Is Fat Intake a Risk Factor for Fat Gain in Children?
Eric Jéquier
Institute of Physiology, University of Lausanne, 1005 Lausanne,
Switzerland
Address correspondence and requests for reprints to: Dr. Eric Jéquier, Institut de Physiologie, University of Lausanne, Case postale, CH-1000, Rue du Bugnon 7, CH-1005 Lausanne, Switzerland.
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Introduction
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The prevalence of obesity in children and
adults is increasing worldwide. This demonstrates that the primary
cause of obesity lies in environmental and behavioral changes rather
than in genetic modifications. Among the environmental influences on
body weight regulation, the percentage of fat energy of the everyday
diet plays an important role. In many low-income countries, the
percentage of fat energy in the everyday diet increases in people who
reach a higher socioeconomic level, and this is accompanied by an
increased prevalence of overweight and obesity. The passive
over-consumption of energy-dense, high-fat diets combined with the
decline in physical activity are the two main factors that account for
the rising prevalence of obesity. The latter probably explains why
several epidemiological studies report a trend of a decreased fat
consumption in United States, while obesity prevalence is rising
(1). The well-documented fact of dietary underreporting by
obese people (2), however, is to be taken into account
when assessing the results of such epidemiological studies, because
worldwide the prevalence of overweight and obesity is significantly
related to the percentage of fat energy in the diet
(3).
Here, several lines of evidence are presented to illustrate why dietary
fat does affect obesity development. There are four questions that are
relevant to the relationship between dietary fat and obesity
development: 1) Is there a difference in the efficiency of energy
utilization from carbohydrate vs. fat? 2) What are the
effects of dietary fat and carbohydrate on postingestive fuel
selection? 3) Does a high-fat diet promote excessive energy
intake by passive over-consumption? and 4) Does a low-fat diet
influence the regulation of body weight?
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Nutrient-induced thermogenesis: efficiency of energy utilization
from carbohydrate vs. fat
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After food ingestion, there is an increase in energy expenditure,
a phenomenon called "nutrient-induced thermogenesis" or the thermic
effect of food. This rise in energy expenditure mainly results from the
absorption, the processing, and the storage of nutrients
(4). The thermic effect of carbohydrate was found to be
greater than that of fat (68% vs. 23% of the energy
content of ingested nutrients for carbohydrate and fat, respectively).
The reason for this difference in the thermic effects of fat and
carbohydrate is the higher energy cost for storing glucose as glycogen
than the cost for processing and storing fatty acids as fat. In
practical terms, these results show that the efficiency of energy
utilization is greater for fat than for carbohydrate, particularly when
either fat or carbohydrate is consumed in excess. Because the thermic
effect of nutrients is a loss of energy for the body, the lower the
thermic effect, the higher the proportion of nutrient energy that is
available for useful energy requiring processes or for weight gain.
Maffeis et al. (5) report that a
high-fat meal induces a lower thermogenic response than a isocaloric,
isoproteic low-fat meal given to children. Although the meal-induced
thermogenesis was 30% lower with the high-fat meal compared with the
low-fat meal, this energy saving only represents about 2% of total
24-h energy expenditure.
It is important to assess whether the small differences in the
efficiency of carbohydrate and fat energy utilization that are measured
within 5 h following a meal are also observed when meals are given
under eucaloric conditions for prolonged periods of time.
Administration of isoenergetic formulas to adult individuals with
various percentages of carbohydrate (1585% energy as carbohydrate
with 15% of energy as protein and the balance of energy as fat) did
not induce any significant variation in energy needs as a function of
percentage fat intake (6). Other studies on the effects of
imposed isoenergetic low- or high-fat diets in obese and nonobese women
showed that isoenergetic shifts from dietary fat to dietary
carbohydrate within the generally recommended range had no effect on
energy metabolism. Only diets with a very high carbohydrate and a very
low fat content induced significant increases in either sleeping
metabolic rate or in the thermic effect of a high carbohydrate meal
(7).
Thus, imposed isoenergetic diets with various percentages of
carbohydrate and fat modify energy metabolism only slightly and can be
considered as comparable energy sources to cover energy needs. It is
important to emphasize that the concept of a comparable efficiency of
energy utilization between carbohydrate and fat calories arises from
experimental conditions of imposed isoenergetic diets with various fat
and carbohydrate contents. This concept, however, does not take into
account two aspects of nutrient physiology that may affect the subjects
eating behavior under conditions of everyday life (i.e. the
postingestive fuel selection and the specific effects of nutrients on
food intake regulation). Evidence has accumulated recently showing that
high-fat, energy-dense meals favor passive over-consumption, a
mechanism that very likely contributes to explain the increasing
prevalence of obesity (8).
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Effects of dietary fat and carbohydrate on postingestive fuel
selection
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After a meal, the metabolic fuel mix oxidized depends on the
plasma concentration of glucose, free fatty acids, amino acids, and on
hormonal responses, among which insulin secretion plays a major role.
The carbohydrate content of a meal is the major determinant of insulin
secretion, the main hormone that controls fuel disposal. Insulin
promotes glucose uptake and oxidation in insulin-sensitive tissues. By
stimulating glycolysis at several steps and by activating the pyruvate
dehydrogenase complex, insulin controls the conversion of glucose to
acetyl-CoA and its entry into the Krebs cycle in insulin-sensitive
tissues. In addition, insulin suppresses the activity of the
hormone-sensitive lipase and, therefore, inhibits lipolysis and lipid
oxidation. As a result, after a high carbohydrate meal, glucose
oxidation is promoted whereas fat oxidation is inhibited
(7). The main driving mechanisms, which influence fuel
selection between carbohydrate and fat oxidation, are glucose
availability and the postprandial insulin response.
The metabolic priority for carbohydrate oxidation accounts for the fact
that carbohydrate balance is well controlled; under habitual stable
food intake conditions, carbohydrate balance is reached over a 24-h
period. This means that nearly all the amount of carbohydrates ingested
over a whole day is oxidized within 24 h. The fact that
carbohydrate balance is well controlled is also related to the relative
limited amount of body glycogen storage (maximal storage capacity,
500800 g glycogen in an adult man). Furthermore, the daily
carbohydrate intake corresponds to about 50% of the glycogen storage
capacity. Thus, the half-life of dietary carbohydrate after ingestion
is about 24 h, whereas that of dietary fat is much longer because
of the very large body pool of adipose tissue triglycerides.
A biochemical process that could invalidate the concept of carbohydrate
balance is de novo lipogenesis (i.e. the
conversion of glucose into fatty acids and triglycerides). It is
commonly believed, and often stated in biochemical textbooks, that
hepatic de novo lipogenesis from glucose is an important
metabolic pathway in humans. If it was true, dietary carbohydrate might
be an indirect source of fat accumulation in adipose tissue through
hepatic de novo lipogenesis. The concept of nutrient balance
would then be invalidated because one dietary macronutrient
(i.e. carbohydrate) could influence the balance of another
macronutrient (i.e. fat). Two different methods of
investigation have been used to assess de novo lipogenesis
in humans: indirect calorimetry and stable isotopes techniques.
Indirect calorimetry allows measuring net de novo
lipogenesis (i.e. the difference between de novo
fat synthesis and fat oxidation). A significant net lipogenesis has
been observed in humans only with experimental massive carbohydrate
overfeeding (9), a condition that does not occur in
everyday life. Under these exceptional conditions, de novo
lipogenesis is strongly stimulated and hepatic lipogenesis only
accounts for a small portion of de novo fat synthesis,
suggesting that adipose tissue lipogenesis may play a role.
Under spontaneous feeding conditions, however, isotopic measurements of
de novo lipogenesis show that only 23% of glucose carbon
atoms are converted into fatty acids; the latter are secreted by the
liver, after esterification into triglycerides, as very low-density
lipoprotein. Even with a high carbohydrate diet, hepatic de
novo lipogenesis does not exceed 510 g fatty acids synthesized
per day (10). Thus, human obesity does not result from the
conversion of glucose into lipids, and dietary carbohydrates cannot be
considered as nutrients directly responsible for the development of
obesity. However, dietary carbohydrates indirectly induce a reduction
in fat oxidation, and, for this reason, they may play a role in the
excessive weight gain leading to obesity. This may occur in children
who drink large quantities of soft drinks with a high sugar
content.
The influence of carbohydrate on body weight regulation is also
dependent on the effects of nutrients on food intake control. It is not
possible to eat excessive amounts of carbohydrates because of the bulk
effect of most carbohydrate rich meals that promotes satiation and
satiety.
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Does fat intake promote excessive energy intake by passive
over-consumption?
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The effects of nutrients on satiation and satiety have been
much studied recently. Satiation corresponds to the suppression of
hunger after the ingestion of a certain amount of food whereas satiety
describes the period of time of absence of hunger between meals. It is
important to assess the satiating capacity of the nutrients because the
ability of the different macronutrients to stimulate satiety and to
suppress subsequent food intake is not equal. There is a hierarchy in
the ability of the three macronutrients to suppress subsequent food
intake. Proteins have the greater satiating capacity; carbohydrates,
which are also able to decrease the amount of food ingested at the next
meal, follow them. By contrast, lipids have a less potent satiating
effect than proteins and carbohydrates (11). Meals with a
high lipid content favor passive over-consumption because the
high-energy density promotes energy intake. In addition, the
fat-induced appetite control signals are too weak to prevent excessive
energy intake from a fatty meal, and the satiating effect is relatively
small in relation to the amount of the ingested energy.
According to the concept of oxidation hierarchy, carbohydrate and
protein intake elicits an acute autoregulatory increase in their
oxidation, with a suppression of fat oxidation. It is interesting to
emphasize that the hierarchy in the capacity of the macronutrients to
elicit satiety (protein > carbohydrate > fat) is similar to
the priority of fuel selection of macronutrients following a meal. It
has been hypothesized that a stimulus generated at the level of fuel
oxidation, presumably in the liver, provides a feedback signal that
links the oxidative metabolism of fuels to the control of food intake.
The effect of high-fat meals on spontaneous food intake has been
studied in short-term and long-term covert manipulation studies
(11). Both types of studies show a positive relationship
between dietary fat content and energy balance. An interesting finding
of long-term manipulation studies of dietary fat is the absence of
compensation of energy intake with high-fat diets even after 14 days of
positive energy balance. In addition, it has been established that
passive overconsumption is related to the energy density of foods.
High-fat diets are more energy dense than high carbohydrate diets, and
the former favor hyperplagia.
The passive over-consumption of high-fat diets is also due to the fact
that people tend to consume a similar bulk of food regardless of its
composition (11). With high-fat, energy-dense diets more
calories are passively ingested than with high carbohydrate diets. The
improved taste and texture of fatty foods further enhance the increased
energy consumption of high-fat diets.
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Does a reduction in the fat content of the diet influence the
regulation of body weight?
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It is remarkable that only a very small difference between energy
intake and energy expenditure can account for weight gain in the
development of obesity. If energy intake would exceed energy
expenditure by 1% everyday, this would result in a gain of 1 kg
adipose tissue after 1 yr! This explains why it is so difficult, or
even impossible, to demonstrate the precise mechanism of weight gain in
a given individual. By contrast, it is possible to test whether a
decrease in the percentage of fat energy (combined with a concomitant
increase in carbohydrate energy) may be a useful approach to induce
long-term weight loss in overweight and obese patients.
In a meta-analysis of low-fat diets (12), it was found
that these diets induced about 5 kg weight loss in comparison with the
control groups. The amount of weight loss was related to the degree of
reduction in dietary fat and to the pretreatment body weight. An
advantage of this dietary approach in the treatment of obesity is the
implementation of behavioral changes: the patients have to change their
habitual food choice, and there is some evidence that the benefit of
the weight loss may be long-lasting in patients who adhere to these
dietary recommendations.
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Other advantages of low-fat diets
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It is fortunate that low-fat diets are not only useful for
preventing or treating obesity, but they are also recommended to reduce
the risk of coronary heart diseases and of certain types of cancer.
Low-fat diets are relatively rich in carbohydrates, and this has
created some concern about their nutritional value (13).
The isoenergetically replacement of fats by carbohydrates has been
shown to lower both high-density lipoprotein (HDL) and low-density
lipoprotein cholesterol plasma levels. Because the lowering of HDL
cholesterol is considered to be associated with an increased risk of
coronary heart diseases, the recommendation to favor low-fat, high
carbohydrate diets has been criticized. It is interesting to note that
the drop in HDL cholesterol was found to be very small when the higher
carbohydrate diet is fed ad libitum instead of
isoenergetically. Furthermore, the physiologic reduction of HDL
cholesterol plasma levels with a low fat diet is not detrimental; on
the contrary, the incidence of atherosclerosis is reduced in
populations with low-fat diets. Low-fat diets associated with more
fruits, vegetables, and fibers have also been shown to reduce blood
pressure.
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Conclusion
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Low-fat, high carbohydrate diets are to be recommended for the
prevention of obesity. The two main criticisms, which have been
reported against the implementation of low-fat, high-carbohydrate
diets, are their alleged lack of efficacy in eliciting weight loss and
their potential adverse effect in cardiovascular disease prevention.
These criticisms are not justified for the following reasons: low-fat
diets have been shown to promote moderate weight loss over 1 yr or
more, and no study has ever reported an increased incidence of
cardiovascular diseases with low-fat diets. In addition, an improved
insulin sensitivity and a decrease in impaired glucose tolerance
accompany even a modest weight loss in obese subjects. It is,
therefore, appropriate from a public health perspective to promote a
reduction in fat intake as an important goal for the prevention of
obesity and obesityinduced diabetes. Although the beneficial
effects of low-fat diets have been mainly studied in adult subjects,
there are many reasons to believe that the main concepts described
above do also apply to adolescents. For infants and children, the
nutritional advice must, of course, take into account the energy cost
of growth and development; long-term studies for obesity prevention
using low-fat diets need to be carried out in children. A practical
issue is to improve the poor compliance of obese-prone individuals to
adhere to a low-fat diet on a long-term basis. Another reason
for concern with high carbohydrate, low-fat diets is the amount of
highly refined and processed carbohydrate in the diet, because an
excess of sugar intake has been associated with the development of
diabetes mellitus. Therefore, diets should contain a sufficient amount
of cereal fiber and grains, and the amount of refined carbohydrate must
be kept low.
It is relevant to emphasize that the control of nutrient intake only
concerns one side of the energy balance equation. The other side,
energy expenditure, is highly dependent on the degree of physical
activity. A low level of daily physical activity is a factor that
contributes to the positive energy balance, which may lead to obesity.
This is particularly well documented in children who spend several
hours per day watching television programs. Because exercise of
moderate intensity mostly stimulates fat oxidation, one understands why
a lack of physical activity favors a positive fat balance and body
weight gain. It is, therefore, important to stimulate fat oxidation by
promoting physical activity.
Received November 3, 2000.
Accepted November 15, 2000.
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