The Pennington Biomedical Research Center Prevention of Childhood ...

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The Impact of Early Nutrition on Health and

Disease

Melinda S. Sothern, PhDPrevention of Childhood Obesity

LaboratoryPennington Biomedical Research Center

Louisiana State University (LSU)

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Increasing Prevalence of Overweight Children

0

5

10

15

20

25

30

35

1960 1980 2000

At Risk for Overweight Overweight

Source: U.S. Centers for DiseaseControl; Ogden, et al, JAMA, 2002

>85th percentile for Body Mass Index >95th percentile for Body Mass Index

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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

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As children mature, their weight condition is a stronger predictor of adult obesity.100%

50%

0%Age 6 Age 12 Age 21

YearsParent’s WeightChild’s Weight

80% of overweight 12 year olds will become

obese adults.

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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 J Med, 1997

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Prevalence of Obesity in Young Adulthood If the child is overweight the risk is...

Age No ParentsObese

>1 ParentObese

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

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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

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GENETICS PERMITS OBESITY.ENVIRONMENT CAUSES OBESITY.

Hill & Dietz

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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, 1996; Neel, 1962

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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.


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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)


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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.


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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.


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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.


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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, 1989

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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, 1989

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Fetal Origins Hypothesis

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

Barker, 1995; Barker, 2002

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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

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Reduced number of nephrons: Leads to increased blood

flow through each glomerulus (kydney)

Eventually leads to glomeruli-sclerosis

High blood pressure


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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.


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Setting of hormones and metabolism High blood glucose

concentrations negatively impact glucose transportinto the muscles.

Decreased muscle growth


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Increased vulnerability to adverse environmental influences in later life.

Low SES and poverty Psychosocial consequences

associated with low social class.


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The Four Birth Phenotypes

Thin

Short

Short and Fat

Large Placenta

Barker, 1999

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Thin: Insulin resistance during childhood

Metabolic syndrome Adaption to undernutrition though endocrine and metabolic changes.

Barker, 1999

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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 trunkBrenner, 1993; Keller, 2003; Phillips, 1996

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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.


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Large Placenta Disproportionately large

in relation to the baby’s weight

Increased blood pressure Adaptive response to

extract more nutrients from the mother.


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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; Gershwin, 2000

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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


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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


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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


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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.


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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.


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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.

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Anything is Better than Sitting!

Flex at Your DeskHot Seat (chair squats) Raise the Roof (overhead press)Stand and stretchOff the Wall (wall push-ups)Tippy Toes (calf raise)Music break (dance to one song)Stand like a tree and balanceReward positive behavior with

indoor or outdoor play periods

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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, 2001

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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, 2001

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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

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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.


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Feeding during Catch-Up Growth

Getting bigger faster is detrimental

Optimal neurodevelopmental outcome is achieved with: Slower growth rate of pre term

infants Breastfeeding


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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; Eriksson, 2002

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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, 2000; King, 2003

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Low Pre-pregnancy BMI Strongest predictors of pre-

term birth and fetal growth retardation

Interacts with smoking and stress.


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Pre-gestational Diabetes Increased risk of fetal growth

restriction

Related to the increased incidence of chronic hypertension and diabetic nephropathy.


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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.


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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


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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


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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


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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


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Short Inter-pregnancy Intervals Closely spaced pregnancies (<18

months)

Insufficient time to replace nutrients used during the previous pregnancy


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Early Pregnancy Within 2 years of menarche

Low nutrient reserves because of recent use of nutrients to facilitate growth.


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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.


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Summary

Increased adiposity at both end of the birth weight spectrum:1) Higher BMI = Higher Birthweight

2)Higher central obesity = low birth weight


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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, 1999

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30 Minute Rule


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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; Dietz, 2001

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There is evidence for a significant relationship between breastfeeding and future obesity.

Breastfeeding may reduce the risk for adult obesity and metabolic disease.


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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.


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Breast feeding is associated with improved immune function.

Obesity may be associated with inflammatory disease.


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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

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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

Food Preferences

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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.


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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.


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Nutrition Tips for Kids at Risk for Obesity &

Chronic Disease

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“I do like vegetables…That’s why I hate to see them brutally killed and eaten!”

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Let baby’s appetite determine what and how much to feed.

Teach young children that it’s OK to leave food on the plate.

Nutrition and At-Risk Youth

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Observe the child’s eating and physical activity behaviors.

Schedule frequent sessions with the pediatrician for advise and monitoring.


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Discourage consumption of high sugar beverages.

Select healthy fruits and snacks as treat foods, i.e. grapes, raisins, etc.


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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.


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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.


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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.


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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.


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Create a safe home food environment:

Allow infrequent consumption of non-

nutritious foods away from the home.

Downsize: Place foods in serving size containers.


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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, 2001

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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, 2001

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Parent TipEven if your child is geneticallydesigned 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, 2001

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30 Minute Rule


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Any Questions?Any Questions?

Say: Time to Play!

Katy Kangaroo

Patty Panther

Molly Monkey

The Pennington Biomedical Research Center Prevention of Childhood ...

Health & Medicine

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