Where is the A in MCH? A Life-Course Perspective on Adolescent Health

1. Where is the A in MCH?A Life-Course Perspective on Adolescent Health Michael C. Lu, MD, MPH Associate Professor Department of Obstetrics & Gynecology David Geffen School of Medicine at UCLA Department of Community Health Sciences UCLA School of Public Health AMCHP Web Conference November 17, 2006

2. Life-Course Pespective • A way of looking at life not as disconnected stages, but as an integrated continuum

3. Life-Course Pespective • To improve adolescent health, we must promote MCH. • To improve MCH, we must promote adolescent health.

4. MCH Adolescent Health

6. Children 6-18 Overweight Source: National Center for Health Statistics, National Health and Nutrition Examination Survey Note: Estimate not available for 1976-1980 for Hispanic; overweight defined as BMI at or above the 95th percentile ofr the CDC BMI-for-age growth charts

7. Fetal Origin of Obesity

8. Fetal Programming • The process whereby a stimulus or insult, at a sensitive or ‘critical’ period, has lasting or lifelong impact on health or function. Barker DJP. Mothers, babies and health in later life. Edinburgh: Churchill Livingstone. 1998.

9. Prenatal Programming ofChildhood Overweight & Obesity

10. Maternal Diabetes & Intrauterine Hyperglycemia Intrauterine Hyperinsulinemia (Fetal Pancreatic β Cells) Prenatal& Postnatal Hyperleptinemia Preadipocyte Differentiation Programmed Insulin Resistance Adipocyte Hyperplasia Postnatal Hyperinsulinemia Hypothalamic Leptin Resistance Pancreatic β- Cell Leptin Resistance Hyperphagia Hyperinsulinism Adipogenesis Prenatal Programming of Childhood Obesity Dysregulation of the Adipoinsular Feedback System Maternal Diabetes & Intrauterine Hyperglycemia Maternal Diabetes & Intrauterine Hyperglycemia Maternal Diabetes & Intrauterine Hyperglycemia Intrauterine Hyperinsulinemia (Fetal Pancreatic β Cells) Intrauterine Hyperinsulinemia (Fetal Pancreatic β Cells) Intrauterine Hyperinsulinemia (Fetal Pancreatic β Cells) Prenatal& Postnatal Hyperleptinemia Prenatal& Postnatal Hyperleptinemia Preadipocyte Differentiation Programmed Insulin Resistance Programmed Insulin Resistance Prenatal& Postnatal Hyperleptinemia Preadipocyte Differentiation Programmed Insulin Resistance Adipocyte Hyperplasia Adipocyte Hyperplasia Adipocyte Hyperplasia Postnatal Hyperinsulinemia Postnatal Hyperinsulinemia Postnatal Hyperinsulinemia Hypothalamic Leptin Resistance Hypothalamic Leptin Resistance Pancreatic β- Cell Leptin Resistance Pancreatic β- Cell Leptin Resistance Hypothalamic Leptin Resistance Pancreatic β- Cell Leptin Resistance Hyperphagia Hyperphagia Hyperphagia Hyperinsulinism Hyperinsulinism Hyperinsulinism Adipogenesis Adipogenesis

11. EpigeneticsVolume Control for Genes R.A. Waterland, R.A. Jirtle, "Transposable elements: targets for early nutritional effects on epigenetic gene regulation," Mol Cell Biol, 23:5293-300, 2003. Reprinted in the New Scientist 2004

12. Adolescent Health MCH

13. Allostasis • Maintain stability through change

14. Stress Photo: http://www.lam.mus.ca.us/cats/encyclo/smilodon/

15. Allostasis McEwen BS. Protective and damaging effects of stress mediators. N Eng J Med. 1998;338:171-9.

16. Allostatic Load McEwen BS. Protective and damaging effects of stress mediators. N Eng J Med. 1998;338:171-9.

17. Allostatic Load • Wear and tear on the body from chronic stress

18. Allostasis Insulin Response Plasma Glucose Time

19. Allostatic Load Plasma Glucose Insulin Resistance Time

20. Allostasis vs. Allostatic Load McEwen BS, Lasley EN. The end of stress: As we know it. Washington DC: John Henry Press. 2002

21. Summary • Life-Course Perspective • A way of looking at life not as disconnected stages, but as an integrated continuum • Fetal Programming • The process whereby a stimulus or insult, at a sensitive or ‘critical’ period, has lasting or lifelong impact on health or function. • Allostasis • Maintain stability through change • Allostatic load • Wear and tear on the body from chronic stress