of other macronutrients such as fat and
starch in the small intestine. Moreover, the slower
digestion and absorption rate of carbohydrates in high
fibre foods would lead to a reduced postprandial blood
glucose response, which increases satiety and, over a
long term, could improve insulin sensitivity and influence fuel partitioning to favour fat oxidation35. Findings from many, if not all, studies indicate a beneficial
role of dietary fibre in weight control36,37.
Free sugar and fructose
Free sugars are a collection of added sugars and
concentrated sugars in honey, syrups and fruit juices38.
Foods high in free sugars have been proposed to
contribute weight gain because they are normally low in
fibre and micronutrients, high in ED and palatability
which could easily cause overconsumption7. Over the
past decades, the food industries in the USA and some
other countries have increasingly used high fructose
corn syrup in manufactured foods such as soft drinks,
baked goods, and desserts. This trend is in parallel with
the trend in obesity in the US39. Fructose follows a
different metabolic pathway as compared to glucose:
insulin is not increased, leptin is not increased but
reduced, and ghrelin is suppressed to a much lesser
degree. This will lead to a reduced satiety and a positive energy balance7,40. In addition, fructose ingestion
favours de novo lipogenesis, which could increase adiposity and cardiovascular risk. Consumption of fructose-sweetened beverages has been found to increase
visceral adiposity and lipids and to decrease insulin
sensitivity among overweight or obese people41.
Sugar-sweetened beverages (SSB)
Sugar-sweetened beverages (SSB) generally contain
a large amount of liquid energy, which is poorly compensated and may result in excess energy intake42. In
addition, added sugars in the SSB are absorbed rapidly,
which may promote visceral fat accumulation due to
the insulin resistance and increased de novo hepatic
fatty acid synthesis caused by the added sugars43,44.
Increased consumption of SSB, mainly soft drinks and
fruit juices, is considered as a main driving force for
weight gain and obesity, especially among children
and adolescents45. Although large high-quality clinical trials are lacking, the evidence in general supports
that consumption of SSB is a probable risk factor for
obesity46.
Glycaemic index and glycaemic load
The glycaemic index (GI) is a quantitative measure
of carbohydrate quality based on the blood glucose
response after consumption47. Glycaemic load (GL)
measures the entire blood glucose-raising potential of
dietary carbohydrates and is calculated as the product
of GI and total carbohydrates48. It has been suggested
that low GI or GL diets can help to prevent body
weight gain and stimulate weight loss49. This is because
the mild blood glucose and insulin response following
a low GI or GL diet consumption could stimulate a
higher satiation and satiety, thus leading to a decrease
in energy intake50, regulate energy partitioning resulting in a reduced fat storage51, and limit the decrease of
the resting metabolic rate under energy restriction52,53.
However, findings in literature are inconsistent. For
example, some trials found that low GI and low GL
diets are more effective in promoting body fat loss
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(~1∞∞kg more) than comparison diets54,55, but not the
others56,57. Some cohort studies found that GI was
positively associated with a change in weight or waist
circumference, but not GL34,58. Some found low GI
diets associated with a lower weight and waist circumference gain in women, but not in men59.
IV. PROTEIN
INTAKE
Protein has a higher satiety value than iso-energetic
quantities of other macronutrients, and therefore
higher protein intake could decrease total energy
intake60. Also, protein has a greater thermogenic effect
and may therefore result in an increased energy expenditure61. In the USA, the consumption of protein, both
at absolute level and as percentage of total energy
intake, has remained relatively stable during the past
decades, while the obesity prevalence has increased dramatically62,63. Although these secular trend data do
not support the hypothesis that protein plays an important role in the development of obesity, several recent
studies have observed an inverse association between
protein intake and obesity64,65. Furthermore, some
researchers proposed the so-called ‘protein leverage
hypothesis’, which means that the body must be supplied with a certain level of dietary protein66. When
a protein-rich diet is consumed, this demand can be
easily reached with a lower level of fat and carbohydrate thus total energy intake, otherwise a higher
amount of total energy must be consumed to obtain
enough protein.
Popular weight loss diets
I. ATKINS
DIET
The Atkins diet, the most popular weight-loss diet
to date, was first introduced in the 1970s by Dr. Atkins.
It involves restricting carbohydrates severely (< 20∞∞g
per day for the induction phase and < 50∞∞g per day
after for the ongoing weight loss phase) to produce
ketosis. The underlying reasons for the weight loss
effects of the Atkins diet include the satiating effect of
protein, possible appetite suppression effect of ketosis, reduced energy intake caused by restrictive food
choices, and the greater loss of water and glycogen60.
In addition, the reduced carbohydrate intake could
lead to a lowered insulin response thereby promoting
lipolysis and causing body fat loss67.
In a one-year intervention study conducted by
Dansinger et al., the Atkins diet was not associated with
a larger weight loss as compared to the other popular
weight loss diets68. A large dropout rate was observed
and the sustained adherence to an assigned diet, rather
than the type of diet, was the main determinant of
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weight loss and cardiac risk factor reduction in this
study68. In another study, the Atkins diet produced a
substantially larger weight loss and improvement in
cardiovascular risk factors as compared to other weight
loss programs at the initial stage, but most of the lost
weight was regained during the weight maintenance
phase69. In the study by Gardner et al. weight loss was
significantly larger in the Atkins diet group at
12∞∞months70, but the greater speed of relapse may
implicate that the difference between the groups would
disappear if the study continues. Therefore, there is
still insufficient evidence to make recommendations
for or against this diet71.
Dietary quality comparison of a range of popular
weight loss diets has shown that the Atkins diet had
the lowest score (worst quality)72,73. The high fat - especially saturated fat - and cholesterol contents of the
Atkins diet is the major concern due to the potential
hazardous effect on cardiovascular risks67,71. Longterm prospective studies investigating the impact of
the Atkins diet on the morbidity and mortality of
CVD are lacking. Furthermore, this type of diet is
inherently low in whole grains, cereals and fruits and
therefore may be nutritionally inadequate: low in vitamins E, A, thiamin, B6, folate, calcium, magnesium,
iron, potassium, and dietary fibre6.
II. WEIGHT WATCHERS
Weight Watchers® is a commercial weight loss program based on long-standing medical advice. The diet
emphasizes a high fibre, low ED and small portion
size68.
In a 2-year randomized trial with more than 400
obese subjects, the weight losses at 1∞∞year and 2∞∞years
were greater among subjects in the Weight Watchers®
group (4.3∞∞kg at 1∞∞year and 2.9∞∞kg at 2∞∞years) as compared to those in the control group (1.3∞∞kg and 0.2∞∞kg,
respectively)74. However, in another trial comparing
the effects of Weight Watchers® with other popular
weight loss diets, including the above mentioned Atkins
diet, none of these diet plans led to a significantly
larger weight loss at 1∞∞year68.
The dietary quality evaluation has revealed that the
Weight Watchers® and the Ornish diet (discussed later)
have a relatively higher quality compared to other popular weight loss diets implicating their potential benefits for CVD prevention73. No foreseeable safety problem has been reported for the Weight Watchers®.
III. ORNISH
DIET
The Ornish dietary plan was first described by Dr.
Ornish in his book Eat More, Weigh Less and is basically a vegetarian diet which is characterized as a strict
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restriction on high fat foods (∞∞<∞∞10% of total energy
intake), including oils, nuts, seeds, meat, poultry, and
fish. It is very high in carbohydrates, such as fruits,
vegetables, legumes and whole grains75. These foods
are generally healthy with a potential to reduce the risk
of many chronic diseases including CVD, diabetes and
cancer.
Low fat diets could result in more weight reduction
as compared to control diets in clinical trials of short
term. In long-term studies (>= 1∞∞year), however, the
impact of the fat percentage was low76. In the two
recent clinical trials comparing the effects of the Ornish
diet with the Atkins diet and other popular weight loss
diets on weight, the Ornish diet did not provide extra
benefits in 12∞∞months68,70. Nevertheless, there was no
trend of relapse in weight loss from the 6th month to
the 12th month of the intervention70. This is in line
with earlier evidence showing that a low fat, high carbohydrate diet has a better long-term effect for maintaining weight loss77.
Because meat and fat intake is extremely low,
following the Ornish dietary plan may cause vitamin
E, B12 and zinc deficiency6.
IV. ZONE
DIET
The Zone diet was introduced by Dr. Sears in 1995
advocating a “40:30:30” ratio of calories from carbohydrates, proteins, and fats, respectively. This represents a 0.75 ratio of protein to carbohydrates, which is
approximately three times the ratio of 0.25 according
to the conventional dietary recommendation78. The
“Zone” is a term for a metabolic state in which the
human body operates at optimal efficiency: the insulin
to glucagon ratio is reduced, allowing the excess body
fat to be burned and leading to the production of good
anti-inflammatory eicosanoids79.
Short-term studies have found that high protein
diets are more effective for preventing weight regain
and preserving fat free mass80,81. Several long-term
intervention studies have found that a high protein diet
is associated with improved weight maintenance and a
reduced CVD risk. For example, Clifton and colleagues
have observed that a higher protein (protein to carbohydrates ratio∞∞=∞ 46:34) intake led to a larger weight loss
after 1∞∞year as compared to those reporting a higher
carbohydrates diet (ratio∞∞=∞ 17:64)82. In the OmniHeart
study, substitution of carbohydrates with protein has
been associated with lowered blood pressure, improved
lipid levels, and reduced estimated cardiovascular
risk83. But, recent clinical trials comparing the effect of
the Zone diet with the Ornish diet and the Atkins diet
failed to observe any significant benefits of the Zone
diet in promoting body weight or fat loss or preserving lean body mass68,70. Therefore, the currently available scientific literature does not support a beneficial
role of the Zone diet for weight control and general
health79.
Although long-term data on the risk of a high protein diet is still lacking, protein, especially from animal
sources, is generally associated with total fat, saturated
fat, and cholesterol. Therefore long-term high protein
consumption may cause an increased risk of CVD60.
It is also of concern that a high protein diet may have
potential deleterious effects on the kidneys84. Moreover, a relatively low level of carbohydrate intake may
lead to a low intake of vitamins and fibre.
Challenges to dietary research
In spite of the wide awareness of the obesity problem, there are actually only a few high-quality longterm dietary intervention studies on weight change.
One of the potential reasons is the low compliance
rate. It is very difficult to promote a substantial and
sustainable lifestyle behaviour change, due to all kinds
of internal and external barriers85. For example, in the
above mentioned study by Dansinger et al., 42% of
participants did not complete the study at 12∞∞months
and the main reasons for the dropout were either ‘dislike the diet’ or ‘unable to adhere’68. In another study
comparing the weight loss effects of 4 diets with different macronutrient composition by Sacks et al.86,
protein intake difference between the high-protein-diet
group and the average-protein-diet group was intended
to be 10% of energy, but the actual difference was only
1-2% difference87.
Another main challenge in dietary intervention
trials, as well as in observational studies with dietary
exposures, may be the inaccuracy of dietary measurements, especially among obese individuals88. This may
limit the strength of the conclusions derived. To overcome this problem, some dietary intervention trials
provided all the foods and beverages, free of charge, to
the study participants, through either a study supermarket89 or controlled-feeding program90. This promotes a better monitoring of the food consumption,
avoids reporting errors, and may also increase compliance. However, it may cause a tendency of over-eating and is not of benefit for the establishment of a sustainable behaviour change. New technologies, such as
metabonomics, may provide more accurate measurements of dietary exposures in the future91.
Conclusion and recommendation
The fundamental point for weight control is the
energy balance. Multiple dietary approaches are available to prevent excessive energy intake, such as increase
the intake of fruits and vegetables, choose small portion
size, and stay away from sugar-sweetened beverages.
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For body fat loss, the degree of energy deficit is the
predominant determinant and adherence determines
whether the lost weight will be regained. Maintaining
a healthy body weight is a lifelong task therefore people
should choose a diet best suited to his or her food preferences, budget, lifestyle, daily challenges and medical
conditions to maximize long-term adherence. More
importantly, being physically active and having a balanced nutritionally adequate diet are critical for health,
where the ultimate purpose of losing extra weight lies.
A diet high in healthy substances, such as low GI complex carbohydrates, fibre, MUFAs, n-3 PUFAs and
plant protein, but low in calories and harmful or less
healthy compounds such as SFA, trans-fatty acids,
cholesterol, free sugars and red meat may be optimal.
Acknowledgment
Dr. Du’s PhD research (doctoral thesis: Dietary
determinants of obesity. Maastricht University, 2009.
ISBN: 978-90-9024757-1) was supervised by dr.
Daphne L. van der A (National Institute for Public
Health and the Environment (RIVM), the Netherlands), professor Edith M.J. Feskens (Wageningen
University), and professor Wim H. M. Saris (Maastricht University).
Funding
The research project was financially supported by
the pan-European program DiOGenes, which is the
acronym of “Diet, Obesity and Genes” (Contract n°.
Food-CT-2005-513946).
Conflict of interest: none declared.
References
1. WHO. Global Strategy on Diet, Physical Activity and
Health-Obesity and Overweight Geneva, 2003.
2. Swinburn BA, Sacks G, Lo SK, Westerterp KR, Rush EC,
Rosenbaum M, Luke A, Schoeller DA, Delany JP, Butte NF,
Ravussin E. Estimating the changes in energy flux that characterize the rise in obesity prevalence. Am J Clin Nutr 2009;
89: 1723-8.
3. Woods SC, Seeley RJ, Cota D. Regulation of food intake
through hypothalamic signaling networks involving mTOR.
Annu Rev Nutr 2008; 28: 295-311.
4. de Graaf C, Blom WA, Smeets PA, Stafleu A, Hendriks HF.
Biomarkers of satiation and satiety. Am J Clin Nutr 2004; 79:
946-61.
5. McMinn JE, Sindelar DK, Havel PJ, Schwartz MW. Leptin
deficiency induced by fasting impairs the satiety response to
cholecystokinin. Endocrinology 2000; 141: 4442-8.
383
6. Freedman MR, King J, Kennedy E. Popular diets: a scientific review. Obes Res 2001; 9 (Suppl 1): 1S-40S.
7. van Dam RM, Seidell JC. Carbohydrate intake and obesity.
Eur J Clin Nutr 2007; 61 (Suppl 1): S75-99.
8. Hill JO, Drougas H, Peters JC. Obesity treatment: can diet
composition play a role? Ann Intern Med 1993; 119 (7 Pt 2):
694-7.
9. Romon M, Lebel P, Velly C, Marecaux N, Fruchart JC,
Dallongeville J. Leptin response to carbohydrate or fat meal
and association with subsequent satiety and energy intake.
Am J Physiol 1999; 277 (5 Pt 1): E855-61.
10. McKeown NM, Meigs JB, Liu S, Rogers G, Yoshida M,
Saltzman E, Jacques PF. Dietary carbohydrates and cardiovascular disease risk factors in the Framingham offspring
cohort. J Am Coll Nutr 2009; 28: 150-8.
11. Rolls BJ. The relationship between dietary energy density
and energy intake. Physiol Behav 2009; 97: 609-15.
12. Ello-Martin JA, Roe LS, Ledikwe JH, Beach AM, Rolls BJ.
Dietary energy density in the treatment of obesity: a yearlong trial comparing 2 weight-loss diets. Am J Clin Nutr
2007; 85: 1465-77.
13. Ledikwe JH, Rolls BJ, Smiciklas-Wright H, Mitchell DC,
Ard JD, Champagne C, Karanja N, Lin P-H, Stevens VJ,
Appel LJ. Reductions in dietary energy density are associated
with weight loss in overweight and obese participants in the
PREMIER trial. Am J Clin Nutr 2007; 85: 1212-21.
14. Savage JS, Marini M, Birch LL. Dietary energy density
predicts women’s weight change over 6 y. Am J Clin Nutr
2008; 88: 677-84.
15. Bes-Rastrollo M, van Dam RM, Martinez-Gonzalez MA,
Li TY, Sampson LL, Hu FB. Prospective study of dietary
energy density and weight gain in women. Am J Clin Nutr
2008; 88: 769-77.
16. Iqbal SI, Helge JW, Heitmann BL. Do energy density and
dietary fiber influence subsequent 5-year weight changes in
adult men and women? Obesity (Silver Spring) 2006; 14:
106-14.
17. Du H, van der A DL, Ginder V, Jebb SA, Forouhi NG,
Wareham NJ, Halkjaer J, Tjonneland A, Overvad K,
Jakobsen MU, Buijsse B, Steffen A, Palli D, Masala G,
Saris WH, Sorensen TI, Feskens EJ. Dietary energy density
in relation to subsequent changes of weight and waist circumference in European men and women. Plos ONE 2009;
4: e5339.
18. He K, Hu FB, Colditz GA, Manson JE, Willett WC, Liu S.
Changes in intake of fruits and vegetables in relation to risk
of obesity and weight gain among middle-aged women.
Int J Obes Relat Metab Disord 2004; 28: 1569-74.
19. Vioque J, Weinbrenner T, Castello A, Asensio L, Garcia de
la Hera M. Intake of fruits and vegetables in relation to
10-year weight gain among Spanish adults. Obesity (Silver
Spring) 2008; 16: 664-70.
20. Buijsse B, Feskens EJ, Schulze MB, Forouhi NG, Wareham
NJ, Sharp S, Palli D, Tognon G, Halkjaer J, Tjonneland A,
Jakobsen MU, Overvad K, van der A DL, Du H, Sorensen
TI, Boeing H. Fruit and vegetable intakes and subsequent
changes in body weight in European populations: results
from the project on Diet, Obesity, and Genes (DiOGenes).
Am J Clin Nutr 2009; 90: 202-9.
21. Rolls BJ. The Supersizing of America: Portion Size and the
Obesity Epidemic. Nutr Today 2003; 38: 42-53.
22. 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: 562-8.
93779_ActaCardio_65-4_01_10-4287
384
04-08-2010
10:57
Pagina 384
H. Du et al.
23. Rolls BJ, Engell D, Birch LL. Serving portion size influences
5-year-old but not 3-year-old children’s food intakes. J Am
Diet Assoc 2000; 100: 232-4.
24. Zoumas-Morse C, Rock CL, Sobo EJ, Neuhouser ML.
Children’s patterns of macronutrient intake and associations
with restaurant and home eating. J Am Diet Assoc 2001;
101: 923-5.
25. Bowman SA, Vinyard BT. Fast food consumption of U.S.
adults: impact on energy and nutrient intakes and overweight
status. J Am Coll Nutr 2004; 23: 163-8.
26. Hill JO, Melanson EL, Wyatt HT. Dietary fat intake and
regulation of energy balance: implications for obesity. J Nutr
2000; 130 (2S Suppl): 284S-288S.
27. Maffeis C, Schutz Y, Grezzani A, Provera S, Piacentini G,
Tato L. Meal-induced thermogenesis and obesity: is a fat
meal a risk factor for fat gain in children? J Clin Endocrinol
Metab 2001; 86: 214-9.
28. Astrup A, Grunwald GK, Melanson EL, Saris WH, Hill
JO. The role of low-fat diets in body weight control: a metaanalysis of ad libitum dietary intervention studies. Int J Obes
Relat Metab Disord 2000; 24: 1545-52.
29. Field AE, Willett WC, Lissner L, Colditz GA. Dietary fat
and weight gain among women in the Nurses’ Health Study.
Obesity (Silver Spring) 2007; 15: 967-76.
30. Howard BV, Manson JE, Stefanick ML, Beresford SA,
Frank G, Jones B, Rodabough RJ, Snetselaar L, Thomson
C, Tinker L, Vitolins M, Prentice R. Low-fat dietary pattern and weight change over 7∞∞years: the Women’s Health
Initiative Dietary Modification Trial. JAMA 2006; 295:
39-49.
31. Forouhi NG, Sharp SJ, Du H, van der A DL, Halkjaer J,
Schulze MB, Tjonneland A, Overvad K, Jakobsen MU,
Boeing H, Buijsse B, Palli D, Masala G, Feskens EJ,
Sorensen TI, Wareham NJ. Dietary fat intake and subsequent weight change in adults: results from the European
Prospective Investigation into Cancer and Nutrition cohorts.
Am J Clin Nutr 2009; 90: 1632-41.
32. Hu FB, Manson JE, Willett WC. Types of dietary fat and
risk of coronary heart disease: a critical review. J Am Coll
Nutr 2001; 20: 5-19.
33. Bray GA, Lovejoy JC, Smith SR, DeLany JP, Lefevre M,
Hwang D, Ryan DH, York DA. The influence of different
fats and fatty acids on obesity, insulin resistance and inflammation. J Nutr 2002; 132: 2488-91.
34. Ma Y, Olendzki B, Chiriboga D, Hebert JR, Li Y, Li W,
Campbell M, Gendreau K, Ockene IS. Association between
dietary carbohydrates and body weight. Am J Epidemiol
2005; 161: 359-67.
35. Pereira MA, Ludwig DS. Dietary fiber and body-weight regulation. Observations and mechanisms. Pediatr Clin North
Am 2001; 48: 969-80.
36. Liu S, Willett WC, Manson JE, Hu FB, Rosner B, Colditz
G. Relation between changes in intakes of dietary fiber and
grain products and changes in weight and development of
obesity among middle-aged women. Am J Clin Nutr 2003;
78: 920-7.
37. Du H, van der A DL, Boshuizen HC, Forouhi NG, Wareham NJ, Halkjaer J, Tjonneland A, Overvad K, Jakobsen
MU, Boeing H, Buijsse B, Masala G, Palli D, Sorensen TI,
Saris WH, Feskens EJ. Dietary fiber and subsequent changes
in body weight and waist circumference in European men
and women. Am J Clin Nutr; 91: 329-36.
38. Mann J. Free sugars and human health: sufficient evidence
for action? Lancet 2004; 363: 1068-70.
39. Baker CW. Free sugars and human health. Lancet 2004; 364:
662; author reply 662-3.
40. Wylie-Rosett J, Segal-Isaacson CJ, Segal-Isaacson A. Carbohydrates and increases in obesity: does the type of carbohydrate make a difference? Obes Res 2004; 12 (Suppl 2):
124S-9S.
41. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer
AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang
W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer
EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C,
Hellerstein MK, Berglund L, Havel PJ. Consuming fructosesweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in
overweight/obese humans. J Clin Invest 2009; 119: 1322-34.
42. Mattes RD. Dietary compensation by humans for supplemental energy provided as ethanol or carbohydrate in fluids.
Physiol Behav 1996; 59: 179-87.
43. Schwarz JM, Linfoot P, Dare D, Aghajanian K. Hepatic de
novo lipogenesis in normoinsulinemic and hyperinsulinemic
subjects consuming high-fat, low-carbohydrate and low-fat,
high-carbohydrate isoenergetic diets. Am J Clin Nutr 2003;
77: 43-50.
44. Hill JO, Prentice AM. Sugar and body weight regulation.
Am J Clin Nutr 1995; 62 (Suppl 1): 264S-273S; discussion
273S-274S.
45. Gill TP, Rangan AM, Webb KL. The weight of evidence
suggests that soft drinks are a major issue in childhood and
adolescent obesity. Med J Aust 2006; 184: 263-4.
46. Gibson S. Sugar-sweetened soft drinks and obesity: a systematic review of the evidence from observational studies
and interventions. Nutr Res Rev 2008; 21: 134-47.
47. Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H,
Baldwin JM, Bowling AC, Newman HC, Jenkins AL, Goff
DV. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981; 34: 362-6.
48. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing
AL, Willett WC. Dietary fiber, glycemic load, and risk of
non-insulin-dependent diabetes mellitus in women. JAMA
1997; 277: 472-7.
49. Ludwig DS. Dietary glycemic index and the regulation of
body weight. Lipids 2003; 38: 117-21.
50. Ball SD, Keller KR, Moyer-Mileur LJ, Ding YW, Donaldson D, Jackson WD. Prolongation of satiety after low versus moderately high glycemic index meals in obese adolescents. Pediatrics 2003; 111: 488-94.
51. Stevenson EJ, Williams C, Mash LE, Phillips B, Nute ML.
Influence of high-carbohydrate mixed meals with different
glycemic indexes on substrate utilization during subsequent
exercise in women. Am J Clin Nutr 2006; 84: 354-60.
52. Pereira MA, Swain J, Goldfine AB, Rifai N, Ludwig DS.
Effects of a low-glycemic load diet on resting energy expenditure and heart disease risk factors during weight loss.
JAMA 2004; 292: 2482-90.
53. Du H, van der A DL, Feskens EJ. Dietary glycaemic index:
a review of the physiological mechanisms and observed
health impacts. Acta Cardiol 2006; 61: 383-97.
54. Thomas DE, Elliott E, Baur L. Low glycaemic index or low
glycaemic load diets for overweight and obesity. Cochrane
Database Syst Rev 2007; 3: CD005105.
55. de Rougemont A, Normand S, Nazare JA, Skilton MR,
Sothier M, Vinoy S, Laville M. Beneficial effects of a 5-week
low-glycaemic index regimen on weight control and cardiovascular risk factors in overweight non-diabetic subjects.
Br J Nutr 2007; 98: 1288-98.
93779_ActaCardio_65-4_01_10-4287
04-08-2010
10:57
Pagina 385
Dietary determinants of obesity
56. Das SK, Gilhooly CH, Golden JK, Pittas AG, Fuss PJ,
Cheatham RA, Tyler S, Tsay M, McCrory MA, Lichtenstein AH, Dallal GE, Dutta C, Bhapkar MV, Delany JP,
Saltzman E, Roberts SB. Long-term effects of 2 energyrestricted diets differing in glycemic load on dietary adherence, body composition, and metabolism in CALERIE: a
1-y randomized controlled trial. Am J Clin Nutr 2007; 85:
1023-30.
57. Sichieri R, Moura AS, Genelhu V, Hu F, Willett WC. An
18-mo randomized trial of a low-glycemic-index diet and
weight change in Brazilian women. Am J Clin Nutr 2007;
86: 707-13.
58. Du H, van der A DL, van Bakel MM, Slimani N, Forouhi
NG, Wareham NJ, Halkjaer J, Tjonneland A, Jakobsen MU,
Overvad K, Schulze MB, Buijsse B, Boeing H, Palli D,
Masala G, Sorensen TI, Saris WH, Feskens EJ. Dietary
glycaemic index, glycaemic load and subsequent changes of
weight and waist circumference in European men and
women. Int J Obes (Lond) 2009; 33: 1280-8.
59. Hare-Bruun H, Flint A, Heitmann BL. Glycemic index
and glycemic load in relation to changes in body weight,
body fat distribution, and body composition in adult Danes.
Am J Clin Nutr 2006; 84: 871-9; quiz 952-3.
60. St Jeor ST, Howard BV, Prewitt TE, Bovee V, Bazzarre T,
Eckel RH. Dietary protein and weight reduction: a statement for healthcare professionals from the Nutrition Committee of the Council on Nutrition, Physical Activity, and
Metabolism of the American Heart Association. Circulation
2001; 104: 1869-74.
61. 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: 1135-41.
62. Norris J, Harnack L, Carmichael S, Pouane T, Wakimoto P,
Block G. US trends in nutrient intake: the 1987 and 1992
National Health Interview Surveys. Am J Public Health 1997;
87: 740-6.
63. Cavadini C, Siega-Riz AM, Popkin BM. US adolescent food
intake trends from 1965 to 1996. Arch Dis Child 2000; 83:
18-24.
64. Due A, Toubro S, Skov AR, Astrup A. Effect of normal-fat
diets, either medium or high in protein, on body weight in
overweight subjects: a randomised 1-year trial. Int J Obes
Relat Metab Disord 2004; 28: 1283-90.
65. Halkjaer J, Tjonneland A, Thomsen BL, Overvad K,
Sorensen TI. Intake of macronutrients as predictors of 5-y
changes in waist circumference. Am J Clin Nutr 2006; 84:
789-97.
66. Simpson SJ, Raubenheimer D. Obesity: the protein leverage
hypothesis. Obes Rev 2005; 6: 133-42.
67. Crowe TC. Safety of low-carbohydrate diets. Obes Rev 2005;
6: 235-45.
68. Dansinger ML, Gleason JA, Griffith JL, Selker HP,
Schaefer EJ. Comparison of the Atkins, Ornish, Weight
Watchers, and Zone diets for weight loss and heart disease
risk reduction: a randomized trial. JAMA 2005; 293: 43-53.
69. Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C,
Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S.
A randomized trial of a low-carbohydrate diet for obesity.
N Engl J Med 2003; 348: 2082-90.
70. Gardner CD, Kiazand A, Alhassan S, Kim S, Stafford RS,
Balise RR, Kraemer HC, King AC. Comparison of the
Atkins, Zone, Ornish, and LEARN diets for change in weight
and related risk factors among overweight premenopausal
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
86.
87.
88.
385
women: the A TO Z Weight Loss Study: a randomized trial.
JAMA 2007; 297: 969-77.
Bravata DM, Sanders L, Huang J, Krumholz HM, Olkin I,
Gardner CD. Efficacy and safety of low-carbohydrate diets:
a systematic review. JAMA 2003; 289: 1837-50.
Kennedy ET, Bowman SA, Spence JT, Freedman M, King
J. Popular diets: correlation to health, nutrition, and obesity.
J Am Diet Assoc 2001; 101: 411-20.
Ma Y, Pagoto SL, Griffith JA, Merriam PA, Ockene IS,
Hafner AR, Olendzki BC. A dietary quality comparison of
popular weight-loss plans. J Am Diet Assoc 2007; 107: 178691.
Heshka S, Anderson JW, Atkinson RL, Greenway FL, Hill
JO, Phinney SD, Kolotkin RL, Miller-Kovach K, Pi-Sunyer
FX. Weight loss with self-help compared with a structured
commercial program: a randomized trial. JAMA 2003; 289:
1792-8.
Ornish D. Was Dr Atkins right? J Am Diet Assoc 2004; 104:
537-42.
Willett WC. Dietary fat plays a major role in obesity: no.
Obes Rev 2002; 3: 59-68.
Toubro S, Astrup A. Randomised comparison of diets for
maintaining obese subjects’ weight after major weight loss:
ad lib, low fat, high carbohydrate diet v fixed energy intake.
BMJ 1997; 314: 29-34.
US Department of Agriculture. Nutrition and your health:
dietary guidelines for Americans, Washington DC, 2005.
Cheuvront SN. The Zone Diet phenomenon: a closer look
at the science behind the claims. J Am Coll Nutr 2003; 22:
9-17.
Lejeune MP, Kovacs EM, Westerterp-Plantenga MS. Additional protein intake limits weight regain after weight loss in
humans. Br J Nutr 2005; 93: 281-9.
Westerterp-Plantenga MS, Lejeune MP, Nijs I, van Ooijen
M, Kovacs EM. High protein intake sustains weight maintenance after body weight loss in humans. Int J Obes Relat
Metab Disord 2004; 28: 57-64.
Clifton PM, Keogh JB, Noakes M. Long-term effects of a
high-protein weight-loss diet. Am J Clin Nutr 2008; 87: 239.
Appel LJ, Sacks FM, Carey VJ, Obarzanek E, Swain JF,
Miller ER, 3rd, Conlin PR, Erlinger TP, Rosner BA, Laranjo
NM, Charleston J, McCarron P, Bishop LM. Effects of protein, monounsaturated fat, and carbohydrate intake on blood
pressure and serum lipids: results of the OmniHeart randomized trial. JAMA 2005; 294: 2455-64.
Luyckx VA, Mardigan TA. High protein diets may be hazardous for the kidneys. Nephrol Dial Transplant 2004; 19:
2678-9.
Wing RR, Goldstein MG, Acton KJ, Birch LL, Jakicic JM,
Sallis JF, Jr., Smith-West D, Jeffery RW, Surwit RS. Behavioral science research in diabetes: lifestyle changes related to
obesity, eating behavior, and physical activity. Diabetes Care
2001; 24: 117-23.
Sacks FM, Bray GA, Carey VJ, Smith SR, Ryan DH, Anton
SD, McManus K, Champagne CM, Bishop LM, Laranjo
N, Leboff MS, Rood JC, de Jonge L, Greenway FL, Loria
CM, Obarzanek E, Williamson DA. Comparison of weightloss diets with different compositions of fat, protein, and
carbohydrates. N Engl J Med 2009; 360: 859-73.
Katan MB. Weight-loss diets for the prevention and treatment of obesity. N Engl J Med 2009; 360: 923-5.
Zhang J, Temme EH, Sasaki S, Kesteloot H. Under- and
overreporting of energy intake using urinary cations as
93779_ActaCardio_65-4_01_10-4287
386
04-08-2010
10:57
Pagina 386
H. Du et al.
biomarkers: relation to body mass index. Am J Epidemiol
2000; 152: 453-62.
89. Due A, Larsen TM, Mu H, Hermansen K, Stender S,
Astrup A. Comparison of 3 ad libitum diets for weight-loss
maintenance, risk of cardiovascular disease, and diabetes: a
6-mo randomized, controlled trial. Am J Clin Nutr 2008; 88:
1232-41.
90. Bos MB, de Vries JH, Feskens EJ, van Dijk SJ, Hoelen DW,
Siebelink E, Heijligenberg R, de Groot LC. Effect of a high
monounsaturated fatty acids diet and a Mediterranean diet
on serum lipids and insulin sensitivity in adults with mild
abdominal obesity. Nutr Metab Cardiovasc Dis 2009 Aug 17.
[Epub ahead of print].
91. Fave G, Beckmann ME, Draper JH, Mathers JC. Measurement of dietary exposure: a challenging problem which may
be overcome thanks to metabolomics? Genes Nutr 2009; 4:
135-41.