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Early Nutrition's Role in Childhood Obesity

This document discusses the impact of early nutrition on health and disease. It summarizes research showing that factors like low birth weight, parental obesity, and an obesogenic family environment can increase children's risk of becoming overweight or developing chronic diseases. The document also examines developmental plasticity and the fetal origins hypothesis, which propose that nutritional experiences early in life can have long-term metabolic and health effects by programming the body's physiology and susceptibility to later health risks.

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0% found this document useful (0 votes)
15 views93 pages

Early Nutrition's Role in Childhood Obesity

This document discusses the impact of early nutrition on health and disease. It summarizes research showing that factors like low birth weight, parental obesity, and an obesogenic family environment can increase children's risk of becoming overweight or developing chronic diseases. The document also examines developmental plasticity and the fetal origins hypothesis, which propose that nutritional experiences early in life can have long-term metabolic and health effects by programming the body's physiology and susceptibility to later health risks.

Uploaded by

api-27074757
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd

The Impact of Early

Nutrition on Health and


Disease

Melinda S. Sothern, PhD


Prevention of Childhood Obesity
Laboratory
Pennington Biomedical Research Center
Louisiana State University (LSU)

Jump to first page


Increasing Prevalence
of Overweight Children
35
30
25
20
15
10
5
0
1960 1980 2000
At Risk for Overweight Overweight

>85th percentile for Body Mass Index


Source: U.S. Centers for Disease >95th percentile for Body Mass Index
Control; Ogden, et al, JAMA, 2002 Jump to first page
Risk Factors for Obesity and
Chronic Disease

Socioeconomic Status

Ethnicity

Parental Obesity - under 6 years of age

Body Mass Index - over 6 years of age

Critical development periods
 Birth - Low Birth Weight
 5-9 years (adiposity rebound)
 Puberty (12-15 years of age)

Formula versus Breastfeeding

Poor Nutrition - Food Preferences

Sedentary Behaviors Jump to first page
As children mature, their weight condition
is a stronger predictor of adult obesity.
100%
80% of overweight 12
year olds will become
obese adults.

50%

0%
Parent’s Weight
Age 6 Age 12 Age 21
Child’s Weight Years Jump to first page
Parental Obesity

If both parents are non-obese the child
has only a 7% chance of developing
obesity.


If one parent is obese the risk of
developing obesity is increased to 40%.


If both parents are obese the risk for
developing obesity doubles to 80%.
Whitaker, et al, NE JtoMed,
Jump 1997
first page
Prevalence of Obesity
in Young Adulthood
If the child is overweight the
risk is...
Age No Parents >1 Parent
Obese Obese
1-2 8% 40%
3-5 24% 62%
6-9 37% 71%
10-14 64% 79%
15-17 54% 73%
Whitaker, et al, NE J Med, 1997 Jump to first page
Obesigenic Families

A recent study examined the self-reported physical
activity and dietary intake patterns of parents and
changes in weight status (body mass index and skin
folds) over 2 years in offspring.

 Girls of parents with high dietary intake and low


physical activity (obesigenic) had significantly greater
increases in weight status.

 Family environment may explain increased weight


status in children over and above genetic
susceptibility.
Davison and Birch, Int’l J of Ob 2002
Jump to first page
GENETICS PERMITS OBESITY.
ENVIRONMENT CAUSES OBESITY.
Hill & Dietz
Jump to first page
Early Nutrition and
Children
 Metabolic changes
accompany excess body fat
during critical periods of early
development.

 These changes promote an


increased risk for Type 2
diabetes in adolescence and
adulthood.
McGarry, 2002; Ong, 2000; Barker, 1995; Law,
Jump1996; Neel, 1962
to first page
Early Nutrition and
Metabolic Health
 The intrauterine period is a
critical period for the
development of metabolic
abnormalities later in life.

 A programming response is
established by the interaction
of the infant and their early
environment.
McGarry, 2002; Ong, 2000; Barker, 1995; Law,
Jump1996; Neel, 1962
to first page
Birth weight and
Overweight Children
 Low birth weight is associated
with impaired insulin
sensitivity, obesity and
cardiovascular risk factors
later in life.

 The relationship may be due


to intrauterine growth
retardation (IUGR)
McGarry, 2002; Ong, 2000; Barker, 1995; Law,
Jump1996; Neel, 1962
to first page
Birth weight and
Overweight Children
 IUGR causes metabolic
disorders and ultimately
promotes diabetes mellitus.

 The impact of IUGR is


exacerbated in susceptible
populations exposed to
early environments
conducive to obesity.
McGarry, 2002; Ong, 2000; Barker, 1995; Law,
Jump1996; Neel, 1962
to first page
Jump to first page
Jump to first page
Jump to first page
Jump to first page
Birth weight and
Overweight Children
 Law and Dietz propose that
weight and adiposity are
entrained during early life.

 Research points to nutrition-


induced changes in the
hypothalmic-pituatary-
adrenal axis in the mother
and the fetus.
McGarry, 2002; Ong, 2000; Barker, 1995; Law,
Jump1996; Neel, 1962
to first page
Birth weight and
Overweight Children
 The local availability of nutrients
during pregnancy, especially
protein intake, has strong
implications for future metabolic
health.

 Adjustments to protect brain tissue


preferentially over visceral and
somatic growth result in an altered
metabolic profile.
McGarry, 2002; Ong, 2000; Barker, 1995; Law,
Jump1996; Neel, 1962
to first page
Developmental
Plasticity
 A critical period when a system
is plastic and sensitive to the
environment.

 Followed by a los of plasticity


and a fixed functional capacity.

West-Eberhard, 1989Jump to first page


Developmental
Plasticity

 One genotype can give rise to


a range of different
physiological or morphological
states in response to different
environmental conditions
during development.

West-Eberhard, 1989Jump to first page


Fetal Origins
Hypothesis

 Chronic diseases originate in


developmental plasticity, in
response to under-nutrition
during fetal life and infancy.

Barker, 1995; Barker, 2002


Jump to first page
Fetal Origins
Hypothesis
 Three processes explain why
individuals born with low birth
weight are more vulnerable to
later chronic disease:
 Reduced number of nephrons
 Setting of hormones and
metabolism
 Increased vulnerability to
adverse environmental
influences in later life.
Brenner, 1993; Keller, 2003; Phillips, 1996
Jump to first page
Fetal Origins
Hypothesis
 Reduced number of
nephrons:
 Leads to increased blood
flow through each
glomerulus (kydney)
 Eventually leads to
glomeruli-sclerosis
 High blood pressure

Brenner, 1993; Keller, 2003; Phillips, 1996


Jump to first page
Fetal Origins
Hypothesis
 Setting of hormones and
metabolism
 Undernourished infant
establishes a “thrifty” way of
handling food
 Persistence of a fetal
response to maintain blood
glucose concentrations to
the brain.
Brenner, 1993; Keller, 2003; Phillips, 1996
Jump to first page
Fetal Origins
Hypothesis
 Setting of hormones and
metabolism
 High blood glucose
concentrations negatively
impact glucose transportinto
the muscles.

 Decreased muscle growth

Brenner, 1993; Keller, 2003; Phillips, 1996


Jump to first page
Fetal Origins
Hypothesis
 Increased vulnerability to
adverse environmental
influences in later life.

 Low SES and poverty


 Psychosocial consequences
associated with low social
class.

Brenner, 1993; Keller, 2003; Phillips, 1996


Jump to first page
Jump to first page
The Four Birth
Phenotypes
 Thin

 Short

 Short and Fat

 Large Placenta

Barker, 1999 Jump to first page


The Four Birth
Phenotypes
 Thin:
 Insulin resistance during
childhood
 Metabolic syndrome

 Adaption to undernutrition

though endocrine and


metabolic changes.

Barker, 1999 Jump to first page


Four Birth Phenotypes
 Short:
 Short stature in relation to head
circumference
 Reduced abdominal circumference
 Liver dysfunction
 Elevated LDL cholesterol
 Elevated plasma fibrinogen
 Brain sparing circulating adaptations
 Cardiac output is diverted to the
brain at the expense of the trunk

Brenner, 1993; Keller, 2003; Phillips, 1996


Jump to first page
The Four Birth
Phenotypes
 Short and Fat
 Insulin deficient
 High rates of non-insulin
dependent diabetes
 Maternal hyperglycemia
 Imbalance in the supply of
glucose and other nutrients
to the fetus.

Brenner, 1993; Keller, 2003; Phillips, 1996


Jump to first page
The Four Birth
Phenotypes
 Large Placenta
 Disproportionately large
in relation to the baby’s
weight
 Increased blood pressure

 Adaptive response to

extract more nutrients


from the mother.
Brenner, 1993; Keller, 2003; Phillips, 1996
Jump to first page
Pre-Pregnancy BMI
 Genetic and nutritional
components

 Low BMI is a marker for low


tissue nutrient reserves

 High BMI is a marker for


elevated glucose and fatty
acide concerntrations
Hay, 2003; Neggers, 2003; Catalano, 2003;
JumpGershwin,
to first page2000
Jump to first page
Pre-Pregnancy BMI
Results of study of 6690 women:
Normal weight and below the Institute
of Medicine (IOM) recommendations
= an increased risk of small-for-
gestational-age infants.

Higher than the IOM = increased


incidence of Cesarean Delivery

Hay, 2003; Neggers, 2003; Catalano, 2003;


JumpGershwin,
to first page2000
Weight Gain during
Pregnancy
Results of study of 6690 women:
Women gaining 11.5-16 kg =
moderately high risk for macrosomia
(fetal obesity, with excessive adipose
tissue development)

Women gaining >16 kg were at


greatest risk for macrosomia

Hay, 2003; Neggers, 2003; Catalano, 2003;


JumpGershwin,
to first page2000
Gestational Diabetes

 Common in gestational
diabetes
 Abnormally high plasma
glucose and fatty acid
concentrations produce high
fetal levels.
 High levels lead to excessive
insulin production
Hay, 2003; Neggers, 2003; Catalano, 2003;
JumpGershwin,
to first page2000
Gestational Diabetes
 Produces excessive fetal
adiposity characteristics
 Infants remain obese into
childhood.
 Adolescents develop early signs
of insulin resistance
 Propagation of the diabetic
condition has been passed on for
five generations in animal studies.
Hay, 2003; Neggers, 2003; Catalano, 2003;
JumpGershwin,
to first page2000
Nutrient Intake during
Pregnancy
 Fatty acid intake contributes to
growth of lipid tissues in the
fetus.
 Essential fatty acid nutrition is
correlated with reduced fetal
growth and head
circumference.
 Fish oil supplementation in the
third trimester improves
neonatal neurodevelopment.
Hay, 2003; Neggers, 2003; Catalano, Jump
2003;toGershwin,
first page 2000
Jump to first page
30 Minute Rule
Research indicates that after
30 minutes of mental work the
ability to concentrate begins to
decline.
Sitting burns only 33-50
calories per hour.

Jump to first page


Anything is Better than Sitting!
 Flex at Your Desk
 Hot Seat (chair squats)
 Raise the Roof (overhead press)
 Stand and stretch
 Off the Wall (wall push-ups)
 Tippy Toes (calf raise)
 Music break (dance to one song)
 Stand like a tree and balance
 Reward positive behavior with
indoor or outdoor play periods
Jump to first page
Childhood Growth and
Chronic Disease
 Rates of disease is predicted
more strongly by rates of weight
gain than by the measure of
childhood BMI.

 Compensatory growth when


under-nutrition is followed by
improved nutrition

Huxley, 2002; Barker, 2002; Middowson, 1972; Metcalfe,


Jump 2001
to first page
Childhood Growth and
Chronic Disease
 Compensatory growth reduces
life-span.

 Rapid growth is associated with


persisting hormonal changes
that promote large body size.

Huxley, 2002; Barker, 2002; Middowson, 1972; Metcalfe,


Jump 2001
to first page
Childhood Growth and
Chronic Disease
 Small and thin babies lack
muscle.

 Muscle deficiency persists


because the critical period for
development is before birth.

 Rapid, weight gain leads to high


fat to muscle ratio and eventual
insulin resistance.
Huxley, 2002; Barker, 2002; Middowson, 1972; Metcalfe, 2001; Erikkson, 2002
Jump to first page
Feeding during Catch-
Up Growth
 Infants with a slower rate of
intrauterine growth are unlikely
to ever grow normally.

 Low nutrient intake and reduced


growth in SGA infants is
associated with improved insulin
sensitivity.

Hay, 2003; Neggers, 2003; Catalano, Jump


2003;toGershwin,
first page 2000
Feeding during Catch-
Up Growth
 Getting bigger faster is
detrimental

 Optimal neurodevelopmental
outcome is achieved with:
 Slower growth rate of pre term
infants
 Breastfeeding
Hay, 2003; Neggers, 2003; Catalano, Jump
2003;toGershwin,
first page 2000
Catch-up Growth
Hypothesis.
 Aggressive feeding to induce
catch-up growth, especially
high fat intake, is strongly
associated with:
 Obesity
 Insulin resistance
 Diabetes in later life.

Cianfarani, 1999; Erikson, 2003;Jump


Eriksson, 2002
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
 Low Pre-pregnancy BMI
 Pre-gestational Diabetes
 Malnourishment
 Smoking
 Caffeine
 Compromised Immune System
 Maternal stress response
 Short Inter-pregnancy Intervals
 Early Pregnancy
 Multi Fetal Pregnancy

Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,


Jump 2000; King, 2003
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
Low Pre-pregnancy BMI
 Strongest predictors of pre-term
birth and fetal growth retardation

 Interacts with smoking and


stress.

Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,


Jump 2000; King, 2003
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
Pre-gestational Diabetes
 Increased risk of fetal growth
restriction

 Related to the increased


incidence of chronic hypertension
and diabetic nephropathy.

Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,


Jump 2000; King, 2003
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
Malnourishment
 Deficient or excessive consumption
and/or absorption of select nutrients

 Disease, diet-nutrient interactions,


drug-nutrient interactions and
lifestyle habits (alcohol and
tobacco) affect absorption.

Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,


Jump 2000; King, 2003
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
Smoking
 Pregnant smokers have poorer
nutrient intakes of most
micronutrients.
 Pregnant smokers require more
micronutrients.
 Smoking combined with caffeine is
negatively associated with birth
weight
Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,
Jump 2000; King, 2003
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
Smoking and Caffeine
 Pregnant smokers have poorer
nutrient intakes of most
micronutrients.
 Pregnant smokers require more
micronutrients.
 Smoking combined with caffeine is
negatively associated with birth
weight
Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,
Jump 2000; King, 2003
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
Compromised Immune System
 Disease state compromises nutrient
uptake
 Poor nutrition compromises the
immune system
 Chronic infection leads to maternal
catabolism and nutrient competition
between mother and placenta

Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,


Jump 2000; King, 2003
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
Stress in Early Pregnancy
 Work strain
 Poor nutrition
 Stress on neuro-endocrine-immune
interactions increases the risk for
infections
 The timing of prenatal stress is the
most important factor

Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,


Jump 2000; King, 2003
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
Short Inter-pregnancy Intervals
 Closely spaced pregnancies (<18
months)

 Insufficient time to replace nutrients


used during the previous pregnancy

Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,


Jump 2000; King, 2003
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
Early Pregnancy
 Within 2 years of menarche

 Low nutrient reserves because of


recent use of nutrients to facilitate
growth.

Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,


Jump 2000; King, 2003
to first page
Nutritional Risk Factors for Fetal
Growth Restriction and Pre-
Term Birth
Multi-fetal Pregnancy
 Weight gain is positively and
llinearly related to birth weight in
twin pregnancy

 Declining weight gain late in


pregnancy is associated with low
birth weight twins.

Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,


Jump 2000; King, 2003
to first page
Jump to first page
Summary

Increased adiposity at both end of


the birth weight spectrum:
1) Higher BMI = Higher
Birthweight

2)Higher central obesity = low


birth weight

Naggers, 2003; Catalarc, 2003; Gershwin, 2000; Matthews, 2000, Brown,


Jump 2000; King, 2003
to first page
Summary

Once the fetus is programmed by either


under-nutrition and growth restriction, or
over-nutrition and obesity, metabolic
disease is inevitable.

Prevention of childhood obesity is critical


and may have lifelong, multi-
generational , impact.

Snoeck, 1990; Singhal, 2003, Hay, 1997, Albertsson-Lwikland, 1997; Neggers, 2003; Cianfarani,
Jump to first page 1999
30 Minute Rule
Research indicates that after
30 minutes of mental work the
ability to concentrate begins to
decline.
Sitting burns only 33-50
calories per hour.

Jump to first page


Anything is Better than Sitting!
 Flex at Your Desk
 Hot Seat (chair squats)
 Raise the Roof (overhead press)
 Stand and stretch
 Off the Wall (wall push-ups)
 Tippy Toes (calf raise)
 Music break (dance to one song)
 Stand like a tree and balance
 Reward positive behavior with
indoor or outdoor play periods
Jump to first page
Breast feeding Obesity
& Chronic Disease
 Recent research strongly
suggests that postnatal
nutrition is an important
factor in the development:
 obesity,
 insulin resistance

 dyslipidemia

 other chronic diseases.


Von Kries, 1999; Liese, 200; Das, 2001;
JumpDietz,
to first2001
page
Breast feeding Obesity
& Chronic Disease
 There is evidence for a
significant relationship
between breastfeeding and
future obesity.

 Breastfeeding may reduce the


risk for adult obesity and
metabolic disease.
Von Kries, 1999; Liese, 200; Das, 2001;
JumpDietz,
to first2001
page
Breast feeding Obesity
& Chronic Disease
 The prevalence of obesity in 5-6 year-old
children who were never breast fed is
almost double that of breast fed children.

 The risk of childhood obesity declines as


the duration of breast feeding increases.

Von Kries, 1999; Liese, 200; Das, 2001;


JumpDietz,
to first2001
page
Breast feeding Obesity
& Chronic Disease
 Breast feeding is associated with
improved immune function.

 Obesity may be associated with


inflammatory disease.

Von Kries, 1999; Liese, 200; Das, 2001;


JumpDietz,
to first2001
page
Food Attitude and Practices
in Young Children
 How parents present food to their
young children greatly impacts their
food preferences.

 Providing rewards for eating


nutritious foods initially enhances
preference, but has a negative
effect later when the reward is
removed.
Birch, Ch. Dev., 1980 and 1995; Spruijt-Metz, 2002
Jump to first page
Food Preferences
The strategy of
having a child eat a
food in order to obtain
a reward tends to
reduce the child’s
liking for the food she
is rewarded for eating.
Birch, Young Children, 1995
Jump to first page
Food Attitude and Practices
in Young Children
 Pressure to eat and concern for child’s
weight are associated with increased
fat in children.

 If left unattended, children will select


foods they enjoy and leave behind
foods they dislike.

Birch, Ch. Dev., 1980 and 1995; Spruijt-Metz, 2002


Jump to first page
Food Attitude and Practices
in Young Children
 Children will eat less if served
less or if allowed to serve
themselves.

 As children mature, parental


influence is reduced and the
influence of peers may change
food preferences.

Birch, Ch. Dev., 1980 and 1995; Spruijt-Metz, 2002


Jump to first page
Nutrition Tips for
Kids at Risk for Obesity &
Chronic Disease

Jump to first page


Jump to first page
Jump to first page
Jump to first page
“I do like vegetables…
That’s why I hate to see them brutally killed and eaten!”
Jump to first page
Jump to first page
Jump to first page
Nutrition and
At-Risk Youth

 Let baby’s appetite determine


what and how much to feed.

 Teach young children that it’s


OK to leave food on the plate.

Jump to first page


Nutrition and
At-Risk Youth

 Observe the child’s eating and


physical activity behaviors.

 Schedule frequent sessions


with the pediatrician for advise
and monitoring.

Jump to first page


Nutrition and
At-Risk Youth

 Discourage consumption of high


sugar beverages.

 Select healthy fruits and snacks


as treat foods, i.e. grapes, raisins,
etc.

Jump to first page


Nutrition and
At-Risk Youth
 Require that all drinks and foods be
consumed at the kitchen or dining table
or other designated area.

 Schedule mid-morning and mid-


morning healthy snacks - make them
attractive.

Jump to first page


Nutrition and
At-Risk Youth
 Always require children to eat a healthy
breakfast.

 Discourage snacking after dinnertime.

 Children who eat late dinners or snacks


are less hungry in the morning.

Jump to first page


Nutrition and
At-Risk Youth
 Don’t place a moral value on food.

 Teach children that all food is OK; some


is “grow tall or big” food and some is not.

 Never give food as a reward.

Jump to first page


Nutrition and
At-Risk Youth

 Create a safe home food environment:

 Gradually replace non-nutritious foods in


the home. Involve children with shopping.

 Display and keep within reach nutritious


foods naturally low in fat and sugar.

Jump to first page


Nutrition and
At-Risk Youth

 Create a safe home food environment:

 Allow infrequent consumption of non-


nutritious foods away from the home.

 Downsize: Place foods in serving size


containers.
Jump to first page
The Ultimate
Parent Tip
Stop nagging. Praise
children who select healthy
snacks. Ignore unhealthy
nutrition and re-direct.

Offer choices, “Do you want


strawberries, carrots or melon for
your snack.”
Sothern, et al, Trim Kids,
Jump to 2001
first page
What if the Parents say:

You know, I’m big,


my momma was big, my
grandma was
big…..We’re just big
people.

Sothern, et al, Trim Kids,


Jump to 2001
first page
Parent Tip
Even if your child is genetically
designed to be overweight, his
or her environment can be
adjusted to combat this predisposition.
Your child may become chubby
even with adjustments. He or she does
not have to be doomed to a life of ill
health. Weight management is the key.

Sothern, et al, Trim Kids,


Jump to 2001
first page
30 Minute Rule
Research indicates that after
30 minutes of mental work the
ability to concentrate begins to
decline.
Sitting burns only 33-50
calories per hour.

Jump to first page


Anything is Better than Sitting!
 Flex at Your Desk
 Hot Seat (chair squats)
 Raise the Roof (overhead press)
 Stand and stretch
 Off the Wall (wall push-ups)
 Tippy Toes (calf raise)
 Music break (dance to one song)
 Stand like a tree and balance
 Reward positive behavior with
indoor or outdoor play periods
Jump to first page
Patty Panther

Katy Kangaroo Molly Monkey

Say: Time to Play!


Any Questions?
Jump to first page

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