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Childhood
and Adolescent Obesity
What
is Obesity?
Obesity
has been defined as "an increase in
body weight resulting from an excessive
increase in body fat"(Joseph
et al, 1996, p2). The problem
with obesity is not weight or mass but excess
adipose tissue. Adipose tissue
is a "major energy store in the body
and its size can only increase if food (energy)
intake is greater than the bodys energy
demands" (Caterson,
1997, p15).
Some
researchers agree that Body Mass Index (BMI)
is the best tool available to determine
childhood obesity. BMI is the ratio of weight
(kg)/ height(m)2 which gives a reasonable
estimate of adiposity. A person is seen
to be obese if his/her BMI exceeds the cut-off
point for his/her age (Joseph
et al, 1996, p2).
The World Health Organisation recommend
the following guidelines for determining
obesity; (Tienboon
et al, 1992, p21).
| Age
(years) |
BMI(kg/m) |
| <14
|
19-20 |
|
15 |
25 |
| >16 |
28 |
Growth
charts, such as weight-for-age and weight-for-height,
are more frequently used to determine if
children are overweight/obese rather than
using BMI. The use of BMI is usually
inappropriate for infants, children and
adolescents because of different rates of
gain in weight and height during development.
Prevalence
in Australia
In
Australia approximately 50% of men and 33%
of women are overweight or obese, and about
16% of adolescents are obese. It has been
found that approximately 80% of obese adolescents
become obese adults (Joseph et al, 1996, p2), however, the risk of
obese children becoming obese adults is
less clear.
It
is difficult to measure overweight and obesity
in children as they are continuously growing
(Caterson, 1997, p12). The prevalence of obesity
in Australian children is not well known
with figures between 12.5% and 30% suggested
(Caterson, 1997, p13). A study by Dugdale (1982)
found by using a standard weight for height
measurement, that 10% of Australian boys
and 13% of Australian girls were classed
obese. Using the same measure, an additional
22% boys and 20% of girls were classed as
overweight (Dugdale, 1982, p132).
A
study by Hitchcock
et al (1986) investigated a selected
sample of Perth primary and secondary school
children. The study found children of lower
social rank and those with a southern European
background were over-represented among the
overweight children (greater than the 90th
percentile for BMI), particularly in adolescence.
Children with an Asian background who were
11 years of age and younger were over-represented
among the underweight children (less than
or equal to the 10th percentile for BMI).
A
study by Harvey et al
(1993) investigated the distribution
of body mass index of more than 800 randomly
selected Australian school children aged
7-15 years. The distributions of BMI in
Australian children were then compared to
those from a representative sample from
the United States. It was found that the
prevalence of overweight in Australian children
aged 12-14 years was lower than that in
children of the same age in the United States.
Causes
of Obesity
Many
theories suggest causes for obesity. It
does, however, appear to be a multifactorial
condition which can not be easily explained.
Genetic, endocrinal and nutritional factors
as well as low activity levels have
been linked with the development and onset
of obesity.
Genetics
There
appears to be no consensus surrounding what
percentage makes up the genetic contribution
towards obesity. Some studies suggest that
genetic factors account for 25-40% of the
aetiology of obesity (Caterson, 1997, p15). Other studies advise
the genetic contribution being from 5-25%
(Kimm,
1995, p1010).
Some
studies have suggested that families with
a low Resting Metabolic Rate (RMR) are more
likely to gain weight (Caterson,
1997, p15).
It has also been found that when an individual
reduces their weight their RMR lowers, this
is may be why many individuals find it difficult
to maintain their new weight.
Some
23 genes have been linked to obesity. The
specific action of each gene is not known.
Some genes have a connection with the tendency
to put on abnormal fat and others have been
linked with the actions of lipoprotein lipase
(LPL) and/or apoB100 (Caterson,
1997, p115).
An
abnormal endocrine gland is often blamed
for producing obesity. However this is not
a common cause of obesity (Caterson,
1997, p18).
The
Environment
"While
genetic factors may underlie obesity, they
are not sufficient. The gene pool has been
stable for many generations and therefore
there needs to be an environment or lifestyle
change for these genetic factors to be expressed
and overweight and obesity to occur. The
two obvious and important factors are eating
and activity"(Caterson,
1997, p17).
Eating
Food
consumption quality and quantity are important
factors influencing obesity. Most adult
people with obesity will admit that they
are excessive eaters. It is also noted that
the quality of the food eaten by some obese
people includes high levels of dietary fat,
which are only partly used for energy and
mostly used for body stores (Caterson,
1997, p17).
Not
all obese individuals overeat all the time,
often they eat reasonably normally and healthily
but now and then binge. This is common in
women in response to emotional stress, but
also found in some men (Caterson, 1997, p17).
Activity
The
majority of the literature available has
reported that children and adolescents are
more active than adults. In spite
of this, concerns have been raised as to
whether they are exercising enough to confer
current as well as future health benefits.
Modern
lifestyle has seen a reduction in both voluntary
and incidental activities. This is an important
influence on weight gain and the increase
in obesity in the last decade (Caterson,
1997, p18).
A
number of studies of children and adolescents
have discovered significant correlates of
inactivity associated with factors such
as age (younger more active), gender (males
more active), ethnicity (Caucasian more
active), socioeconomic status (affluent
more active), school type and location,
season, peer activity participation, perceived
future health problems and perceived health
status. What seems to be emerging, from
both anecdotal and scientific reports is
that children's activity levels decline
throughout the teenage years.
Some
studies have found that the prevalence of
obesity in children is directly related
to the hours of television viewed.
Other studies, however, have failed to establish
a direct correlation. Critics of television
have suggested that television watching
induces laziness, passivity, hyperactivity
and/or many other undesirable conditions.
There are two main reason why television
watching may contribute to obesity.
Firstly, it results in less activity as
television watching replaces more active
pursuits and secondly, television viewing
decreases the metabolic rate. (Caterson,
1997, p18)
(Klesges et al, 1993, p281)(Kimm, 1995, p1010).
A
study of children and television viewing
in the United States by Gortmaker
et al (1996),
estimated that more than 60% of overweight
incidences in the population can be linked
to excessive television viewing time. However,
a study by Robinson
et al (1993) found that the hours of
after school television viewing had no significant
association with baseline or longitudinal
change in BMI or tricep skinfold thickness.
Health
Implications
Obesity
in adults has been associated with an increase
risk of ;
Cardiovascular disease & Hypertension
Non-insulin dependent diabetes mellitus
Gallbladder disease
Cancers of the breast, colon, endometrium
and prostate.
Sleep apnoea
Increase risk of morbidity and mortality
Osteoarthritis- this is induced by the excess
weight of obesity and can be a major problem.
If inadequately managed it can be a barrier
to adequate weight loss. The obese also
have an increase of arthritis in non-weight
bearing joints, for example the hands (Caterson,
1997, p21).
Serious
physical complications associated with high
weights in children are rare. These
do include, however, cardiomyopathy, pancreatitis,
orthopaedic disorders, respiratory disorders
such as upper airway obstruction and chest
wall restriction. These are largely
restricted to the severely obese and are
of low prevalence (Joseph et al, 1996, p2) (Caterson, 1997, p20) (Dietz, 1998, p518)
In
adolescents, obesity confers significant
cardiovascular risks, abnormal glucose tolerance,
hypertension, and lipid profile abnormalities.
Social
Implications of Obesity
The
most immediate consequences of overweight
during childhood and adolescence are psychosocial.
The
social implications of obesity are a major
problem area that is often neglected. "The
obese, do less well academically, have poorer
job prospects and lower self esteem. This
latter often caused by repeated failures
at weight loss. Children see obesity as
a disability worse than losing a limb"
(Caterson,
1997, p21). Obese individuals
generally lead socially isolated lifestyles
(Joseph et al, 1996,
p2).
Obese
children are often taller than their non-overweight
peers, they are apt to be viewed more mature.
This is an inappropriate expectation that
may result in adverse effects on their socialisation
(Dietz,
1998, p518).
Treatment
for Obesity
The
goal of managing a child with obesity is
to regulate body weight while ensuring adequate
nutrition for growth and development. Ideally
alleviation of obesity would also cause
positive physiological and psychological
change (Epstein,
1998, p554).
Restricting
food, in particular fat, intake is not recommended
for young children as there is a risk of
compromising growth. Energy dense snacks
should be replaced with more nutritionally
sound choices as much as possible.
Care
should be taken not to be too overzealous
in restricting foods that may be considered
nutritionally undesirable. Being overly
restrictive in a child's food choice may
be a counter productive strategy as it may
lead to can increased desire for a food
items to which access has been restricted
(Birch,
1999, pg 1268). Children should
be directed to more healthy alternatives
as much as possible.
Most
importantly, attention should be placed
on increasing physical activity levels,
which is central to tackling obesity in
children.Exercise by itself does not cause
major weight loss, but rather promotes changes
in body composition by reducing adiposity
and increasing muscle mass
(Caterson, 1997, p23).
The
best form of exercise is prolonged low intensity
exercise, for example walking. Vigorous
exercise, which is physical activity that
makes an individual puff and pant, should
be promoted especially for younger age groups
for more immediate health benefits.
Parents
play an important role in preventing and
managing childhood obesity as they are important
food providers and role models. They should
attempt to provide healthy meals and snacks
and encourage regular exercise.
The
treatment of paediatric and adolescent obesity
is optimistic compared to adult obesity.
This may be due to the following reasons;
Support through the family
Generally,
children and adolescents have not had eating
and activity problems as long as obese adults.
Treatment at an early age prevents the development
of excess adipose cells where adult treatment
involves shrinking adipose cells. (Epstein,
1998, p554)
(Caterson, 1997,
p24).
Treatment
of obesity using a common intervention contributes
to mixed results. As stated by Epstein et al, 1998, p565 "research has identified
many aetiologic factors of obesity,
including genetics, metabolic, biochemical,
environmental, psychological and physiological
variables. However, at an individual level
it is probably rare for all of these factors
to be involved in development and maintenance
of obesity". Through the development
of better assessment techniques interventions
more appropriate to each individual can
be implemented.
At
present it is felt that the treatment of
obesity may be most effectively achieved
using a multi-component program, based on
behavioural management principles
(Zakus, 1982, p11).
With
increasing rates of children and adolescents
experiencing eating disorders, undue emphasis
on specific weight targets should be avoided.
A weight loss regime may be avoided when
overweight is not extreme.
Nutrition
It
has been recognised that nutrition intervention
is ineffective as the only treatment for
paediatric obesity (Epstein, 1998, p555). The long term efficacy
of weight loss programs is not good, the
most important component is behaviour modification
and follow up (Caterson,
1997, p20).
It
has been suggested that people at risk of
obesity should be offered nutrition advice
in combination with increasing their activity
levels (Caterson,
1997, p21).
Behaviour
When
given a choice, obese children often pick
sedentary activity instead of engaging in
physical activity as they find physical
activity less reinforcing than sedentary
activity compared to their non-obese peers
(Epstein,
1998, p564).
One
method to increase physical activity is
to reduce their access to sedentary behaviours
that leads to a modification in their environment.
However, Epstein et al, 1998 stated that
it is important to let the child have control
of activity choice. Children should be supported/
reinforced for decreasing sedentary activities
and choose to replace them with physical
activity (Epstein,
1998, p565).
Prevention
Techniques
Joseph
et al (1996)
found that it is possible to improve knowledge
about obesity and its prevention, either
directly among teachers or indirectly among
children, through the use of simple techniques
such as seminars and educational activities.
Prevention
is the best long term therapy for obesity.
However as Caterson, 1997, p25 stated "Many approaches
have been trialed to date and they have
been uniformly unsuccessful in whole population
terms".
References
Barlow,
S., Dietz,
W. (1998) Obesity
Evaluation and Treatment: Expert Committee
Recommendations. American Academy
of Pediatrics, 102;3. pp626.
Baur,L.(1996)
Body
composition and body fat in children and
adolescents, Asia Pacific Journal
of Clinical Nutrition, 5;2. pp100.
Caterson,I.(1997) Obesity Part of
the Metabolic Syndrome,
The Clinical Biochemist Reviews, 18;1. pp11-21.
Dietz,W.
(1998) Health Consequences
of Obesity in Youth: Childhood,
Pediatrics, 101;3S. pp518-525.
Birch,
O.J. (1999) Restricting access to
palatable food affects children's behavioural
response, food selection, and intake
Am J Clin Nutr, 69, pp1264 1272.
Dugdale,A.
(1982) How obese are Australian children?
J Food Nutr. 39;3. pp132-133.
Epstein,L.,
Myers,M., Raynor,H., Saelens,B.(1998)
Treatment Of Pediatric Obesity,
Pediatrics, 101;3S. pp554-570.
Goran,M.
(1998) Measurement
Issues Related to Studies of Childhood Obesity:
Assessment of Body Composition, Body Fat
Distribution, Physical Activity, and Food
Intake.Pediatrics, 101;3S. pp505-518.
Gortmaker,S.
Must, A. Sobol, A. Peterson, K. Colditz,G.
Dietz,W. (1996) Television
Viewing as a Cause of Increasing Obesity
Among Children in the United States 1986-1990,
American Medical Association, 150;4, pp356-362.
Harvey,P.,
Althaus,M. (1994) The
distribution of body mass index in Australian
children aged 7-15 years, Aust
J Nutr Diet, 51. pp151-153.
Hitchcock,N.,
Maller,R., Gilmour,A. (1986) Body size
of young Australians aged five to 16 years,
Med.J.Aust. 145. pp368-372.
Joseph,K.,
Ang,K., Ngo,K., Yim,G. (1997) Obesity
in Children, Internet Journal of Health
Promotion, URL; http://www.monash.edu.au/health/IJHP/1996/2.
Kimm,S.(1993)
The
role of dietary Fiber in the Development
and Treatment of Childhood. Pediatrics,
96;5. pp1010-1014.
Klesges,
R. Shelton,
M. Klesges, L.(1993) Effects
of Television on Metabolic Rate: Potential
Implications for Childhood Obesity.
Pediatrics, 91;2. pp281-286.
Robinson.T,
Hammer. N, Killen. L, Kraemer, J. Wilson.
H, Hayward. D, Taylor, C. Barr, C.(1993).
Does
Television Viewing Increase Obesity and
Reduce Physical Activity? Cross-sectional
and Longitudinal Analyses Among Adolescent
Girls. Pediatrics, 91;2. pp273-280.
Rosenbaum,M.
Leibel, R. (1998) The
Physiology of Body Weight Regulation: Relevance
to the Etiology of Obesity in Children,
Pediatrics,101;3S. pp525-539.
Ross,K.,
Daniels,L., Douglas,H.(1980) The
obese child: observations in the gymnasium
of the Adelaide Children's Hospital,
Med.J.Aust.2. pp80-84.
Tienboon
P., Wahlqvist M., Rutishauser I. (1992)
Early
Life Factors Affecting Body Mass
Index and Waist-Hip Ratio In Adolescence,
Asia Pacific J Clinc Nutr, 1. pp21-22.
Wilcken,
D., Lynch,J.,
Marshall, M. (1996) Aussie Kids Are Getting Fatter,
Choice. 164. pp22-25.
Zakus,G.
(1982) Obesity
in Children and Adolescents: Understanding
and Treating the Problem, Social
Work in Health Care, 8;2. pp11-29.
Last
Updated: March 27, 2001.
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