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 95 th 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 of Childhood Overweight & Obesity

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

11. Epigenetics Volume 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.  Maintain stability through change Allostasis

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 Plasma Glucose Time Insulin Response

19. Allostatic Load Plasma Glucose Time Insulin Resistance

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