Huberman Lab - Dr. Shanna Swan: How to Safeguard Your Hormone Health & Fertility
Episode Date: November 4, 2024In this episode, my guest is Dr. Shanna Swan, Ph.D., professor of environmental medicine and reproductive health at the Mount Sinai School of Medicine. Dr. Swan is the world’s leading expert on the ...harmful impact of chemicals in our food, water, cosmetics, and various household and consumer products on our hormones, and the consequences for fertility and overall reproductive health. She explains how exposure to phthalates and other endocrine disruptors adversely impacts fetal development, puberty, and the adult brain and body. We discuss the global decline in human fertility due to disruptive environmental toxins, such as pesticides, and certain foods and beverages we consume. We discuss practical strategies to minimize exposure to harmful chemicals, such as phthalates, bisphenol A (BPA), BPS, and PFAS. This includes reducing disposable plastic use, making healthier food preparation, consumption, and storage choices, and selecting personal and household products that don’t contain harmful toxins. This episode allows you to assess your risk of exposure to endocrine disruptors accurately and empowers you to take control of your hormone health and fertility. Access the full show notes for this episode at hubermanlab.com. Thank you to our sponsors AG1: https://drinkag1.com/huberman LMNT: https://drinklmnt.com/huberman ROKA: https://roka.com/huberman BetterHelp: https://betterhelp.com/huberman Function: https://functionhealth.com/huberman Timestamps 00:00:00 Dr. Shanna Swan 00:02:58 Sponsors: LMNT, ROKA & BetterHelp 00:06:49 Environmental Chemicals, Fertility, Hormones, Phthalates 00:13:30 Phthalate Syndrome, Animal Data, Male Offspring 00:19:11 Phthalate Syndrome in Humans, Pregnancy & Babies 00:27:30 Hyenas; Phthalate Syndrome in Males 00:32:49 Sponsor: AG1 00:34:22 Polycystic Ovary Syndrome (PCOS), Mothers & Female Offspring 00:39:03 Anogenital Distance & Sperm Count 00:45:03 Sperm Count & Fertility 00:49:24 Sponsor: Function 00:51:11 Sperm Count Decline 00:58:19 Sperm Quality & Pesticides 01:04:12 Atrazine, Amphibians, Sexual Dimorphism, Behavior 01:09:00 Preschoolers, Phthalate Exposure, Sexually Dimorphic Behaviors 01:14:08 Tools: Lowering Exposure to Endocrine Disruptors, Fertility 01:24:52 Tools: BPA, BPS, BPF & Can Linings; Drinkware; Plastics & Microwave 01:30:07 Tools: Buying Organic; Skin Products, Fragrance; Sunscreens, Consumer Guides 01:32:58 Funding 01:34:31 Tools: Distilling Water, Shoes, Clothing, Food Sourcing; Building Materials 01:40:12 Europe vs. US Chemical Safety, REACH Program 01:46:20 Tool: Pregnancy & Fetal Health 01:49:23 Plastics & Environmental Concern; Fertility 01:55:26 Sperm Quality, Fertility, Cell Phone, Temperature 01:58:04 Other Animals & Fertility Decline, Ecosystems 02:01:58 Advancing Technologies, Fertility, Offspring & Adverse Effects 02:06:02 Tool: Consumer Guides, Personal & Household Products 02:09:39 Tool: Receipts; Thyroid System; Non-Stick Pans 02:15:18 Zero-Cost Support, YouTube, Spotify & Apple Follow & Reviews, Sponsors, YouTube Feedback, Protocols Book, Social Media, Neural Network Newsletter Disclaimer & Disclosures
Transcript
Discussion (0)
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,
even in household items,
impact the developing fetus, children and adults at the level of their reproductive biology.
So things like testosterone and estrogen
and the pathways within the brain and body
that are impacted by testosterone and estrogen,
but also how all of those things in our environment
and that we put into our body impact our health
on a daily basis and our long-term health.
So 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 things like polycystic ovarian syndrome are increasing in women, and what we can do about it.
In fact, during much of today's discussion,
Dr. Swan emphasizes the things that you can do
every single day, and that in fact,
turned 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.
So by the end of today's episode,
you will be highly informed by the world expert
on endocrine disruptors and environmental toxins. And you will also be highly informed in terms of
how you can have agency, how you can 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 to consumer
information about science and science related tools to the general public.
In keeping with that theme,
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And now for my discussion with Dr. Shawna Swan.
Dr. Shawna Swan, welcome.
Dr. Andrew 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.
You didn't know I was there, but incredible stuff that you've been doing as a researcher,
as a public educator, as 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?
And if so, which are the ones that you think about?
And perhaps if you could just mention
a few of the more salient, maybe even shocking,
but salient results that you've observed over the years.
Like what was the kind of like, whoa, 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 somebody who walks out into the world
and looks for things that could be messing up our biology,
messing up our health.
And yet you've found some.
So if you could just share with us what you've observed
and what you find really compelling and important
for people to know about, we can dive in there.
That was a lot of questions.
I could probably talk for a long time.
Feel free.
I won't speak until you're done.
No, but I want to break it up.
Let's break it up.
So I think the first question about was,
are there forces, chemicals, agents in the environment
that can affect our reproductive health?
Yes?
Okay, so my answer to that is yes.
I think there's no question about that.
The question comes down to when and in whom,
and what dose and so on and so forth.
But whether there are, let's just say broadly, things, yes, of course.
The category that I focus on are manmade, primarily manmade chemicals. Although I do also include the influence of other factors,
factors of choice, for example, sleep, exercise,
that kind of thing, 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.
And so my thesis is that chemicals in the environment,
that's a very broad class,
so we'll have to say some chemicals in the environment
at the right time to the right organism affect fertility.
Okay? So, and let me just say fertility is one area to the right organism affect fertility, okay?
So, and let me just say fertility is one area
that I've focused on, but actually this class of chemicals
that I'm primarily interested in are those
that affect the body's hormones.
So those are known as hormone disrupting chemicals
or endocrine disrupting chemicals,
hormone altering chemicals, whatever, you know, there's a lot of names,
but that helps you focus on where to look for the effects.
Because if it's hormone altering, you can now have something to really ask,
okay, here's a chemical, does it affect a hormone?
Which hormone? When? How?
And then you start, that's almost an, you know, laying out an hormone, when, how?
And then you start, that's almost an, you know, laying out an experiment right there,
right?
So, focusing in on hormone disrupting chemicals, I think is useful.
Absolutely.
Yeah.
And I think 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
sperm and egg quality.
Right.
So I'm a reproductive epidemiologist.
I got there in 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.
Right?
That's what they're designed to do, change your body's hormones, your reproductive hormones.
So it's interesting, you know, 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,
actually, trying to figure out,
were there adverse effects of oral contraceptives?
If so, you know, for whom and when and how much and so on.
And so, that was a very great study.
And coming forward in time,
I studied environmental chemicals, not so much pharmaceuticals, for quite a while when
I was at the California Department of Health Services.
And then I had an aha moment. I was flying to Japan with my friend John Brock,
who's a chemist at CDC, wonderful chemist.
We had long flights, we were talking about this and that,
and he says, 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 have shown something they are calling the phthalate syndrome.
And so he explained.
What is NTP?
National Toxicology Program, sorry.
Thank you.
For using alphabet.
No, it's quite all right.
National Toxicology Program, a governmental research center.
And their job is to look at chemicals
and see what is the toxicity.
So it could be reproductive,
it could be carcinogenicity,
it could be neurotoxicity, that's what they
do.
And so they had signaled out these phthalates as being reproductively toxic and specifically
to males and specifically when exposure is in utero.
Pregnant mom is exposed to phthalates and somehow the fetus is disrupted.
If you don't mind, I'd like to know, is 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, let's just assume it goes
through the placental barrier into the fetus and is
impacting fetal development.
Right.
So in those experiments, it was through food.
But we are exposed in all those ways you mentioned.
Every way that something can get into our body, thallies get in there.
But let's come back to that.
Let me go to the experiment at NTP.
So what they did at NTP, National Toxicology Program, they fed mother rats various doses of these various thalates.
And what they found was no changes in the females
are not that they found at that time.
The female offspring?
Female offspring, sorry.
But in the male offspring, they found that the genitals were,
I summarize it by saying, incompletely masculinized.
So I'll explain what that is.
So for that, I have to back up and say something
you probably know very well, but I'll just explain it.
The genital tract initially is a ridge.
It's a single ridge.
It's the same in males and females.
It's not sexually dimorphic at the beginning.
And then under the influence of testosterone
in a very specific window called the male programming window
in rats, it stays, I think, nine to 12 of gestation.
So a very short window.
To orient people, I think rat mouse gestation
is about 21 days or so.
Yeah.
Okay.
So, for us, it'll be early first trimester.
Okay.
But that comes later.
So, at that time, if they feed their mother
that chemical in her food,
then her male offspring are born
with changes in his genitals, or more likely
to.
And so what they tend to have is a smaller penis, less descent of the testes, more likely
to have undescended testicles.
There are internal changes that we didn't get into in our human study because we can't look there, but
the epididymis there changes and so on.
The whole genital tract is altered.
And the most important measure for me, as it turned out, and for humans, and perhaps
for animals, is something that the animal scientists had studied for a long time, for actually 90 plus years, but
had never been studied in humans.
And 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. Now you're a physician and I challenge you
to think of any syndrome aside from alcohol.
Feel alcohol syndrome, of course, there's a syndrome.
But note what syndrome is attached to a chemical class.
Just for technical purposes, I'm a PhD, not a clinician,
but I worked on neural development for many years
and then prior to that, some endocrine stuff.
So I'm facile with the general terms.
One that comes to mind would be, for instance,
the thalidomide babies, right?
A miscarriage, anti-miscarriage drug
that changed limb development.
That's a very extreme example.
I would say for in human normal development,
what I'm most familiar with are the early organizing effects
of androgens that convert to estrogen on external phenotype,
which is basically nerd speak for during development,
the Y chromosome produces,
it leads to the production of a number of genes
and eventually proteins through RNA, et cetera,
that are including testosterone and dihydrotestosterone
that in the brain organizes the brain male
and causes the growth of the penis or organizes,
meaning it sets up the penis to then during puberty
when the penis is exposed to testosterone and estrogen
and DHT, it's a bunch of things, not just testosterone,
the penis grows.
Right.
And lots of other things.
Right, lots of other things, right?
So the word soup that I just put forward
is basically saying that there are a lot of things So the word soup that I just put forward
is basically saying that there are a lot of things in development where hormones set up a potential
to respond to other hormones later.
It's not that testosterone grows the penis
during development, it does that,
but more so it establishes a potential for the penis
to grow when exposed to things later during puberty.
Do I have that right?
Right, right.
As far as the name goes, which is the phthalate syndrome,
there is thalidomide.
It's not usually called the thalidomide syndrome,
but it could be.
You saw you're right about that,
but it's extremely rare.
And there is no environmentally,
you know, chemical in the environment as opposed to a pharmaceutical that is given a syndrome.
So this is very, very unique.
And so 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
alcohol, fetal alcohol syndrome and thalidomide syndrome.
Right.
Yeah.
So when, well, at this point it was only animals, right?
Because John was telling me about the NTP study, which was in rats.
And so I thought, wow, you know, I like puzzles.
So my first question was, is this happening in humans?
You might ask that, you know, as a natural thing to ask.
Great question.
And then I thought, how would we find out?
And answering that question took me 10 years.
Okay. It took me 10 years. And so if you think about, okay, phthalate in the mother, changes in the genitals of
the offspring, connect them.
How do we do that?
So we have to start with phthalates in the mother.
So how do we know 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 woman's urine coincidentally.
If you will, I thought, well, save it. You know, it's not expensive and not hard. Minus
80 degree freezers doesn't take a lot of room, put it in there.
So I had this urine saved from pregnant women.
And then I knew from John that we could look in the urine
for phthalate metabolites.
So 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.
And 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 fetus. So then I thought, okay, then maybe there's a change in the babies.
So then I had to get the babies.
So 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, right?
How willing were parents to let you do that? That seems-
They were okay.
Most of them were okay with that.
Were they?
Yeah, yeah.
Well, they trusted us.
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, I think
about a month, 12 months old. So not ideal maybe because the rats had been measured at
birth, the rat genitals have been, but that's what we could do at that time.
Yeah. The reason I ask is there's always the potential for ongoing phthalate exposure to
the newborn.
Absolutely. phthalate exposure to the newborn. Sure, absolutely. But I suppose in either case, you're able to draw some potential link between, or potentially
draw a link, I have to be careful with my language there, between phthalate exposure
in utero and ex-utero and these external biomarkers.
Yeah.
I mean, given that the critical window is quite short and quite early, by the way, let
me just say, when the rats, they did a lot of work on this critical window.
And when the rat moms were exposed before day nine,
it did nothing.
And when they were exposed after day 12, it did nothing.
So it was only the exposure during that critical window
is very delicate, and it's by the way,
true of the brain as well.
So teasing out what is the critical window
is one of the challenges that we have
when we work with these chemicals.
So I wasn't so much worried about exposure
in the delivery room and, you know,
in their feed as in the first year of life,
because I knew that it was unlikely to change these measures.
Do other things, but maybe, but not these measures.
So then the question became kind of what you're asking is what do we measure?
What do we actually measure?
And if you think about a newborn rat or 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, you know, when you spread a boy's legs.
And so I got a pediatrician in Los Angeles who worked with me on how to make that translation
and how to do this exam.
And that took us quite a while because we really wanted
to come as close as we could.
What was clear was that the anus part of it was easy.
You go to the center of the anus, so that was easy.
Then what's the other landmark?
What's the genital landmark?
So it turns out there are in males too,
and in females there are two as well.
So let's just talk about males.
For males, the best place to measure and actually closest to the rat measurement is the place
where the tissue changes where the scrotum inserts.
It goes from rougated to smooth tissue, and at that point it's pretty clear.
Pretty easy to measure.
The other measure, and that was the anus scrotal distance.
And the other measurement we took was the anal-penile distance, and that was the insertion,
the anterior insertion of the penis.
The part closest to the body?
Close to the head, yeah.
Closest to the head.
Yeah.
And that was not so obvious because you don't have a change in tissue there. So where exactly do you put your caliper and um?
We had a lot of discussion about do you press down?
You know how where exactly do you make that mark and
actually, the anus coronal is the measurement
with the least variance,
because you can measure most precisely,
but the anal penile is another measurement.
And then you can do something similar in females,
and we did that, but that's,
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.
And what we finally did was bring the mothers in,
bring the babies in, and got three measurements.
And then on every 10th 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 had done been done this way in humans
there was a Mexican study that
tried to do this and I
Never learned very much about it, and I was excited that they had done this
But I'm not sure how it relates to this. I just mentioned that out of honesty
you know there's somebody in Mexico did this.
But to my knowledge, this is the first time it was used as a toxicological measure in
humans.
Right.
So we were, we did that study.
We related those measurements to what CDC had measured in the urine of our women collected while they were pregnant.
And we found the phthalate syndrome.
Could you explain what the correlation was
between phthalate metabolite levels, which is I believe.
Not by number, cause I don't remember it anymore,
but there was a significant, let's just take the AGD.
The AGD of mothers who had higher levels of three,
the most antiandrogenic phthalates,
I'll tell you what those are in a minute,
had significantly shorter anegental distance.
And then I have to say that, which I haven't said
and should have, that anal genital distance
is sexually dimorphic.
So it tends to be 50 to 100% longer in males than females.
That makes sense if you think about
what's going in that space.
There's a lot of real estate in males between the anus
and, you know, let's say the penis, penile insertion,
much more than in females.
So it's natural that that will be longer,
but that's, I began doing some work
looking at other species, and it turns out
that that's true in all mammalian species,
except two, and one is the hyena.
All right.
And one is the elephant. So in the hyena. All right. And one is the elephant.
So in the hyena, I'm just saying this
because you would be amused by it.
Well, I-
You know about hyenas?
I do, I know more about hyena genitalia
than I'd like to admit.
And I can tell you why after you educate us,
but I'll keep my explanation brief,
but I'm very familiar with hyena genitalia.
So I know Stephen Glickman who works with a, you might know him too, he works in Berkeley
with a...
He was my instructor when I was a graduate student at Cal.
And I used to run in Tilden Park, I suppose I'll tell it now.
And there was a colony of wild hyenas, but they were behind chain link.
Yes. It's actually a favorite hike of but they were behind chain link. Yes.
Actually a favorite hike of mine
up the Strawberry Canyon Trail.
Yeah, I did that trail.
A good friend of mine, Brian Prendergast,
who's now a professor at the University of Chicago,
worked on the Prairie Vols
that were also housed at that facility.
And a fun thing to do was to go see the hyenas with Steve.
They're brutally dangerous animals.
And Steve has tons of stories about them.
We should probably resist our temptation to spiral into that.
Maybe sometime I'll do a little evening chat podcast
where I tell Steve Glickman stories.
He's a delightful person.
And yeah, those, let's just say this,
the female hyenas have clitorises larger
than some of the male hyena penises,
and those females give birth through those clitorises.
Yes.
As we both know.
So you will not be surprised to know
that the female HDD is longer than the male.
Right, because they're heavily androgenized.
Exactly.
As I recall by androstenedione.
Actually, I don't know that.
It became popular during the era of steroids
in professional baseball because androstenedione
was being used pretty frequently in baseball at that time.
Anyway, we have to be, we could go down the spiral of-
But also in terms of behavior, the female is the alpha.
Right.
They eat first.
Yes.
They're physically and hierarchically dominant
in hyenas.
So it's really interesting, isn't it,
that they would have a longer, more masculine
intergenerational distance.
Elephants we won't go into now,
but they're kind of midway in many things.
So including they're about equal
in genital distance in males and females.
Other than that, humans and other species,
male genital distance is 50 to 100% longer.
However, so three phthalates, diethylhexyl phthalate,
DEHP, dibutyl phthalate, DBP, and butylbenzoyl
phthalate, BBZP, are the most anti-androgenic testosterone-lowering phthalates, and those
are the ones that were associated with a shorter intergenital distance in males.
In human males.
Human males and animal.
So we replicated that animal study in humans.
And then, because you know this is how it is in science, I had to do it all again, right?
So I started a whole new study.
And that study is still going on.
The children are still being followed.
I think we started in 2012.
The first paper on inogenital distance came out in 2005.
It had a pretty big impact.
So these are studies where you're looking at the endogenital distance in relatively
newborn humans, then tracking that distance.
No, that's a different...
Tracking is another study.
Okay.
This is just two studies on demonstrating the Salley syndrome in human males.
So the first one I described, the second one the replication,
and the second one is the one that's going on still.
So, and what it does to their reproductive function,
we don't know the kids are only 12 years old now.
So, we would like to know that and we will know that.
Okay, but I have another answer for you about that.
So, we started the second study,
and the second study which is called TIDES,
which is the Infant Development and Environment Study,
by the way, these are both in four cities
in the United States.
And there we did it right.
So we got the urine in the first,
early urine, because we knew that could be important.
We didn't have that option in the first one.
Remember those urine samples were accidental.
We got them when we could, right?
And we got repeated urines, one in each trimester to look at the effects in different trimesters.
And then we examined the babies at birth, which is what the rats.
So we came much closer to replicating the rodent study
and we saw it again.
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More phthalate exposure equates to shorter analgenital distance in males.
It was approaching the distribution in females.
It sounds like the distributions moved more closely together.
Yes.
Right.
Although it wasn't the females that moved.
Sorry.
The male distribution-
Became more like the female.
Became more-
Right.
Feminized. Could say feminized, but more female-like in its.
But these boys also had smaller penises,
less descend of the testes, smaller scrotums.
So they were smaller.
Everything was in their genital areas.
All the secondary sex characteristics of puberty in males,
Adam's apple, facial hair growth,
thickening of the vocal cords,
therefore lowering the voice, et cetera.
Are those all later activating effects of hormones
or are there precursors to those that are present in males?
Because in mice, as I recall,
like I couldn't tell you, like we call it in the laboratory,
people always chuckle at this, but it's like sexing the animals tell you, like we call it in the laboratory, people always chuckle at
this, but it's like sexing the animals when you look to determine if it's a male or female.
When they're really young, you have to look carefully at first, right?
And then you get pretty good at it.
As they get older, it gets easier.
But when the mice are feet down, back up, you can't you know, you can't really tell.
You can't really tell.
As the mice get older, their testicles become visible in the males from 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.
Of maleness.
And so I do want to say one thing about females because then that'll lead me to my
conclusion about the role of
this measure
so
If the mother is exposed to more testosterone than expected
You might expect that her female
Offspring would have a more male in a genital distance.
Is that the case?
Yes.
So it's a bidirectional?
Yes.
Can we also presume that if the mother either secretes or is exposed to more androgen, then
the males can become hyper male?
No, we'd never, I don't know what that would be.
We never saw anything that would be hyper male.
So the yes I said to you was the result of a study where we looked at the girls born
to women with PCOS.
So women with PCOS, as you know, have excess testosterone.
Polycystic covariance.
Sorry.
Polycystic covariance.
That's good.
We've talked about it a little bit before in the podcast.
It's associated with, my understanding is it's associated with elevated levels of androgens.
That's right.
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, we're not elevated androgens. Yes.
Not just, we're not talking about pregnant moms anymore.
Exactly.
And so in our study, population, we did a search for women who had diagnosis of PCOS
and took that as a marker of higher testosterone exposure and then looked at the girls.
And yes, those girls had a longer quote more masculine in your general distance.
What age group were you looking at?
In the infants.
In the infants.
Oh, the PCOS was at pregnancy.
At the time they were pregnant.
So presumably people between their like somewhere in their 20s out to their 40s.
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.
They do not, their daughters do.
Their daughters do, thank you for that clarification.
Their daughters.
And 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 even get, you know, fluid and so on.
So this tells you, this is like a readout
of what was in the fluid at the time.
So then your next question was,
what does this mean for later fertility?
Yes?
Yeah, what is the impact of this early androgen exposure What does this mean for later fertility? Yes? Yeah.
What is the impact of this early androgen exposure to female offspring or let's just
say reduction in functional androgen exposure to male offspring?
The reason I'm using these loop-de-loop languages, as you probably know, but for the audience,
not trying to complicate things here,
but a lot of the masculinizing effects of hormones
in fetal development is actually testosterone
that's converted into estrogen,
so it can get pretty tricky.
Right.
And, but maybe for 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.
It's just that people form such strong associations falsely
that testosterone is male, maleness, and that's not true,
and estrogen is femaleness, and it just gets really murky.
But for the time being,
It's femaleness and it just gets really murky. But for the time being, you identified an external biomarker of fetal androgen, AKA
masculinization via the mother.
That's right.
Got it.
Okay.
So then we asked the question you've asked and many people asked, who cares?
Why would we worry about a boy having a slightly smaller anegonal distance?
Well, I can tell you there are many boys that are probably worried about it right now.
Right.
They've probably got the ruler and the calipers out right now.
But I'm going gonna answer that question.
Right.
So I told you that our kids are too young.
They're not producing sperm right now, right?
So we had to go to an adult population, right?
And so we went to a population of college students
in Rochester, New York.
And what we did there was make an assumption population of college students in Rochester, New York.
And what we did there was make an assumption, which is 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, who did these studies said-
His name is Earl Gray?
Yeah.
That's cool.
Yeah. He said, His name is Earl Gray? Yeah. That's cool. Yeah.
He said, AGD is forever.
Aneogenital distance is forever.
Now, what that means is it's not like
your aegidinal distance today
is what it was when you were born.
Of course, you're a bigger person,
but that means adjusted for body size, right?
So if you assume that AGD is forever,
if you're born with a short for your size AGD, then
when you're 20, you'll have a short for your size AGD, okay?
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 anal genital distance, we're getting a reflection of what it was when they
were born.
And 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
you can do anything.
And so what we did was we measured their antigenal distance and then we got them to give us a
semen sample and complete a questionnaire and things you do in a study.
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 to recall all the details,
but you're adjusting for body size and body weight.
Height, weight, what are the factors that would scale here
that would allow you to normalize?
In other words, what you're trying to do is backtrack
to what it likely was at infancy.
No, we didn't actually try to go back.
Let me just tell you what the results were.
In this group of men, if they had a longer antigeneral distance, they had a higher sperm
count.
Got it.
So you would correlate those two measures.
Right.
And then 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.
If we wanna say something about early AGD and sperm count.
So it's easy to say AGD is related to sperm count
because we measured that, we saw that,
a correlation that's published.
Okay, if we wanna 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.
For these guys in Rochester, we didn't measure their AGD at birth.
Were there any conditions of being a participant in the study such as refraining from alcohol,
cannabis, et cetera, in the 90 days prior?
No. No. I don't think so. 90 days being the duration of a spermatogenesis.
Yeah, I don't remember that.
These are college students,
so presumably some of them are drink.
Okay, so, but in the end it was a robust link.
And then Mike Eisenberg, who you might know at Stanford.
Yeah, my colleague at Stanford,
he's been on this podcast.
Yeah, yeah, yeah, good, good.
He's a colleague of mine too.
And he looked at men in a fertility clinic
and those who had born children
and those who had not born children.
And the men who had born children had a longer
in a general distance than men who had never born a child.
Never born, but were trying.
Yes.
Right.
These were not people who opted out.
These were. Exactly. These were not people who opted out. These were-
Exactly.
Exactly.
These were people who were having challenges with fertility versus success with fertility.
By the way, the question of how you measure AGD in an adult man is a different question
than how you measure it in the newborn.
We did a lot of work on that and Michael helped with that too. So it sounds like, oh, and may ask where the sperm counts that were on the, let's just
say the lower, like the lower quartile, where the quote unquote lower sperm counts, like
functionally lower.
Cause I always wonder about this.
Like it's come up in a number of discussions, like with Robert Sapolsky, with Mike Eisenberg.
And now I'm asking you, you know, when we hear that sperm counts are going down, are they going
down to the point where fertility is impacted?
That's really one of the, I think, functional questions.
So let's lay aside the question of AGD, right?
That's really interesting, but let's talk about sperm count.
Okay. That's really interesting, but let's talk about sperm count.
There's a beautiful study among pregnancy planners out of Denmark quite a long time
ago.
In that study, what they did was take 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, right?
Time to pregnancy in relation to...
And what they showed is a really interesting curve, which has never been corrected to my
knowledge.
It's what I use and what I think people use, which is that if you...
I wish I could draw it here.
You should have a board and wipe it.
The problem is a lot of people are listening, but maybe we can talk people through it.
Yeah, yeah.
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, so you're looking at sperm count
along the x-axis and months to conception, and what you see is that if you have no sperm,
you don't have no conception. If you go up to around 40, 45, there's a steep increase.
So the more sperm you have- 40, 45 million?
Million per milliliter.
And this is million per milliliter.
So just pure concentration, not number of motile sperm.
This is just how many sperm?
We're not talking about quality.
We're just talking about number.
No, no, no.
Just the number.
Okay.
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.
And then around 45 to 50 starts to level off. And then after that, after certainly after 100, probably 75, it doesn't matter at all.
So 100 million sperm per milliliter of semen.
Yes.
So can you see this?
Okay.
So when people say, does sperm count matter for fertility?
Yes. 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 we just have too many sperm.
I mean, I don't, but you miss, you know.
And there's-
So nature runs a probability game.
Overproduced sperm.
Right.
Some of those will be high quality,
some will be low quality.
Exactly.
Depending on their age, when they were,
that is when they were generated.
Or their conditions.
Or their conditions, how much heat exposure, et cetera.
So nature runs a probability game.
Hoping that the best quality sperm will fertilize the egg.
So below 45,000, excuse me, below 45 million sperm per milliliter of semen, the sperm count
really matters.
It drops off precipitously.
That's right.
Once you get up to 75, 100 million per milliliter of sperm, then-
It's all good.
You're good to go.
Right.
And sperm counts range anywhere from,
it could be low eight, nine, 10 million per million
in the very low situation.
It could be zero.
It could be zero in some people, right?
All the way up to 400 million.
There's a huge range.
That's right.
And that's a function of age, it's a function of genetics,
it's a function of presumably phthalate exposure.
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We were on to the fact that sperm counts are dropping.
There's a relationship to anal genital distance and there's a relationship between anal genital
distance and phthalate exposure.
And then I asked the question, you know, okay, we're hearing about sperm counts dropping,
but is it 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.
We can talk about that a little bit later.
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.
Right, so let's go back to sperm count
because we haven't really talked about that.
It's a kind of a different path.
And my introduction into phthalates
was not through sperm count, right?
It was through this question of my colleague asking me, you should look at this and challenged,
and I looked at it and that was really,
really interesting journey that I went on.
Okay, so that, but there was
a separate for a while journey that I was on.
That started in the late 1990s when I was asked to
join a committee of the National Academy of Sciences.
And 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.
Because at that time, it was like, well, yeah, we hear about this, but should we care?
And so 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.
Wow.
That's a huge drop.
That's what, we're seeing worse than that, by the way, now.
So, okay.
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 and I looked at it
and I thought, eh, I don't think so.
That was my initial reaction.
And that was because, first of all, I didn't know who had written this.
I just saw it in a journal and it was not very big and not very many figures,
not very much data.
And I thought of it and I thought, that's a big claim for a little
paper.
But I'll look at it, because it's important.
And so what I did then was to think about all the factors that we epidemiologists call
confounders, things that might have caused that decline if it wasn't real biologically.
And so we could think of some of them together.
Maybe the method of counting sperm had changed so that later methods counted fewer sperm
in the same sample.
That's certainly possible.
But it turned out that wasn't the case because they actually had all used the same method.
And 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, right?
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, fertility. And maybe they smoked more and maybe,
and so on and so forth. So what I did was to get the 61 studies, go through them, and try to extract information
on all the factors that could explain the decline.
So 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.
Right.
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.
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
... I mean, a lot of weed, and I always say, okay, well, there are a number of other factors,
right?
But alcohol, there's frequency of ejaculation, right?
The requirement to abstain for 48 to 72 hours to up to five days prior, et cetera, all these factors that men may or may not faithfully report,
but you assume that if some are telling the truth
and some aren't, that there's an equal distribution of that.
So all the different things, right?
This is so very different than looking at, for instance,
ovarian reserve, like the number of eggs,
where you use ultrasound and you use AMH levels.
And sure, things can impact that, but it's a little different than when taking sperm counts.
So thank you for doing the study so carefully and for repeating them so many times. I mean,
many of the studies that you've done are, 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 and there was an update I noticed online.
So you are extremely thorough.
And it probably reflects your early training in math and statistics and probability theory.
You're not somebody to just kind of go in and go, oh yeah, like in these people that
eat a few too much of this, then there's a little less of that. So I just want to,
if today's discussion feels like we're really, we're leavening through this, that's intentional.
And it's important for people to hear these kinds of claims are not the sort of thing
that you could, people 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.
Well, good scientific method, yeah.
Yeah, and I would say especially
with human epidemiological work
because of the number of potential confounding variables.
Right, right.
So when I saw that and actually did another study
to select my own studies and not accept
her 61 studies that had been published that Elizabeth Carlson had published.
So new studies came up to more recent times, went back further, did it again, found exactly
the same thing.
Okay.
So there were three, you know, three looks at that and I thought, okay, I'm going to
accept this now. This is sperm count is declining.
And why?
That turned to the why, okay?
Because up and down now, we hadn't said anything about why.
We just said, is it doing that?
Yes, okay.
Now we believe it is declining, why?
And 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 environment.
And so what is it about the environment that could do this?
So I asked, OK, in the environment, there could be things that are making sperm decline.
So if you think about how you might look at that, you might design the study that I design
next, which is another study.
And by the way, this preceded the AGD.
So we had four cities in the United States that we picked with different environments,
and then we got men to come in and 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?
And 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 I can't ask a guy in the street to give me a semen sample right now.
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?
And what I decided was to sample 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.
And we know what we're looking at.
So that's what we did.
So this is a, the semen study is the study of partners of pregnant women.
And of course, they'll have slightly higher semen quality because they got their partner
pregnant.
And so, we had their urine, we had their blood, and we looked at their semen quality.
And then we decided to look at pesticides.
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 a agricultural
belt where there was spraying all the time for soybeans and so on.
Those men had half as many moving sperm as men in Minneapolis.
Whoa.
Whoa.
Huge, Right? And 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, and showed that five pesticides
were significantly higher in the men with the low sperm parameters.
That include motility and morphology, you know, all the parameters.
So these are pesticides that are being sprayed in the air on crops.
You mentioned soybeans.
What other types of crops?
I don't know.
I don't remember.
So plant and fruit crops, presumably.
Yeah, whatever they were growing in Columbia, Missouri at that time.
And just to make sure I understand, it's not that the men need-
Soybeans, corn and soybeans.
Corn and soybeans.
But we're not talking about eating corn and soybeans.
We're talking about living in an area where pesticides are being used by, I guess, is
it still called dust crop?
Yeah, we didn't go into how they got these.
We just looked in their urine and there were the metabolites.
The metabolites 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.
Okay.
We don't know.
But this was not a particularly, we didn't sample farmers only or anything like that.
So it was 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.
Whoever happened to come in to the prenatal clinic and agree to be in our study, the male's
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 triazine pesticides.
Atrazine was the most widely used and it's a huge use around the world.
I mean, it's highly, you know, one of the most,
the largest commercial pesticides.
So these were very big players in the pesticide field.
A relevant theme there would be,
maybe we could take a moment and talk about atrazide
and its effect on male sexual behavior in amphibia.
And we'll come back to the sperm studies
because when I was a graduate student
at UC Berkeley, I had the wonderful experience of taking a course from the now, I think you
mentioned he's a dean.
There are multiple deans on campuses, Tyrone Hayes is a wonderful researcher who established
a link through his research between atrazine exposure and male sexual behavior of amphibia.
Could you elaborate on that result?
Yeah.
So 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 to how much.
And he showed that the...
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.
Tried to mate with other male frogs, presumably unsuccessfully.
Well, they mounted them.
He has photos of the males mounting males.
And so presumably this is a neural change that occurred, neuroendocrine change, but
ultimately neural since mounting behavior is controlled by, actually we now know the
hypothalamic nuclei that control this. David Anderson who's been on this podcast has people in his laboratory that,
including a former graduate student of mine,
working on this specific issue of what the circuitry is.
That's a remarkable result.
It's been kind of, you know, 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, I don't want to say partner, because it is mating, the
frogs aren't monogamous, but sexual preference are significantly impacted by this atrazine.
Yes.
And it suggests that there are other environmental chemicals can as well. And I don't know if we'll have time to go there, but I did work on neurodevelopmental
outcomes in relation to prenatal phthalate exposure.
And so I think the overarching idea here is that the brain, like the genitals, is sexually
dimorphic.
And there's many people, by the way,
who will take offense at that.
Really?
Yeah.
I think there's, I mean, going back to the work
of Frank Beach and the psychology department
at UC Berkeley, showed this in beagles.
It's been shown in pretty much every species.
But I'm just telling you that-
But it's not a better or worse.
I think this is what people need to hear.
Like dimorphic does not mean better or worse.
It means different.
Right, right. And that this is what people need to hear. Like dimorphic does not mean better, worse. It means different. Right.
Right.
And that there are, for example, advantages to spatial reasoning in a male, which are
related to testosterone.
Right?
You know that.
I mean, I think they're...
Yeah.
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, the hypothalamus is known to be sexually dimorphic, dependent
on testosterone converted into estrogen during development, et cetera, et cetera.
And there's just so much evidence of this.
How it links to behaviors is can, 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 or 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, like I have much better sense of
direction than my husband.
And you go, well, yeah, like, you know, and then you go, well, does that mean that she
has higher testosterone than him?
And then maybe in that, and pretty soon you're in almost a 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.
But look, there is a very simple, outdated questionnaire, and it's play behavior.
It's called the PSAI.
It's been used for years.
Have you heard of it?
This is rough and tumble play.
Yes.
Yeah.
Yes.
And there are 24 questions on there, and they are sexually dimorphic, I guess you could
say that.
You know, my child likes to play with dolls.
My child likes to play dress up. my child likes to play dress-up,
my child likes to play rough and tumble, et cetera.
And we gave that questionnaire to our population
and looked at the answers that the mothers gave,
both in our population, by the way,
and a Swedish population of a colleague there,
Carl Bornahag and Gustav Bornahag.
What we found, higher phthalate levels, these antiandrogenic phthalates were associated
with less masculine male typical play in our male boys.
So, you know.
This is phthalate exposure.
In utero.
To the mom, baby is born in the young human child.
Yeah, four year, I think it was four years of age.
Four years of age, less rough and tumble type play.
That's right.
Among the boys whose mothers were exposed to more phthalates
during a critical period
of development.
Now you can see that's a politically loaded issue now.
Well, I think we're... Let's have some fun with this in the scientific sense.
The notion of dimorphism is, okay, male and female brains are different, right?
And male, female defined in almost all those studies as presence of a Y chromosome.
Then people say, well, there's XYY and then there's XXY.
Okay, but most of the time you're talking about XX chromosome or XY chromosomes at birth.
Forget everything else for the moment.
These are always distributions.
This is what I think people need to know.
This is not two hills of data separated by a valley.
These are overlapping distributions.
You get males with a quote unquote female-like distribution, you get females with a quote
unquote male-like distribution.
I think as long as we acknowledge that, then we're just talking statistics. Right.
We're not placing any cultural
or any value on it really whatsoever.
Right.
But if you could make the analog
to the intergenerational distance,
it's kind of similar.
You know, you have the same exposure,
salad exposure, you have something changed statistically.
We don't see huge differences in the boys' genitals.
And we don't see huge, I don't, we know,
these kids have not been scanned,
so we don't know how their brains look.
But based on their answers, we don't see huge differences.
We see tendencies, we see they are more likely,
if they had been exposed to these phthalates,
to want to play dress up and have tea parties.
More likely, doesn't mean that they're all going to, dress up and have tea parties more likely.
Doesn't mean that they're all going to,
but that's the direction and so on.
So I think we have to just think
about more likely not absolute, yeah.
And of course there are also the socio-biological variables
such as if a young boy has a sibling that's a sister,
there's more likely to be dresses around,
right?
She's going to-
We can control for that.
If he has two older brothers, there might be more rough and tumble play happening in
the house.
And I have some friends that are women who have older brothers and those women are, some
of them roll jujitsu or do-
And I know some women who are only children who do martial arts and fight, right?
So I think that none of this is deterministic as we know.
But let me just add, we did control
for the sex of the sibling, older sibling,
and we also asked about the parents' attitude
just towards same-sex play.
So how would you feel if your child,
your male child played with dolls?
Would you be discouraging?
Would you encourage,
because it has a lot to do with what's in the house.
You know, if you say, did your child play with dolls?
Well, what if there were no dolls?
This is super interesting to me.
I don't want to reveal too much,
but I grew up, just because it's not,
it's just an N of one,
but I grew up in a household where I have a sister,
but then after a certain age, I received very strong messages about what sorts of play were gender
appropriate.
I think I also just naturally defaulted to, there were a bunch of boys that lived in my
neighborhood.
They had older sisters, so all the sisters hung out together.
It's kind of interesting.
All the younger brothers pretty much hung out together.
And the guys that didn't have siblings or had brothers or siblings.
So there was a really strong divergence.
But I grew up in the, that was in the 70s and early 80s when things were, let's just
say culture was more dimorphic then.
Clearly.
I mean, there were television shows like All in the Family, which the entire basis of the
show was the wife going back to work and the husband being confused about it.
I mean, nowadays people will go like, what?
That's wild.
I have to ask because I know people are wondering, and I'm wondering, what are some non-pesticide
sources of phthalates that we have agency over, that we can take control over?
Right.
So let me correct you.
It's not the sources of phthalates necessarily. Pesticides,
there are phthalates in pesticides, but that's not the worst player in the story. If you
look at the different classes of exposures that are hormonally active, right? Pesticides are, phthalates are, bisphenols,
like bisphenol A.
BPA.
BPA, certain metals are, there's the PFAS chemicals,
there's all these different classes, right?
And if we want to go, excuse me,
into what in our daily life exposes us to these things.
That's another story that we can talk about, but they're going to be different depending
on the class, right?
So let's throw our arms around all of those for the moment.
And I'll just ask you, given that you're an expert in this area, what are the top three
to five sources of endocrine disruptors that we have agency over?
And let's forget about pregnancy for the moment, since we're all out of the womb if we're listening
to this.
Some people will be pregnant as they listen to it, but would you say it's drinking out
of plastic bottles?
Is it laundry detergent?
Is it rubber tires that are cascading down on us through the air and we're inhaling them?
Presumably all of the above, but which ones that we have agency over do you think are
the most, let's just say, concerning where people could make better choices?
I would say foodborne exposures,
exposures in the food, in the food packaging,
in the food storage, in the food, in the cooking utensils.
We can go through the various things,
but we're doing that all the time.
We're eating all the time.
We're getting food into us, and these are bringing in in a way that we have some control
over some agency over, you know, we can make changes in our foods.
Very close to that is drink, you know, food and beverage.
So first of all, I've talked about this a lot.
I've written about it in my book.
I'm also, as you know, involved in a movie where in the movie, that might be a good time
to talk about that. What we do in the movie, the movie is about six couples that are infertile.
They haven't been able to conceive in 12 months, that's the definition.
And then a company that I work with, Million Marker out of Berkeley, has a trained staff
that interviews them, not only them, but anyone
who signs into this company, interviews them and ask them what they use.
What do they use for their facial care?
What do they use for their shampoo?
What do they use for their cleaning products and their laundry detergent?
And what do they store their food in, and on and on and on. So this is long inventory that they take
of all products that people are aware of using, okay?
And based on that, we identify likely bad players
in the list.
So how we do that is another, you know,
we can talk about that later.
But then in the film, and in this little, it's actually an experiment that I designed
and we're called an intervention.
And we are then intervening in their exposures by changing out these things that they told
us.
So we will tell them, you know, don't use any product with fragrance, for example.
That's a major source of exposure to phthalates.
Any product.
Any fragrance product.
If fragrance is added.
So no perfume, no lotions, soap with fragrance.
Right.
Even essential oil fragrances like lavender.
Essential oil is a tricky.
Right, it's a mix.
It's a mix, yeah.
So I'm going to, that's guarded.
But anything, you know. Spray deodorants It's a mix. Yeah. So I'm going to... That's guarded. But anything, you know...
Spray deodorants, roll-on deodorants.
Laundry detergent.
Shampoo.
Yep. And if you can smell it, it's probably affecting your hormones.
I'm so happy about this answer. Not because I have any stake in any company related to
fragrance-free stuff, but I have a very strong sense of smell, and I either love or hate smells, and I hate synthetic smells.
Going through the duty-free, especially in a European airport with all the perfumes,
and I'm just, I was going to hold my breath.
It feels like I'm breathing poison.
I know.
Well, you are, actually.
Yeah.
Yeah.
In some sense.
And most soaps, right. Yeah. Yeah. In some sense.
And most soaps, right.
Yeah.
Super interesting.
So that's your primary intervention, is to tell them get rid of anything with fragrances.
No.
That's only one thing we get rid of.
So then we talk about how the plastics that they use to store their food, food storage
containers, try to get them to get rid of those if they're made of plastic.
We try to get them to get rid of their non they're made of plastic. We try to get them to get rid of their non-stick pans
because of the PFAS chemicals that are in those
and so on and so forth.
So we go through all steps of their life
and try to tell them how to make changes
that will reduce their exposure.
But presumably also changes,
like if the man is obese, for instance,
you might have him walking a bit more.
No, no, no.
You don't touch any of that?
Well, you see, Andrew, if we did that,
we would be mixing up two interventions.
We would be mixing up an obesity intervention.
I see, this is a study.
I'm sorry, I thought that this group is missioned
with helping couples get pregnant.
No, no, this is a study to look at what happens
if you make these product-related changes.
Great.
Just product-related changes.
Right.
Exactly.
Love it.
Okay.
Thank you for that clarification.
We would love to do and probably will do another study, separate one on obesity.
And a lot of these chemicals, just to let you know, are obesogens.
They increase obesity.
There's a book out called Obesogens.
You can read about them.
And so there you know, it's very, you know,
there is some overlap.
So by reducing some of these chemicals
that are in your food storage containers,
you're also reducing Obesogens.
So it's not a clear, you know, yes, no.
We gave them a box, each couple, I went to their house,
six couples around the United States with a big box.
And in this box are these alternative products.
And so, you know, straws and bamboo spoons and $500 per box, I think it was approximately,
it had to do with their personal exposure.
And then they made these changes. Now, unlike another study that you reported,
they are at the end quite happy to keep doing this,
by the way.
They love this.
They love doing this.
It was so gratifying to see that they felt,
in many, many ways, their life got better.
I'm pretty careful in what I,
so I hesitate to say this because the data is not hard,
but the impression is that they are happy, happier.
They're sleeping better, they report more energy
and so on and so forth, having made these changes.
We need to follow that up with hard data.
I'm not writing that.
I'm not, you know, but I can say, and I can write,
that they felt very positive and are,
we're gonna go back and see if they did continue.
We need to do that.
But at the end of the six, of the three months,
they, and hopefully in six months, they will,
they are still making these changes in their lives.
Did you collect data on whether or not
they were able to conceive
after having made these changes?
Yes, we did, but I actually can't talk about that.
Can't talk about it until the babies are born.
Just kidding.
And we did get their sperm count at the beginning
and the end and had some very interesting data on that.
Too early to report.
Yeah, too early to report.
Let me ask you this then.
I appreciate that the not wanting to share specific results until all the data are in
and it's published.
If somebody listening were having trouble conceiving for 12 months or more, are the sorts of replacement interventions, product interventions that
you're talking about here, things that you would at least feel comfortable saying might
be a good place to start or to explore?
Absolutely.
Absolutely.
There's no harm.
None of the changes are putting people at risk or doing anything that could be harmful
to them. I'm sure of that could be harmful to them.
I'm sure of that.
We're very careful.
Some are going to be cost saving.
I think that's where drinking out of plastic bottles far less, if at all.
Just for reasons related to wanting to reduce waste, I use a mason jar or I use these or
ceramic.
Although you'll probably tell me that the lining on the ceramic mug might have endocrine disruptors.
No, I don't.
Okay, great, okay.
Well, then I'll keep drinking.
But it's very reassuring to me that there are things
that we can do in terms of cost saving elimination
or replacement of consumables.
Buying in bulk.
That can improve endocrine status,
maybe fertility also.
Which you can buy in bulk,
bring a container to the store and fill it up, a fertility also. If you can buy in bulk, bring a container to the store
and fill it up, a glass jar,
instead of buying something in plastic,
you're winning on both ends
because those bulk products are cheaper.
One of the things I did with the couples
was go shop with them.
And we went around and we looked at various products.
And for example, we looked at the produce
and there was the option to buy freestanding
bunches of lettuce, heads of lettuce, or wrapped up in plastic bunches of lettuce.
And I said, let's compare the price.
I actually didn't know until we did it.
But the freestanding unwrapped lettuce was cheaper.
And I think that's, you know, because that makes sense, because there's work involved
in wrapping it up
and in the container and so on.
And so not only are you getting something
that's more toxic, but it's more expensive.
When it comes to reducing BPA exposure
and some of these forever chemicals that you mentioned,
seems like reducing fluid intake from plastic vessels
is going to be number one.
The primary source of BPA is in the lining of cans.
So any drink or soup or anything that comes in a can
is going to be-
Any can, all cans.
Any can, unless it's a high end,
elite company that's made the change from BPA to an alternative lining.
And they'll say that.
And by the way, BPA has some bad relatives, such as BPS and BPF.
And maybe you'd be interested in this story.
So when it came out that BPA was estrogenic, which is what it is, and by the way, it's
kind of the evil twin of phthalates because phthalates are anti-androgenic and BPA is
estrogenic, and phthalates make plastic soft and BPA makes plastic hard.
You don't want either.
Okay.
So when this came out that this was a bad thing,
the manufacturers started selling things that say BPA free.
I'm sure you've seen that.
The trick is that instead of BPA, they use BPS.
Sneaky rats.
And BPF.
And these are chemicals.
These are lookalikes.
They're analogs.
And they're just as harmful.
Sneaky, sneaky, sneaky.
I'm not a conspiracy theorist, but it's just so dirty.
It's so dirty.
Right now is a really important time to be having this discussion because there's been
a lot of movement on Capitol Hill and there's been a lot of movement on social media about
trying to call attention to metabolic syndromes and highly processed foods and issues like this.
It's become unfortunately politicized.
I hear this stuff and I just think to myself, the only good faith that we can really trust
is our own desire to be healthier and to have our families and friends be healthier and
to try and 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.
They're going to do what they're going to do.
We just have to be informed as opposed to trying to dismantle the systems that led to
this, which just seems it like 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, now that I'm 49, I feel like.
But what you're saying is really important.
If I look at a can, it says BPA free.
It doesn't mean anything.
It could say have BPSs or other endocrine disruptors.
So drinking out of glass vessels, drinking out of ceramic vessels-
Metal.
Metal, but not cans, not metal cans, not aluminum cans.
Right, not cans, no.
Goodness.
Okay.
You can get a metal water bottle that's not lined with BPA.
Steel.
Steel, yeah.
Steel.
Yeah.
Is it true that microwave safe just means that the plastic won't melt in the microwave,
but it's-
Do never, never put plastic in a microwave.
So here's the story.
The BPA phthalates plasticizers are added to the plastic, but they're not chemically
bound to it.
Okay?
So, if you put anything in a container that has these chemicals in it, they will, and
then put it in a hot environment, they will come out of the plastic and go into the food.
So, if you, in a microwave microwave or you put your bottle in the car
and the sun comes in and it warms up the bottle
and then the stuff goes into your water.
You don't wanna mix these chemicals and your food,
but if you do, the worst thing is to do it
in a heated environment.
I think about all the food that was consumed in college
in the 90s and 2000s, like the cup of noodles with the styrofoam,
the things in packaging.
Stuff like that 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,
grass-fed, grass-finished 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?
We have to do that experiment, I don't know.
Yeah.
So I guess, so it sounds to me like not drinking out of cans,
not drinking out of plastic bottles.
It's gonna be not microwaving plastic ever.
And in general, just avoiding plastic intake.
If you can afford it, buy organic.
So you're going to avoid the pesticides, and then phthalates are actually added to pesticides.
And they're added because they increase absorption.
So you know that 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, absorption.
Anything that's absorbed in the body
is gonna have phthalates in it.
And it also holds scent and color.
So it's added to those scents and it's also added
to your lipstick and to your color, you know,
whatever you put on your face and so on.
Anything that holds scent and color,
that's gonna be phthalates.
I'm sorry.
I've been accused online of being a sunscreen truther.
I'm not 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 dermon-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 chemicals-based sunscreens are safer.
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, et cetera.
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 Environmental Working Group?
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 them.
They have consumer guides.
And in those consumer, so Environmental Working Group, I'm not part of them, but I like their
work.
And in these consumer guides, you can put in the product and they have categories.
You can put sunscreen.
If we had time, we could do it right now. And then you can put the name of your sunscreen 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.
And then if the number is less than 10,
it'll tell you why.
Are they independent of any funding?
Yeah.
That question will probably come up for you too.
People will say, where did she get her funding?
You know, people get very suspicious about this.
I can tell you.
Yeah, that'd 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, second sperm decline analysis
and the publicity of my book.
So it's a foundation.
So it's philanthropy.
Yeah, it's philanthropy.
And it's actually not a lot of money.
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 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 the,
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 psychological
and emotional issues.
Yeah, yeah.
Yeah, okay.
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 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, our water, I worry about the water.
I studied water for a long time in my past life. So we actually distill our water. So we have a
tabletop distiller. My husband, Stephen, 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.
No, distilling.
Okay.
Yeah. So it's steam 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.
Somebody 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 whenever I can think about it.
We can't use too much because you'd be too busy.
You always do that.
But he does it once a day.
It's just the two of us.
So water is important.
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 PFAS chemicals.
So that's actually, I'm not 100% good on that,
but we try to do that.
And I'm careful with the products I put on my face.
I check them out the way I suggested,
environmental working group.
And I go to the farmer's market.
I always buy organic, always buy organic.
But I know that's a cost issue for some people
and an availability issue for some people.
In San Francisco, you can do that.
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 it turns out there's a lot of, 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 erring toward cotton as opposed to synthetic materials.
Synthetics, right.
And the dyes are important.
So 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 I'm just saying that's another area that
I think people will soon be paying attention to. There's also the area that is much more
difficult, which is what's in building materials and furniture. But a lot of these PFAS and
the flame retardants 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 it's really challenging to think about
if you were gonna do this right,
and you were gonna 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
and you do the inverse of everything that's there.
The inverse of everything that's there,
including alcohol intake,
which is robust on the Simpsons.
But interesting, so, and when it comes to food sourcing,
like a 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 farmer's market,
but this stuff can get pretty tricky, pretty expensive.
And most people listening are not gonna be, you know,
living in Sonoma where they might have a neighbor
that has chickens or something.
Yeah.
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, and I know it's okay.
But I know that's not the case everywhere.
So I think being aware, honestly, is a really big step. If you are 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, young 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 toys and sippy cups.
And my understanding is that BPAs were banned
from sippy cups.
Thalates.
Thalates, excuse me.
Based on my work.
Based on your work.
Thank you so much.
Thank you for the clarification truly
and for the work that led to that.
We have this 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, So, there are literally laws in place and restrictions in place to make sure that 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.
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 lotions, et cetera, that you're aware of,
that are prominent here in the US?
Maybe that's a good filter to play some of this choice-making through. et cetera, that you're aware of that are prominent here in the US.
Maybe that's a good filter to play some of this choice making through.
Europe has had a policy called reach and under reach, you have to show that a chemical is
safe before it's put into the marketplace.
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 years, $10 million, by the way.
So if you're going to wait for that, I don't know, given the number of chemicals out there,
80,000 or more, forget it.
So I think the reach policy of testing before something's put in the market is making a
big difference in Europe.
I think that's one reason why they're much better off.
Are those animal tests or animal and human tests that they're doing over there?
Whatever defines safety, it depends on the chemical, it depends on what the product is.
I can't answer that in general.
So that might 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.
So you know that, you might not know,
but should know that phthalates are very prevalent
in the hospital setting.
There, if you think of a tube, you know,
to dialysis, to chemotherapy, to IV, it's all
plas, that's all phthalates, right?
And that's going into your body.
And there was a recently a 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.
Yes. DEHP bag. Yes. The bags could not contain these endocrine disruptors.
Yes.
DEHP specifically.
DEHP.
Diethylhexylthalite, the most anti-androgenic saline.
So that was a great step forward, 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, BeBron, 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,
polyolefin.
And the problem is that we're not sure about the safety of polyolefin. And the problem is that we're not sure about the safety
of polyolefin.
So it gets really difficult.
You can say remove DHP, 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.
No, that's okay. 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 the 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.
Yeah, I'm thinking about this.
A former president of Stanford, who also happened to be a family friend years ago, he's since
passed Don Kennedy when he retired as president of Stanford.
My understanding is that he went and directed the FDA.
And I was just thinking to myself, when did this happen?
Because I know he was super into health.
He was like an avid runner.
He was very fit well into his seventies.
He had a 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 there's a lack of interest
in health at the level of, it was like the FDA.
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 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, but maybe they're more
significant issues.
Who knows?
The seed oil crowd is pretty intense and I like olive oil anyway, so I err to that.
But I think if people are interested in limiting their exposure to these endocrine disruptors,
one of the key questions that's gonna come up again
and again, especially in light of PCOS and sperm counts is,
we can't control what happened to us during pregnancy.
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 that there's plasticity and resilience to this system?
So God forbid if somebody was exposed to a lot of these things early on, can they, 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 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 his sperm count.
He can stop and his sperm will be restored.
He can get his 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 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 in within your child.
So germ cells are not germs as in infectious germs.
Right, right, right.
It's the cells that will produce the egg and sperm
that germinate, hence the word germ.
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 gen...
Some labs say it's seven generations.
I don't know if that's true,
but certainly three generations are affected.
And so I should mention my book.
Can I mention that?
Yeah, please, I'll mention it.
Yeah, I believe I mentioned it in my introduction.
Yeah. 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
You need very practical things you can do and also websites you can go to and links you can go to now this
Came out in a while ago. So 21 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 the sorts of things you're talking about?
Is there a whole field of this, of 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 you're the most public facing and prominent.
I guess my question is, is the NIH funding a lot of this sort of thing?
Absolutely.
We're an army and it's not international.
There is now a global plastics treaty
under negotiation by the way.
Tell us about the plastics treaty.
People are trying to create, get passed by various countries
an international plastics treaty.
I can't, I don't wanna talk a lot about it.
I'm not involved in that process,
but in the process you could could see, if you looked into
there, hundreds of scientists and concerned citizens and activists and people in legislation
who are working specifically on the chemicals in plastic.
Now, plastic is really a bad actor,
but it is not the only bad actor.
So I wanna just mention that plastic is really important,
but 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 you asked about scientists in this area, Including our exposure to plastic is huge.
You asked about scientists in this area.
Yes, there's a huge amount of science going on for this.
It's funded by NIH and it's funded by the EU and primarily, I think those are the two
funders of Scandinavia has funding within Scandinavian countries.
There's a lot of work and a lot of very good people working really hard, but it's a huge
problem.
It's been here since, well, plastic started to rise in popularity in 1950.
We have 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.
And control of infectious disease.
And control of infectious diseases.
But lifespan is definitely increasing.
Whereas the use of plastics has clearly increased.
And so I guess one could argue that we're living longer, but we are less robust than we were,
less reproductively competent. Is that- The people that are reflected in that long
or 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,
and there were other things, of course,
but not as they are today.
So 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 industries somehow driving that longevity.
Absolutely not.
Absolutely not.
I think what it's driving is 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 so this is a 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?
This is true in other countries as well.
Yes, absolutely, absolutely.
It's all over the world.
And the decline in fertility, in my mind,
is probably, well, one of the biggest challenges
we're facing now, because it's everywhere,
it's very acute, and there's only limited things
we can do to counter it.
There's a wonderful website, 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
put in, you know, plug in a country or a year and see what the fertility rate in each country
in the world each year, and you can see that. And what you see is that a decline, about the same rate as sperm decline, by the way,
about 50% in 50 years.
And 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, 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,
or we can talk about it.
I don't know if you want to go into that,
but it's not just burn count for sure.
You know along those lines,
let's talk about egg count and quality.
You mentioned the PCOS results earlier.
Before we were on Mike,
you mentioned an interesting study that you did
about the use of electric blankets
and assessing whether or not the use of electric blankets
had impacted egg
number or quality in women?
And the answer was?
Actually what we looked at in women, I'm sorry to correct you, but it was the outcome of
their pregnancy, their fertility and if they got pregnant, how did that turn out?
Excuse me.
Thank you for that clarification.
But I'm sure there'd be a lot of other studies that have looked at that.
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 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 for sperm count and motility, aka quality, 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,
I'm gonna be careful here,
impact sperm count and motility quality,
but direct effects of EMFs on sperm,
there's no evidence that it is disrupting sperm,
at least to my knowledge.
Honestly, I have to say, just gonna say I don't know,
but I do know that heat is related
to fertility and sperm count.
And 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, there's less. So, 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 we'll see what they find.
Yeah, the data on sitting more than a few hours a day, on having legs that are very
large as a consequence of obesity, or even just that are large, heating the scrotum.
And those data are fairly, 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 the features that it does
to move the testicles further or closer to the body.
Getting back to egg count and quality, there's some evidence that girls are entering puberty
earlier 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 I think that's right. I think there is growing evidence that earlier fewer...
It's also called premature ovarian failure,
so that women are just not producing the eggs
as long as they used to, yeah.
But, I just wanna say something about the fertility.
Can we go back to fertility?
Please.
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, fewer children are being born.
A, 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 delay childbearing till they're no longer as fertile, 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 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 so the decline in fertility in non-human species
cannot be attributed to delayed childbearing
or use of contraception or entering the workforce.
Or rent crisis, right.
And it's interesting because 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 it was about to go distinct.
Like the Florida panther.
Or we hear that there are these species
that are like there's a very small subset of them left.
The black-footed ferrets in Montana,
I think one ferret, his name is Scarface,
sired something like 300 litters that then led to the,
eventually they started outbreeding
because if you do too much inbreeding,
obviously it's not good.
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.
When the black-footed ferrets, I know it might sound kind of silly, but 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 on bugs.
I'm not an expert in this, but one doesn't have to be an expert
to understand.
You move one pin here and the whole web moves.
You move one node and the whole web reconfigures.
That's what nature has been doing for millions of years, right?
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
an outrageous sci-fi movie.
No, that's 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.
Ixie, the literally gentle grabbing of one's sperm and forcing it to fertilize the egg
is something we've covered on this podcast in our fertility episode with Natalie Crawford
and a solo episode that I did.
There are questions that people have, reasonable questions about whether or not the offspring
of those types of scenarios are the same as the genetic probability experiment, as you
mentioned before, of having 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 for example, I don't know if you've heard
of gametogenesis, so it is now possible to create
an embryo from a sperm cell,
from a skin cell, skin cell can produce
a sperm cell and an egg cell.
So you give it the right transcription factors
and you can-
So this is kind of interesting, exciting and scary, right?
This is like the, what is it?
I think the vultures, the females,
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-party IVF.
I don't know if you're aware of this.
This was developed where there's a mitochondrial disease.
You can take the two eggs, one from the intended mother.
You take the nucleus, so you get the
DNA, you put it into an egg of somebody where the DNA has been removed, but where the spindles,
which are rich with mitochondria, are from 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.
And in theory.
Legal issues must be.
But in theory, this would allow women of any age,
provided they still have eggs, to have their DNA propagated
forward, because the DNA can be put into a younger egg that they still have eggs to have their DNA propagated forward
because the DNA can be put into a younger egg
that has the spindle quality that allows for,
the production of more cells.
I mean, this can and has been done in humans.
Yeah. Yeah.
So we're, I mean, you and I won't think of all the things
that will be developed in the next 10, 20 years
to meet the challenge of declining fertility
by ordinary conception.
I mean, I think that's how we're gonna solve
this problem for us.
We're going to just be smarter and smarter
about how to do a medically assisted conception.
And then the question is going to be an alternative to do a medically assisted 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.
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 in a test tube or
whatever.
And then you can say, well, maybe that's because the father was infertile and he's got inheritance
from the father from that.
You know what I'm saying?
So you can't know whether the, 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.
Yep.
Yeah.
Super challenging, fascinating problem.
So in anticipation of this sit down together,
I put a question out on X, formerly known as Twitter.
I let people know that I was hosting an expert
in endocrine disruptors, in phthalates,
and pesticides reproductive implications, et cetera.
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, 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, difficult
word to say, can also be effective,
etc.
There were a lot of questions about cosmetics and laundry detergents.
I don't know if we discussed laundry detergents.
What do you use in terms of laundry detergent?
Presumably one can find-
I don't even remember.
Okay.
Don't go by my products.
Okay.
For one thing, I'm not gonna be pregnant anytime soon.
I believe there are some solutions related to that.
Like instead of bleach, people can use hydrogen peroxide.
I can't speak about specific products actually.
Okay.
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 company.
Well, they are a company.
Look at Million Marker.
I think you'd be interested.
Okay.
Great.
And the person who runs that, Jen Hua, is a who, and a friend of mine, and we're going to be
writing a grant together.
And she participated in the film.
So our participants sent their...
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 wanna think about it, might be interesting.
And then if you pay another hundred,
I think you get this counseling and so on, blah, blah, blah.
So you can see the different levels.
But she knows all about products.
I don't know about product, because it's a moving target.
And also I don't like to talk about product names
because it sounds like I'm endorsing them.
So.
Right, and we won't expect you to give product names
and I'll follow your recommendation that you just gave.
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.
I saw that.
It's wild. It's so scary.
It's so scary.
I sent it to Rogan and he, I won't,
he was like, whoa, his version of whoa.
I was like, I also said, whoa.
He probably said, holy shit, right?
Or worse.
No, no, I'm not gonna say what it said,
but it was, he didn't curse.
There were a number of questions about household items.
Again, we're 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 find the ones that don't?
Yes.
Okay.
Receipts, how serious is it?
Should we be concerned about the BPAs and other endocrine disruptors on receipts?
Yes.
And my suggestion is just ask for an electronic receipt
and then you don't have to deal with it.
But they're definitely absorbed into your body.
Any impact of endocrine disruptors
of the sort we've talked about today on the thyroid system?
Yes. Presumably on the thyroid system. Yes.
Presumably in the bad direction.
Yeah, I mean, this is an interesting point.
Let me just say another word about it.
So there was an ongoing study in the Faroe Islands
off of Denmark, and they studied PFAS chemicals
and showed that people who fished there, there were fish
people and they ate the fish and they were getting high levels of PFAS in their body
and had, and this is published, effects on their immune response.
So my concern, and I don't know if anyone's looked at this, is given everyone's
vaccination feeling, 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 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?
Things like sweating.
Are there ways to improve liver clearance of these endocrine disruptors?
The answer to that depends on the class of chemicals.
So the chemicals that are water soluble, in particular 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 PFAS chemicals, pesticides are...
So 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, et cetera?
Lots of questions about atrazine,
questions about ointments and fragrances you've covered.
And I must say that as I scroll through these hundreds
of questions, if not more,
you've done an amazing job at clarifying for us
what's known, what is not known,
and essentially where it's a probably should avoid, definitely avoid,
and look, we just don't know.
Right.
And I- Well, you know, I have to distinguish
between we 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, sure, sure.
Right?
It's a huge field.
So, you know, maybe with some, you know,
ask the question of chat GPT.
Yeah, we'll be certain to ask chat GPT
and we will be certain to ask other experts in these areas.
But 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 this chemist that you mentioned,
that you stored the urine of those pregnant women,
that you analyzed it and that you've gone down this path
of exploring things that are really disruptive
to our health and
potentially to the existence of our species.
As we talked about earlier, there is the possibility that we go extinct not because of a meteor
but because we fail to replace ourselves and that we fail to replace ourselves because
we destroy our biological ability to replace ourselves.
I think it's hard for people to internalize that very real possibility because we destroy our biological ability to replace ourselves. I think it's hard for people to internalize that very real possibility because we feel
ourselves sitting in traffic with thousands of other people and go, there's too many people,
right?
This kind of thing.
But 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 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, especially in terms of consumables that they've spent their hard-earned
money on, have been-
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 possibility
and a sense of agency over these things.
And I love that you weave your math
and statistics and probability theory background
into all of this, because what comes through
is 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.
Thank you.
It's been really fun.
Thank you for joining me for today's discussion
with Dr. Shauna 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.
Also, I should mention that if you're interested
in learning more about microplastics
and endocrine disruptors,
I did a solo episode of the Huberman Lab podcast
on that topic,
and that is also linked in the show note captions.
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