Obesity Joel
and sweet
Grinker,
Theories
taste1’
Ph.D.
of obesity
Obesity
is a disorder
intake emphasized physiological, cognitive social and sensory components in feeding, i.e., peripheral or hepatitic metabolism (1 2), conditioned satiety (3-5), hyperinsulinemia (6), early nutritional or genetic effects on adipose cell morphology (7, 8), external responsiveness (9 1 0) and epidemological and cultural factors (11 12). In studies of human obesity it is often impossible to distinguish causation from correlation since the behavioral and metabolic pathology of the obese is a combination of genetic predisposition, cultural variables, the cognitive and social consequences of obesity and early is excessive.
in which
Various
theories
food
have ,
,
,
,
,
environmental
influences.
Because
of
these
confounding experimentally
factors in human obesity, the produced obese rat and mouse (electrolytic or chemical lesions or the region of the ventromedial hypothala-
VMH),
mus, rat
(Zucker)
the
genetic
and
mouse
obesities (ob/ob obese
and the dietary produced been used as model systems. While the inheritance of obesity documented in rodents (13-15), for
a genetic
component
based
on
occurs
in only
is clearly evidence
in human
epidemological seven
of both and AVY) rat have all
obesity
studies. percent
of
is
Obesity the
negative
correlation class
adults females
In the 1078
and (17,
between
has been children 19).
genetic The
documented and both
children
animal
obesities,
American
Journal
obesity
in males
early ofClinical
velopment of obesity is associated with both hypertrophy and hyperplasia of adipose tissue (20, 21). In experimentally produced obesity as a result of lesioning of the VMH, the obesity is primarily associated with hypertrophy of the adipose depots. In normal rats, adipose cell proliferation is generally complete by the time of weaning (22, 23).
In humans,
early
onset
of obesity
is usually
associated depots,
with hyperplasia of the adipose but individuals with late onset obesity can be hypercellular (24) Obese children are reported to show a different developmental pattern of cell proliferation (25) than normal nonobese controls. Recent studies suggest that even mature animals can increase the measurable number of adipose cells when stimulated to overeat by high fat or high carbohydrate diets (26, 27). Different strains of rats (Osborne-Mendel Sprague Dawley and Zucker leans) demonstrated differential responsiveness to high fat feeding; the amount of weight gained and the consequent increases in adipose cell number were greatest in the Osborne-Mendel and least in the lean Zucker rat. When the Osborne-Mendel rat was returned to the standard laboratory diet it never fully returned to normal body .
,
In
weight.
,
contrast,
a 25%
Sims
(28) in body
reported
in adult normal weight human volunteers without accompanying increases in adipocyte number and a full return to normal body weight. Individuals may show variability in the degree of hyperplastic or hypertrophic response to overfeeding (29). Subjects in the experimental feeding study were selected only if they reported no previous weight problems. These studies raise the achieving
born of normal weight parents, 40% of the children born in families with one obese parent, but 80% of the children in families with two obese parents (16). The 40% incidence of obesity is not dependent upon the occurrence of maternal obesity (1 1). Studies have also shown a consistent relationship between socioeconomic factors and the incidence of obesity (17, 18). A strong social
2
increase
weight
and
both and
deNutrition
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/6/1078/4650651 by Denise Hannibal user on 22 May 2018
I
From New
2
Supported
enue,
the Rockefeller University, York, New York 10021.
by NSF
Grant
BNS
1230
76-09957
Institute of Health Grant 5 ROl HD03719, tion Foundation Grant 485 to the author.
31:
JUNE
1978,
pp.
1078-1087.
Printed
York
Av-
National and
Nutri-
in U.S.A.
OBESITY
question atable or
of foods
whether the overeating may itself be a cause
a consequence
overweight. whether “elasticity”
of
of palof obesity
predisposition
to
An additional question there exist differential degrees in the control of food intake.
Taste responsiveness and maintenance
In its simplest asked,
some
AND
is of
and the development of obesity
form
the
question
can
be
does
obesity result from hyperresponsiveness to the sensory qualities of the diet or is hyperresponsiveness to sensory qualities merely a correlate of obesity? Both obese man and animals over-respond or over-consume foods that are highly “palatable” (see Reference 30 for a discussion of “finickiness” in VMH obesity; Reference 31 for genetic obesities; and Reference 32 for a discussion of palatability and human consumption) Palatable foods such as fats and carbohydrates are defined in a logically circular fashion as those foods that rats will over-consume (33, 34). Little information is available concerning the preferences or hedonic profiles between obese and normal weight animals. Several experiments in human subjects measured both the hedonic rating for various foods (ice cream, crackers, cake) and intakes of these same foods. In at least three separate experiments (32, 35, 36) overweight subjects, (moderate overweightdefined as from 1 5 to 40% above ideal weight based on actuarial tables of desirable weight for height and sex; Metropolitan Life Insurance Co. Statistical Bulletin 1958, and extreme overweight-defined as more than 40% overweight), showed greater intake of foods rated good compared to intakes of food rated less pleasant. Although normal weight subjects also had intakes correlated with preferences, the relationship was less pronounced. These experiments demonstrate that obese animals and humans will over-consume liked or palatable foods to a greater degree than normal weight controls. They fail to provide information on differ.
ences
in sensory
Over-indulgence drates has been cause
more
of
human
prevalent
processing.
in sweets or carbohyspecifically postulated as a obesity (37). One of the myths about factors associ-
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/6/1078/4650651 by Denise Hannibal user on 22 May 2018
SWEET
TASTE
1079
ated with the genesis of obesity is that obese individuals have a “sweet tooth”, that they prefer sweet tasting substances in greater degree than normal weight individuals and that they are particularly unable to restrain themselves in the face of tempting sweet foods. If, in fact, the myth were true, it would logically follow that there might be differences in some measurable parameter of taste that would help to provide a physiological clue to the genesis or maintenance of the obese state. There are few direct observations or questionnaire studies comparing the actual daily intake for sweets between obese and normal weight subjects. One study reported no differences between the preferences for desserts of varying sucrose concentrations by obese and normal weight subjects (38) Self reports by obese teenagers showed a lower daily carbohydrate (bread, sweets, and sugar) consumption than that reported by normal weight children (39) and similar findings have been reported for obese adults (40) The lack of significant differences in fatty acids of adipose tissue between obese and normal weight subjects does provide some support for the assumption that the proportions of dietary fat carbohydrate, and protein for obese and normal weight individuals are similar (40a). There have been several studies of the development of sweet preference and consumption in obese infants. Nisbett and Gurwirtz (4 1) report that heavy (although not fatter) infants (>3540 g) consumed proportionally more sweetened formula than did normal weight or low birth weight infants. Desor (42) reported that only the intake of low birth weight infants could be reliably differentiated from that of normal or heavy birth weight infants. Infants weighing less than 2722 g consumed lesser amounts of sweet carbohydrates (sucrose dextrose lactose, fructose) in three minute ingestion tests than did infants weighing greater than 3175 g. Finally, Grinker (43) has reported that low birth weight infants (
and sweet
Grinker,
Theories
taste1’
Ph.D.
of obesity
Obesity
is a disorder
intake emphasized physiological, cognitive social and sensory components in feeding, i.e., peripheral or hepatitic metabolism (1 2), conditioned satiety (3-5), hyperinsulinemia (6), early nutritional or genetic effects on adipose cell morphology (7, 8), external responsiveness (9 1 0) and epidemological and cultural factors (11 12). In studies of human obesity it is often impossible to distinguish causation from correlation since the behavioral and metabolic pathology of the obese is a combination of genetic predisposition, cultural variables, the cognitive and social consequences of obesity and early is excessive.
in which
Various
theories
food
have ,
,
,
,
,
environmental
influences.
Because
of
these
confounding experimentally
factors in human obesity, the produced obese rat and mouse (electrolytic or chemical lesions or the region of the ventromedial hypothala-
VMH),
mus, rat
(Zucker)
the
genetic
and
mouse
obesities (ob/ob obese
and the dietary produced been used as model systems. While the inheritance of obesity documented in rodents (13-15), for
a genetic
component
based
on
occurs
in only
is clearly evidence
in human
epidemological seven
of both and AVY) rat have all
obesity
studies. percent
of
is
Obesity the
negative
correlation class
adults females
In the 1078
and (17,
between
has been children 19).
genetic The
documented and both
children
animal
obesities,
American
Journal
obesity
in males
early ofClinical
velopment of obesity is associated with both hypertrophy and hyperplasia of adipose tissue (20, 21). In experimentally produced obesity as a result of lesioning of the VMH, the obesity is primarily associated with hypertrophy of the adipose depots. In normal rats, adipose cell proliferation is generally complete by the time of weaning (22, 23).
In humans,
early
onset
of obesity
is usually
associated depots,
with hyperplasia of the adipose but individuals with late onset obesity can be hypercellular (24) Obese children are reported to show a different developmental pattern of cell proliferation (25) than normal nonobese controls. Recent studies suggest that even mature animals can increase the measurable number of adipose cells when stimulated to overeat by high fat or high carbohydrate diets (26, 27). Different strains of rats (Osborne-Mendel Sprague Dawley and Zucker leans) demonstrated differential responsiveness to high fat feeding; the amount of weight gained and the consequent increases in adipose cell number were greatest in the Osborne-Mendel and least in the lean Zucker rat. When the Osborne-Mendel rat was returned to the standard laboratory diet it never fully returned to normal body .
,
In
weight.
,
contrast,
a 25%
Sims
(28) in body
reported
in adult normal weight human volunteers without accompanying increases in adipocyte number and a full return to normal body weight. Individuals may show variability in the degree of hyperplastic or hypertrophic response to overfeeding (29). Subjects in the experimental feeding study were selected only if they reported no previous weight problems. These studies raise the achieving
born of normal weight parents, 40% of the children born in families with one obese parent, but 80% of the children in families with two obese parents (16). The 40% incidence of obesity is not dependent upon the occurrence of maternal obesity (1 1). Studies have also shown a consistent relationship between socioeconomic factors and the incidence of obesity (17, 18). A strong social
2
increase
weight
and
both and
deNutrition
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/6/1078/4650651 by Denise Hannibal user on 22 May 2018
I
From New
2
Supported
enue,
the Rockefeller University, York, New York 10021.
by NSF
Grant
BNS
1230
76-09957
Institute of Health Grant 5 ROl HD03719, tion Foundation Grant 485 to the author.
31:
JUNE
1978,
pp.
1078-1087.
Printed
York
Av-
National and
Nutri-
in U.S.A.
OBESITY
question atable or
of foods
whether the overeating may itself be a cause
a consequence
overweight. whether “elasticity”
of
of palof obesity
predisposition
to
An additional question there exist differential degrees in the control of food intake.
Taste responsiveness and maintenance
In its simplest asked,
some
AND
is of
and the development of obesity
form
the
question
can
be
does
obesity result from hyperresponsiveness to the sensory qualities of the diet or is hyperresponsiveness to sensory qualities merely a correlate of obesity? Both obese man and animals over-respond or over-consume foods that are highly “palatable” (see Reference 30 for a discussion of “finickiness” in VMH obesity; Reference 31 for genetic obesities; and Reference 32 for a discussion of palatability and human consumption) Palatable foods such as fats and carbohydrates are defined in a logically circular fashion as those foods that rats will over-consume (33, 34). Little information is available concerning the preferences or hedonic profiles between obese and normal weight animals. Several experiments in human subjects measured both the hedonic rating for various foods (ice cream, crackers, cake) and intakes of these same foods. In at least three separate experiments (32, 35, 36) overweight subjects, (moderate overweightdefined as from 1 5 to 40% above ideal weight based on actuarial tables of desirable weight for height and sex; Metropolitan Life Insurance Co. Statistical Bulletin 1958, and extreme overweight-defined as more than 40% overweight), showed greater intake of foods rated good compared to intakes of food rated less pleasant. Although normal weight subjects also had intakes correlated with preferences, the relationship was less pronounced. These experiments demonstrate that obese animals and humans will over-consume liked or palatable foods to a greater degree than normal weight controls. They fail to provide information on differ.
ences
in sensory
Over-indulgence drates has been cause
more
of
human
prevalent
processing.
in sweets or carbohyspecifically postulated as a obesity (37). One of the myths about factors associ-
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/6/1078/4650651 by Denise Hannibal user on 22 May 2018
SWEET
TASTE
1079
ated with the genesis of obesity is that obese individuals have a “sweet tooth”, that they prefer sweet tasting substances in greater degree than normal weight individuals and that they are particularly unable to restrain themselves in the face of tempting sweet foods. If, in fact, the myth were true, it would logically follow that there might be differences in some measurable parameter of taste that would help to provide a physiological clue to the genesis or maintenance of the obese state. There are few direct observations or questionnaire studies comparing the actual daily intake for sweets between obese and normal weight subjects. One study reported no differences between the preferences for desserts of varying sucrose concentrations by obese and normal weight subjects (38) Self reports by obese teenagers showed a lower daily carbohydrate (bread, sweets, and sugar) consumption than that reported by normal weight children (39) and similar findings have been reported for obese adults (40) The lack of significant differences in fatty acids of adipose tissue between obese and normal weight subjects does provide some support for the assumption that the proportions of dietary fat carbohydrate, and protein for obese and normal weight individuals are similar (40a). There have been several studies of the development of sweet preference and consumption in obese infants. Nisbett and Gurwirtz (4 1) report that heavy (although not fatter) infants (>3540 g) consumed proportionally more sweetened formula than did normal weight or low birth weight infants. Desor (42) reported that only the intake of low birth weight infants could be reliably differentiated from that of normal or heavy birth weight infants. Infants weighing less than 2722 g consumed lesser amounts of sweet carbohydrates (sucrose dextrose lactose, fructose) in three minute ingestion tests than did infants weighing greater than 3175 g. Finally, Grinker (43) has reported that low birth weight infants (
