Dr. Shanna Swan: How to Safeguard Your Hormone Health & Fertility

**Welcome to the Huberman Lab Podcast**, where we discuss science and science-based tools for everyday life. I'm Andrew Huberman, and I'm a professor of neurobiology and ophthalmology at Stanford School of Medicine. My guest today is Dr. Shauna Swan. Dr. Shauna Swan is a professor of environmental medicine and public health at the Mount Sinai School of Medicine. She is a world expert in how exposure to various toxins and compounds in the food and environment impact our reproductive health.

She focuses on how these compounds in our air, in our food supply, in our water supply, in cosmetics, and even in household items impact the developing fetus, children, and adults at the level of their reproductive biology. This includes things like testosterone and estrogen and the pathways within the brain and body that are impacted by these hormones. She also discusses how all of these environmental factors and what we put into our bodies impact our health on a daily basis and our long-term health.

During today's discussion, you will learn why fertility rates are indeed dramatically dropping from year to year and have been for quite some time now. You'll also learn why testosterone levels are dropping, why sperm counts are dropping, why conditions like polycystic ovarian syndrome are increasing in women, and what we can do about it. In fact, throughout today’s discussion, Dr. Swan emphasizes the things that you can do every single day that turn out to be very simple. They involve certain things to do and certain things to avoid in order to limit your exposure to these environmental toxins and their impact.

By the end of today's episode, you will be highly informed by the world expert on endocrine disruptors and environmental toxins. You will also be well-informed in terms of how you can have agency and take control of your health in relation to these various compounds.

Before we begin, I'd like to emphasize that this podcast is separate from my teaching and research roles at Stanford. It is, however, part of my desire and effort to bring zero-cost consumer information about science and science-related tools to the general public. In keeping with that theme, I'd like to thank the sponsors of today's podcast.

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Now for my discussion with Dr. Shauna Swan.

**Dr. Shauna Swan:** Welcome Dr. Andrew Huberman.

**Huberman:** Thank you! I'm super excited for today's conversation. I've followed your work for a number of years. I've seen some of your appearances on other podcasts, and I got to see you speak while we were both in Copenhagen. I was in the audience, and you didn't know I was there. But incredible stuff that you've been doing as a researcher, a public educator, and a writer.

Let's kick off by just asking the basic question: Are there things in our environment, including our food, that are diminishing our reproductive and overall health? If so, which are the ones that you think about? Perhaps you could mention a few of the more salient, maybe even shocking, results that you've observed over the years. What was the kind of "wow" result or results that have really steered your attention in the last couple of decades?

And I'll just say what we were talking about before we were on the microphone, which is that you are a skeptic. You are not someone who walks out into the world looking for things that could be messing up our biology and health, and yet you've found some. So, if you could share with us what you've observed and what you find compelling and important for people to know about, we can dive in there.

**Dr. Swan:** That was a lot of questions! I could probably talk for a long time.

**Huberman:** Feel free; I won't speak until you're done.

**Dr. Swan:** No, but I want to break it up. Let’s break it up. So, I think the first question was: Are there forces, chemicals, or agents in the environment that can affect our reproductive health? Yes.

Okay, so my answer to that is yes; there's no question about that. The question comes down to when, in whom, at what dose, and so on and so forth. But whether there are broadly, things—yes, of course.

The category that I focus on are man-made, primarily man-made chemicals. Although I do also include the influence of other factors—factors of choice, for example, sleep and exercise. We can talk about that, but let’s just focus here on the chemicals because I think that's what led me to do a lot of my research and to write the book that I wrote.

My thesis is that chemicals in the environment—a very broad class—at the right time and to the right organism can affect fertility. Let me just say fertility is one area that I focused on. This class of chemicals that I'm primarily interested in are those that affect the body's hormones.

Those are known as hormone-disrupting chemicals or endocrine-disrupting chemicals—hormone-altering chemicals, whatever. There are a lot of names, but that helps you focus on where to look for the effects. If it’s hormone-altering, you can now really start to ask, “Okay, here’s a chemical. Does it affect a hormone? Which hormone? When? How?” Then you start laying out an experiment right there.

Focusing in on hormone-disrupting chemicals, I think, is useful.

**Huberman:** Absolutely. Much of what we’ll talk about today probably centers on the estrogen and testosterone pathways as they relate to masculinization or feminization of the brain and body—and, of course, sperm and egg quality.

I’m a reproductive epidemiologist. I got there on an indirect path; I think probably my work on oral contraceptives led me there most directly, and oral contraceptives are endocrine-disrupting chemicals—that's what they're designed to do: change your body's hormones, your reproductive hormones.

So it’s interesting; way back when, when I worked on the study at Kaiser on oral contraceptives—which was the largest study of its kind in the world—trying to figure out whether they had adverse effects, and if so, for whom and when and how much. This was a very great study.

Coming forward in time, I’ve studied environmental chemicals, not so much pharmaceuticals, for quite a while when I was at the California Department of Health Services. Then I had an "aha" moment. I was flying to Japan with my friend John Brock, who’s a chemist at CDC, a wonderful chemist. You have long flights and you’re talking about this and that. He said, “Shauna, you should look at phthalates.” I’m going, “Why should I look at phthalates? I never heard of phthalates.”

He said, “Well, we can now measure them at the CDC, and we see they’re in everybody. They’re in women of reproductive age.” Fact one. Fact two: Colleagues at the NTP (National Toxicology Program) have shown something they are calling the phthalate syndrome.

He even explained what the NTP is. It’s the National Toxicology Program—a government research center. Their job is to look at chemicals and see what is the toxicity; it could be reproductive, it could be carcinogenicity, it could be neurotoxicity—that’s what they do.

They had singled out these phthalates as being reproductively toxic, specifically to males and specifically when exposure is in utero, meaning when a pregnant mom is exposed to phthalates and somehow that affects the fetus.

**Huberman:** If you don't mind, I'd like to know—is the mom ingesting phthalates in the form of food? Is she inhaling phthalates? Are they landing on her skin? What are the modes of entry into the body of the mom that assuming it goes through the placental barrier into the fetus and is impacting fetal development?

**Dr. Swan:** In those experiments, it was through food. But we are exposed in all those ways you mentioned—every way something can get into our body. Phthalates get in there.

But let’s come back to the experiment at NTP. What they did at NTP was they fed mother rats various doses of these phthalates. What they found was no changes in the females or not that they found at that time. But in the male offspring, they found that the genitals were, I summarize it by saying, incompletely masculinized.

To explain that, I have to back up and say something you probably know very well. Initially, the genital tract is a ridge; it’s a single ridge. It’s the same in males and females; it’s not sexually dimorphic at the beginning. Then, under the influence of testosterone during a very specific window—called the male programming window in rats, it’s days 9 to 12 of gestation, a very short window.

To orient people, rat/mouse gestation is about 21 days or so. At that time, if they feed their mother these chemicals in her food, then her male offspring are born with changes in his genitals.

What they tend to have is a smaller penis, less descent of the testicles, and they are more likely to have undescended testicles. There are internal changes that we didn’t get into in our human studies because we can’t look there, but the epididymis—there are changes, and so on.

The whole genital tract is altered, and the most important measure, for me as it turned out and for humans, is something that animal scientists had studied for a long time—for actually 90-plus years—but had never studied in humans. That is the distance from the anus to the genitals.

This collection of changes in the male genitals was given the name the phthalate syndrome.

**Huberman:** Now, you're a physician, and I challenge you to think of any syndrome aside from alcohol. You know, the fetal alcohol syndrome, of course; that’s a syndrome. But what syndrome is attached to a chemical class?

**Dr. Swan:** Just for technical purposes, I'm a PhD, not a clinician. But I worked on neural development for many years, and prior to that some endocrine research, so I’m familiar with the general terms. One that comes to mind would be, for instance, the thalidomide babies—that’s a very extreme example.

So you're right about the name, which is the phthalate syndrome; there is thalidomide, but it’s not usually called the thalidomide syndrome. However, it could be.

There is no environmental chemical in the environment that is, as opposed to a pharmaceutical that is given a syndrome. So this is very unique. And I thought, “Wow,” John’s telling me this on the plane, right? Something in the environment that is basically having an endocrine and body disruptive effect at least on par with fetal alcohol syndrome and the phthalate syndrome?

What I thought was, at this point, it was only animals because John was telling me about the NTP study which was in rats. And so I thought, "Wow, you know, I like puzzles." My first question was: Is this happening in humans?

You might ask that; it's a natural thing to ask. Great question! Then I thought, "How would we find out?" Answering that question took me 10 years.

If you think about it, how do we connect phthalate exposure in the mother to changes in the genitals of the offspring? How do we do that? Well, fortunately or not, I had stored a lot of urine from pregnant women from a study that I was doing on sperm count.

I just got the women's urine coincidentally, if you will. I thought, "Well, save it, you know? It’s not expensive and not hard,"—80-degree freezers, doesn’t take a lot of room—so I had this urine saved from pregnant women.

Then I knew from John that we could look in the urine for phthalate metabolites. These are products that the body forms when they're exposed to phthalates, and you can measure them in urine. So I thought, "Okay, I could get that urine; I could look at the phthalate metabolites, and then I’d know what the mother was exposed to."

Based on the animal data, we have good evidence that it actually makes its way to the fetus. So then I thought, "Okay, then maybe there’s a change in the babies." So then I had to get the babies.

Fortunately, I had done this study on pregnant couples—pregnant women and their partners—and I was able to call them and say, “Would you come in and let us measure your baby’s genitals?”

**Huberman:** How willing were parents to let you do that? That seems like a stretch.

**Dr. Swan:** They were okay; most of them were okay with that. They trusted us, you know; they had been in a study with us, and we were reputable. Those babies were still young, but not newborns, so this was a while later. The babies that we actually got were, on average, about 12 months old.

So not ideal maybe because the rats had been measured at birth—but that’s what we could do at that time.

**Huberman:** The reason I asked is there's always the potential for ongoing phthalate exposure to the newborn.

**Dr. Swan:** Absolutely, but I suppose in either case you’re able to draw some potential link or potentially draw a link, I have to be careful with my language here, between phthalate exposure in utero and ex utero and these external biomarkers.

Given that the critical window is quite short and quite early, let me just say the rats did a lot of work on this critical window. When the rat moms were exposed before day 9, it did nothing, and when they were exposed after day 12, it did nothing. So it was only the exposure during that critical window that was very delicate.

This is, by the way, true of the brain as well. Teasing out what the critical window is one of the challenges we have when we work with these chemicals. So I wasn’t so much worried about exposure in the delivery room, in their food, as in the first days of life, because I knew it was unlikely to change these measures.

**Huberman:** So, what do we measure? What do we actually measure?

**Dr. Swan:** If you think about a newborn rat or a mouse, their genitals are pretty small, and it’s very difficult to know exactly how that corresponds to the human genital system and what you see at birth.

So I got a pediatrician in Los Angeles who worked with me on how to make that translation and how to do this exam. That took us quite a while because we really wanted to come as close as we could to what was clear was that the anus part of it was easy. You go to the center of the anus, so that’s easy.

Then what's the other landmark? What's the genital landmark? It turns out there are two in males and there are two in females as well. But let’s just talk about males. For males, the best place to measure—actually closest to the rat measurement—is where the tissue changes, where the scrotum inserts where it goes from rugae to smooth tissue.

That point is pretty clear, pretty easy to measure. The other measure that was the anoscrotal distance, and the other measurement we took was the anopenile distance.

That was the insertion, the anterior insertion of the penis—the part closest to the body, the closest to the head. That was not so obvious because you don’t have a change in tissue there.

So where exactly do you put your caliper? We had a lot of discussion about pressing down, how we do it, how we make that mark. The anoscrotal distance is the measurement with the least variance because you can measure most precisely, but the anopenile distance is another measurement.

Then we can do something similar in females, and we did that, but we maybe don’t have to go into that now. So we designed this exam, and we did a lot of work to make sure it was repeatable across examiners.

What we finally did was bring the mothers in, bring the babies in, and got three measurements. On every tenth baby, we got an independent examiner to get three measurements so we could look at within and between examiner variation.

You understand this is the first time this has been done this way in humans. There was a Mexican study that tried to do this, and I never learned much about it. I was excited that they had done this, but I’m not sure how it relates to this, so I just mention that out of honesty.

You know, someone in Mexico did this, but to my knowledge, this is the first time it’s been used as a toxicological measure in humans. We did that study; we related those measurements to what the CDC had measured in the urine of our women collected while they were pregnant. We found the phthalate syndrome.

Could you explain what the correlation was between phthalate metabolite levels, which I believe were not by number because I don’t remember them anymore, but there was a significant—let's just take the anogenital distance of mothers who had higher levels of three of the most anti-androgenic phthalates.

I’ll tell you what those are in a minute—had significantly shorter anogenital distance.

**Huberman:** It sounds like that the distributions of the male measurements moved more closely together to the female distribution.

**Dr. Swan:** Yes, although it wasn’t the females that moved; the male distribution became more feminized. These boys also had smaller penises, less descent of the testes, and smaller scrotums.

So they were smaller; you know, everything in their genital area—are all the secondary sex characteristics of puberty in males—Adam's apple, facial growth, thickening of the vocal cords, lowering the voice, etc.—are those all later-activating effects of hormones, or are there precursors to those present in males?

Because in mice, as I recall, we call it in the laboratory; people always chuckle at this, but it’s like “sexing” the animals when you have to determine if it’s male or female when they’re really young. You have to look carefully at first, and then you get pretty good at it because as they get older it gets easier.

But when the mice are feet down back up, you can’t really tell. As they get older, their testicles become visible in the males, even from above.

But you know, as far as I know, there aren’t really external markers. So you may have found the one truly external biomarker of maleness.

I do want to say something about females because then that'll lead me to my conclusion about the role of this measure. If the mother is exposed to more testosterone than expected, you might expect her female offspring would have a more male anogenital distance. Is that the case?

**Dr. Swan:** Yes, so it’s a bidirectional effect.

**Huberman:** Can we also presume that if the mother either secretes or is exposed to more androgens, then the males can become hyper-male?

**Dr. Swan:** No, we’ve never seen anything that would be considered hyper-male, so yes, I said to you that we did a study where we looked at girls born to women with PCOS (polycystic ovary syndrome).

So women with PCOS, as you know, have excess testosterone. These women often have facial hair, and, you know, not just the moms but the people—the women with PCOS have elevated androgens, not just—sorry, we’re not talking about a pregnant mom anymore.

In our study population, we searched for women who had a diagnosis of PCOS and took that as a marker of higher testosterone exposure, then looked at the girls. Yes, those girls had a longer, quote, more masculine anogenital distance.

**Huberman:** What age group were you looking at in the infants?

**Dr. Swan:** Oh, the PCOS was at diagnosis at pregnancy at the time they were pregnant, so presumably girls from somewhere in their twenties to their forties.

**Huberman:** So adult human females who have PCOS tend to—we know they have higher levels of androgens—but they also have more male-like anogenital distance.

**Dr. Swan:** They do not; their daughters do.

**Huberman:** Thank you for that clarification.

**Dr. Swan:** Yes, the daughters. So put this together: This measure is a look inside the womb at the androgen level that the fetus is exposed to at that time, which is amazing because you can’t go in there without disturbing—you know, you can't, and so this is very early, first trimester.

You can’t get, you know, fluid in so on. This tells you this is like a readout of what was in the fluid at the time.

Then your next question was: What does this mean for later fertility?

**Huberman:** Yes, what is the impact of this early androgen exposure in female offspring or, let’s just say, reduction in functional androgen exposure for male offspring?

The reason I’m using this loop-to-loop language, as you probably know, but for the audience, I’m not trying to complicate things here, but a lot of the masculinizing effects of hormones in fetal development are actually testosterone converted into estrogen.

So it can get pretty tricky, but for the sake of simplicity today, we’ll just stick with androgen effects on masculinization, with the understanding that some of those effects are the consequence of testosterone being converted into estrogen.

So you identified an external biomarker of fetal androgen—aka masculinization—via the mother.

**Dr. Swan:** That’s right.

**Huberman:** Got it. Okay, so then we ask the question that you’ve asked, and many people have asked: Who cares? Why would we worry about a boy having a slightly smaller anogenital distance?

**Dr. Swan:** I can tell you there are many boys probably that are worried about it right now; they’ve probably got the ruler and calipers out right now, just you know…but I’m going to answer that question.

So I told you that our kids are too young; they’re not producing sperm right now, so we had to go to an adult population, and so we went to a population of college students in Rochester, New York.

What we did there was make an assumption based on animal data. It's true in animals; we've been following the animal path here all along.

So in the animals, my colleague Earl Gray did these studies—his name is Earl Gray, yeah, that’s cool—and he said, “AGD is forever.”

Anogenital distance is forever. Now, what that means is it's not like your anogenital distance today is what it was when you were born; of course, you're a bigger person. But that means adjusted for body size.

So if you assume that AGD is forever, if you’re born with a shorter-for-your-size AGD, then when you’re 20, you’ll have a shorter-for-your-size AGD.

Can we assume that? Okay. So if we assume that, then if we get these college students to come in and we can measure their AGD, we're getting a reflection of what it was when they were born.

Then we can get their sperm count, and then we can see if they’re related, and that’s what we did. So we got this population of volunteers, paid them $75, and one of the guys said, “For 75 bucks, you can do anything.”

What we did was we measured their anal distance and then got them to give us a semen sample, complete a questionnaire, and things you do in a study.

Well, we’ll link to that study, but I have a couple of questions about the controls in that study, just for sake of people understanding how a study like this would be done.

I don’t expect you’ll recall all the details, but you’re adjusting for body size and body weight; height, weight—what are the factors that would scale here?

What you're trying to do is backtrack to what it was likely at birth.

**Dr. Swan:** No, we didn’t actually try to go back to what it was; we let me just tell you what the results were in this group of men—if they had a longer anogenital distance, they had a higher sperm count.

**Huberman:** So you were correlating those two measures.

**Dr. Swan:** Right!

If we wanted to say something about—we didn’t try to say anything about how it was when they were born; we just said, “Okay, we’ll take that assumption that this reflects their early AGD.”

So it's easy to say AGD is related to sperm count, because we measured that, and we saw that correlation. That’s published; okay? If we want to say their early AGD at birth and their sperm count—that's a leap of faith in some sense because we don’t have their early measurements.

For these guys in Rochester, we didn’t measure their AGD. Were there conditions of being a participant in the study such as refraining from alcohol, cannabis, etc. in the 90 days prior? This being the duration of spermatogenesis?

I don't remember that; these are college students, so presumably some of them are drinkers. Okay, so but in the end, it was a robust link.

Then, Mike Eisenberg, who you might know—my colleague at Stanford—he's been on this podcast. He’s a colleague of mine too, and he looked at men in infertility clinics and those who had born children and those who had not.

Those who had born children had a longer anogenital distance than men who had never born a child but were trying, yes.

**Huberman:** Right!

These were not people who opted out; these were people who were having challenges with fertility versus success—

By the way, you know, the question of how you measure AGD in an adult man is different than how you measure it in a newborn, and we did a lot of work on that.

Michael helped with that too, so it sounds like…

Oh, and may I ask, were the sperm counts that were on the, let’s just say, the lower quartile—were the “lower sperm counts,” like functionally lower?

Because I always wonder about this. It’s come up in a number of discussions, like with Robert Sapolsky, Mike Eisenberg, and now I’m asking you: When we hear that sperm counts are going down, are they going down to the point where fertility is impacted? That’s really the question.

So, I’m going to—I hate to put you on the spot—but let’s lay aside the question of AGD for a second.

**Dr. Swan:** Right, that’s really interesting!

**Huberman:** But let’s talk about sperm count.

**Dr. Swan:** If you look at a beautiful study among pregnancy planners out of Denmark, quite a long time ago, they took couples that were trying to conceive—that had never or not recently—I can’t remember—used oral contraceptives, and then they saw what the sperm count was and how long it took them to conceive, the time to pregnancy, in relation to—and what they showed is a really interesting curve, which has never been corrected to my knowledge.

So, it’s what I use and think people use, which is if you—I wish I could draw it here. I wish I had a board, a whiteboard. The problem is a lot of people are listening—but you might think about it.

So just think about a curve where you go all the way down to zero—that would be no sperm—and then as the probability of conceiving is zero—you’re looking at sperm count along the x-axis and months to conception.

What you see is that if you have no sperm, you don’t have conception. If you go up to around 40-45 million per milliliter, and this is million per milliliter—so just pure concentration, not the number of motile sperm—that’s just how many sperm.

We’re not talking about quality; we’re talking about number, and when you have 45 to 50 million per milliliter and below, it matters a lot what your sperm count is.

You know, people say it doesn’t matter? Yeah, if you get in this range where the probability of conception is dropping off really rapidly, it matters a lot.

Then around 45 to 50, it starts to level off, and then after that—after certainly after 100, probably 75—it doesn’t matter at all.

**Huberman:** So, 100 million sperm per milliliter?

**Dr. Swan:** Yes! So can you see this? So when people say, “Does sperm count matter for fertility?” Yes, it matters a lot if it’s low, and no, it doesn’t matter at all if it’s high.

So you just—as nature runs a probability game, overproduced sperm, right? Some of those will be high quality; some will be low quality, depending on their age when they were generated or their conditions—heat exposure, etc.

So nature runs a probability game that’s hoping that the best quality sperm will fertilize the egg.

**Huberman:** Right!

So below 45 million per milliliter, the sperm count really matters; it drops off precipitously.

**Dr. Swan:** That’s right!

Once you get up to 75 to 100 million per milliliter of sperm, then it's all good to go.

**Huberman:** Right!

Sperm counts range anywhere from, you know, it could be low 8-10 million per milliliter in the very low situation; it could be zero in some people, right?

All the way up to 400, yeah, million.

**Dr. Swan:** That's right; there’s a huge range.

That’s a function of age, it’s a function of genetics, it’s a function of, presumably, phthalate exposure.

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**Dr. Swan:** We were onto the fact that sperm counts are dropping, and there's a relationship to anogenital distance. There’s a relationship between anogenital distance and phthalate exposure.

Then I asked the question: If sperm counts are dropping, but are they functionally relevant? Is that one of the reasons why fertility is dropping? We’ve also got the female side, where we've got women with elevated androgens.

So we can talk about that a little bit later.

And then, of course, we have the socio-biology piece, where people are opting out or it’s also economics in some cases—opting out of having kids.

Let’s go back to sperm count, because we haven’t really talked about that. It’s a kind of a different path. My introduction to phthalates was not through sperm count, right? It was through this question my colleague asked me: “You should look at this,” and I looked, and that was a really, really interesting journey that I went on.

But there was a separate journey that I was on, and that started in the late 1990s when I was asked to join a committee of the National Academy of Sciences. That committee was assembled to look at the question of whether hormonally active chemicals—endocrine-disrupting chemicals—in the environment posed a threat to human health.

At that time, it was like: “Well, yeah, we hear about this, but should we care?” That committee wanted to consider a study that had come out of Denmark a few years earlier, which claimed that sperm count had dropped 50% in 50 years.

**Huberman:** Wow, that’s a huge drop.

**Dr. Swan:** That's what we're seeing now—worse than that, by the way.

They said to me, I was the only statistician on the panel, “Would you look at this and see if we need to consider this in our deliberations?” And as I mentioned, I’m skeptical.

I looked at it and thought, “I don’t think so.” That was my initial reaction. First of all, I didn’t know who had written this; I just saw it in a journal. It was not very big and didn’t have very many figures or very much data.

That was a big claim for a little paper, you know? But I'll look at it because it’s important.

What I did then was think about all the factors we epidemiologists call confounders—things that might have caused that decline if it wasn’t real or biological.

So we could think of some of them together—maybe the methods of counting sperm had changed, so that later methods counted fewer sperm in the same sample. That’s certainly possible, right?

But it turned out that wasn’t the case because they actually had all used the same method. Maybe the men had changed, so maybe there’s a—you can’t get a sperm count at random; you have to get somebody to volunteer.

So who were these men? Were they very different? You know, in the early part of the study and the late part of the study in a way that maybe in the late part of the study there were men with lower sperm count and they were more concerned; maybe they were more obese.

That’s pretty plausible. Obesity is related to sperm count and fertility.

So what I did was get the 61 studies, go through them, and try to extract information on all the factors that could explain the decline. I created a multivariable model and ran that model, and to my astonishment when I was done, the slope of the decline was exactly the same to the first decimal place.

It had not explained anything, and I was like, “Oh my God. This looks like it might be real.”

And for those listening, what Dr. Swan is describing is being the excellent scientist that she is. She went and looked for all the things that could impact the result that were not related to what the main conclusion seemed to be, which is that sperm counts were going down over time.

And this is really important because I think what we’re talking about here in parallel to the main conversation is how to do really great science, especially in human populations that are out there living—some of these men probably smoke some cannabis.

I’m not saying that reduces sperm count; it might reduce sperm motility; however, we covered that in the podcast.

Now all the cannabis folks go, “Well, so-and-so got so-and-so pregnant when they were doing a lot of weed.” I always say, “Okay, well, there are a number of other factors, right?”

You know, frequency of ejaculation, the requirement to abstain for 48 to 72 hours, up to five days prior, etc.—all of these factors that men may or may not faithfully report.

But you assume that if some are telling the truth and some aren’t, then there’s an equal distribution of that.

So all the different things, right?

This is very different than looking at, for instance, ovarian reserves, like the number of eggs, where you use ultrasound and you use AMH (anti-Müllerian hormone) levels.

Sure, things can impact that, but it’s a little different than taking sperm counts.

**Dr. Swan:** So thank you for doing these studies so carefully and for repeating them so many times. Many of the studies that you’ve done are extensive; you’ve done follow-up on these sperm count studies across multiple years.

As you said, the first study was in 1992; then you did one in 2017; then there was one again. I noticed online there was an update.

So you are extremely thorough, and it probably reflects your early training in math and statistics and probability theory—you're not someone to just go in and go, “Oh, yeah.”

Like, if these people that eat a few too much of this, then there's a little bit less of that. I just wanted to say that.

If today’s discussion feels like we're really laying through this, that’s intentional, and it’s important for people to hear that claims like these are not the sort of thing that people make.

They make them all over the board, but work like this needs to be done with an extremely meticulous eye and consideration of all the variables.

**Dr. Swan:** Well, good scientific method!

I would say, especially with human epidemiological work, because of the number of potential confounding variables, right?

So when I saw that and actually did another study to select my own studies and not accept her 61 studies that Elizabeth Carlson had published, so new studies came up to more recent times and went back further—did it again and found exactly the same thing.

So there were three looks at that, and I thought, “Okay, I’m going to accept this; now this is sperm count is declining.”

Why? Okay, now we hadn’t said anything about why; we just said: Is it doing that? Yes.

Okay, if now we believe it is declining, why? So then I thought quite a lot, and talked to people and ruled out genetics, because it was too fast.

It’s two generations; it’s too fast: 50 years, two generations. So if it’s not genetics, then it’s the environment.

So what is it about the environment that could do this? So I asked, “Okay, in the environment, there could be things that are making sperm decline.”

If you think about how you might look at that, you might design the study that I designed next, which was another study. And, by the way, this preceded the AGD study.

So just note that. We had four cities in the United States that we picked with different environments, and then we got men to come in.

We used the same equipment at each place; we used the same method of selecting the men. The technicians were trained centrally at UC Davis.

We had very good quality control—so samples were sent around every quarter to make sure that everybody was measuring things the same way.

We didn’t want drift, right? Then we got their urine, and that’s how I had those urine samples.

So if you wanted to do this study and you wanted to get a representative sample of men, where would you go? Because you can’t—I can’t ask a guy in the street to give me a semen sample.

It’s not something you get very—you know? So I thought, “How can I get a representative sample, which would teach me something about a larger population called the parent population.”

So here’s a sample; it should represent the parent. So how do I ensure that?

I decided to sample the partners of pregnant women because pregnant women all come to medical care—almost all—and if their partners will give a semen sample, then we have a representative sample.

We know what we’re looking at. So that’s what we did.

**Huberman:** This is the semen study?

**Dr. Swan:** Yes, this is the study of partners of pregnant women.

And, of course, they’ll have slightly higher semen quality because they got their partner pregnant. But, we had their urine; we had their blood, and we looked at their semen quality.

Then we decided to look at pesticides, and the reason we look at pesticides was because there was a lot of gradation across our four centers in pesticide use.

What we found was really extraordinary: that men who were living in Central Missouri, where I was living at the time, who were in the middle of an agricultural belt where there was spraying all the time—soybeans and so on—those men had half as many moving sperm as men in Minneapolis.

**Huberman:** Whoa! Whoa! Huge!

**Dr. Swan:** Right! Then we went one step further, and within Missouri, we looked at a sample of men who had very high sperm parameters and very low sperm parameters.

We showed that five pesticides were significantly higher in the men with the low sperm parameters, which included motility and morphology.

**Huberman:** You mentioned soybeans; what other types of crops?

**Dr. Swan:** I don't remember; I don’t know.

**Huberman:** Okay, so not just the crops, but we're not talking about eating corn and soybeans; we're talking about living in an area where pesticides are being used.

**Dr. Swan:** Yes; we didn’t go into how they got these; we just looked in their urine, and these were the metabolites.

You don’t get in their urine unless they were exposed—exposed through the air or exposed by eating corn and soybeans; we don’t know.

We don’t know, but this was not a particularly—you know, we didn’t sample farmers only or anything like that.

Whoever came into the—remember how we got these men? Their wives were pregnant; they were having prenatal care at the University of Missouri, so that’s where we got them.

**Huberman:** Whoever happened to come in to the prenatal clinic and agreed to be in our study became the male… Their urine was measured for these pesticides.

I’m sure a number of people, including myself, are wondering: In what other products are these five pesticides present?

Are these commonly used pesticides, or is it something about…?

They’re called the “the ‘active’ pesticides;” one of these—atrazine is one of the most widely used and it has huge use around the world; I mean it’s one of the largest commercial pesticides.

**Huberman:** A relevant theme there would be: maybe we could take a moment and talk about atrazine and its effect on male sexual behavior in amphibians.

**Dr. Swan:** Absolutely.

When I was a graduate student at UC Berkeley, I had the wonderful experience of taking a course from Tyrone Hayes, who is a wonderful researcher. He established a link through his research between atrazine exposure and male sexual behavior of amphibians.

Yes, could you elaborate on that result?

**Dr. Swan:** Tyrone first caught frogs in the wild in environments that were more or less exposed to atrazine and showed effects on development and sexual behavior.

Then, in his lab, he actually exposed them. So, he knew exactly who was exposed and how much, and he showed that—and I can’t tell you what percent or what—you know, but a significant number of frogs exposed to this pesticide atrazine chose to mate with other male frogs.

They tried to mate with other male frogs—presumably unsuccessfully, well, they mounted them.

He has photos of males mounting males, and so presumably this is a neural change that occurred—a neuroendocrine change—but ultimately, neural.

Since mounting behavior is controlled by, actually, we now know—the hypothalamic nuclei that control this—David Anderson, who has been on this podcast, has people in his laboratory that include a former graduate student of mine working on this specific issue of what the circuitry is.

That’s a remarkable result, and it’s been kind of used and misused out there in the media and in popular culture.

But if nothing else, it suggests that the organization of the neural circuits and neuroendocrine pathways that control sexual behavior—in this case, mating behavior—are significantly impacted by this atrazine.

**Dr. Swan:** Yes. And it suggests that there are other environmental chemicals that can do this as well. I don't know how if we’ll have time to go there, but I did work on neurodevelopmental outcomes in relation to prenatal phthalate exposure.

So I think the overarching idea here is that the brain, like the genitals, is sexually dimorphic.

**Huberman:** Absolutely.

There are many people, by the way, who will take offense at that.

**Dr. Swan:** Really?

**Huberman:** Yeah, I think there’s—

I mean, going back to the work of Frank Beach in the psychology department at UC Berkeley, I know he showed this in beagles.

It's been shown in pretty much every species as you know.

But it’s not a better-worse thing; I think people need to hear it; it’s not what it is. Dimorphic does not mean better or worse; it means different.

There are, for example, advantages to spatial reasoning in a male that are related to testosterone.

So, I mean, my understanding of this literature—and I’m not an expert in this particular aspect, which is the behavioral phenotypes—but you know, like the medial preoptic area of the hypothalamus is known to be sexually dimorphic dependent on testosterone converted into estrogen during development, etc., etc.

There’s just so much evidence of this.

How it links to behaviors is, I think, can be reasonably placed into ethologically relevant, evolutionarily logical arguments when talking about rodents or beagles or even rhesus macaque monkeys.

I think where people get a bit inflamed is when people try and take the sexual dimorphisms that have been observed in animal brains—even in human brains—and tack those to specific abilities or lesser abilities.

I think that’s when people sort of go, “Wait a second!”

Then they go, “Well, does that mean she has higher testosterone than him?” and then maybe—and then pretty soon you're in almost at no man’s land, a no-person’s land of confounding variables.

But I really appreciate that you raised this and also that you said it, and I didn’t, because I feel safer that way!

**Dr. Swan:** Yes, there is a very simple outdated questionnaire, and it’s play behavior—it’s called the PSAI (Parent Sex-Atypical Items), it’s been used for years. Have you heard of the Rough and Tumble play?

Yes, yes!

There are 24 questions on there, and they are sex-typical—you could say, “My child likes to play with dolls,” “My child likes to play dress-up,” “My child likes to play rough and tumble,” etc.

We gave that questionnaire to our population and looked at the answers both in our population and in a Swedish population by a colleague there—Carl Borag and Gustaf Borag.

What we found is that higher phthalate levels—these anti-androgenic phthalates—were associated with less masculine male-typical play in our male boys.

So this is exposure, right?

So this is association, but these boys weren't tested; so yes!

So this is interesting!

So this is a super interesting area of work because it leads you from anogenital distance into behavioral measures, and so far we can make associations only—but these associations, obviously, are going to make a lot of people insecure!

Let’s not dwell on what's happening now; let’s focus on what we can do to reduce those outcomes.

**Huberman:** I agree!

So I think now is a really important time to be having this discussion because there’s been a lot of movement on Capitol Hill and a lot of movement on social media, and there has been a lot of focus on trying to call attention to metabolic syndromes and highly processed foods and issues like this, and it’s become, unfortunately, politicized.

I mean, I hear this stuff, and I think to myself, the only good faith that we can really trust is our own desire to be healthier.

To have our families and friends be healthier, and to try to consume and not consume things on the basis of that.

My belief is that we can’t trust any larger agency to either protect or harm us. It’s like they’re going to do what they're going to do; we just have to be informed instead of trying to disassemble the systems that led to this, which just seems infinitely complicated.

Maybe you can do that, but I’m far less optimistic. Now that I’m 49 years old, I can say things like this.

But what you're saying is really important. If I look at a can and it says “BPA-free,” that doesn’t mean anything; it could have BPS or other endocrine disruptors.

So, drinking out of glass vessels, drinking out of ceramic vessels, metal mugs… is it true that "microwave-safe" means it just means that the plastic won’t melt in the microwave—but you should never put plastic in a microwave?

**Dr. Swan:** So here’s the story: The BPA and phthalates are plasticizers added to the plastic, but they’re not chemically bound to it.

If you put anything in a container that has these chemicals in it and then put it in a hot environment, they will come out of the plastic and go into the food.

If you do that in a microwave or if you put your bottle in the car and the sun comes in and it warms up the bottle, then the stuff goes into your water—you don’t want to mix these chemicals into for your food.

But if you do, the worst thing is to do it in a heated environment.

**Huberman:** I think about all the food that was consumed in college in the 90s and 2000s, like the cup of noodles—it’s a huge change!

And frankly, food cooked in plastic packaging too—is pretty straightforward to eliminate once one understands and decides.

Then we start getting into the more nuanced thing of like, “Okay, you can buy a really nice tasting, anyway, organic grass-fed steak, but it's wrapped in plastic!”

Or you can go to the butcher, but most people don’t have time to go to the butcher, or you can get strawberries at the farmer’s market, blueberries at the farmer’s market, which is what I try to do; but sometimes I buy strawberries at the market and they have those plastic flip-top things and, of course, I recycle the plastic—how bad is it if you rinse the strawberries off with good, clean water that were in the plastic container?

**Dr. Swan:** We have to do that experiment—I don't know!

So, I guess it sounds to me like not drinking out of cans, not drinking out of plastic bottles is going to be the first step.

Not microwaving plastic ever, and, in general, just avoiding plastic intake if you can afford it.

Buy organic, because you’re going to avoid the pesticides, and you know phthalates are actually added to pesticides, and they’re added because they increase absorption.

So you know… the...

**Huberman:** How are pesticides tested for exposure levels?

**Dr. Swan:**You can measure the metabolites and see that.

There are a number of different methodologies that scientists use.

Of course, that's usually done in studies—but I wish it was paired with super intense educational campaigns regarding tested levels.

Getting back to substances like phthalates, there are many that can affect males that are not tested, and for which exposure level is not properly noted.

We also know that stress is a significant area; researchers can show that extreme stress can deplete Androgens or testosterone in females, leading to higher estrogen levels—bear in mind you must control for this variable too.

The more people can become educated on this, the better our public health environment can be in understanding these underlying causes and remedies, and perhaps physicians can advocate for lifestyle changes and responsibility in their patients that can lead to significantly better health options and reproductive health overall!

You want your pesticides to get into the plant right and to kill the bad stuff, and insects. So, the same property of phthalates that makes them good for pesticides also makes them good for our hand cream. Just mentioning absorption—anything that's absorbed in the body is going to have phthalates in it. It also holds scent and color, so it's added to those scents, and it's also added to your lipstick and to your colored, you know, whatever you put on your face, and so on. Anything that holds scent and color, that's going to be th—

Um, sorry, I've been accused online of being a sunscreen truther. I'm not a sunscreen truther. I'm going to keep repeating this as many times as I can. I understand that UV damage to the skin can cause certain cancers. I get that. I agree with that. The data are pretty clear to me based on having researched this pretty extensively and talked to many, many people, including dermatology oncologists, that mineral-based sunscreens, like zinc oxide and titanium dioxide— but certainly zinc oxide—are safer than the chemical sunscreens.

A lot of people get upset when I say that and they say, “Well, in Europe there's tons of evidence that the chemical-based sunscreens are safe.” Okay, fine. You use them. I'm not going to. The point being that UV damage is bad. There are ways to protect ourselves from the sun—including physical barriers like clothing, hats, etc.—but pretty much all sunscreen that I'm aware of is designed to be absorbed.

So what do we do if we want to get some UV protection from whatever kind of sunscreen we deem safe for ourselves, but we want to avoid these exposures to these other things? What do we do? Do we have to hunt really carefully for the right sunscreen?

Yeah, I think that's a good idea. Are you familiar with the Environmental Working Group?

Uh, is another one out of the Bay Area.

No.

Oh, okay. I don't know actually where they are. They're pretty big.

Sounds familiar, but I'm not—I can't say I'm familiar with—

They have consumer guides, and in those consumer guides, you can put in the product. They have categories. You can put sunscreen. If we had time we could do it right now—but, and then you can put the name of your sunscreen, and it'll give you a number. If the number is less than 10, it'll tell you why—

Are they independent of any, like, funding?

That question will probably come up for you too. Um, people will say, “Where did she get her funding?” You know, people get very suspicious about this; I can tell you.

Yeah, that would be great.

Yeah, so I am a tenured professor at Mount Sinai—get some salary there because I'm only part-time—and I have a funder, one funder, who funded my sperm decline analysis and the publicity of my book. So he's a, he's a foundation—I won't say—philanthropy.

Yes, philanthropy.

Yeah, and it's actually not a lot of money, so no. And so there's no reason to think that anything that you're telling us is linked to, like, the food industry or an alternative product or anything.

I'm very, very careful not to endorse any product because I don't want that complication.

Yeah, thanks for clarifying that. I wasn't suspicious, but um, I think nowadays people have just been taught to—you know—appropriately so—they've been taught to say, “Well, wait, where does this funding come from?” Because a lot of the studies about that led to the food pyramid, for instance, people were under the impression that somehow that was biased by companies that were funding the work.

And I don't know. I haven't done the forensics on that. I don't have the time or the energy.

All I know is that, when it comes to what people eat, when it comes to what people put on their body, it becomes a very personal thing and it's woven in with a lot of—um—psychological and emotional issues.

Yeah, okay. Um, what are a few things that you do and/or avoid in light of what you know about these endocrine disruptors? And by the way, it goes without saying that you're in spectacular cognitive and physical shape for any age, but it's really remarkable.

I feel comfortable sharing this because someone else published it online recently—you are soon to enjoy your what birthday?

89th.

89th birthday? Amazing!

And um, with all the talk about longevity, cognitive and physical longevity, everyone's thinking—including me—like, what does she do? Well, she avoids all these endocrine disruptors, and she has a wonderfully rich life of curiosity and other things.

But yeah, what are some other things that you do and avoid in light of what you know, for which there may or may not be a controlled study? But I think we're all just curious.

We'll frame this as what you do.

So, water. I worry about the water. I studied water for a long time in my past life, so we actually distill our water. We have a tabletop distiller. My husband, Steven, cleans it out. There's a lot of gunk in it, by the way, even though it's San Francisco that has clean water. At the end of the day, after you've distilled the water, there's a lot of gunk.

So you distill the water?

So this is not reverse osmosis, distilling.

Okay.

Yeah, so it's steamed distilled, and then it condenses in a glass container, and then we put that in glass containers in the fridge.

And it tastes really good, by the way. Really, really... Someone was just over and he said, “This tastes like melted snow.” I thought it was lovely.

And you use that for drinking, for coffee, for tea, for cooking too?

If you make rice, you're using distilled?

Actually, no. No, but for ice cubes and, you know, whenever I can think about it—we can't use too much 'cause we'd be too busy always—but he does it once a day. That it's just the two of us. So water is important.

Um, we try to leave our shoes at the door.

Tell me about that one.

Well, dust that you bring in contains a lot of the particularly the phthalate chemicals. And so that's actually—I'm not 100% good on that, but we try to do that.

Um, and I'm careful with the products I put on my face. I check them out the way I suggested, you know, Environmental Working Group.

Um, and I go to the farmers' market. I always buy organic. Always buy organic.

Um, but I know that's a cost issue for some people and an availability issue for some people. But in San Francisco, you can do that.

Um, some areas where I don't do more of what I should—I think I'm starting to be aware of the chemicals in clothing. We haven't talked about that, but there's—turns out there's a lot, particularly in—it’s a problem for workout wear because you're absorbing so much, you're sweaty, you're hot, and you're bringing these chemicals into your body.

And that may be one of the interventions that we do—get a bunch of athletes to use safe clothing and traditional clothing and see what their body burden is. That's how you know.

So, um, airing toward cotton as opposed to synthetic material?

Right. Right. And the dyes are important, so you don't want— you want maybe plant-based dyes. It's not my area of expertise. I have a colleague who I work with on this, and I'll go with her advice.

But, um, I'm just saying that's another area that I think people will soon be paying attention to.

Um, there's also the area that is much more difficult, which is what's in building materials and furniture.

But, um, a lot of these phthalates and the toxins are in our furniture and in our building materials.

And trying to think about how to build—I was asked about safety in a new village that's being built in California, by the way—and um, it's really challenging to think about if you were going to do this right, and you were going to build a town that was toxic-free, how would you do that?

I'm thinking about that—I'm thinking about the opener of The Simpsons and doing the exact opposite.

Where, like, in the opener of The Simpsons there's like a three-eyed fish, and there's the chemical plant—and I'm just thinking. You just look at the opener of The Simpsons, you do the inverse of everything that's there, the inverse of everything that's there, including alcohol intake, um, you know, which is robust on The Simpsons.

Yeah, right. But, um, interesting.

So, when it comes to food sourcing, like, non-fruit, non-vegetable food sourcing, is there anything we can do? I mean it's so hard for people to get eggs from farms—I mean, you can if you go to a farmers’ market, but this stuff can get pretty tricky, pretty expensive, and most people listening are not going to be, you know, living in Sonoma where they might have a neighbor that has chickens or something.

Um, it's a hard problem.

It is a hard problem. And I think maybe people asking for it more would help.

I don't know. I mean, in San Francisco I'm lucky because I can just get, you know, just on the phone, Fresh Direct, order the and I know it's okay.

Um, but I know that's not the case everywhere.

So, um, I think being aware, honestly, is a really big step. If you're aware that this is something you want to change, you will find ways to change it.

It's interesting because a few years back there was a lot of discussion about dyes in children's toys in particular—

Toys from overseas, right?

Remember, kids are not, you know, babies are always gnawing on stuff and teething and there was a lot of attention, like, “Hey, like what's in these sippy cups?”

And my understanding is, uh, toys and sippy cups—and my understanding is that BPAs were banned from sippy cups—

Excuse me, based on my work.

Based on your work. Thank you so much for the clarification, truly.

And for the work that led to that.

Um, we have this—you know—um, innate, thankfully innate reflex to protect our young, as does every—most every species.

Thank goodness. And we know that baby skin is more absorbent than older skin. We know.

And so there are literally laws in place and restrictions in place to make sure that some of this stuff is minimized in young kids.

But then we sort of, after age 12, we're kind of like: “Okay, well, it's a free-for-all. It depends on your budget where you go.”

And so we can't rely on governing bodies to do this.

But I think it's a useful conversation, especially given your relationship to Scandinavia, which is a fun one to elaborate on to illustrate some of the discrepancy between the US and Europe.

What sorts of chemicals are banned in Europe—in food, in lotion, etc.—that you're aware of that are prominent here in the US?

Maybe that's a good filter to place some of this choice-making through.

Europe has a policy called REACH, and under REACH, you have to show that a chemical is safe before it's put into the marketplace.

Not so!

What the way our system is here is put in the marketplace and then if somebody gets worried about it, they might do a study, they might find harm.

Remember how long it took me to find that phthalate connection? It was 10 years, two studies, 10 million dollars, by the way. So if you're going to wait for that—I don’t know what, you know, given the number of chemicals out there, 80,000 or more—forget it!

You know, so I think the REACH policy of testing before something's put in the market is making a big difference in Europe, and that's—I think that's one reason why they're much better off.

Are those animal tests?

Um, or animal and human tests that they're doing over there?

Whatever defines safety. It depends on the chemical; it depends on, you know, what the product is—I can't answer that in general, but...

So that'd be a good avenue for changing legislature here, right? To install something similar to REACH?

Absolutely, but it's not going to happen. I don't think.

No, no, because there's too many forces against that.

It's very, very hard for manufacturers to make changes.

I'll give you one example, um, so you know that. You might not know, but should know that phthalates are very prevalent in the hospital setting.

If you think of a tube, you know, for dialysis, for chemotherapy, for IV—it's all phthalates, right? And that's going into your body.

And there was a recent bill passed in California that DEHP could not be in IV bags.

It's fantastic!

Success in the actual bag?

Yes, the bags could not contain these endocrine disruptors—not DEHP specifically, di-2-ethylhexyl phthalate, the most anti-androgenic phthalate.

So, so that was a great step for—but that's like one chemical, right, in one product, and that was a battle.

So you see how hard it is to do this?

Extremely hard.

There's a company I'll give you, BBRW, which makes hospital products, and they are very forward-thinking.

And they set up a factory in Florida to make alternative IV bags out of another product, um, polyolefin, and the problem is that we're not sure about the safety of polyphenols.

So it gets really difficult. You know, you can say, “Remove DEHP,” but now we scientists have to say, “What does it mean for a chemical to be safe?” And we don't know that.

I don't mean to disillusion you and your listeners; you know, that's a huge challenge that we're up against.

We know it's safer; we know it's safer. And we know what the bad actors are, and we know things we don't want to be exposed to, but we have to be careful when we think about what do we want to put in instead.

Is that?

Yeah, yeah.

I’m thinking about this—um, a former president of Stanford who was also, happened to be a family friend years ago.

Um, he has since passed, Don Kennedy. When he retired as president of Stanford, I think he ended up directing the FDA.

And I was just thinking to myself, like, um, when did this happen?

Um, because I know he was super into health. He was like an avid runner. He was very fit, well into his 70s.

Yeah. Hip replacement, kept running, or maybe it was knee replacement—I don’t know. The guy was obsessed with health, and so I don't think that, um, there’s, there’s a lack of interest in health at the level of things like the FDA, and um, but there’s clearly a problem.

And I'm just trying to think of solutions, and it seems to all boil down to what we can take control of in our home.

Like when we go to a restaurant, it’s challenging to know like what they’re doing in the kitchen, and at some point it becomes neurotic to, you know, although I know people that won’t go to restaurants where they use seed oils.

There’s this whole new thing cropping up about avoiding seed oils, um, but maybe they're more significant issues—who knows?

Um, the seed oil crowd is pretty, pretty intense.

Um, and I like olive oil anyway, so I air to that.

But I think if people are interested in limiting their exposure to these endocrine disruptors, one of the key questions that's going to come up again and again, especially in light of PCOS and sperm counts, is we can't control what happened to us during pregnancy, right?

But once we have some sense of agency over what we put into our body and how we put it into our body, do you think there's a, um, that there's, um, plasticity and resilience to this system?

So you know, God forbid, if somebody was exposed to a lot of these things early on, can they, you know, by making changes, can they rescue themselves to any degree?

No!

So it's really just dependent on what your parents did?

Yes!

That's not to say that your own exposure cannot change things further and make things worse.

But here’s a, here’s a fact: if a male’s mother smokes when he’s in the womb, then he has a—this is a Danish study, by the way—50% reduction in sperm count if his mother smoked while he was in the womb.

How much smoking are we talking?

I don’t know. I don’t remember.

But the reason I bring this up is because there’s nothing he can do to change that.

Okay, if he smokes as an adult, he has, I think, a similar reduction in the sperm count. He can stop and his sperm will be restored; he can get a sperm health back.

But whatever happened in the womb stays in the womb, if you will. It’s developmental—it’s not going to, you know, it's going to be there for life, and that's true of the brain as well.

So, um, I think anybody who's thinking of conceiving a pregnancy or pregnant has a responsibility to really learn how to reduce their exposure because these things are, by the way, passed on for several generations.

It's your child and your child’s child because the germ cells for your grandchild are going to be carried within your child.

So germ cell are, um, not germs as in infectious germs; it's the cells that will produce the egg and sperm that germinate—hence the word germ, right?

So it's a huge responsibility, and I think people should take it very seriously that they have, you know, they're going to be affecting the health of subsequent generations.

Some labs say it's seven generations; I don’t know if that’s true, but certainly three generations are affected.

Um, so I should mention my book.

Can I mention?

Please! I'll mention, yeah. I believe I mentioned it in my introduction, but yeah, please!

So in Countdown—two words, by the way, because if you say Countdown one word, you won't find it—but Countdown, we have two chapters on things you can do, very practical things you can do, and also websites you can go to and links you can go to.

Now, this came out in, um, a while ago—2021—so there are many more things now, but I think it's a good start.

How lonely are you in this expedition of identifying endocrine disruptors in food, in pesticides, in, um, in the sorts of things you're talking about? Like, is there a whole field of this—of, um, excellent people? Are you a small team of people that are against the grain?

I mean, I confess I don't know many people doing the sorts of work that you're doing, but I—you know—you're the most public-facing and prominent, and I—my question is like, is the NIH funding a lot of this sort of thing?

Absolutely! We're an army. And it's not—it’s international.

And there is now a global, um, plastics treaty under negotiation, by the way.

Tell us about the plastics treaty!

People are trying to create, get paid by various countries, um, an international plastics treaty.

I can't—I don't want to talk a lot about it; I'm not involved in that process.

But in the process, you—if you looked into it—there are hundreds of scientists and concerned citizens and activists, and you know—people in legislation who are working specifically on the chemicals in plastic.

Now, plastic is really a bad actor, I—but it is not the only bad actor.

So I want to just mention that plastic is really important, but you know pesticides are not plastic and so on.

So there are many other classes that you have to worry about.

But certainly controlling our exposure to plastic is huge, and, um... though you asked about scientists in this area—yes, there’s a huge amount of science going on for this—in this.

There’s—and it's funded by NIH and it's funded by, um, the EU—and, um, primarily, I think those are the two funders.

Scandinavia has funding in, you know, in Scandinavian countries.

So there's a lot of work and a lot of very good people working really hard, but it's a huge problem and it's been here since—well, plastic started to rise in popularity in 1950.

So we have like 75 years to battle against, and it's not going down anytime soon!

Lifespan is increasing pretty significantly, presumably in large part because of the reduction in smoking, um, and control of infectious diseases—

Control of infectious diseases.

Um, but lifespan is definitely increasing, um, whereas the use of plastics has clearly increased.

And so, uh, I guess one could argue that we're living longer, but we are less robust than we were.

Less, um, reproductively competent?

Is that, uh—the people that are reflected in that longer lifespan were not necessarily exposed early in life, which is when it's most critical.

So, you know, I was born in 1936; there was no plastic then!

There was no, you know, um, and there were other things, of course, but not as they are today.

So, um, I don't think that you can make the inference that because we're living longer, plastic growth— you know, the growth of the plastics industry is somehow driving that longevity.

Absolutely not!

Absolutely not! I think what it's driving is a decrease in fertility.

And what's happening is that the shift in populations is pretty dramatic.

We're getting—you know, the pyramid used to be like this—I'm making a triangle with my arms, showing very few people on top and a lot of people on the bottom—but what's happening is that that's getting inverted.

So we're getting more and more people on top and fewer and fewer people on the bottom.

Birth rates are way down!

Birth rates are way down!

And this is an enormous problem for societies because the people in that small support group at the bottom can't drive the society to support the large growth on top.

You see what I'm saying?

Is this true in other countries as well?

Yes! Absolutely!

It's all over the world!

And the decline in fertility, in my mind, is probably one of the biggest challenges we're facing now because, um, it's everywhere.

It's very acute and there's only limited things we can do to counter it.

Um, there's a wonderful website called, it's by the World Bank, put out by the World Bank, it's called Fertility Data.

And if you go in there, you can see what is the fertility rate every year.

But you can plug in, you know, a country or a year or a—you can see what the fertility rate in each country in the world each year.

And you can see that, and what you see is that, um, a decline about the same rate as sperm decline, by the way, about 50% in 50 years.

And, um, the critical point for fertility is two.

So what's that mean?

That's called replacement!

And that's two people replace themselves with a total fertility rate of two—actually 2.1 because you have a little bit of loss, but 2.1, you're good to go!

A society, when you fall below that, you're shrinking, and there are many countries in the world that are below that, including the United States.

And for example, the worst I've seen is actually South Korea, which is at 0.78.

Wow.

Japan is at one.

Wow!

So large parts of the world are just not replacing themselves.

And why that is is maybe another discussion, but—or we can talk about it; I don't know if you want to go into that.

But um, it's not just sperm count, for sure.

Yeah. Along those lines, let's talk about egg count and quality.

Uh, you mentioned the PCOS results earlier.

Um, before we were on mic, uh, you mentioned an interesting study that you did about the use of electric blankets, um, and assessing whether or not the use of electric blankets had impacted, um, egg number or quality in women.

And the answer was—

What we looked at in women—I'm sorry to correct you—but was the outcome of their pregnancy, their fertility, and if they got pregnant, how did that turn out?

Excuse me, so thank you for that clarification.

But, um, I’m sure there’ll be a lot of other studies that have looked at that.

You know, I just have been away from that field for a long time, but so far, I don't see convincing evidence that the use of cell phones or, um, you know, other exposures to electromagnetic radiation are affecting our pregnancies and our fertility.

That's not to say it's not happening, but I have not looked at it, and I don't like to make statements about things I haven't looked at.

My understanding of the cell phone data, uh, for sperm count and motility, aka quality, um, is—I discussed a meta-analysis covering this on the podcast previously—is that there are some heat effects of cell phone use and keeping the phone in the pocket that may—that may, I want to be careful here—impact, um, sperm count and motility, uh, quality.

But, um, direct effects of EMFs on sperm, there's no evidence that it is disrupting sperm, at least to my knowledge.

I honestly—I have to say, just going to say I don’t know.

But I do know that, um, heat is related to fertility and sperm count.

Right! And, um, you can look at the birth rates as a function of the month of conception, and you can see that, for example, in warm months, in warm climates, uh, there’s less—yeah!

So the heat does play a role! But how much that’s tied to cell phone use, I think that’s something that’s now under investigation by a lot of groups and, um, we’ll see what they find.

Yeah, the data on sitting more than a few hours a day on, um, having legs that are very large as a consequence of obesity or even just legs that are large—uh, heating the the scrotum—those data are fairly, um, I would say solid in terms of the relationship to reducing sperm count.

Heat is not good for sperm, which is why the scrotum has its, um, the features that it does to move the the testicles further or, um, closer to the body.

Um, getting back to egg, um, egg count and quality, there's some evidence that, um, girls are entering puberty earlier, um, but that women are also undergoing perimenopause and menopause earlier.

Do we know what that is the consequence of?

There are several new papers, actually, on the menopausal age, showing relation to a number of chemicals, but I can't quote them to you right now.

I don't remember which class it was that they looked at.

But, um, I think that's right. I think there is growing evidence that earlier—you know, fewer—it's also called premature ovarian failure—

Um, so that women are just not producing the eggs as long as they used to.

Yeah, but um [Music].

Um, the—I just want to say something about the fertility.

Can we go back to fertility, please?

Um, so when this comes up—and I'm sure you've seen the literature—there's a lot of literature on this that say fertility is going down, you know?

Fewer children are being born. People say, “Well, that's a good thing because it's less of a load on the planet,” which is another discussion.

And then they say, “Well, this is due to choice, that people are choosing to have fewer children, and they're choosing to, um, delay childbearing till they're no longer as fertile.”

Uh, they're using more contraception; women are more educated, they're entering the workforce—all of these social factors are given as the reason for decline in fertility.

And, um, I just need to point out whenever I hear this that it’s not just human fertility that's declining.

The number of species that are becoming extinct is increasing rapidly.

And there have been for at least 40 years evidence that those pesticides that affect us are affecting animals as well.

And, um, so the decline in fertility in non-human species cannot be attributed to delayed childbearing or use of contraception.

Right, right!

And it's interesting because, um, we hear—we usually hear first about species that are about to go extinct, that are badly endangered.

I don't know what the proper language is, but is about to go extinct, um, like the Florida panther, right?

Or, you know, we hear that, you know, there are—there are a very small subset of them left.

Uh, the black-footed ferrets in Montana, I think, one ferret—the name is, um, Scarface, SED?

Something like 300 left!

Then they led to the EV—they started out, um, outbreeding because if you do too much inbreeding, obviously, it's not good.

And but then they were able to at least partially recover, maybe fully recover those populations.

And people forget the domino effect of these ecosystems when one species is compromised.

Like when the black-footed ferrets—I know it might sound kind of silly, but, um, were compromised in terms of their populations, the prairie dog population went up, the grasses were getting eaten far more, and then there's all these downstream consequences.

You know, I'm not an expert in this, but one doesn't have to be an expert to understand, like, you move one pin here and the whole web moves, and um... and so, or you move one node and the whole web reconfigures.

And, um, that’s what nature has been doing for millions of years, right?

But, um, at some point, it is conceivable—no pun intended—that we are going to be the species on the endangered species list, right?

I mean, that's not like a—an outrageous sci-fi movie, like, right?

Like at some point humans might be added to the endangered species list, with the exception that we have— we’re very clever and so we found a lot of ways to do medically-assisted, you know, conception, right?

IVF—the—the literally you—gentle grabbing of one sperm and forcing it to, um, fertilize the egg, um, is something we've covered on this podcast in our fertility episode with Natalie Crawford in a solo episode that I did.

Um, there are questions that people have reasonable questions about whether or not the, um, the offspring of those types of scenarios are the same as the—the genetic, um, probability experiment, as you mentioned before, of having, you know, 200 million sperm and then letting nature select the one that is most robust in that environment.

Yeah! And you know, the number of technologies is increasing; we're a very clever species.

And, um, for example, I don't know if you've heard of gametogenesis.

So it is now possible to create, um, an embryo from a sperm cell from a skin cell.

A skin cell can produce, um, a sperm cell and an egg cell, and you give it the right transcription factors, and you can, you can—

So this is kind of interesting, exciting, and scary, right?

This is like the, um, what is it? I think the vultures—the females, uh, there's some way in which two female vultures or maybe a single female vulture can create offspring in the absence of a male.

There’s also a three-parent IVF; I don't know if you're aware of this, where this was developed—where there's a mitochondrial disease.

You can take the, uh, two eggs, one from the intended mother—you take the nucleus, so you get the DNA—you put it into an egg of somebody that, um, where the DNA has been removed, but where the spindles, which are rich with mitochondria, are from a typically a much younger host.

And then you use a sperm.

So it's actually three parents: it's the spindle of one mom, the DNA of another mom, and a sperm.

They do this in the UK for mitochondrial disease.

It's still illegal in the United States, as far as I understand.

And it's done in other countries.

Um, and in theory, legal issues must be, yeah.

But in—but in theory this would allow women of any age, provided they still have eggs, um, to have their DNA propagated forward.

Because they could—the DNA can be put into a younger egg that has, um, the spindle quality that allows for, um, you know, the production of more cells.

I mean this canon has been done in humans.

Yeah!

So we're—I mean, you and I won't think of all the things that will be developed, you know, in the next 10, 20 years to meet the challenge of declining fertility by ordinary conception.

I mean, I think that's—that's how we're going to solve this problem for us.

We're going to just be smarter and smarter about how to do medically-assisted um, conception.

And then the question is going to be—and it'll take time to know this—is whether there are effects in the offspring, adverse effects in the offspring.

Um, it’s a little tricky because, for example, if you use the sperm of an infertile couple and you see, let's say, the son is subfertile—that's born that way—but you do it, you know, in a test tube or whatever.

And then you can say, “Well maybe, um, that's because the father was infertile, and he's got inheritance from his father from that...” You see what I’m saying?

So you can't know whether if you see an adverse effect in an offspring—you have to be very careful that it's not something that they've gotten because of problems that led the couple to seek assisted reproduction.

You see?

You follow me?

Yep!

Yeah, um, super challenging, fascinating problem!

So, in anticipation of this sit-down together, uh, I put a question out on X—formerly known as Twitter—um, I let people know that I was hosting an expert in endocrine disruptors, in phthalates and pesticides, reproductive, uh, implications, etc., and I asked for questions.

And they came up with a huge number of excellent questions, many of which you've already answered!

Things like, um, is tap water safe? What can we do to our tap water? You mentioned you distill water.

My understanding is that reverse osmosis, provided there's remineralization—excuse me, difficult word to say—can also be effective, etc.

Um, there were a lot of questions about, um, cosmetics and laundry detergents.

Um, I don't know if we discussed laundry detergents—what do you use in terms of laundry detergent?

Um, or—that is presumably one can find...

I don't even remember!

Okay! Don’t go by my product!

Okay!

For one thing, I'm not going to be pregnant anytime soon.

No! Um, the, uh, I believe there are some solutions, um, related to the—like instead of bleach, people can use hydrogen peroxide!

Can't speak about specific products, actually.

Um, you know, I can tell you who can—you might like to talk to her.

So remember I mentioned Million Marker, the company that did the inventory?

Not the comp—well, they are a company—but um, so they look at—Million Marker, I think you’d be interested, okay?

Yeah!

And the person who runs it, Genoa, is a Chinese American, um, who—and a friend of mine!

And we're going to be writing a grant together, um, and she participated in the film.

So, if you go to Million Marker, you log on, and if you agree to pay whatever it is, $199, I think you send your urine in. They give you a kit, you send your urine in, and they test it for all these things in your urine.

So you know what's in your body.

You might want to think about it, might be interesting.

And then, if you pay another $100, I think, you get this counseling and so blah, blah, blah.

You can see the different levels of—but she knows all about products.

I don't know about products because it’s a moving target—I don’t—and also I don't like to talk about product names because it sounds like I'm endorsing them.

So, um, right, and we won't, um, expect you to give product names and um, I'll follow your recommendation that you just gave.

Um, somebody asked about food dyes—just generally the dyes in foods.

I saw an incredible study recently that Science magazine covered—so Science magazine, very reputable, of course—yellow number five; I forget what the precise name is, but the thing that makes Cheetos really bright—they put it on the bellies of adult mice and it literally makes them translucent!

Oh yeah—I saw that!

You can see the organs!

It’s wild!

It’s so scary!

I sent it to Rogan and he—uh, I won’t—he was like, “Whoa!”

His version of “Whoa...”

I was like, “I also said 'Whoa!'”

He probably said “Holy—” right?

No, he—no, I'm not going to say what he said, but it was—he didn't curse!

There were a number of questions about household items—again, not looking for specific products, but for instance, soaps, body wash, cleaning sprays, floor cleaners, laundry-related cleaners.

Do any or all of these contain endocrine disruptors unless one is careful to, to find the ones that don't?

Okay.

Um, receipts—how serious is it? Should we be concerned about the BPAs and other endocrine disruptors on receipts?

Yes! So—I suggest is just ask for an electronic receipt, and then you don't have to deal with it.

Yeah, but they're definitely absorbed, you know, into your body!

Any impact of, um, endocrine disruptors of the sort we've talked about today on the thyroid system?

Yes, presumably in the bad direction!

Not, yeah!

I mean this is an interesting point. Let me just say another word about it.

So, um, there was an ongoing study in the Faroe Islands off Denmark, and they studied phthalate chemicals and showed that, um, people who fished there, there were Fisher people, and they—they ate the fish, and they were getting high levels of phthalates in their body and had—um, this is published—um, effects on their, um, immune response.

So my concern—and I don't know if anyone's looked at this—is given everyone's vaccination, like are our, is our response to vaccination now altered by these chemicals?

I don't know, but I think it's a really interesting question!

But there, there is a whole field of the effect of these chemicals on the thyroid system, and there's a lot of evidence that it's adverse.

Can these endocrine disruptors be detoxed from the body? Is there anything that we can do? What's the quickest ways?

Um, things like sweating—are there ways to improve liver clearance of these endocrine disruptors?

That answer to that depends on the class of chemicals.

So the chemicals that are water soluble—particularly the phthalates and the bisphenols—leave the body in a matter of hours. You don't have to do anything; you just have to stop taking them in!

Right? The forever chemicals, the phthalates, chemicals, pesticides—they're, and though—but it has to do with how they're handled by the body.

Are they put into the—you know, if they're water soluble, you pee them out.

If they're fat-soluble, they're going to be around for a long time, so it just depends on the chemical structure of the chemical of the compound.

There was a question about non-stick pans; you covered that earlier.

If someone had to pick between non-stick coated pans versus seasoned iron pans—no question! Iron!

There's no risk associated with seasoned iron pans.

A number of other questions, such as why does Europe have such more stringent laws, etc.?

Um, lots of questions about atrazine, questions about ointments and fragrances—you've covered.

And I must say that, um, as I scroll through these hundreds of questions, if not more, um, you've done an amazing job at, um, clarifying for us what’s known, what is not known, and essentially where it’s probably should avoid, definitely avoid, and look—we just don't know, right?

Um, and well, you know, I have to distinguish between “we don’t just don’t know” and “I just don’t know.”

It's not—I mean, there are many things that I don't know, sure! It’s a huge field!

So, you know, maybe with some, you know, ask the question of chat GPT.

Yeah, we will be certain to ask chat GPT, and we will be certain to ask, um, other experts in these areas.

But, um, I just want to make very clear—I and everyone listening and watching truly appreciate the work that you've been doing in this area for a number of years.

We're so grateful that you took that airline flight with your, this chemist, um, that you mentioned, um, that you stored the urine of those pregnant women, that you analyzed it, and that you've gone down this path of exploring, you know, things that are really disruptive to our health and potentially to the existence of our species as, um, you know, as we talked about earlier, there is the possibility that we go extinct, um, not because of a meteor, but because we fail to replace ourselves!

Um, and that we fail to replace ourselves because we destroy our biological ability to replace ourselves!

I think it's hard for people to, um, internalize that very real possibility because we feel ourselves sitting in traffic with thousands of other people and going, “There's too many people!”

Right?

This kind of thing.

But, um, I want to thank you for the work that you've been doing and continue to do, for your willingness to write books and to educate the public on podcasts like this and others because, um, these are topics that are pretty emotionally loaded for people.

I don't think anything gets people quite as inflamed as the idea that what they've been ingesting and exposed to, um, especially in terms of consumables that they've spent their hard-earned money on, have been, um, harming them, harming them and their offspring, and generations to follow.

That there's something that really lands deep in that way!

But you've also offered us a lot of, um, possibility and a sense of agency over these things, and I love, um, that you weave your math and statistics and probability, uh, theory background into all of this because what comes through is, um, intense curiosity, intense rigor, and a real desire to do good.

So thank you so much for joining us, and please come back again as you make more discoveries!

It's been really fun!

Thank you for joining me for today's discussion with Dr. Shana Swan.

To learn more about her work and to find a link to her excellent books on these topics, please see the links in the show note captions.

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