Winchester 150dpi 1.5x2.2

Dr. Paul Winchester is the Medical Director of the NICU at Franciscan St. Francis Health and a Professor of Clinical Pediatrics at Riley Children’s Hospital in Indianapolis, Indiana. He also conducts research on the epidemiology of birth defects, including the effects of prenatal exposure to pesticides.

On this episode, Dr. Winchester talks about how his background in farming informs his work today and shares a number of sobering findings from research in his field, such as the fact that women who conceive during peak pesticide months are more likely to have a child with birth defects, a preterm pregnancy, or both; not to mention that the effects of pesticide exposure are not limited to those directly exposed, but can be seen and felt generations later…

Tune in to hear about

  • Pesticides: why we depend on them, and how they affect us
  • Birth defects and preterm pregnancy as they relate to pesticide exposure
  • Falling fertility rates
  • The top two leading causes of infant deaths in our nation
  • The percentage of pregnant women who carr DDT in their bodies

Listen at the link above, on iTunes, Stitcher, Google Play or wherever you get your podcasts!

Transcript: Rootstock Radio Interview with Dr. Paul Winchester

Air Date: July 30, 2018

Welcome to Rootstock Radio. Join us as host Theresa Marquez talks to leaders from the Good Food movement about food, farming, and our global future. Rootstock Radio—propagating a healthy planet. Now, here’s host Theresa Marquez.

THERESA MARQUEZ: Hello, and welcome to Rootstock Radio. I’m Theresa Marquez, and I’m here today with Dr. Paul Winchester, who is the Medical Director of the Neonatal Intensive Care Unit at St. Francis Health, and professor of Clinical Pediatrics at Riley Children’s Hospital in Indianapolis, Indiana. And Dr. Paul is also a researcher. So, Dr. Paul, it is an honor to have you speaking with us today.

PAUL WINCHESTER: Honor to be here.

TM: You know, I always love to start out by asking the folks who talk on the show how they got started in what they’re doing. And you have be described by your colleagues as someone who is so admired for their both compassion and enthusiasm for babies and their health and everything about babies. How’d you get there?

PW: Well that’s more of an organic question than we probably have time for. But yeah, why babies? Actually, growing up on a cattle ranch in Montana, my dad’s dream was to—having grown up himself on a homestead, herding sheep at age four, even though he became an educated PhD animal geneticist, we still had to live on the farm and raise prize cattle and sheep. So I’m one of the few baby doctors that knows how to shear a sheep.

But I was delivering babies long before I came into the human [unclear—world? (sounds like “grill”)], because we were delivering baby lambs and baby cows. I was also the family baby doctor. When the cat had kittens I had to crawl up there and make sure they were okay, and I became the baby doctor. And I think just the growing up on the farm and having this sort of sense of every problem doesn’t really come with a set of instructions—you kind of just have to solve it. And if you solve it correctly you won’t be looking for black cows in the middle of the night. If you figure out how to keep the gate closed at night you won’t—you’ll keep it closed!

TM: Some basic things, huh?

PW: Basic things. Other prevention things, you know? Anyway, so having a farm background certainly connects me with food production and farming. Really those are more of my people in some ways.

TM: You know, I was reading that you came to Indiana in, was it 2001? And at that time they weren’t counting the incidents of birth defects, and a lot of things they weren’t tracking. For you it was, your work was like, wow, why don’t we track these things and figure out what’s going on.

PW: Yes, when I came here, I had already been a director of nurseries in Colorado Springs; Overland Park, Kansas; and Manchester, New Hampshire—a lot of places around the country. So I was kind of used to how much, how many birth defects I should expect to see in a given month and in a community hospital. And I was surprised at how many I was seeing, and I asked my colleagues about it. And if you work in a referral center, the main university hospital, you’re always referred the sickest babies. So for them, it was normal to have all the sickest and problems.

But the question is, is the state of Indiana having more birth defects than other states? I thought I could start that way. And I thought the place that would know that would be the CDC, who gets paid by the government to track health care and public health. They called me back and said that Indiana was one of 12 states that didn’t count birth defects and didn’t have a birth defect registry. This has changed since then. But then, in 2001, that many states in the supposedly most advanced industrial country was not tracking defects, reminding you that CDC has named birth defects the leading cause of infant death in the U.S. for the last 30 years. So imagine that. Imagine not counting the leading cause of infant death in a fifth of the states. It was almost beyond comprehension.

I have to confess to you that when I heard this I immediately said to myself, “It’s because we’ve never had a woman president,” because we could never imagine a woman letting the leading cause of infant death not be a priority. That’s the level of the CDC. That’s just an example of what happens if you only have a male perspective on the universe.

So we started using birth certificates, collecting all the data from all the states through the CDC birth fatality data to study it. And what we did to correlate with our birth defect data was a treasure trove of data that we obtained from colleagues in the U.S. Geological Survey. They have a major center here in Indianapolis and their warehouse for this data, the NAWQA national water study, was housed in Tacoma, Washington, and they were very generous in sharing with us their data.

What was really extraordinary about it is they had measured the water—river water, surface water—in watersheds all over the country and every month of the year, and in peak months, multiple times. And so they kind of had a profile of the concentration of pesticides for the whole country. And that’s an amazing, if you will, at least one way to measure the pesticide environment for the whole country. Now, it varies a little bit from north to south. The planting season in the southern states is a little earlier than the northern states. But the general pattern was very, very characteristic. It showed that early in the spring, the May and June phase of planting was associated with the peak pesticide months in all water systems. There was a trough in August and then a resurgence of pesticides in the fall. Nitrates followed this very characteristic curve. So, since everything peaked in June, we called it the June Effect, but there was also a dimple in the fall that we saw as well.

TM: Yeah, that post-harvest time.

PW: Well, yeah, I didn’t really know what the farmers… We weren’t really farmers in Montana so much as we were raising cattle, so the most we got into was growing hay. So I didn’t really know what the evolution of corn and soybean planting had become. But there’s a pre-harvest administration that really caught me by surprise, except that I was looking for it because I could already see—what I basically found was the birth defects fit the profile of pesticides like a hat. Women who conceived in the peak pesticide months had more chance of having a birth defect than women who conceived in low pesticide months.


TM: And this came all out of that data from Indiana and from—

PW: The U.S. Geological Survey.

TM: Oh my goodness!

PW: Just ginormous. Sandy Williamson, who used to work for them, was my mentor there and was so generous. The thing that I realized kind of as I—I’ve had to kind of evolve because I’m a Pollyanna, not a conspiracy person, and it’s taken me a while to just sort of come to grips with the fact that the things that we’re not doing are the things that are kind of scary.

So when we published this paper, I think the thing that struck me at the time the most and depressed me the most was the fact that I did it. It should have been done years ago. They’ve had this data for years. When I realized that the CDC and the basic of the U.S. government was not counting birth defects in a fifth of the states, that troubled me too. It said somehow we’ve got our priorities wrong.

TM: Well, you know, I’m wondering whether they still were collecting that data.

PW: Well, what they had, what I used for the data was birth certificates. And there’s a whole agency now within the CDC that calls themselves the Birth Defect Registry people. And most of the time they spend is denigrating all the other data. They’ve never let me talk at their conference—it’s interesting. You wonder why. But, in other words, the implication is that there’s some politics that underly this. There are certain things you’re not allowed to do, say, or comment on.

You know, when you’re looking then at this sort of like background environmental footprint that’s ginormous, it’s huge—at the time, all I had were service water data. But I had already assumed that you couldn’t have that big a background of environmental data and have it not somehow be reflected in pregnant mothers. I wasn’t finding—I didn’t have funds to measure pesticides in 50 million women, but I had this equally large sample of water for which millions of dollars have been spent to measure. And you can’t have that much water, a story like that in the water, that isn’t somehow reflected.

So since then, my research has extended beyond that. But I first used that water data to extend it to the second-leading cause of infant death, which is preterm birth. And we used the California pesticide use data for that. California has really good pesticide use data by county and by time. And they actually weren’t very generous with their outcome data, but we got it from the CDC anyway. And we correlated the likelihood of having a preterm birth, and the likelihood of having a short pregnancy was directly related to how many pesticides were used in your county and what month you delivered. So if you had a baby in the peak pesticide month of June in the high pesticide county, you have a significantly shorter pregnancy and a much higher risk of preterm birth.

So now we have the first leading cause of infant death and the second leading cause of infant death correlated with these pesticides. And we’re starting to be able to tell a story that we found actually fairly easy to tell. You could find these correlations everyway. Abdominal wall defects, pyloric stenosis, severity of hypospadias—it just went on. And of course, all of these correlations are just the first step in a quest for understanding. Where the critics would say those are just correlations, they don’t mean causation, and they’re right. But the other side of that is that 50 million live births shouldn’t have correlated with anything. If you’re throwing darts at random, you shouldn’t have a hat-shaped curve. And our curves were highly significant.


TM: If you’re just joining us, we are talking to Dr. Paul Winchester, who is the Medical Director of the Neonatal Infant Care Unit at the Franciscan St. Francis Health. And he’s also a professor of Clinical Pediatrics at Riley Children’s Hospital. And we’re having a rather fascinating conversation about what Dr. Winchester found about the low birth weights of children and other, number one and number two causes of death of children.

And, Dr. Paul, I wanted to switch gears and ask you a little bit about the research that you’ve done with animals. And I was really fascinated when you just told us about the fact that you were raised on a farm and that you were raised around animals all the time and was one of the kids who was in charge of the births. Did that correlation that you were seeing between low birth weights and other information that you were digging out of the U.S. Geological Survey, did that kind of lead you to this animal research?

PW: Yeah, so there are a few other little pieces to this. When I was doing questions of what led up to premature birth, I had found, I had discovered another thing that my advance degrees in experimental psychology had not prepared me for, which was that all these risk factors were in fact heritable. Nobody had implied that prematurity was heritable or that anything else was heritable. But my own extensive surveys of all the women that, when we started this prematurity prevention program, we started asking them. And we were shocked to find that there was almost nothing, whether it was smoking or the abnormal uterus, but even behavioral things that sort of increase your likelihood of preterm birth—all of them seemed to run in families. And this had been ultimately extended to our discovery that even genetic links that have been missed by the geneticists are somehow there.

So I meet, at one of our pediatric conferences in San Francisco, Mike Skinner, who is this University of Washington–Pullman scientist researcher that, he has an extensive background in molecular biology. And he discovered that in a rat model that a little pesticide exposure for just a week at a very low dose that leaves the pregnancy completely unharmed and the fetus unharmed can nevertheless show up as disease later in their adult life.

So this is the kind of problem that you would miss if you were an EPA safety inspector or a researcher in toxicology. In other words, these doses were not toxic but were doing something to these adult animals. And through another serendipitous accident of his lab, one of these adult-exposed animals was bred, and he was able to see what happened in the next generation and the next. And mind you, these exposed fetuses, their descendants are being compared to the descendants of unexposed fetuses. So we have a control group, where pesticides versus not.

And what he discovered was that diseases were showing up in the adults of all the generations. And by the third generation, animals could not have possibly been exposed directly or even through their cellular gametes to the chemical, so they were inheriting a disease that their great-grandmother got exposed to, a pesticide. And this basically created a whole new area of biology called transgenerational epigenetic inheritance. Now, needless to say, there’s a whole lot of Darwinians out there that didn’t believe that such a kind of inheritance could occur. So he had to take on a lot of—I don’t know we would call it—a received wisdom that turned out to be false. It turns out the environmental exposures can cause inherited problems in the offspring.

TM: That’s pretty big.

PW: Yeah, well, it’s huge. No wonder he got the Genius Award from Discovery magazine [Ingenuity Award from Smithstonian magazine] and many, many other awards.

TM: This is Dr. Skinner?

PW: Yeah, Dr. Michael Skinner from University Washington–Pullman. And so the combination of his molecular genetics skills and using the three-generation rodent model, he is able to do in three years what you could never, ever do in humans, which is to see what are the consequences of exposing a pregnancy to a very small dose of DDT, for instance. What happens to the third generation of the offspring?

Now, the reason these are relevant questions is because we have, in a separate set of work, the National Institutes of Health has had to admit that the pregnant mothers today are all carrying chemicals in their bodies, many of which have been banned for years. Like DDT is found still in a 100 percent of pregnant mothers.

TM: One hundred percent?! That’s alarming! That means me!

PW: Well, yeah. The list of chemicals is pretty long. It includes pretty much all the chemicals that have ever been created. The worst ones, though, are the ones that were created to be immortal. So PCBs, for instance, they were made to be put in transformers and not be oxidized by heat—in nonflammable oils, if you will. Monsanto, with General Electric, made these transformer oils that were very effective at providing the lubrication that was needed but not starting on fire. The problem is, PCBs are immortal molecules. They’re artificially made and they can’t be degraded by normal biological mechanisms.

Imagine having a company that said, “One day, everybody in America is going to have one of my apples in their pantry.” That’s the dream of an entrepreneur, right? Well, Monsanto and Dow Chemical have exceeded that by a scale that’s incomparable. Every life-form on the planet has a PCB level and a flame-retardant level, and a phthalate level, and a bisphenol A level, and a dioxin level. These molecules, many of which have now been recognized to be toxic and their manufacture has ceased, have nevertheless become part of our biosphere. They’re part of us. They’re in the atmosphere, they’re in the snow, they’re in the rain, they’re in the water, and every June they peak. It’s that kind of thing. And sadly, this sort of—I call it the detritus of the age of chemistry—is now a layer in the geological strata that you can measure. One’s a core sample in Puget Sound, as they’re doing. In fact they just recorded mussel shells in the Puget Sound area have oxycodone—have opioids in them.

So what we have discovered is that the chemicals don’t—there’s no barrier between where they’re applied and where they end up. They end up in us. We’re one of the top food chain members. And what we didn’t realize is just how extensive this exposure is.

TM: And it sounds also that also we didn’t realize that it’s going to go on for generations.

PW: Yeah, so the original mechanism of harm that we use to qualify safety of a chemical is kind of modeled after a toxicology model in which you start giving doses to an animal. And the lowest dose is first, and then higher and higher doses. And you discover where, in this incremental increase in doses, where the LD50 is in that—where half of them die. You know, that kind of—literally 50 percent lethal dose. And that’s just in the organism.

But when we start to look at infants or pregnant mothers, those kind of assays have been harder to do. They’re not nearly as often done, actually. But it’s the same idea. If I give this much dose to this animal, what happens to the pregnancy? And if nothing happens, if there’s no abortion or miscarriage, if the fetus doesn’t have malformations, it’s considered safe.

And that’s exactly what Mike found. Actually, at the time, he was hoping to see something, and he didn’t find anything—which is a tiny dose of vinclozolin which was administered at 4 percent of the minimal lethal dose, very tiny dose. And so he thought pretty much he’d failed, that there was nothing to be found. And fortunately he let these animals grow up to be adults, and fortunately it only takes six months for a rat to become an adult. And that’s when he started to see things that were abnormal: low sperm counts, polycystic ovaries, premature onset of puberty, cancer, shortened lifespan, obesity, behavioral problems—it’s just, the list goes on.

TM: So I’m wondering, what would be the equivalent age in a human? What would a six-month rat—is that an adult?

PW: So he’s just passed into adulthood. Now, what we’re seeing, one of the first things he can detect in a rat is the onset of puberty is abnormal. And so for us, that’s age 10 to 12. And we have already noticed that worldwide both girls and boys are getting younger and younger at their age of puberty. The average age of puberty onset has dropped almost a full three years over this time period.

TM: Gee, that’s a lot!

PW: Yeah, it’s mind-boggling. Now, independently you might have thought, well, that’s just a sign of the nutrition—better nutrition or something. But every chemical that Mike has tested has caused disruptions in onset of puberty. And we’ve just recently tested atrazine, which is the most heavily used herbicide next to Roundup, and sure enough, it causes onset of puberty problems. And when I say it causes them in the adult animals, I’m referring to the third-generation animals where it couldn’t possibly have been caused a direct exposure. It was caused by a disruption in their DNA, which we call an epigenetic change.

TM: You know, I just want to stop for one second there and remind our listeners that atrazine, which we allow here in the United States, is actually banned in many, many other countries, at least something like 50 or 60 countries.

PW: Yeah, it was finally, in France it was found to be present in 30 percent of the pregnant mothers. And it’s found in virtually 100 percent of the streams and rivers in the U.S. And in fact, it’s allowed in the drinking water up to four parts per billion. Unfortunately, that’s ten times higher than is needed to turn a male frog into a hermaphrodite, according to Tyrone Hayes’s work from Berkeley.


TM: I know that we’re starting to run out of time. And I was reading, not the full abstracts, but some summaries of the abstracts that Dr. Skinner did, and I just wanted to make sure we touched on this one. It was about the ethical considerations of “intergenerational environmental justice,” he’s calling it. What are some of those ethical considerations that you feel aren’t being taken into consideration as we use atrazine and so many of these new pesticides, like 2,4-D, dicamba. Where was Dr. Skinner going with this “ethical considerations”?

PW: Well, you could start with what are the ethical considerations in a country which doesn’t count the leading cause of infant death in a fifth of its states? What are the ethics of that? How is that possible? First of all, if you’re not counting at all, then you don’t even know there’s a problem. So when we retrospectively counted the birth defect rate in Indiana it was higher than the national average. So they didn’t have a problem for 20 years, but they did. They chose not to look at it.

But extend beyond that: if the current EPA standards for safety of chemicals does not even include the epigenetic consequences, the very thing that now we have 20 years of data showing happens when you get exposed in utero to these chemicals. By the way, these influences, these epigenetic influences, they start at adolescence. So if you’re going to ask, is this chemical safe to have in virtually every pregnant mother, the next question, and you know that we just published it, 94 percent of pregnant mothers have Roundup in their bodies when they’re making a baby. That’s the leading herbicide in the country and it’s being sold because [unclear – GMO?] seeds can be manufactured that are resistant to weed killer. And on its face it sounds like a perfect farmers’ solution to weeds and productivity.

But if that same chemical has now made its way into every pregnant mother, we need an order of magnitude of higher level of safety than is currently being measured. It’s not even used as a measure of safety. And yet we can find that its cousin, atrazine, does imprint the DNA and alters not just the exposed fetus but the third-generation offspring and produces in them the very diseases which, if taken to their extreme, would imply that the human race is really on a path to extinction through these chemicals.

And every single chemical so far tested has reduced the fertility of both males and females. And it’s especially hard on male sperm. So sperm quality in the third-generation offspring is diminished significantly, both in motility and quality. This is happening with every chemical that we find, and every mother has at least 20 to 30 chemicals like that in her body when she’s making her fetus.

TM: Dr. Winchester, thank you again for joining us today. It’s been a really fascinating interview to learn about how all these things connect.

PW: You’re welcome, and thank you for asking me.

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