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Poor Fetal and Infant growth: Antecedents of childhood obesity Alan Jackson Institute of Human Nutrition Division for Developmental Origins of Adult Disease.

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Presentation on theme: "Poor Fetal and Infant growth: Antecedents of childhood obesity Alan Jackson Institute of Human Nutrition Division for Developmental Origins of Adult Disease."— Presentation transcript:

1 Poor Fetal and Infant growth: Antecedents of childhood obesity Alan Jackson Institute of Human Nutrition Division for Developmental Origins of Adult Disease University of Southampton

2 Evidence base for rational interventions in public health 14,000 deaths each day

3 ActivityInitial treatmentRehabilitationFollow-up days1-2days 3-7weeks 2-6weeks 7-26 Treat or prevent: hypoglycaemia hypothermia dehydration Treat infection Correct electrolyte imbalance Correct micronutrient deficiencies Begin feeding Increase feeding to recover lost weight (“catch-up growth”) Stimulate emotional and sensorial development Prepare for discharge without ironwith iron

4 Key to effective treatment: gain metabolic control correct metabolic imbalance provide nutrient rich food intake case mortality 5-10%,from 30-50%

5 During last two years; three meetings of direct relevance 1. Fetal Origins of Adult Disease International Congress: Brighton broad scientific community: multidisciplinarity 2. USAID/Wellcome Trust: Merton small workshop for experts address focussed considerations 3. USAID/Wellcome Trust: meeting of potential funders of research and implementation to explore potential for collaborative/integrated approach.

6 International Congress Fetal Origins of Adult Disease: “Barker” hypothesis: programming of function During early life nutrient exposure sets metabolic behaviour and thereby determines the risk of chronic disease during adult life.

7 Early Life Origins of Health and Disease Evidence of a relationship between birth weight and risk of non-communicable disease in adult life: - Type II diabetes - Hypertension - CVD - Obesity - Other …….

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9 Early Life origins of disease: Evidence from wide range of international studies Metabolic changes already evident in childhood by 5 years of age

10 Fig. 1. Mean Z-scores for height, weight and BMI during childhood in 290 people who later developed Type 2 diabetes within a cohort of 8760 men and women. At any age, the mean Z-score for the cohort is set at 0 while the standard deviation is set at 1

11 Fig. 2. Mean BMI in 6060 children according to the age of adiposity rebound

12 Fetal origins of hyperphagia, obesity and hypertension and postnatal amplification by hypercaloric nutrition. Vickers, Breier, Cutfield, Hofman, Gluckman: Am J Physiol Endocrinol Metab 2000; 279: E83-E87

13 Diet Dietary patterns: national surveys. Carbohydrate: sucrose, glycaemic response Micronutrients: folate vitamin A riboflavin Iron Zinc Iodine

14 Risk of fetal death by maternal smoking and micronutrient supplementation. Wu et al, 1998 Regular supplements before pregnancy recognised Regular supplements after pregnancy recognised Number smoked per day NOYESNOYES > trend< 0.05>0.05<0.05

15 Nutrition as a Preventive Strategy Against Adverse Pregnancy Outcomes USAID/Wellcome Trust, July, 2002 Overview evidence base and plausibility Infection and inflammation genital tract infection, malaria, HIV Metabolic eclampsia, diabetes, underweight Life and fitness smoking, alcohol, social stress Fetal and infant macronutrients, micronutrients

16 During early development, plasticity allows fetus/infant to acquire the metabolic capability to deal as best it might with the environment to which it is exposed. Directly, or indirectly through maternally mediated signals. Later exposure to an environment, or environmental signals which are substantially different, likely to generate metabolic stress. Small size at birth, marks environmental limitation and developmental constraint, which is ill-fitted for later environmental which is energy dense. Greater the energy richness/nutrient poverty of diet, the greater the metabolic stress

17 General phenomenon, Demonstrated human disease outcomes: cardiovascular disease type 2 diabetes mental health cancer Animal models vary in detail, timing and exposure fundamental mechanisms operating in different contexts Outcome unbalanced development neuro-cognitive/obesity

18 Nature of the problem: - expressed as energy balance (obesity), relationship between activity and energy (food) intake - energy derived from macronutrients, partitioning between lean and adipose tissues - macronutrient partitioning protein, EAA and Non-essential nitrogen CHO: simple sugars, complex carbohydrates Lipids: SFA, monounsaturated, n-3,n-6 FA - capability for partitioning: metabolic capability: mineral, vitamin and trace element status

19 Quality and quantity of diet: - macronutrient quality AND - micronutrient density per unit energy consumed Nutrient poor energy sources displace nutrient rich foods, Effect most marked at low levels of energy expenditure Leading to: - poor quality pregnancy - low birth weight - increased risk of obesity


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