Nutrition and the Lifelong Continuum

Nutrition and the Lifelong Continuum
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 ASTPHND Annual Meeting Baltimore, MD June 14, 2010 Thank you very much, Dean. And good morning to you all. I’m delighted to be here this morning. I want to first thank Dean for inviting to speak at Maricopa. It’s been a great privilege working side by side with Dean on the CDC’s Select Panel on Preconception Care; he’s been a national leader championing the cause of preconception health and healthcare and so I’m very honored to be invited by Dean to speak here this morning.

“If you want 1 year of prosperity, grow grain
“If you want 1 year of prosperity, grow grain. If you want 10 years of prosperity, grow trees. If you want 100 years of prosperity, grow people.” Chinese Proverb To quote Lewis Carroll “If you don't know where you are going, any road will take you there.” So before we can reinvent MCH, we need to figure out where we are going. We need to do some collective visioning about where we are going, and I think this CityMatCH conference has been a great start.

Let me start with my grandma. I call her ama. She’s in her 90’s now
Let me start with my grandma. I call her ama. She’s in her 90’s now. This is a picture when she was in her 70’s. You see a big trophy behind her which she won playing city-wide croquet tournament in the senior citizen league. Now my ama did not grow up playing croquet. I don’t think she ever got to play anything because she was born into a real poor family. Like most girls back then she never got to go to school and is illiterate. When my grandpa die she became a young widower with six kids to raise on her own. She struggled to put food on the table and still managed to put one kid through college which was my uncle who went to the National Taiwan University which was unheard of back then for a kid from a poor family. In fact my uncle graduated top of his class and got a full ride to go to Notre Dame where he got his PhD in civil engineering and that’s how we got to come to America because we had an uncle here. My ama is very sick right now and so please keep her in your thoughts and prayers because if you like, you’d love her.

Life-Course Perspective
A way of looking at life not as disconnected stages, but as an integrated continuum I was asked to talk about the life-course perspective, as a way of providing a context for our dialogues about preconception health and healthcare over the next 3 days. Simply stated, the life course perspective is a way of looking at life not as disconnected stages, but as an integrated continuum. It is a conceptual framework, some people might even call it a paradigm shift, which recognizes that each stage of life is influenced by the stages that precede it, and it in turn influences the life stages that follow it.

Life Course Perspective
This may be particularly important for all of us in MCH, where one developmental stage often gets disconnected from another. In perinatal health, we focus so much on events occurring in the 9 months of pregnancy we forget that there are a great deal of life course influences on perinatal outcomes, and a great deal of perinatal influences on life course outcomes. For example, in explaining the Black-White gap in infant mortality, for decades we searched for maternal risk factors during pregnancy rather than looking at the mothers’ cumulative life course experiences. The danger of focusing solely on risk factors during pregnancy is not only that it doesn’t adequately explain the disparities, but more importantly it can misguide public health programs and policies. For two decades we thought if we could get women universal access to good quality prenatal care, then we can do something about reducing infant mortality and racial disparities in this country. Many of us recognize now that to expect prenatal care, in less than nine months, to reverse all the cumulative disadvantages and inequities over the life course of the woman, may be expecting too much of prenatal care. If we as are serious as a nation about improving birth outcomes and reducing disparities, we have to start taking care of women and families not only during pregnancy, but before and between pregnancies and indeed, across their entire life course. Lu MC, Halfon N. Racial and ethnic disparities in birth outcomes: a life-course perspective. Matern Child Health J. 2003;7:13-30.

Life Course Perspective
Early programming Cumulative pathways Prevention of childhood obesity The life-course perspective consists of two components: an early programming component, and a cumulative pathways component. I will now briefly describe each component, and then reframe our thinking about preconception health and healthcare from a life-course perspective.

Early Programming

The early programming model posits that experiences early in life – including when you were just a baby inside your mother’s womb – these early life experiences can influence your health and function for life.

Barker Hypothesis Birth Weight and Coronary Heart Disease
Age Adjusted Relative Risk Much of this originates from the work by David Barker and colleagues. Through a remarkable series of studies, Barker and his colleagues were able to show an association between low birth weight and coronary heart disease, Rich-Edwards JW, Stampfer MJ, Manson JE, Rosner B, Hankinson SE, Colditz GA et al. Birth weight and risk of cardiovascular disease in a cohort of women followed up since Br Med Jr 1997;315:

Barker Hypothesis Birth Weight and Hypertension
Law CM, de Swiet M, Osmond C, Fayers PM, Barker DJP, Cruddas AM, et al. Initiation of hypertension in utero and its amplification throughout life. Br Med J 1993;306:24-27.

Barker Hypothesis Birth Weight and Insulin Resistance Syndrome
Odds ratio adjusted for BMI hypertension, and diabetes later in life. Now when we think of the risk factors for heart disease, we think of smoking and high blood pressure and cholesterol and obesity and so forth  but low birth weight? What does low birth weight have anything to do with heart disease forty to fifty years later in life? Barker and his colleagues hypothesized that there are these critical periods in development during which the functions of an organ or system are being programmed, and if things don’t go right; if something goes wrong with fetal programming then that organ or system may never function optimally over the entire life course. For example, if you were undernourished inside the womb, especially in the second trimester when your pancreas was developing, you end up with a smaller pancreas than the average adult, and a smaller pancreas might not be able to handle a sugar load as well, leading to increased susceptibility for the development of diabetes mellitus. The Barker Hypothesis was met with a great deal of skepticism initially, but over the past decade a growing body of evidence from animal and epidemiological studies now support this whole idea of early programming. Barker DJP, Hales CN, Fall CHD, Osmond C, Phipps K, Clark PMS. Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (Syndrome X): Relation to reduced fetal growth. Diabetologia 1993;36:62-67.

Maternal Stress & Fetal Programming
Let me give you 2 examples that further illustrate the lifelong impact of early programming, starting with stress. If your mom was stressed out when she was pregnant with you

Prenatal Stress & Programming of the Brain
Prenatal stress (animal model) Hippocampus Site of learning & memory formation Stress down-regulates glucocorticoid receptors Loss of negative feedback; overactive HPA axis Amygdala Site of anxiety and fear Stress up-regulates glucocorticoid receptors Accentuated positive feedback; overactive HPA axis We know that there are two areas in the fetal brain that are particular vulnerable to the neurotoxic effects of glucocorticoids: the hippocampus and the amygdala. The hippocampus is a site of learning and memory formation; rat pups that are exposed to prenatal stress have a tougher time learning new tasks. The amygdala mediates anxiety and fear, and prenatally stressed rats showed more anxiety and fear in aversive situations. Welberg LAM, Seckl JR. Prenatal stress, glucocorticoids and the programming of the brain. J Neuroendocrinol 2001;13:

Prenatal Programming of the Hypothalamic-Pituitary-Adrenal Axis
More importantly, the hippocampus and the amygdala regulates the hypothalamic-pituitary-adrenal axis, which mediates our fight or flight response. Now I want you to think of the hippocampus as a brake pedal on the hypothalamic-pituitary-adrenal axis; it brakes the HPA axis. And I want you to think of amygdala as the accelerator pedal; it accentuates the action of the HPA axis. Prenatal stress increases the release of glucocorticoids from fetal adrenal glands, which can downregulate glucocorticoid receptors in the hippocampus, and at the same time upregulate glucocorticoid receptors in the amygdala. So you are making the brake pedal less sensitive to negative feedback, and making the accelerator pedal more sensitive to positive feedback. What do you get? You end up with a fetus with a hyper-reactive HPA axis. Welberg LAM, Seckl JR. Prenatal stress, glucocorticoids and the programming of the brain. J Neuroendocrinol 2001;13:

Epigenetics What is fascinating to me about all this fetal programming business is this phenomenon called epigenetics. Epigenetics is basically volume control for genes. You can turn up or down, or switch on or off gene expressions based on your prenatal exposures. And you can do that simply by putting a chemical group – in this case it’s a simple methyl group – CH3 with one carbon and 3 hydrogen atoms – if you put a methyl group right in front of the DNA, which blocks the gene from ever being expressed. Whereas if you take away that methyl group, then the gene is allowed to freely express itself. Generally speaking, methylation turns off or silences gene expression, whereas de-methylation turns on gene expression. So prenatal stress can determine the amount of glucocorticoid receptors that gets expressed inside the brain simply by methylating or demethylating the DNA. This is fascinating to me because you can now have two people with the exact same genetic code, but they can have very different output of stress hormones depending on whether the genes are turned on or off, which has to do with whether or not their DNA’s are methylated or demethylated, which has to do with whether or not their moms were stressed out during pregnancy, attesting to the important and potentially lifelong impact of maternal stress during pregnancy on children’s health and development. Gibbs WW. The Unseen Genome: Beyond DNA. Scientific American 2003

Epigenetics Same Genome, Different Epigenome
Let me give you another example of epigenetics. What do the mice in this picture have in common, and how are they different? Obviously, some are brown and some are yellow. But would you guess that they have the identical gene that control their coat color? It turns out that the brown mice were born to mothers who were fed a diet high in folic acid which is a methyl donor, and the gene that naturally expresses yellow fur is methylated or silenced, and so they were born brown instead. More importantly, they are also less susceptible to obesity, diabetes, and cancer compared to the yellow mice. So despite having the same gene as the yellow mice, the brown mice had different color and less obesity, diabetes, and cancer simply because their mothers ate a folate-rich diet during pregnancy. This is one of the first and best studies to show that early nutrition can influence DNA methylation, and that such epigenetic changes can have lifelong and even intergenerational impact on disease risk. R.A. Waterland, R.A. Jirtle, "Transposable elements: targets for early nutritional effects on epigenetic gene regulation," Mol Cell Biol, 23: , Reprinted in the New Scientist 2004

Prenatal Programming of Childhood Obesity
A second example of early programming I will give you is about childhood obesity.

Epidemic of Childhood Overweight & Obesity
Children 6-18 Overweight You all know that there is an epidemic of childhood obesity going on in this country. Over the past 3 decades, the rate of childhood overweight has doubled for white kids and tripled for black kids. The question is could your predisposition to overweight and obesity be programmed in utero? Source: National Center for Health Statistics, National Health and Nutrition Examination Survey Note: Estimate not available for for Hispanic; overweight defined as BMI at or above the 95th percentile ofr the CDC BMI-for-age growth charts

Prenatal Programming of Childhood Overweight & Obesity
My students and I recently completed a systematic review of the literature on prenatal programming of childhood obesity and found a number of prenatal factors that are linked to childhood obesity including maternal diabetes, smoking, and poor nutrition.

Prenatal Programming of Childhood Obesity
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 The mechanisms are being mapped out in animal models. Maternal diabetes, especially if poorly controlled, leads to overproduction of insulin by the fetus. This fetal hyperinsulinemia leads to overgrowth of fat cells in the body and overproduction of leptin, resulting in downregulation of leptin receptors in the brain and the pancreas. Normally leptin tells your brain to stop eating. If you get leptin resistance in the brain you are going to keep eating. Normally leptin tells your pancreas to stop producing insulin. If u get leptin resistance in the pancreas you are going to keep producing excess insulin and laying down more fat cells. So before the child was ever born, she is already predisposed for a lifelong struggle with overweight and obesity due to relative insulin, leptin, and glucocorticoid resistance that was programmed in utero. And then you add on top of that a fast food nation that supersizes everything, and that may be partially what is driving this whole epidemic of childhood obesity and early onset type II diabetes in our nation. So if we want to prevent childhood overweight and obesity, what do we have to do? We probably have to do more than just talk about school lunches and physical activities. Not that those are unimportant. But by the time that baby is born, you’ve lost half of the battle already. And so if we want to stem the tide of childhood obesity in our country, we have to start much earlier than that, starting with prenatal care or, better yet, with preconception care by helping women achieve better glycemic control, better nutrition and quit smoking before they get pregnant. 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) Preadipocyte Differentiation Programmed Insulin Resistance Programmed Insulin Resistance Prenatal& Postnatal Hyperleptinemia Prenatal& Postnatal Hyperleptinemia Preadipocyte Differentiation Programmed Insulin Resistance Prenatal& Postnatal Hyperleptinemia 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

Cumulative Pathways The second component of the life-course perspective is the cumulative pathways model, which posits that chronic stress creates wear and tear on your body’s adaptive systems, leading to decline in health and function over time.

Let’s take the example of stress again
Let’s take the example of stress again. This time mom doesn’t have to be stressed out during pregnancy, but rather it’s the chronic stress and strain, the daily wear and tear that women experience that cause them to have higher stress reactivity. How does this happen? What happens when you are stressed? What happens when you see a saber tooth tiger? You run! Your body activates the fight-or-flight response -- the hypothalamic-pituitary-adrenal system and the sympatho-adrenal-medullary system -- to put out more stress hormones -- CRH and ACTH and cortisol and catecholamines -- to help you run faster. Photo:

Allostasis: Maintain Stability through Change
But what happens after you got away? Your heart rate slows down, your blood pressure comes down, and you body calms down. The amazing thing about the human body is that it is self-regulating; it knows to shut itself off once the stressor has been removed. This is called allostasis – maintaining stability through change. Allostasis works by a negative feedback mechanism, which is found common to many biological systems. It works very much like a thermostat. When the temperature falls below a preset point, it turns on the heat. Once the temperature reaches that preset point, the heat is turned off. In the stress response, the HPA axis produces cortisol. Cortisol, in turn, feeds back to the brain to shut off the HPA axis. McEwen BS. Protective and damaging effects of stress mediators. N Eng J Med. 1998;338:171-9.

Allostastic Load: Wear and Tear from Chronic Stress
But what happens when there is no where to run? In the face of repeated or chronic stress, the body loses the ability for self-regulation so you can turn it on, but you can’t shut it off. Biologically speaking, tonically elevated levels of cortisol start to down-regulate the glucocorticoid receptors in the brain leading to the loss of negative feedback. So we find in animals and humans who are chronically stressed that they walk around with higher circulating levels of stress hormones, and if they were to be exposed to some natural or experimental stressors, they put out out much more CRH and cortisol that could increase their vulnerability to preterm labor during pregnancy McEwen BS. Protective and damaging effects of stress mediators. N Eng J Med. 1998;338:171-9.

HPA Axis & Immune System
Chikanza 2000 And what does stress do to your immune system? In general stress depresses the immune system. This may explain why women who are chronically stressed are more susceptible to infections like bacterial vaginosis, which could increase their risk for preterm labor during pregnancy. It turns out that this is only half of the story. In the face of an infection, your body activates the immune system to fight off the infection. But as soon as the battle is being won, the body starts to shut off the immune response to avoid a potentially damaging inflammatory overshoot. This occurs largely through activation of the hypothalamic-pituitary-adrenal axis by inflammatory cytokines. Again, the amazing thing about the body is that it is self-regulating. In the face of chronic and repeated stress, however, the body loses that ability for self-regulation. Biologically speaking, the tonically-elevated levels of cortisol start to down-regulate the glucocorticoid receptors inside the immune cells so you lose that counter-regulation from the hypothalamic-pituitary-adrenal axis. So we find in animal and some humans who are subjected to chronic and repeated stress is that they can turn on the immune response, but they have a really tough time shutting it off, and so they get an excessive output of pro-inflammatory and TH-1 cytokines in response to an infection, even one as innocuous as bacterial vaginosis, that could potentially cause them to go into preterm labor.

Stressed vs. Stressed Out
Increased cardiac output Increased available glucose Enhanced immune functions Growth of neurons in hippocampus & prefrontal cortex Stressed Out Hypertension & cardiovascular diseases Glucose intolerance & insulin resistance Infection & inflammation Atrophy & death of neurons in hippocampus & prefrontal cortex This is when you go from being stressed to being stressed out. When you are stressed, your body activates a sympathetic response which leads to increased cardiac output. When you are stressed out, you can’t shut off the sympathetic response which in the long run leads to hypertension and cardiovascular diseases When you are stressed, your body activates the HPA axis to produce cortisol which increases blood glucose as fuel. When you are stressed out, your body can’t shut off the HPA axis which in the long run leads to glucose intolerance and insulin resistance. When you are stressed, your immune functions are actually enhanced. But when you are stressed out, as we talked about, you become more susceptible to infection and inflammation. When you are stressed, your hippocampus and prefrontal cortex actually grow in size. These are learning centers inside your brain that help you learn from your mistakes. But when you are stressed out, these neurons don’t grow; they atrophy and die. So acute stress helps you learn; that’s why we keep such vivid memories of a stressful event like when Kennedy was shot or 911. But chronic stress makes you forget and you start to lose your memory if you are under chronic stress.

Allostasis & Allostatic Load
Bruce McEwen uses this diagram to illustrate allostatic load. The lower image is an image of allostasis – maintaining stability through change. The upper image is one of allostatic load – if you put kilo sumo wrestlers on a seesaw what is going to happen? It is going to break. McEwen BS, Lasley EN. The end of stress: As we know it. Washington DC: John Henry Press. 2002

Rethinking Preterm Birth
And what would happen if you were to enter pregnancy carrying kg sumo wrestlers on your back? You are not going to get healthy pregnancy or optimal fetal programming. I recently served on the IOM Committee on Understanding Prematurity, which put out its report earlier this summer.

Sequelae of Preterm Birth
75% Perinatal Mortality 12.3% As you all know, preterm birth is a leading cause of infant mortality and childhood disabilities in this country. The 12% of babies born each year account for about 75% of all perinatal mortality and half of all neurological disabilities in children. 50% Neurologic Disabilities 21 5

Racial & Ethnic Disparities Preterm Births
Percent of Live Births Year 2010 Goal … nearly twice as likely to be born premature, … NCHS 2009 30

Racial & Ethnic Disparities Very Preterm Births
Percent of Live Singleton Births Year 2010 Goal … and three times as likely to be born very premature. NCHS 2009 31

Racial & Ethnic Disparities Infant Mortality
Deaths Per 1,000 Live Births Year 2010 Goal An African American baby born today is still twice as likely to die within the first year of life than a White baby. NCHS 2009 32

Rethinking Preterm Birth
Vulnerability to preterm delivery may be traced to not only exposure to stress & infection during pregnancy, but host response to stress & infection (e.g. stress reactivity & inflammatory dysregulation) patterned over the life course (early programming & cumulative allostatic load) During Committee meetings, there were some discussion about the need to rethink the causes and prevention of preterm birth from a life-course perspective. You see. We used to think the preterm birth is the result of some precipitating event like stress or infection occurring around time of the onset of labor. We now think that the origin of preterm birth occur much earlier than that, and that your vulnerability to preterm delivery may be traced to not only exposure to stress & infection during pregnancy, but host response to stress & infection (e.g. stress reactivity & inflammatory dysregulation) patterned over the life course (early programming & cumulative allostatic load). And this is why prenatal care may be too little too late. By the time a woman starts prenatal care, there may be little that her doctor can do to quickly get those 500 kg sumo wrestlers off her back. If we want to do something about preventing preterm birth in this country, we really need to start taking care of women’s health long before they get pregnant.

Preterm Birth & Maternal Ischemic Heart Disease
Smith et al Lancet 2001;357: And just in case you think this is all about the baby, think again. The same stress reactivity and immune-inflammatory dysregulation that lead to preterm birth will go on in the next years to wreak havoc in mom’s blood vessels, heart, and other vital organs. In this study, women who had a preterm birth …. . Thus we can reframe preterm birth not only as a children’s health issue, but as a women’s health issue – that preterm birth may be an early sign of things to come – it may herald the development of hypertension, heart disease, and other chronic diseases mediated by stress and inflammation. Kaplan-Meier plots of cumulative probability of survival without admission or death from ischemic heart disease after first pregnancy in relation to preterm birth

Prevention of Childhood Obesity
So what does this all mean for your strategic planning? How might the life-course perspective guide the development of your strategic plan for the next 5-7 years?

Preventing Childhood Obesity
1. Prevention has to begin before birth First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

White House Task Force on Childhood Obesity
Recommendation 1.1: Pregnant women and women planning a pregnancy should be informed of the importance of conceiving at a healthy weight and having a healthy weight gain during pregnancy, based on the relevant recommendations of the Institute of Medicine First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

OB Prenatal Care 1.0 Medical Receptionist Assistant Ultrasound
Nurse Manager Ultrasound Tech Probably not this. This is what it looks like in prenatal clinics around the country. The big know-it-all OB supported by an office staff.

OB Prenatal Care 2.0 High Risk OB Primary & Nutritional Specialty Care
Counseling Receptionist Medical Assistant OB Teratogen Information Services Mental Health Nurse Manager Ultrasound Tech But the problem is, I don’t know it all, especially things that matter. So this is what prenatal care 2.0 looks like. This is beginning to like a patient-centered medical home for pregnancy, and I believe that every pregnant woman in America should have a medical home Social Services Oral Health Family Support

Medical Home Prenatal Care 3.0 High Risk OB WIC Family Planning
Primary & Preventive Services Nutrition Counseling Medical Home Teratogen Information Services Preconception & interconception Care Family Support Health Education But the problem is, I don’t know it all, especially things that matter. So this is what prenatal care 2.0 looks like. This is beginning to like a patient-centered medical home for pregnancy, and I believe that every pregnant woman in America should have a medical home Prenatal care Oral Health Mental Health

Prenatal Care 3.0 Nutrition Reproductive Potential NHV FRC PED 10 20
Optimal Health Development Prenatal Care 3.0 Nutrition Lower Health Development Trajectory Reproductive Potential Medical Home for Women’s Health Medical Home for Adolescent Health NHV FRC PED Pediatric Medical Home 10 20 30 40 Years

Recommendation 1.3: Hospitals and health care providers should use maternity care practices that empower new mothers to breastfeed, such as the Baby-Friendly hospital standards First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Recommendation 1.4: Health care providers and insurance companies should provide information to pregnant women and new mothers on breastfeeding, including the availability of educational classes, and connect pregnant women and new mothers to breastfeeding support programs to help them make an informed infant feeding decision First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Recommendation 1.5: Local health departments and communitybased organizations, working with health care providers, insurance companies, and others should develop peer support programs that empower pregnant women and mothers to get the help and support they need from other mothers who have breastfed First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

2. Prevention has to begin before conception Second, prevention has to begin before conception. By the time a woman gets conceives, it may be too late for you to get those kg sumo wrestlers off her back quickly enough to optimize fetal programming. If we want to prevent childhood obesity, we have to start before pregnancy, and an important objective of preconception care has to be to restore allostasis …

Early Prenatal Care Is Too Late To Prevent Some Birth Defects
The heart begins to beat at 22 days after conception The neural tube closes by 28 days after conception The palate fuses at 56 days after conception The heart begins to beat at 22 days after conception, and the neural tube closes by 28 days after conception. If you do the math, that’s 5 to 6 weeks after the last menstrual period for women with 28-day cycles. Most women haven’t started prenatal care yet, and many women aren’t even aware that they are pregnant, and yet some of the most vital organs are already formed. This is why early prenatal care is too late. By the time the woman comes in for prenatal care, there may not be much you can do about preventing some birth defects.

Early Prenatal Care Is Too Late To Prevent Implantation Errors
But the heart and neural tube aren’t even the first things to form. The placenta begins to form very early in pregnancy, beginning with implantation at 7 days after conception. This is important because we now know that many pregnancy complications that manifest late in pregnancy may have their origins early in pregnancy, right around the time of implantation and placentation. Take preeclampsia, as an example. One of the most consistent pathologic findings of preeclampsia is poor, shallow placentation; something went awry with trophoblastic invasion early in pregnancy, possibly as a result of some immunologic or inflammatory dysfunction or dysregulation, so that the placenta implants poorly onto the uterus; This poor, shallow placentation plays a major role in the pathogenic processes leading to preeclampsia, so that by the time you start prenatal care, it may be too late to reverse the implantation errors and alter the course of the pregnancy. Norwitz ER, Schust DJ, Fisher SJ. Implantation and the survival of early pregnancy. N Engl J Med Nov 8;345(19):

Early Prenatal Care Is Too Late To Prevent Obesogenic Chemical Exposures
Dioxins Endocrine disruptors Disrupt neruodevelopment Disrupt immune development May promote development of childhood obesity and diabetes Lipophilic Half life of up to 7 years Crosses the placenta easily The heart begins to beat at 22 days after conception, and the neural tube closes by 28 days after conception. If you do the math, that’s 5 to 6 weeks after the last menstrual period for women with 28-day cycles. Most women haven’t started prenatal care yet, and many women aren’t even aware that they are pregnant, and yet some of the most vital organs are already formed. This is why early prenatal care is too late. By the time the woman comes in for prenatal care, there may not be much you can do about preventing some birth defects.

Recommendation 1.7: Federal and State agencies conducting health research should prioritize research into the e!ects of possibly obesogenic chemicals. First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Early Prenatal Care Is Too Late To Restore Allostasis & Optimize Fetal Programming
Bruce McEwen uses this diagram to illustrate allostatic load. The lower image is an image of allostasis – maintaining stability through change. The upper image is one of allostatic load – if you put kilo sumo wrestlers on a seesaw what is going to happen? It is going to break. McEwen BS, Lasley EN. The end of stress: As we know it. Washington DC: John Henry Press. 2002

Interconception Care So what does this all mean for your strategic planning? How might the life-course perspective guide the development of your strategic plan for the next 5-7 years?

3. Prevention has to change not only individual behaviors, but also physical & social environments Second, prevention has to begin before conception. By the time a woman gets conceives, it may be too late for you to get those kg sumo wrestlers off her back quickly enough to optimize fetal programming. If we want to prevent childhood obesity, we have to start before pregnancy, and an important objective of preconception care has to be to restore allostasis …

Access to healthy, affordable food Convenient physical access to grocery stores and other retailers that sell a variety of healthy foods; Prices that make healthy choices affordable and attractive; A range of healthy products available in the market place Adequate resources for consumers to make healthful choices, including access to nutrition assistance programs to meet the special needs of low-income Americans First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Food Desert in Urban America

Food Desert in Rural America

Recommendation 4.1: Launch a multi-year, multi-agency Healthy Food Financing Initiative to leverage private funds to increase the availability of a!ordable, healthy foods in underserved urban and rural communities across the country. First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Recommendation 4.2: Local governments should be encouraged to create incentives to attract supermarkets and grocery stores to underserved neighborhoods and improve transportation routes to healthy food retailers. First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Recommendation 4.5: Encourage the establishment of regional, city, or county food policy councils to enhance comprehensive food system policy that improve health First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Recommendation 4.7: Provide economic incentives to increase production of healthy foods such as fruits, vegetables, and whole grains, as well as create greater access to local and healthy food for consumers. First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Increasing physical activity in schools and in activities outside of school in the community with the built environment to improve the accessibility of parks and playgrounds; in indoor and outdoor recreational settings First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Recommendation 5.3: State and local educational agencies should be encouraged to increase the quality and frequency of sequential, ageand developmentally- appropriate physical education for all students, taught by certi#ed PE teachers First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Recommendation 5.10: Communities should be encouraged to consider the impacts of built environment policies and regulations on human health. First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Recommendation 5.12: “Active transport” should be encouraged between homes, schools, and community destinations for afterschool activities, including to and from parks, libraries, transit, bus stops, and recreation centers. First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

Recommendation 5.13: Increase the number of safe and accessible parks and playgrounds, particularly in underserved and low-income communities First, prevention has to begin before birth. By the time the baby is born, you may have already lost half of the battle already. We need more research on prenatal programming of childhood obesity, looking at factors such as gestational diabetes, poor nutrition, or smoking , but also other perinatal factors such as maternal stress, gestational weight gain, or even environmental toxicants., and we need to use this research to guide the redesign of a new prenatal care that will optimize fetal programming

All this will not be finished in the first 100 days
All this will not be finished in the first 100 days. Nor will it be finished in the first 1,000 days, nor in the life of this Administration, nor even perhaps in our lifetime on this planet. But let us begin. I know this sounds like a lot of work, but that’s because there is no quick fix. To quote President John F Kennedy, all this will not be finished in the first 100 days. Nor will it be finished in the first 1,000 days, not in the life of this Administration, nor even perhaps in our lifetime on this planet. But let us begin. I think back to a conversation I had recently with Magda Peck, whom many of you know as the CEO and founder of CityMatCH. Magda did this amazing project called the invisible heroes of public health where she is going around interviewing people like Bill Foege who eradicated smallpox from the face of the earth, and Julius Richmond who started Head Start. And the one thing that she finds in common with all these heroes, the one characteristic that characterizes all these extraordinary heroes of public health, is what she calls an “unwarranted optimism.” They stayed optimistic in good times and in bad. John F Kennedy (1961)

So as we go forward from this Summit, there are going to be difficult times ahead. If we are ever going to have universal preconception care, or better yet, universal preconception health in this country, there are mountains to climb and valleys to cross. I am reminded of a parable I heard as a child growing up in Taiwan about an old man and his children begin chipping away at a huge mountain that obstructs the way between their home and their fields. When mocked by a wise man for the futility of their efforts, the old man replies that though he himself may not succeed in moving the mountain, his children and his grandchildren will continue the work, and eventually the mountain will be moved.

So let’s start digging. Let’s move mountains
So let’s start digging. Let’s move mountains. And when you leave this Summit in 3 days and go back to your cities, counties and states to continue this great movement all over this great country of ours, I want you to remember one thing from this morning’s lecture. Just one thing. I want you to promise me that you will stay optimistic. Keep your eyes on the prize. Stay optimistic because you have to. And stay optimistic because Mary K and Bob and Brian and Hani and Kay and all you great heroes of public health did for over 20 years. And I’ll give you one more reason to stay optimistic. These are my two little girls. That’s Sasha on the right, Avery in the middle, and Dora who is totally unrelated on the left. Now if the granddaughters of a girl who had to drop out of fifth grade to work in a factory can now grow up in a nation where they can be anything they want to be, that’s enough reason to keep on digging. So let’s keep on digging, and we’ll dig and dig until every valley shall be exalted, every hill and mountain shall be made low, the rough places made plain, and the crooked places made straight; and we’ll find a way to get our children and grandchildren to the Promised Land. Now we might not get there ourselves, but let us begin. And that’s what the life course perspective is all about.

Nutrition and the Lifelong Continuum

Similar presentations

Presentation on theme: "Nutrition and the Lifelong Continuum"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

Nutrition and the Lifelong Continuum

Similar presentations

Presentation on theme: "Nutrition and the Lifelong Continuum"— Presentation transcript:

Similar presentations

About project

Feedback