AMCHP 2005 ANNUAL CONFERENCE
DELIVERING RESULTS, IMPROVING PREGNANCY & BIRTH
February 19-23, 2005
JAMES COLLINS: Okay, good morning. Thank you very much for that warm introduction and for those young people still here we want to maintain that energy. I think I’ve been to a lot of conferences. I’ve never been to an introductory session with such movement and power. It’s very impressive. I’m almost tempted to go to my room and see if I can find a CD, I can just play it and maybe just flash the slides. Maybe that will have more of an impact. And that’s what we want to do this morning is have an impact. What you guys do is critically important to actually addressing and eliminating disparities in pregnancy outcome. My primary focus as a researcher and sometimes I feel handcuffed with the million dollar question, what to do? To set things up for our presentation this morning I’m going to start off by just reviewing some of the general etymology of infant mortality, I’m sure of which 90 percent of you if not all of you are aware of. And then we’ll kind of take it through Dr. Lou’s life course perspective.
Then I’m going to present some data, some research that we’ve performed to examine this more closely. And then we’re going to close it up with some thoughts to try to make things better for all of us. Let’s see if we can get this first slide. Hey, infant mortality rates in this country. Don’t put on the glasses. Don’t strain too hard for those of you in the back. The United States is near the bottom. If this was a linear slide we’d be way near the bottom, but we have two rows and as you guys are well aware of, we rank neither first, fifth, tenth, fifteenth or twentieth, but I think we’re twenty sixth or twenty seventh in the world infant mortality rates. And our position in that internationally has declined steadily since 1960. Apologize for the typo in this slide but approximately 19,000 fewer infant deaths a year could be prevented if the infant mortality rate in this country was lower to that achieved by Japan . And that’s the sum greater than the total number of deaths among all children age one to 15 years. So clearly from a Public Health perspective infant mortality is a very important issue.
Cities with the highest infant mortality rates unfortunately our host city, District of Columbia , leads the ranks. My hometown Detroit , Michigan is close second. Atlanta , Newark , Cleveland , Norfork, Baltimore , my current hometown Chicago , and Philadelphia . Home of Iverson, who just won MVP last night for NBA, just to lighten it up a little bit, all star game. And these cities all have something in common. They have large populations of urban African Americans. And as we see the infant mortality rates are not evenly distributed among the races. The African Americans have the highest infant mortality rates, as you see, almost 14 per thousand, followed by Puerto Ricans and then things start to fall out pretty evenly among Latino whites, Asian Americans, and Whites, between 5 and 6 per thousand. So I’m at 6,000 African American infant deaths a year could be prevented if the infant mortality rate of African Americans was lowered to that of Whites.
The vast majority of African American, and White infant deaths, occur in the first 28 days of life and define neonatal mortality rates. And this slide looks at neonatal mortality rates in this country since 1950. And you see even though the disparity has really been unchanged, there has been significant improvement, particularly since the mid 1960’s all the ‘til today. This is already truly been attributed to the success of neonatal medicine, particularly success caring for small premature infants. If you’re going to be born 800 grams at 27 weeks, there’s no better place to be born in the United States . But a group of infants who weigh that, who in that category will never do as well outcome wise as group of infants who are born at term. And this slide makes the point that though we’ve obtained outstanding birth weights, specific mortality rates, overall neonatal mortality rates are the scourge of our healthcare system. That’s because birth weight distribution is a primary determinate of outcome.
I’m a Neonatologist so I like to measure things. And, what the next slide, thank you? Low birth weight infants account for about eight percent of births, yet the account for two thirds of the deaths. Just over one percent of infants are very low birth weight, approximately 40,000 births a year and yet they account for 50 percent of the deaths, from a form of public health perspective, we really want to get a handle on what’s causing these low birth weight, particularly very low birth weight infants. Approximately 16 percent of very low birth weight infants are moderately to severely handicapped. Neonatology is a lot of things. Inexpensive it is not. All right, next slide. And there’s also the ethical dilemma for caring for extremely premature infants. And this slide looks at the five-decade trend of low birth weight infants in this country. And we see that things have been flat. Despite all of the improvement in what we do, we really haven’t made one major impact on reducing the amount of low birth weight infants.
Approximately two thirds of these infants are born premature. Next slide. This is looking at the five-decade trend for very low birth weight infants. And we see that for African Americans, things have been steadily increasing for unclear reasons, and for whites things have hovered just under one percent, again, almost 99 percent of these infants are born premature. And this slide just reemphasizes what we know looking at the relationship between socioeconomics status. I always pause when I put on this slide because when I first started this line of research approximately 15 years ago, I would have bet everything was driven by socioeconomic status. That is, I would have thought that women who were highly educated, extremely highly educated, master level degrees, doctorate degrees, among that group, the disparity would abate. We found the complete opposite.
The disparity actually widens among those of the highest educated. Even among women with greater than 16 plus years education, African Americans have almost a three fold greater rate of low birth weight infants. Also interesting, the rate of low birth weights among African Americans with greater than 16 years education, actually exceeds that of white women with less than 12 years education. So clearly socioeconomic status by itself does not explain the disparity. This slide was taken from a recent study looking at the pregnancy outcome of women who conceive with assisted reproductive technology. These women almost by definition were highly educated. They also had access to prenatal care and they received frequent prenatal care and we that disparity persisted amongst those outcome measures, term low birth weight, preterm low birth weight, and very low birth weight of African Americans having a two to three greater fold incidence of poor outcome. And now we’re going to change gears a little bit, we don’t do it with music but we’ll try to do it without the music. And we’re going to try to keep the flow going. This just provides kind of an overview. Thank you.
MICHAEL LU: Good morning. I was asked to talk about the life course perspective now. I know some of you have already heard me talk about the racial ethnic disparities from the life course perspective. But for those of you who haven’t, the message is really a simple one. Birth outcomes is the product of not only the nine months or pregnancy, but the entire life course of the woman. Next slide? And disparities and birth outcomes therefore, are the consequences of not only different child exposures during pregnancy but really differential life experiences across the lifespan of the woman. Next slide? Now the life course perspective has two components, an early programming component and accumulative pathways component. The early programming component (inaudible) set experiences early in life that it’s when you were just a baby inside your mother’s womb, has a lot to do with your health and function in the future. So for example, we now know that you’re a lot more likely to become obese if your mother had diabetes during pregnancy.
Next slide? And you’re a lot more likely to become a diabetic yourself if your mother had diabetes during pregnancy. In this study amongst the Pima Indians in Arizona , 70 percent of offspring born to women with gestational diabetes become diabetic before they turn 30. Seventy percent. Just in case that this is all about genetics, amongst women who were pre diabetic, that is that they didn’t have diabetes during pregnancy but developed diabetes later on in life, their offspring don’t show the same risk, suggesting that this may have more to do with the inter uterine environment than genetics.
Next slide? Now we’re beginning to map out that the biological pathways for all of this. We know that if mom’s blood sugar is poorly controlled during pregnancy, well blood sugar crossed the placenta and that causes the fetus to produce a lot of insulin, because fetal hyper-insulin anemia does three things. It causes over growth of fat cells. It causes an insulin resistance. And it causes lepton resistance. Now, you know about insulin resistance but why is lepton resistance important? What does lepton do? Well, lepton tells your brain to stop eating and so if you have lepton resistance inside the brain, you’re going to keep on eating. And lepton tells your pancreas to stop producing insulin and so if you have lepton resistance in the pancreas, you’re going to keep on producing insulin, which will lay down more fat. Now, we know when these babies become adults and get pregnant, they’re also more likely to develop gestational diabetes probably because of this pre programmed insulin resistance.
And that leads to fetal hyper-insulin anemia, leads to lepton resistance and insulin resistance and that’s how the cycle repeats itself. That’s how the risk gets passed on from one generation to the next. And top of that you add a fast food nation that super sizes everything and you see this whole epidemic of childhood obesity and early onset type two diabetes that we’re seeing in this country. So if you want to do something about preventing childhood obesity and diabetes where do you need to begin? Inside the womb. Next slide? Let me give you another example about prenatal programming. Okay. And this is talking about maternal stress. Okay. Now lets suppose that mom was stressed out during pregnancy. Well, what happens? We know that mom’s brain puts out a lot of stress hormones and this placenta, which acts like a second brain also puts out stress hormones. And in a couple of different ways these stress hormones can cross the placenta and in a sense you are bathing the baby in all of these stress hormones, while the baby’s brain is developing, you’re priming the baby’s hypoplamant pituitary adrenal access with all of these stress hormones. What does that do to the baby’s brain?
Could that cause the baby to have higher stress reactivity later on in life? One slide back please. That is when she is exposed to a certain amount of stress that she might put out more stress hormones and if she were to become pregnant 20, 30 years later on, that might actually put her at high risk for preterm delivery. Again, the biological pathways, is getting mapped out. And in the animal models we know that there are two areas of the brain that are particularly sensitive to the and vulnerable to the neuro toxic effects of cortisol and that’s the hippocampus (inaudible). Now I want you to think of the hippocampus on the left there, okay. The hippocampus is the brake pedal. It’s basically breaks the action of the HPA axis. And I want you to think of the imipula on the right, as the accelerator pedal that basically accentuates the HPA axis. So we know prenatal stress caused the fetal adrenals to put out lots of cortisol, which during critical periods of development could down regulate the number of receptors inside the hippocampus and thereby making that negative feedback less sensitive. At the same time it’s going to up regulate the number of receptors inside the imipula and so you’re going to make that positive feedback more sensitive.
Okay. So think about it. You’re making the brake pedal less sensitive and you’re making the accelerator pedal more sensitive. What’s going to happen? You’re going to end up with a baby with a hyperactive HPA axis. And in a way this actually makes a lot of evolutionary sense. Right? Because mom is trying to signal to the baby what the outside environment is like to get the baby ready for the outside world and the outside world is stressful. Mom is going to try to get the baby ready to fight her fight by revving up its HPA axis. And that may have short-term survival advantages but may be have long-term health and developmental consequences. So we’re now getting animal studies to show that prenatal stress is linked to high risk or hypertension and heart disease. And last year, just last year in the human study, it’s been found that prenatal stress was linked to high risk for childhood ADHD. Next slide, please? Now, what’s interesting about all of this is that what’s been proven is actually the DNA. It’s the DNA that’s actually being programmed in the fascinating phenomena called epigenetics.
Okay? How many of you have heard of epigenetics? Okay. Now this is important. Okay? This is going to be very important. Because basically what epigenetics is, it’s a volume control for the genes. You can basically turn up or turn down gene expression based on environmental exposures. So prenatal stress can turn up or down or switch on or off gene expression, the genes that control the amount of (inaudible) receptors that gets expressed inside a brain simply by putting a chemical tag directly onto the DNA, in this case it’s a metho group. Simply by methylating or demethilating DNA. Now this has got profound implications, because now you can have two individuals with the same genetic code. Now in the past we would think that they would be identical, right? If they have the same genetic code, but they can actually end up with very different levels of stressor activities based on whether their DNA is methylated or demethylated, which actually has a lot to do with whether or not their mom was stressed out during pregnancy.
So the debate is no longer about nature versus nurture, but it’s really about the gene environment interaction, including very importantly the prenatal environment, which can turn on or off your gene expression for life. Next slide please? Now I’ll give you one more example of prenatal programming and that’s about inflammation. These days it seems like every single disease is linked to inflammation from heart disease to cancer to your Alzheimer’s and certainly preterm birth. The question is, could these chronic diseases have a fetal origin. Next slide please? Now if you understand inflammation, okay if you understand inflammation you need to know about TH1 and TH2. And these are basically your immune cells that come from your naïve T helper cells, if they’re exposed to TH1 cytokines, where inflammatory mediators start interleukin to and gamma interferon’s and Truman necrosis factors, they turn into TH1 cells. If they’re, on the other hand, they’re exposed to TH1 cytokines they turn into TH2 cells.
Now why is that important? Well it turns out the TH1 cells are very purely inflammatory whereas TH2 cells are thought to be anti-inflammatory because they antagonize the action of TH1 cell. Although anti-inflammatory is probably a misnomer, because we know that these TH2 cells mediates the inflammation that’s involved in things like allergies and asthma. And we know that pregnancy is typically characterized by, a balance between TH1 and TH2. In fact, I’ve been starting thinking, could certain exposure during pregnancy, during critical period of immune development drive your immune differentiation one way or another. That may increase your susceptibility for certain types of diseases later on. So for example, okay, for example, if you were to have a inter uterine infection, well, that usually causes release of these, a lot of these TH1 and a lot of these purely inflammatory cytokines.
Could that drive your immune differentiation more toward TH1? And that might increase your future risk for chronic adult diseases that’s mediated by inflammation. And could this help explain the high rates or higher rates of things like auto immune disease, or nephritis or other types of diseases mediated by inflammation that we see in the African American women? Could that be traced to their higher risk for exposure to inter uterine infections when, they were just a baby inside their mother’s womb. Now suppose, you have other exposures that drive it the other way, drive it more towards TH2? Could that increase your future risk for diseases like asthma and allergies? And what kind of exposure would drive it that way? Well, we know lead does that, dust mites, cigarette smoking, drive you toward more TH2 predominance and could this help explain the link between maternal smoking during pregnancy and childhood asthma.
If you want to do something about preventing childhood asthma, where do you have to start? Inside the womb. Next slide please? Now the cumulative pathways posits that that chronic stress that causes wear and tear on your body’s adaptive systems, which then lead to this decline in health and function over time. And let me give you another example from the stress literature. This time your mom didn’t have to be stressed out during pregnancy, but rather it’s that chronic stress and strain, that daily wear and tear the women go through particularly women of color go through that cause you to have higher stress reactivity. And how does that work? Well, what happens when you’re stressed out? What happens say when you see a saber toothed tiger? You run, right? And what helps you run faster is your body actually activate that fighter flight response, that hyper gland through adrenal access and some pathomegalary system and you’re putting out all of these stress hormones.
The CRH, the ACTH, the cortisol, the calconines to help you run faster away from the tiger. Then what happens after you got away? Your blood pressure comes down, your pulse comes down, and you relax. Right? And that’s the amazing thing about the human body, next slide please, is that it’s self-regulating. It knows to shut itself off once the stressor has been removed. And that’s called allostatic, it’s basically to maintain stability through change, that you maintain stability through change. What happens if you can’t get away? What happens if there’s no where to run? Well, you get eaten, right, so if you don’t, what happens?
In the face of this chronic and repeated stress, your body lose that ability for self regulation and now you can turn it on but you can’t turn it off. And biologically speaking for those of you who are born biologically wrong, and you say what’s happening, you get this tonically elevated level of cortisol, which start to down regulate the glucocard core receptors in side your brain, so you lose that negative feedback. So we find that in animals and humans who are subjected chronic and repeated stress, they actually walk around with higher levels of stress hormones. And if you were to expose them to some natural or experimental stressors that they would put out a lot more of these hormones than others would, and if they were pregnant at the time, that would actually increase their vulnerability to preterm labor. Next slide please? And what does stress do to your immune system? In general stress suppresses your immune system, right? And that may partially explain why women who are under chronic stress are at increased risks for infections like bacterial vaginosus, which then increase your vulnerability to preterm labor.
That turns out to be only part of the explanation, because if you think about it, usually in the face of the infection your body, activate that immune inflammatory response. But as soon as the battle been won, your body starts turning off the immune response to prevent your body from undergoing a potentially damaging and inflammatory over (inaudible). Again, that’s the amazing thing about the human body, it’s self regulating and knows to shut itself off once the battle’s been won. And here again we find in animals and humans who are subjected to chronic and repeated stress is that they lose that ability for self-regulation. And biologically speaking what’s happening is now you get this chronically elevated levels of cortisol, which start down regulating the glucocard core receptors inside the immune cells, so you lose that counter regulation from the HPA axis.
So that in the face of infection, even something as benign, as innocuous as bacterial vaginosus, which is probably one of the weakest infection you could ever hope to get. We find that in some women if they particularly, and I always find in a lot of African American women, that they put it out all of these inflammatory cytokines that too many necrosis factors the interleukins and so forth that could actually activate the biological cascade leading to preterm labor. Next slide please? So the point here is that your vulnerability to preterm labor may have to do not only with exposures to stress infection during pregnancy but really to the stress reactivity and the immune inflammatory disregulation that’s been patterned by a whole life course of chronic stress. So if you want to do something about preventing preterm labor, and preterm birth, what do you have to do? It’s not enough to just do prenatal care. Right? Because you expect prenatal care in less than nine months to reverse all the early life disadvantages and all the cumulative allostatic load over the entire life course, is probably expecting too much of prenatal care.
So if we’re serious about improving pregnancy outcomes and reducing disparities in this country, we really got to take care of women before they get pregnant. Next slide please? Next slide? I’m not just talking about that one visit, three months, preconceptionally. I’m talking about when she was just a baby inside here mother’s womb and the infant and the child and their adolescent and young adults. And we’ve got to do a lot more than just healthcare. All right? We’ve got to take care of all of these underlying causes of chronic stress and allostatic load that wears and tears on maternal health. And that’s what we need to do and that’s what the life course perspective is all about if we really want to improve birth and pregnancy outcome. Now, Jimmy is going to take the theory now and apply some data to it from the trans generational research and from the weathering hypothesis.
JAMES COLLINS: I hope no one’s stressed out this morning because this is not healthy stuff, you know. Sometimes we’ve got to laugh a little bit to relieve stress. Next slide please. Transgenerational factors are defined as those factors, conditions, environments experienced by one generation that relate to the pregnancy outcome of the next generation. I like pictures, basically what we’re talking about is how this little girl, how her birth weight was related to the grandmother’s life experiences. Next slide? For African Americans, the ultimate transgenerational process unfortunately is slavery. Is there something about the legacy of slavery, which contributes to this poor outcome that we still see some 20 years later? Or is it something about the genetic makeup of people who descended from Africa who happen just to be in the United States .
Next slide? And we tried to tease this out a few years ago by doing a study comparing the birth outcome with three cohorts of women who delivered in Illinois over a 15-year period. The first group, U.S. born, African American women, the second group, African born African American women, we don’t know when they came to the United States but we do know that they delivered in the United States, specifically in Illinois, and lastly, U.S. born whites. Next slide? And this is the infamous bell shaped curve of life. In this case we’re looking at birth weight distribution. Don’t strain too hard if you’re in the back again, please. The groups that are very similar are African born African American women, and U.S. born white women. African American born, excuse me, the U.S. born African American women, the curve is shifted to the left by about 260 grams.
Next slide? The mortality is in the tale of the curve. And this slide looks at the tales to find his low birth weight. Again, we see three distinct patterns. The U.S. born African American women having very high low birth weight rates, African born women with the rates close to U.S. born white women. If we look among low risk, that is those who were college educated, married to college educated men and also received early prenatal care, we see that through all three groups. The rates come down, but again the African born blacks are close to U.S. born whites. So what this study led us to think, it’s something about U.S. born black women, it’s something about being here for generations that negatively affects pregnancy outcome as opposed to something that happened in Africa that affected the genetic predisposition to African Americans in the United States .
Next slide? So we thought well lets see what happens to the next generation. That is, we have women who themselves were born in Africa that came to the United States , gave birth to a female. That female grew up in this country, 20, 30, years later, she herself became pregnant and had an infant. Lets see what the low birth weight is among this group here. Next slide? And when this looks at moderate low birth weight rates, we took away the very low birth weight rates just because the way this dataset was setup, women born in the 1950’s, 1960’s had a high mortality rate if you were very low birth weight. So therefore, you would not have survived to give birth. We’re comparing two groups, mothers to daughters. And we see among U.S. born whites that the rates are very similar among mothers and daughters, among foreign born white women, that is women who were born in Europe , rates are very similar. Looking at U.S. born African Americans, again mothers and daughters, very similar.
Then among African, and we also put those who also were born in the Caribbean into the group, we see that daughters start to have a higher moderately low birth weight rates then their mothers. Next slide? We looked at some indirect proxy of socioeconomic status. In this case all that we had was marital status because we didn’t have education. And we see for the first three groups, a very similar trend occurred. But interesting among the African Caribbean’s we see that their mothers, excuse me their daughters, almost have a two fold greater rates of moderate low birth weight than their mothers. So it’s after one generation, their moderately low birth weight starts approximately that of the general African American population. So using the life course conceptional model, it suggests, or provide evidence that something about the life experiences of the mother, which unfortunately negative impacted the pregnancy outcome.
Next slide? So using a life course conceptional model, as Michael setup very well. There are really two hypothesis, which contribute to this. One is the fetal origins. And there’s one natural experiment, which kind of is consistent with this hypothesis, that’s the Dutch famine, which occurred during the 1940’s. And as you are aware, there are a group of women who unfortunately went through the Dutch famine who survived the famine, grew up, 20 or 30 years later had children. Those off spring were growth retarded. The other hypothesis is the weathering hypothesis as we spoke about briefly by Arlene Dronimus and we’ll speak about that also. Next slide? Looking at the fetal origins model of poor reproductive outcome for racial disparity, we decided to use birth weight, so that is maternal birth weight is a marker for a measure of fetal reproductive programming. Not withstanding that this may not be the strongest variable, it is a variable that we had, birth weight.
Next slide? Our hypothesis was the maternal low birth weight is a risk factor for infant low birth weights independent of adult risk status, particularly risk status during the pregnancy. Next slide? In using our transgenerational dataset, the X axis is maternal birth weight and the Y axis is infant low birth weight rates. African Americans are in the white box, whites are in the red box. And we see that for both groups as maternal birth weight increases, the incidence of low birth weight infants declines. Even among the small group who weighed less than a kilo, who survived, we see that for African Americans, almost 30 percent of those mothers grew up and had low birth weight infants as compared to about 15 or 17 percent of whites.
Next slide? This looks at low birth weight rates by maternal birth weights and prenatal care among African Americans. And we use the color check index to find adequate prenatal care utilization. And we that amongst each group of women who received some level of prenatal care, those who were them selves low birth weight had a higher rate of infant low birth weight infants. The group that we’re most concerned about, those received adequate prenatal care, moms who them selves were low birth weight had a two fold greater rate of low birth weight infants them selves compared to mothers who were non-low birth weight. And we’re going to, next slide? We’ll keep looking at that adequate prenatal care group and this time among those who received adequate prenatal care, we stratified this by maternal education.
And we see again in each group as maternal education level improves, then since low birth weight infants decline, which is what you expect, but more importantly we see that maternal low birth weights, those moms who them selves low birth weight had a higher rate of low birth weight infants than those moms who were non low birth weight. Among those moms with greater than 16 years of education, those low birth weight moms had a two fold greater rate of low birth weight infants, then moms who them selves who were non low birth weight. Next slide? Just to really hammer home the point, that in both groups whites and African Americans, moms with them selves low birth weight had a greater rate of low birth weight infants than moms who were non-low birth weight, approximately a two fold greater risk. But interesting looking at the red box, which is in this case maternal non-low birth weight, looking among whites and African Americans, we still see African Americans are higher on the scale than whites.
So clearly maternal birth weight by itself, is not explaining the racial disparity in pregnancy outcome, but it does provide evidence that maternal birth weight is an independent risk factor for poor pregnancy outcome as much as by infant low birth weight. Next slide? Lets transition a little bit, look at the weathering hypothesis. Race is the proxy measure of lifetime exposure to neighborhood poverty. Maybe yes, maybe no? Next slide? Approximately four percent of white infants are born to mothers who them selves reside in impoverished communities. Almost 50 percent of African American infants are born to mothers who reside in poor communities. Next slide? The type of poverty that African Americans are exposed to is also very different than the type of poverty that whites are exposed to. This urban poverty seems to be a stressful independent or a lot of other factors. A
nd this fifth grade pupil, sixth grade pupil from one of the Robert Taylor homes wrote and this was published in the Chicago Tribune about five or six years ago. For the last few days, there’s lots of things been going on, like shooting, killing, dying death, that happens every day, every week, any month. Like they try to kill my cousin, my uncle, almost tried to hurt my grandfather to take his money. Everywhere you go you see people on streets, in abandoned building, breaking in houses, getting stopped by police, every day the same things happen. To me this seems like a very stressful environment and this would be bad for pregnancy outcome. Next slide? So we looked at this from an observation that others have made.
We know that among white there’s a J or U shaped curve in terms of the relationship between maternal, age, and maternal low birth weight rates. That is young maternal age, and advanced maternal age are both risk factors for low birth weight. Among African Americans it’s interesting because really we don’t see this U or J shaped relationship. We actually we almost a linear ratio, relationship with incidence of low birth weight infants actually rising as maternal age increases. Geronomists term the deterioration of reproductive health status over the childbearing years among African Americans as weathering. Next slide? We hypothesize that neighborhood poverty increases the risk of infant low birth weight associated with advancing maternal age among urban African Americans. Next slide? So we want to compare the low birth weight rates of two groups of women, the African American women who resided in non-poor communities and African Americans who reside in extremely poor communities. And we that for both groups, things start to inch their way up as maternal age increases.
However, for those in the extremely impoverished group, even in the early, oh gad, the late 20’s we start to see low birth weight rates start to climb. And by the early thirties, there’s significantly different and that really accelerates into the late 30’s and into the 40’s. Next slide? And this slide kind of summarizes the low birth weight difference between women in their early 30’s compared to women in their early 20’s. And we that among non-impoverished, the risk difference is just under five percent. In extremely impoverished communities, the risk difference is about twice that at about 10 percent. Next slide? Looking among the lowest risk group that we could find, that is first time moms who received adequate prenatal care we see a similar trend with rates starting to slowly start to rise in the extremely impoverished group in the late 20’s and then continuing on to the 30’s.
Next slide? And this slide summarizes that. Again, the low birth weight risk difference, notice women in their early 30’s compared to early 20’s, about four and a half percent in the non-impoverished group compared to about seven and a half percent in the extremely impoverished group. Next slide? Make the same comparison to women in their late 30’s compared to the early 20’s in both groups and we see almost eight percent compared to about 16 percent for those in extremely impoverished. So something is driving the low birth weight rates among African American women who reside in extremely impoverished communities. Kind of make another little transition. Race is a proxy measure of life time exposure to interpersonal racial discrimination. So maybe it’s something about minority status independent of where you live or independent of poverty, which is also bad for pregnancy outcome if you’re African American.
This is a quote from Camara Jones. Race is not a biological construct that reflects innate differences, but a social construct that precisely captures the impacts of racism. So we thought well lets measure, next slide please. Lets address this hypothesis. African American women’s life time exposure to interpersonal race discrimination is an independent risk factor for preterm, very low birth weight. So we performed a study, a case controlled study where actually this time we actually had to collect data. Everything else has been secondary data analysis, which I enjoy. Collecting data is painful. I’d give a high five for everyone that does it on a regular basis. We performed a case controlled study where we actually in retrospect we interviewed women who delivered. Two groups of women, African American women who delivered preterm, very low birth weight infants and African American women who delivered term non-low birth weight infants.
And we administered a structured questionnaire to both groups and we asked them their lifetime experiences with racial discrimination, using two standardized questionnaires. One by Nancy Krieger, which just asks have you ever experienced racial discrimination in five domains, getting work, at work, at school, getting service at a restaurant, or getting medical care. For women who were employed they were asked an additional 10 questions regarding racial discrimination in the work place. Next slide? Responses were dichotomized after daily collection into none or regular, which was any time from a few times a year to a few times a month, at least once a week, to nearly every day. The routine variable we try to control for age, education, blah, blah, blah. And we did a stratified and multi (inaudible) logistic analysis, the control for these traditional confounders.
And this slide kind of summarizes what we found. We found that maternal lifetime exposure, the racial discrimination in one or more domains in infant birth weight. We see that women who delivered preterm very low birth weight infants, almost 16 percent of them experienced racial discrimination in one of those domains compared to just under, over 40 percent of term non-low birth weight infants with an odds ratio of approximately 1.9. Next slide? I looked for those who experienced three or more domains and again we see a difference. Almost 20 percent of preterm very low birth weight infants compared to just over 8 percent of term non-low birth weight infants odds ratio 2.7. Next slide. And we do what we do. Put everything into a logistic model and we see that for one or more domains the odds ratio essentially was unchanged at 2. from 1.9 to 2.3. For three or more domains odds ratio was essentially unchanged, 2.7 to 2.6.
So this suggests that lifelong experiences of racial discrimination or perceived racial discrimination is negatively associated with pregnancy outcome as measured by very low birth weight. Next slide? For the women who were employed, as I said they were administered 10 additional questions and this is just a sample of those questions. You were watched more closely than others because of your race, odds ratio 2.3. Whites often assume that you work in a lower class job then you do and treat you as such, I’m sure almost 2.3. You were treated with less dignity and respect than you would be if you were white, odds ratio 2.0. So that just gives you a sample. Next slide, tries to summarize this. Maternal chronic exposure to interpersonal racial discrimination in the work place, and we that for one or more very low birth weight mothers were almost 50 percent, oh 47 percent experience one or more episodes of racial discrimination on a regular basis on a compared to 35 percent of non-low birth weight controls.
Three or more, we see that 20 percent compared to about nine percent. And we lose (inaudible) to get to seven or more but there’s still a difference of 10 percent compared to just over five percent. Again, this suggests that lifelong experience of racial discrimination is a negative risk factor for pregnancy outcome. Next slide? In summary, the long standing racial disparity in infant outcome cries out for fresh analysis that take into account the pervasive, the multi faceted inequality that is bound up in the historical context of race and begin to capture its affect on human beings over time. Pregnancy while occurring during a limited time period, should not be considered independent of prior life events. Our data highlights that return a low birth weight by a time of exposure to neighborhood poverty in the life long accumulated experience of interpersonal racial discrimination are risk factors for poor reproductive outcome among African American women. We’re going to make a final transition here. I wish we had a little music to help us along but boom, boom, boom.
MICHAEL LU: Next slide please? So what do you make of all these biological and epidemiological data? What’s MCH to do about improving pregnancy and birth outcomes? If Jimmy and I can leave you with just one message to go home with, this is it. You need to go ecological, next slide, you need to go life course. Now what does that mean? Okay I’ll give you a few examples. Next slide? Lets take cigarette smoking. What do we currently do? Well if I have a pregnant woman who comes into my office and she’s smoking cigarettes, what do I do? I sit on my butt and I tell her bad smoking is to her and her baby. Right? How well do you think that works? You still have to do it. But we know that that doesn’t work very well. So what has the public health response been? You created these public media campaigns around smoking and pregnancy and you also created these affordable and accessible smoking cessation programs. How well do you think those work?
They actually work pretty well, in fact, there’s a Cockeran review of about 36 randomized control trials on smoking cessation programs and overall it increased your quit rate by about 50 percent. About 50 percent sounds pretty good until you ask 50 percent of what? AS it turns out that of 100 women who were smoking before pregnancy, about 25 of them would quit just on their own, when they get pregnant. About 10 more of them will quit with usual prenatal care and 50 percent of that, which is five more will quit with these smoking cessation programs. Now unfortunately about one third of them will relapse during pregnancy and about two thirds of them will relapse within six months after delivery. So the vast majority of women who smoke cigarettes before pregnancy will continue to smoke and it’s not because they don’t know better. Why do you think these women smoke? Two things, right? Addiction and stress.
So if you want to prevent smoking during pregnancy what do you have to do? From the life course perspective, you have to prevent women from smoking in the first place, right? We know that 90 percent of women who smoke start smoking before they turn 19. So you really need to intervene much earlier than during pregnancy. And also you’ve got to deal with the stress that maintains smoking as a coping mechanism. So how do you deal with stress? Next slide please? You’ve got to go ecological. It’s not enough to teach a program start dealing with that give them positive coping skills and behavior. You’ve got to deal with the interpersonal level of issues like reducing family violence and strengthening mental involvement and increasing family support, neighborhood and community level factors like addressing neighborhood stressors and increasing reproductive social capital institutional factors like increasing service coordination system integration and using public policy to support working mothers. I’ll talk about some of this.
Next slide please? So speaking of male involvement. You have to have male involvement programs that does more than just collect child support or screen make for STD’s. And it’s not enough to just have interventions like giving knowledge, attitude, behavior and human capital, you got to start working on interpersonal issues that provide marital counseling conflict resolution and generally conciliation to work on neighborhood and community stressors like employment issues and incarceration issues. In many of our largest cities in America on any given day there are more poor black men bars than holding jobs. And talk about how that creates a barrier to real male involvement. And you’ve got to start working on institutional and public policy issues. Right? Because now we have all of these welfare policy and tax policies with earned income tax credit that favors single parent families over two parent families and child support.
Child support that says there’s too much arrears that they can’t pay. And even if they pay, most of it goes to the state and doesn’t get to the child. So you have child support policies in this nation that’s creating this whole cadre of fathers that’s driving them underground. They want to be involved in their children’s lives but can’t. And you really have to start addressing that the racism that’s keeping many black men from living out their true potentials, racism and education and healthcare and housing and jobs and the criminal justice system. Next slide please? Let me talk about the whole idea of social capital. Basic social capital refers to those futures of social organizations, networks, norms, and social trust that facilitate coordination, cooperation, to promote reproductive health within the community. And the question, and basically what it does is describe the connectedness between neighbors and in terms of reproductive health, it describes the connectedness of a pregnant woman to her community.
The question, and there are studies that show that the higher the social capital in the community to lower level that the mortality including infant mortality in the community. But the question is, how do we create social capital. How do we create that sense of community support for pregnant women? Well, there’s this project that I’ve been involved with kind of working with in the organization in south central Los Angeles called Healthy African American Families and I know many of you know and with Loretta Jones and basically they started with this focus group of pregnant women and they asked them about the stressors in their lives. And they asked two more questions. They asked them, what can your family and friends do for you that’s going to help you have a better pregnancy? And what can strangers do for you that’s going to help you have a better pregnancy? And guess what kind of responses they were getting from the pregnant women? From families and friends, more help with washing the dishes, or childcare and a lot of this was actually targeted toward the male partners.
And then from strangers, a lot of it was, well, don’t come up and touch my belly without my permission. They have due respect for privacy. But there were also a lot of things like offer me your seats when I get on the bus. Let me get you to the front of the line. You know, I grew up in Taiwan . In Taiwan when a pregnant woman gets on the bus, you would be so shamed if you stayed seated. When a pregnant woman gets on, everybody stands up. And somehow we lost that in this country so we lost that respect and support for pregnant women and women with young children. And what basically, what Healthy African American Families did is they compiled this list of 100 things that families, friends, and strangers could do to support pregnant women what they call A Hundred Intentional Acts of Kindness For Pregnant Women and that would publicize in churches, in barbershops, in nail salons. And in a sense what they are doing is they’re trying to create our reproductive social capital. Create that support in women’s everyday lives to help them deal with the stressors and to reduce that allostatic load.
Next slide please? We can more effectively use public policy to address stress. Just take the example of maternity leave. Between 1993, when we passed the Family Medical Leave Act, we were the only industrialized nation in the world that did not have a national maternity leave policy. Certainly the family did a lot after 1993 in terms of increasing coverage, but because of all the exemptions for small businesses and part workers, less than have of working mothers in the private sector in the United States have access to guaranteed maternity leave. And less than five percent of mothers have access to paid maternity leave. Now this compares with countries like United Kingdom where they can take a year off with paid leave. Countries like Finland where they can take two thirds of a year off. And my friend Pat Campbell who just moved to Toronto tells me that in Canada you can take a whole year off of paid maternity leave. Now that’s not what I’m suggesting. But certainly we can learn a lot from other countries in terms of better supporting working mothers and reducing the allostatic load in their lives.
Next slide please? So this is a 12 point plan that a number of colleagues and I have been working on that’s going to get published in upcoming issue of ethnicity and disease this year to begin to address the black white gap in birth outcomes from a life course perspective. Now as you can see the first four point move beyond our current focus on focus on prenatal care and start to address the healthcare needs of African American women from preconception to inter conception in the cross of life course. And the next four points move us beyond our current focus on individual behavior and begin to address change in family and community systems. That includes strengthening father involvement, enhancing service coordination systems integration, creating reproductive social capital, and investing in community building. And the last four points move us beyond our current focus on the biomedical model and begin to address the social and economic iniquities that underlie a lot of our health disparities.
That’s about closing our educational gap and reducing poverty and supporting working mothers, undoing racism that Jimmy so eloquently talked about. Now I know we’re asking you to do a lot. All right? Next slide please? And you might say well this is really not our business. We’re not in the business of creating jobs and building houses and doing education, this is not what we do. So lets look at what we do and lets think about how we can go ecological and go life course in terms or our core functions of assessment, assurance, and policy development. So I think in terms of assessment, we’ve got to go beyond our current reliance on birth certificate and hospital discharge data and start to do these multi level assessments of the multiple determinants of pregnancy and birth outcomes. And that may include things like food insecurity and family violence and neighborhood violence and social capital and racial discrimination. And we’ve got to do more than, more play space assessments.
Not just assessment of individual characteristics but neighborhood and community effect. In Los Angeles County were beginning to develop in collaboration with our County Health Department to do this Los Angeles Mommy and Baby Survey based on a multi stage cluster sampling that will allow us to begin to do this type of multi level assessment. And we also need to do more of these kind of longitudinal data linkages. Link databases across time from preconception to inter conception, from one pregnancy to the next, from mother to child, across her life course and perhaps even across generations. In terms of assurance, we need to assure equal access to not just prenatal care but good quality prenatal care and also equal availability and coordination of all these important insulator services like nutritional and mental and oral health services.
Like it doesn’t make sense to ask providers to screen for postpartum depression when there’s no Mental Health Services available at the other end of the referral. So that’s what we need to do and in terms of policy development then we need to work on coverage for inter conception care. Either through Medicaid Waiver, 11/15 waiver or by whatever means necessary. Or better yet, let’s get coverage for
preconceptional care as part of a continuum of women’s healthcare. And we need to use, better use public policies to involve fathers and to support working mothers and would certainly to take on racism as a public health issue just like public health took on violence as a public health issue because there’s no greater violence than what we find in racism. Next slide please?
Now we’re really asking you to do a lot more than you’re currently doing, but we’re really not asking for a quick fix. To paraphrase President Kennedy, all this will not be finished in the first 100 days, nor will it be finished in the first 1000 days, nor in the life of your administrations, nor even perhaps in our lifetime on this planet, but let us begin. Now I get asked these questions all the time and I’m sure Jimmy gets asked these questions all the time, people ask do you ever get discouraged? Do you ever worry about who you might never live to see the day, when we can say that we closed the gap? And I think back to a recent conversation I had with Martha Peck, many of you know her as the founder of CityMatCH. And Martha is actually doing this amazing project called the Invisible Heroes of Public Health, where she’s going around interviewing these great heroes of public health. People like Bill Fahey who banished smallpox from on the face of the earth and people like Julius Fritzman who founded Head Start.
And she says that there’s one thing that she finds in common that’s shared in common amongst all of these great heroes. Okay, one thing, that’s what she calls an unwarranted optimism, unwarranted optimism, that these heroes remain optimistic through the good times and the bad. So despite present difficulties, we’re not discouraged, right? We’re not worried. We’re optimistic because we have to be. And we’re optimistic because we still believe in the dream. Now this is a dream that’s deeply rooted in the American dream. Next slide? WE still believe in this dream that one day our nation will rise up and live out the true meaning of its creed that we hold these truths to be self evident that all men and women are created equal.
Next slide? And we still believe in the dream that one day my little girl Sasha, next slide, I just saw them put her picture in there, back one slide, I’m sorry go back one slide? And Jimmy’s children, and I asked for a picture from, yeah, he’s got teenage boys and so they’re never in the same picture, that they will one day live in a nation where they will not be judged by the color of their skin, but by the content of their character. Now this is a dream that we’re all fighting for, right? In the words of Langston Hughes, next slide, let America be America again. Let it be the dream that it used to be. Oh let America be America again. The land that never has been yet, and yet must be the land where every man is free. So as you go back in the next few days to your home, to New York or Pennsylvania and New Mexico and Alabama , I want you to stay optimistic, because you have to. I want you to remember this dream. Can you go back one slide? Go forward one slide.
Can you go forward one slide? Show the picture of my daughter. This is a dream we’re fighting for, for our children and grand children. It’s about the kind of nation that we want them to go grow up. And so please stay optimistic. And we might never live to see that day when that dream comes true. But that’s okay. Let us begin because that’s what the life course perspective is all about. Thank you very much.