Are chemicals in our products making us sick and obese?

Dr. Rob Lustig discussed newly published landmark research showing how certain environmental toxins can lead to obesity.

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Environmental toxins are one of the eight levers of glucose control—along with food, sleep, exercise, stress management, micronutrients, microbiome, and exposure to sunlight—but perhaps the least discussed. In April, Dr. Rob Lustig published, along with 44 co-authors, an extensive three-part research study on the causes of obesity. The second paper, “Obesity II: Establishing causal links between chemical exposures and obesity,” focuses on the environmental causes of obesity, specifically toxins in our food, water, and products. For the first time, the paper laid out potential causal mechanisms for this connection—what’s happening inside our cells when we are exposed to these chemicals. 

Dr. Lustig is the author of three books: Fat Chance, Metabolical, and Hacking of the American Mind. He is a Professor of Pediatric Endocrinology at the University of California, San Francisco. In a recent episode of our podcast, A Whole New Level, Dr. Lustig talked to Dr. Means about the research. Here’s an edited transcript of that conversation. 

 

 

Dr. Casey Means: We’re talking with Dr. Rob Lustig about obesogens, which are these invisible, small molecules that exist throughout our environment that are minimally regulated and which, through several mechanisms, we’ll talk about today, impact our core metabolic physiology.

These are chemicals that are put into our food, our water. They’re in our air, our soil, our home care products. They’re in our personal care products. They’re in our mattresses. They’re in our furniture. They’re in the containers that we store our food in. 

Rob has published, along with 44 other authors, a series of papers looking at the mechanisms of obesity. One of the three specifically talks about obesogens, which are these compounds in our environment that are now mechanistically shown to cause obesity directly, and may contribute to about 15% of what leads to obesity. The key point is that we’re now showing not just correlation but causality related to obesity.

Since 74% of American adults are dealing with overweight or obesity, this is a topic relevant to almost everyone. And these toxins also affect the genetics of our eggs and our sperm. So they can have an impact on the next generation and our offspring. 

Rob, welcome to A Whole New Level. We’re so excited to have you back.

Dr. Rob Lustig: It’s always my pleasure, Casey. I’d rather spend time with you than anybody else.

Dr. Means: I am so excited about this topic we’re discussing today. It’s so important because it is so under-recognized. So jumping right in, if diet and exercise weren’t enough for us to get on top of, now we realize that chemicals in our food, our water, our air, our personal care products, and our home products actually may directly contribute to weight gain and obesity. And I think this might be fairly shocking to people who already feel like we’re up against a lot in terms of being healthy in the US. So I think my first question for you is, why do you think that this topic has flown so under the radar so far that these chemicals that are everywhere are directly promoting weight gain?

Dr. Lustig: Well, ask the same question about why all these chemicals out there are causing cancer and why they flew under the radar for so long. The fact is you can’t see them. You can’t determine what contains them and what doesn’t. You can’t determine whether there’s cause and effect unless you do large studies, which are hard to do and hard to fund.

The fact of the matter is we had a belief system that said that obesity is due to too much going in and too little going out. It’s all about calories. And if you believe that the problem is calories, then why in the world would you be looking for chemicals that specifically cause weight gain? After all, those chemicals don’t necessarily have any calories.

So there are a lot of reasons that people have ignored this field, but the toxicologists have known about it and have been studying this now for about, I would say 15 years. And I’ve been aware of it since 2007. And the NIH has specifically funded research in this field to try to bring it to fruition, to determine whether or not this is a real cause of obesity that we have to be concerned about or whether this is just another thing along for the ride or just a diversion.

And this paper that’s coming out now, which has 44 authors, all basic scientists, and clinicians in biochemical pharmacology, a real journal, 48 pages long, basically puts the marker down. It’s the line in the sand and says, “This is a real thing, and it is not just correlative. It is causative for obesity.”

Now it is not the whole enchilada. It’s not like everything is an obesogen. I mean, diet still plays a major role. Exercise still plays a supportive role, not a major role, but a supportive role. But these obesogens probably account for a good 15–20% of the obesity problem. And the sad part is most of these obesogens are forever chemicals, and they’re not going away anytime.

 

What are Obesogens?

Dr. Means: Let’s define some terms here. First of all, the paper talks a lot about the term “endocrine-disrupting chemicals,” EDCs. And then, of course, the term obesogen. These might be new to people, so can you talk about what these mean? Also, maybe mention what you mean by forever chemicals and where they are found in our environment?

Dr. Lustig: An obesogen is a chemical that specifically drives fat cell accumulation. That fat cell accumulation can occur in subcutaneous fat, as in “does this swimsuit make me look fat?” or it can drive visceral fat, as in “my belly is fat,” or it can drive liver fat or muscle fat that may not necessarily even show, but will cause chronic metabolic disease.

Obesogens are chemicals that bind to receptors. Receptors are proteins in cells that take information from the outside and alter what happens to the cell on the inside. And in the process, those cells then take up extra energy and lay it down as fat. Now, some of the obesogens are caloric. For instance, fructose is my favorite compound, but most of the obesogens are things that are found in everyday items within the home, outside the home, and in particular things like agricultural products.

So let me give you some places where you might not think about obesogens being. How about vinyl flooring? How about flame retardants? How about electronics? How about pesticides? How about disinfectants? How about thermal paper and resins? How about personal care products like lipsticks? How about drugs, like prescription drugs?

All of these have the capacity to bind to receptors in the body, and several receptors are involved. The important ones are the insulin receptor, the glucocorticoid receptor, PPAR gamma, peroxisome proliferation activated receptor gamma. There’s an aryl hydrocarbon receptor. There’s the farnesoid X receptor. There’s the androstane receptor. 

There are a whole host of receptors, and several chemicals in our environment are promiscuous and will bind to these receptors and cause the cell to change how it processes energy. And in the process, you lay down, fat. So this is a real thing, and the point of the paper was not just to demonstrate that these mechanisms are associated with obesity but actually that they are causative. So we can’t ignore this problem anymore.

 

How Obesogens Work In Your Body

Dr. Means: In terms of what these molecules are doing, they are in some way changing the way that the body is able to make energy, this fundamental core pathway of metabolism. And when that gets perturbed, and we’re not producing energy properly in the body, it causes us to lay down more fat. So, that sounds like a key concept people need to understand is that anything that disrupts our energy-producing pathways of the body can, in turn, lead us to essentially accumulate more fat.

Dr. Lustig: Absolutely. And there are several different mechanisms involved. There’s epigenetics and methylation. There are histone modifications. There’s RNA methylation. There’s chromatin remodeling. There are micro RNAs. And then, of course, there are direct receptor effects of their own. And these mechanisms can occur before birth. In utero, these things can be going on. We have the data to show that women exposed to these compounds end up having offspring that are both more obese and have metabolic syndrome later. And we have found that fetal and early childhood is the most vulnerable time.

So this is a time when you can’t blame the patient. You cannot blame the four-month-old. And the problem is that four-month-olds are exposed to lots of these—for instance, baby bottle nipples have BPA. Or phthalates—these are compounds that are plasticizers that are pretty ubiquitous.

If you ever open a can of food and see a white lining inside, that’s BPA. So it’s in all of our food, and BPA is one of the primary drivers of this problem. When you get a thermal receipt from Target or any other store, there’s BPA in that thermal paper. So we’re all exposed to this stuff all the time, and it has effects on all aspects of energy metabolism within the cells at the molecular level.

And it’s causing changes in epigenetics. It’s changing, not the DNA coding, but the DNA expression. And it binds to these protein receptors to drive fat cell accumulation. It drives mitochondrial dysfunction to cause mitochondria not to function as well, thereby reducing the rate of energy burning. It’s been shown that body temperature has gone down like half a degree across the board over the last 25 years. You cannot explain that based on diet. Why is body temperature lower today than it was 25 years ago? Well, it’s because our mitochondria aren’t burning energy and giving off heat at the same rate. So what’s causing that? Well, it’s very likely these obesogens that are affecting mitochondrial function.

Dr. Means: That is so interesting about the temperature going down and just thinking about our bodies as these poorly working furnaces that are not generating heat appropriately. And when we think about the fact that we’ve got these 37 trillion or so cells in our body and every single one needs cellular energy to function and that we’re surrounded by these invisible chemicals that are essentially making that harder to do, it’s ominous.

You talked about some of the mechanisms. In the paper, you go through dozens of different chemicals in our environment that can lead to problems and are obesogens. And you talk about several mechanisms of how they’re actually doing their harm. You just mentioned epigenetics. You talked about direct receptor targets. You talked about mitochondrial dysfunction.

Can you kind of go through each mechanism briefly? Take us to the level of the cell. 

Dr. Lustig: Okay. So the first thing the audience should know is that there is not one paper. There are three, and they’re being published as a group in Biochemical Pharmacology. And the first one, which I am the first author on, is an overview and also the molecular and biochemical mechanisms by which obesity occurs in cells.

The second lists the obesogens and how they work and demonstrates that they are causative of obesity, not just associated. And then, the third paper is a little bit more technical. It’s on obesity assays. How do you determine whether or not a chemical is an obesogen? What criteria does it have to meet? That’s its own paper. And each paper stands alone.

So the two papers, obesity one and obesity two, are what we’re really talking about today. You have to understand that cells take in information, and they take in information through proteins that are on the surface of the cell or inside the cell. And these proteins are called receptors, and the receptors are for hormones. And there are receptors for chemicals and some chemicals mimic hormones, and some chemicals just bind straight to the chemical receptor.

Now, those receptors can ultimately have effects on adipose tissue differentiation. They can take stem cells and turn them into adipocytes.

Dr. Means: Fat cells.

Dr. Lustig: Basically, you increase the number of fat cells. This is particularly problematic in utero and in the baby. Babies exposed to these chemicals will end up being more obese because they have more fat cells. And it’s often been said that your number of fat cells is determined by the time you are two years old. That’s likely true when we have some data based on atomic bomb testing that has shown us that, in fact, the adipose tissue number doesn’t change that much after age two. Still, the adipose tissue has to grow before the age of two, so these receptors are very, very attuned.

And if you are exposed to these chemicals—and I know this because I took care of these children in Salinas, which is in the middle of the California Central Valley where lots and lots of crops are grown. It’s an agricultural community, mostly immigrants from Mexico. And we’ve done a study along with UC Berkeley called the Chamacos study, where we measured these chemicals in the urine of pregnant women about 25 years ago and have watched what happened to the offspring in terms of cognition, in terms of puberty, in terms of obesity ever since. And what we’ve shown is that the amount of chemicals in the urine of pregnant women specifically predicted what would happen to the child afterward in terms of puberty and obesity.

We now have these data to show that we’re poisoning our fetuses, and the most vulnerable people are the people who are exposed to these at the earliest time points. So that’s one issue. 

A second issue is that, as you know, women are different from men. Women have curves. Those curves are subcutaneous fat, and those curves are determined by estrogen binding to the estrogen receptor.

Well, it turns out that the estrogen receptor is the most promiscuous molecule on the planet. All you have to be to be an estrogen is have two hydroxyl groups 22 angstroms apart. And you’re estrogen. For decades, we’ve known that women who were given DES, diethylstilbestrol, when they were pregnant back in the 1950s ended up with babies with significant congenital disabilities. And so, DES has since been banned, and that’s good, but it turns out that low levels of DES didn’t cause congenital disabilities. It caused obesity. And we’ve now learned that DDT, which was the first pesticide used commercially starting in the 1940s, is an obesogen and caused not just congenital disabilities but significant obesity.

This is, of course, the book that Rachel Carson wrote called Silent Spring back in 1962, which started the environmental movement. Well, guess what? DDT is not around anymore, but its metabolite DDE is, and DDE is an obesogen, and it still can be measured in pregnant women’s urine. This stuff stopped being produced in 1972, but we could measure it in the urine of pregnant women in 1999.

So 27 years later, this stuff’s still around. And the amount of this stuff predicted the obesity in the offspring of those women. This is extraordinarily worrisome because if it’s still around and it’s not going away, what are we going to do? Well, PFOA, perfluorooctanoic acid, also known as Teflon—you don’t see any frying pans made with Teflon anymore. If you have ever seen the movie Dark Waters with Mark Ruffalo (2019), it’s all about the Teflon scandal and what DuPont did to hide the information. The fact of the matter is PFOAs are still around; PFAS, as they’re called, perfluorooctanoic substances.

These things are causing obesity even though they’ve since been taken off the market. And aside from those obvious ones—phthalates, plasticizers, PBDEs, which are flame retardants that are in mattresses and baby clothing—these are all things that are still around and are potentially, in any given baby, causing harm by laying down more fat and causing metabolic syndrome later on. So this is particularly worrisome, and it’s not going away.

Dr. Means: One thing I found striking about this paper, Obesity II, is some of the other mechanisms that were mentioned. You just talked about some of the effects of these small molecules directly on receptors on the cell membrane. Acting almost like estrogen to bind to these receptors we already have and having these downstream cascades. And then the effect on epigenetics, so how our genome is expressed, how it’s folded, and how that can affect our current life, but also can affect the next generation because epigenetic changes can be heritable.

Some of the other mechanisms were how these chemicals impact inflammation in the body, and how they impact oxidative stress. You mentioned mitochondrial dysfunction, the microbiome. And what struck me reading through this was that many of these were the same mechanisms you talked about in chapter seven of your book Metabolical. It’s basically like the overview of systems biology. There are just a small set of core physiologic disturbances that lead to almost all disease.

And some of these in the book that you talk about are oxidative stress, mitochondrial dysfunction, inflammation, and insulin resistance. It’s all the same stuff that we’re talking about how obesogens disturb the body to create obesity. 

That leads me to two questions. It seems like this is a far bigger problem than just obesity. I mean, obesity is a big problem, but it’s almost like the word obesogen limits the magnitude of what’s happening here. Because if it’s affecting all of these different pathways, our core hormonal pathways, our core energy-producing pathways, and our core mitochondrial dysfunction, inflammation, oxidative stress, et cetera, then this could affect all aspects of health. So do you, do you get the sense that these chemicals are not just about making us fat but making us sick in all sorts of other ways?

Dr. Lustig: Well, what you’re describing, Casey, is the fact that there is this larger grouping called EDC that is endocrine-disrupting chemicals. Within that, there is a subset of endocrine-disrupting chemicals called obesogens. So endocrine-disrupting chemicals do what you just said, which is bind to any receptor, cause any epigenetic problem leading into some aspect of cellular metabolic change that can lead ultimately to disease. And that can be reproductive. That can be cognitive. That can be cardiovascular or endocrine, or cancer. These are all endocrine-disrupting chemicals. And there are many, many different types, and there are many different ways they work.

This set of papers is just talking about the subset called obesogens. So all the ones we’re talking about are specifically related to weight gain in some fashion. But if you want to take the whole EDC field, we know about EDCs because we have cancer. We’ve shown 50 ways from Sunday that EDCs are important in the development of cancer, so that’s already on the map.

This set of papers is important because the concept of obesogens has been deep-sixed by a lot of scientists as being not relevant or not the big issue, or it’s still about calories. The fact that we’ve shown in these papers that obesogens are causative—causative, not just correlative—not just the result of a problem, but the cause of a problem is the big reason why I’m happy to talk to you about this now and the big reason why everybody should look at these papers.

The other thing I want to make clear to the audience is that people are focused on food. Hey, I’m focused on food. I wrote several books. I’m focused on food. The fact of the matter is food is more than just its calorie. There are a lot of things in food that shouldn’t be in food.

I mean, there have been a lot of food additives that the food industry specifically adds to stuff like emulsifiers, which can cause inflammation in the intestine, which can lead to leaky gut and, therefore, metabolic syndrome. And that inflammation can ultimately lead to insulin resistance, and the insulin resistance can lead to obesity. Also, how you grow the food. One of the compounds that we spend a lot of time talking about in this paper is a compound that everyone’s now heard of called glyphosate or Roundup.

Who hasn’t heard of Roundup? First made by Monsanto. And then Monsanto was bought by Bayer in Germany. And glyphosate’s been associated with cancer, with lymphoma in particular, but glyphosate has also been shown to be causative of obesity. And glyphosate is in almost every food, so the calories cannot easily be dissociated from the glyphosate. That is part of the calories because glyphosate is an amino acid.

Things get very complicated and hairy in trying to explain all of this. So can you get GMO-free? Can you get glyphosate-free? Can you get herbicide-free food? And the answer is, yes, you can, but boy, oh boy, is it expensive and it’s kind of hard. And there are parts of the country that can’t get it. So this is a perennial problem. This is a problem that’s not going away. And this is a problem that the food industry continues to promulgate and hides behind the concept of calories.

 

Natural and Artificial Obesogens

Dr. Means: That brings me to what is driving this problem? First, I noticed that some of the obesogens are naturally occurring. I think cadmium was one of them and arsenic. And then some of them are synthetic, like glyphosate and like phthalates and things like that. These are industrially manufactured. So can you talk a little bit about how these split between naturally occurring things and synthetically created things? Who’s the bad guy here?

Dr. Lustig: Well, a couple of bad guys, but yes, you’re absolutely right. Most of the obesogens are synthetic chemicals. Only a couple are naturally occurring. You’re right, cadmium is one. Arsenic’s another. Arsenic is found in certain water supplies. Cadmium is found in other products, but the main product with cadmium is cocoa and, in particular, cocoa from South America. I don’t know why, but that’s where there’s a high cadmium burden. Generally, shall we say, cheap cocoa tends to come from South America. I mean, there are cocoa plantations all over the world, but that’s the primary place where you find cadmium.

Most of the other compounds are synthetic in some fashion. They may have started as natural products and then been modified to be synthetic. A lot of them, as I said, are pesticides like DDT and DDE, like glyphosate. So they’re very specifically sprayed on food to keep the pests from getting them to them. Neonicotinoid pesticides. Permethrin, for instance, is another example of that kind of obesogen.

Hey, air pollution. Particulate matter causes inflammation, and inflammation causes insulin resistance, and insulin resistance leads to obesity as well. So diesel exhaust. Now, who would’ve thought diesel exhaust would’ve been an obesogen? But it is. The fact is the closer you live to a freeway, the more weight you gain.

People thought, well, that’s because people who live close to free freeways are of lower socioeconomic status. After all, that’s where they build housing projects, et cetera. And while that’s true, that’s all been factored in. And it has now been shown not just to be associated but causative. We have the mechanisms by which causation occurs.

There are two kinds of causative data. There’s experimental causation where you do interventional data. You don’t do that in humans. You do that in animals. But that we also have what’s known as econometric data, where you can look at natural history studies and you can show that the change in weight or the change in obesity rates are predicted by these changes. They’re not explained by anything else and that they predate the change in obesity.

That’s the point of the paper: explaining what level of data we have to show this. And we also show what aspect of the fat cell process is being affected, whether it’s the differentiation of stem cells into adipocytes, whether it’s the laying down of fat in the liver, whether it’s dyslipidemia in the bloodstream, whether it’s the fatty liver itself, whether it’s a neurological problem, or food, an energy problem, or a mitochondrial problem, or a microbiome problem in the intestine.

We now have the pathways for each of these chemicals. And we discuss the gradation of the veracity of the data, and the quality of the data to demonstrate when we know causation and when we don’t. And boy, oh boy, do we know causation.

 

Why We Need Regulation

Dr. Means: Is there a world in which our computing capabilities get good enough and our understanding of the mechanisms is strong enough that we could screen for chemicals that are being created in the industrial industry and know what’s going to be a problem and what’s not ahead of time or retroactively do this such that we can start eliminating some of these things? What’s the path forward from the industry perspective?

Dr. Lustig: Absolutely. And that’s the reason for the third paper is the obesity assays. The fact is that virtually all of these compounds have been put into our environment without any meaningful regulation or assessment by the FDA or the EPA or the USDA.

Just released into the environment. They’re “safe.” Who says they’re safe and how do you find out if they’re safe? We thought dioxin was safe for decades and only found out about the cancer that dioxin caused 40 years after it started appearing. They started being manufactured in 1902. And it wasn’t until a factory in Seveso, Italy, blew up in the 1960s that we learned about what dioxins were doing.

So how does this stuff get into our environment? How does it get into our food supply? How does it get into our water supply in the first place? The answer is no one’s looking. That’s the real reason. Well, the reason these papers are important is that we now give the government the tools to actually determine whether or not any given compound is an obesogen. And it has to be the government because who else is going to do it? The industry’s not going to do it. They’re the ones perpetrating the crime. Somebody’s got to be watching out. It ultimately is incumbent upon them to use this information to determine what should be allowed and what should not. And thus far, the government’s been asleep at the switch.

Dr. Means: What’s so perplexing to me is that if you Google molecules, which sometimes I’ll do for fun, I’ll just be like, “What’s the structure of this thing?” And it’s like you look at drugs, all of these are just these small molecules. A lot of them are like little molecules, hydrocarbons a few others. And it’s like we are allowing with these industrial chemicals … how is it different than drugs, in a way? These chemicals act on us like pharmaceuticals are, yet they are totally unregulated. And it’s like, what is that distinction between a company that comes up with a food additive or up with some sort of flame retardant and puts it in everything versus developing a drug and then marketing that and then having that go through FDA approval? There’s a really strange disconnect between basically just what people call these things, but they are essentially drugs, right?

Dr. Lustig: That’s exactly right. They’re compounds that are selective poisons. Drugs, medicines that we buy at the pharmacy and stand in line to get our prescriptions are selective toxins. That’s the definition of a drug. It is a selective toxin and these compounds are selective toxins. The only difference between the drug you get at the pharmacy and the drug or chemical that dump into the water supply or the food supply is that they don’t make any claims that it’s going to cure any disease or treat any disease. That’s the difference. If they claim that it was going to cure or treat a disease, then it has to go through all the FDA hoops in order to get approval. If they just dump it into the water, they don’t have to say a damn thing about it. The burden of proof is on you to demonstrate that it’s actually a problem. That’s what happened with Teflon.

How Obsogens Drive Craving

Dr. Means: Something you talk about in the paper is that these obesogens can actually change our desire, our food-seeking behavior, and the way we actually interact with food on the psychological level. If we don’t understand what’s driving us and how we’re hooked on the dopamine roller coaster, we basically don’t understand our behavior and how we’re being controlled by external forces. Maybe just  explain to people how these obesogens can also affect our dopaminergic reward system and impulsivity in our brains and what we should know about that.

Dr. Lustig: We actually got a little flack from the reviewers about including fructose and artificial sweeteners in this paper on obesogens. They said, “How can fructose be an obesogen when it’s caloric?” And the answer is because it lays down more fat than its calories. Yes, it is caloric, but it lays down more fat than its calories.

Dr. Means: Oh, wait. That’s interesting. Is that part of the definition? So you’d expect it to lay down a certain amount of fat but it’s actually doing more. It’s stimulating fat growth in some way, so it fits the criteria of obesogen?

Dr. Lustig: That’s right. So we had to explain that. And the reason is that it’s affecting mitochondria. So if it’s affecting mitochondria, then you’re going to lay down more fat because you’re burning less. And maybe that’s the reason why body temperature’s gone down is because of all the sugar in our environment. I don’t know. I’m not going to tell you I know the answer to that, but it’s not impossible that could be the reason.

Artificial sweeteners. Turns out artificial sweeteners make your brain think sugar is coming, so you release more insulin. Even though they don’t have any calories themselves, because you release more insulin, you drive more energy into fat. So they are an obesogen even though they’re zero calories, as an example. 

The fact is that anything that makes your insulin go up is a potential obesogen and some of those things are specifically added to food on purpose. These things are throughout our food supply. And again, some of them have been there because we didn’t know what caused these problems—for instance, glyphosate; chlorpyrifos is another one. Carboxymethyl cellulose, which is an emulsifier that’s used in ice cream. So you’d say, “Well, of course, ice cream’s fattening.” Well, yes. I’m not saying it’s not, but the fact is that carboxymethyl cellulose makes it more fattening.

Dr. Means: What is this doing to our brain in terms of actually signaling for us to want more food? What’s the mechanism there?

Dr. Lustig: For fructose, it’s a direct mechanism. For other molecules, it’s the insulin. The insulin going up blocks leptin, which causes it. And then for certain compounds like BPA, it appears to have some effects that are consistent with hyperactivity and attention deficit disorder, which then cause food intake as well. The dopaminergic system expresses obesogen targets. And I don’t know why. I don’t have the reason for why that should be, but that does seem to be the case in animal studies.

So that might be some of the reasons, at least, why we see people eating more and out of the blue. And several medicines that people are on, like SSRIs can cause you to eat more. Atypical antipsychotics cause insulin resistance and cause you to eat more. So certain pharmaceuticals that we take for other reasons might also cause increased weight gain and they’re listed in this paper as well.

How Obesogens Span Generations

Dr. Means: Getting back to the epigenetic part of the conversation, some of these impacts of obesogens are heritable. Interestingly, the average Levels customer is a woman between the ages of about 30 and 50, so reproductive of age. And obviously, everyone wants to do their best for their offspring and have the healthiest pregnancy.

You talk about in the paper these sensitive windows of vulnerability for endocrine-disrupting chemicals, including obesogens. And that there are periods of time where we are most sensitive to the effects of these things and some of those are during developmental periods. And you mentioned even in utero.

Can you talk a little bit about those sensitive windows of vulnerability? What this means for how we should maybe be approaching preconception, conception, pregnancy, early child development, differently in our country and individually? And maybe also touch on the heritability part and how these things are actually affecting our germline, meaning like our actual reproductive sex cells.

Dr. Lustig: Several of these compounds do affect the germline. If they affect the germline, it’s likely that it’s not just an obesity issue. There’ll be other issues as well, including reproductive and birth defects and things like that as well.

Dr. Means: Can you define germline for people? Because I think most people don’t know what that means.

Dr. Lustig: Germline means that the eggs or the sperm are affected and therefore once the zygote is made by the egg binding to the sperm entering the egg, now those genetics are fixed.

Dr. Means: The entire offspring cells. All their cells.

Dr. Lustig: That’s right. Scientists have shown that those can persist generation after generation. At least four generations and in some cases, even longer. So it’s not what your mother ate. It’s what your great-grandmother ate that made a difference and what she was exposed to. It’s the gift that keeps on giving throughout the lineage all the way down.

Now, those are things you can’t fix because you had nothing to do with them. The question is what could a pregnant woman avoid that could fix something? Well, one thing she could do is stop smoking. Okay. That’s the easy one. That’s the slam dunk is if you’re smoking, you better stop it. And smoking, secondhand smoke also has been shown to cause an increased BMI and waist circumference in the offspring.

There are probably several reasons, including nicotine. Including the fact that it changes the oxygen tension. The carbon monoxide changes the oxygen tension going to the baby while the baby is developing. So that’s the obvious one.

Another thing that we’re very concerned about is these artificial sweeteners—it turns out that adipocytes have receptors for artificial sweeteners. Why? If they’re noncaloric, why do adipocytes have receptors for artificial sweeteners? So if the mother’s drinking a Diet Coke during pregnancy, that artificial sweetener gets across the placenta and actually causes fat cell differentiation in the fetus, even though it was a Diet Coke? We know that the fructose is a problem. And we know that actually, if you look at the placenta, okay, the placenta of mothers who drink Coke—or not Coke but I mean, soda. I shouldn’t just pick on Coca-Cola because then everybody will go out and drink Mountain Dew instead.

Dr. Means: All soda.

Dr. Lustig: All soda. All soda. Okay, everybody. It’s not just Coke. But there are two parts to the placenta lining. One’s called the labyrinth and one’s called the decidua. And it turns out that if you take in a lot of fructose, the labyrinth gets smaller and the decidua gets bigger. And that ultimately is associated with insulin resistance.

Well, it turns out artificial sweeteners affect that as well. Now why it does that, I don’t know, but it does. So don’t smoke and try to limit your sugar consumption and try to stay away from artificial sweeteners as much as possible. I would say those are the easy things to try to do during pregnancy. Fetal life and early neonatal life are the most susceptible times because that’s the time when your fat cells are still in dividing mode. And you don’t want them to keep dividing unless that’s necessary. That’s what I would say is probably the single lesson for pregnant women.

Dr. Means: When we’re thinking about the sensitive windows of vulnerability for obesogens, is the take-home point that because our fat cells divide only until really a certain point, and then they go into more growth mode? We have a certain number of fat cells early in life and we think that’s still fairly fixed. Getting overweight is a function of them growing as opposed to dividing more. And because that’s happening early in life and obesogens promote laying down more fat cells, that’s part of the reason why it’s such a problem to be exposed to these early on. Is that accurate?

Dr. Lustig: That’s exactly accurate.

Dr. Means: What are those sensitive windows? Is it pregnancy specifically? Is it a wider period?

Dr. Lustig: Pregnancy is the big one without question. Early childhood too.

What We Can Do about Obesogens

Dr. Means: Summing up here: we are surrounded by chemicals and small molecules in our food, water, food additives, food packaging, storage containers for food, cosmetics, personal care products, furniture, electronics, air, pesticides, disinfectants, sunscreens, plastics, household products, antidepressants, and antidiabetic drugs, and cigarette smoke. So just a few places that these chemicals live. 

What’s the strategy here? What do we do? Because it sounds like we’re screwed.

Dr. Lustig: Let’s put it this way. If we do nothing, then we are screwed, yes. The point is that we can do something. First of all, we have to be cognizant of ourselves because no one’s going to protect you better than you can protect yourself. That’s number one. And if you don’t know that this is a problem, then you can’t protect yourself. All right? So that’s why this paper finally getting it out was so important. And like I said, it’s been a long time coming.

This particular paper’s been a year in the making, but we’ve known about the problem since 2007. So that’s number one, education about the problem because you can’t fix a problem if you don’t know what the problem is. 

Second, this paper tells the government, “Hey, you’re on notice. You got to do something and he here’s what you need to do.” We need the government to help us with these things because the food industry and the agricultural tech industry and the chemical industry have basically gotten a free pass for all these years. And that’s why the EPA was developed back in 1970—to stop air pollution and water pollution.

Well, this is environmental pollution and the EPA should be on top of this. But currently, they’re not because they didn’t think obesity was a problem. But they need to start getting their act together. And hopefully, they will now. People need to pressure the government and their congressmen to get the EPA on board with this. The EPA was basically dismantled under the previous administration. You actually had people who were oil drillers running the EPA. So we’ve lost a lot of time on this.

Now, what can individuals do? The answer is to buy organic because a lot of these things are pesticides. Use PFAS-free frying pans, which now are the only ones sold. But if you have old ones, you probably need to get rid of them. Be wary of food preservatives that are added to foods. And basically, eat real food. Real food is the answer here.

And BPA is now known. It’s in all these plastic bottles. It’s in baby bottles. It’s in nipples. These are hard, hard truths and they’re not going to go away easily, but we have to start working at mitigating some of these over time. And it’s not going to happen fast, but you got to start somewhere.

Dr. Means: I’m hearing buy organic. Don’t smoke. Avoid artificial sweeteners—sucralose, aspartame. We’re not talking about natural non-nutritive sweeteners here, like Stevia, monk fruit, or allulose. Is that right?

Dr. Lustig: Well, they can still raise insulin. So they’re not completely innocent, but there are some that are worse than others. Sucralose is famous for causing leaky gut and glucose intolerance. That’s a particularly bad guy in the story. In the paper itself, in figure four, we list all of the bad guys and there are quite a few of them. There’s the aspartame, acesulphame K, saccharin, and sucralose. Stevia’s on there. Neotame, alitame, monk fruit, miraculin. They’re all there. 

Dr. Means: That’s a good clarification. I actually didn’t see, that Stevia and monk fruit were on there. I’m assuming that’s because in some research it’s been shown that they raise insulin?

Dr. Lustig: Yeah. They’re going to drive the insulin receptor and the insulin receptor’s going to lay down fat.

Dr. Means: Generally, things that are sweet may impact our cephalic insulin response, make our brains think something sweet’s coming, and release insulin. 

What about personal care products and home care products?

Dr. Lustig: Parabens are in lipstick and yeah, that’s a big one. These are all concerns.

Let me tell you about a patient that I took care of years ago. There was a five-year-old girl who started developing breasts and so I worked her up for precocious puberty and it turned out that her hypothalamus was fine and her ovaries weren’t even working. So where was she getting the breast from?

I thought maybe she was consuming her mom’s birth control pills. No, that wasn’t it. And we went through everything and finally, I asked the mother, “What do you use in the bath water?” And it turned out, she bathes the kid in Victoria’s Secret bath gel. And I asked her to bring it in and it said right on it for adult use only. And the reason is that it contained genistein, which is a plant estrogen. Phytoestrogens and so cause breast development. Well, guess what? It also causes weight gain.

Dr. Means: The phytoestrogen concept is really interesting because people bring this up a lot with soy. I’m assuming that this is the differential effect in a child. Is that because they’re not making much estrogen pre-puberty, so that any estrogen in the body is going to have a clinical impact?

Dr. Lustig: Exactly.

Dr. Means: In terms of personal care products, I mean this is a topic that’s near and dear to me because I love cosmetics. I love all of it. I love this stuff. And I think that my journey over the years has been very much moving from standard products with fragrances to just as simple as humanly possible. The minimal ingredients like organic Castile soap for almost every soap that I use. Using 100% jojoba oil for moisturizer, things that just don’t have the 50 chemicals.

One of the websites that has been really useful in my figuring out what to use is the Environmental Working Group’s website, which has a list of thousands and thousands of home care and personal care products and ranks them based on toxicity. What are your feelings on EWG?

Dr. Lustig: I use EWG also. And Ken Cook, the head of EWG, is a good friend. And yes, that’s a great place to go to get both sugar information, like in breakfast cereals, and also environmental pollution information on various things. So yes, I strongly recommend them.

Dr. Means: What are your thoughts on air and water filtration? Helpful, not helpful?

Dr. Lustig: Everyone should have an air filter in their house because there’s junk in the air anyway and it’ll help with your allergies. Obviously, hey, don’t live too close to a freeway. What can I say? Particulate matter causes inflammation and inflammation causes insulin resistance and insulin resistance causes weight gain. It’s kind of a problem. How to fix that problem? I don’t know how to fix that problem yet.

Dr. Means: Any other last pearls for people listening to this episode on how they can think about avoiding these things in their life? Any other things that you do in your life or that the research shows are really effective in terms of reducing the body burden of this stuff? 

Dr. Lustig: There is no medicine for this. That people need to understand do not go to your nature path and have him chelate you. It’s not going to work. All right? That’s not the way to answer this problem. The best way to handle this problem unfortunately is avoidance. And that makes it hard and it’s because you can’t see it. How do you avoid something you can’t see? that’s where the education comes in.

Dr. Means: Is there anything we can do to set our bodies up to be more resilient to this type of thing and also to potentially get these chemicals out of our body?

Dr. Lustig: The best way to get these chemicals out of the body is hydration. And that’s about what we’ve got at this point. Maybe we’ll start working on how to find ways of mitigating this problem at a biochemical level, but I don’t know what it is.

What’s Next?

Dr. Means: This lays the groundwork for a lot of future directions. And one of those that would be so interesting to think about is how is each one detoxified by the body? And is it the liver? Is it in the stool? What are the different pathways involved and how can we optimize those things?

There was one last thing I wanted to ask you about, which is that in the paper, there was a mention of how we might be able to in the future personally monitor these things in our bodies to kind of see what’s going on with our toxic burden. What do you think the likelihood of that happening is in the near future?

Dr. Lustig: Well look, we’re already talking about other small molecule monitoring for Levels. We’re talking about various channels that could be wearable. And there’s no reason why we wouldn’t be able to do that for compounds that exist in nature. It would require some engineering, to be sure, but if you’re wearing a wearable, adding a couple of channels to look for other stuff is not so crazy or impossible. Maybe that’ll be the way to do it.

Dr. Means: That’s definitely a world that I think would be interesting because they are invisible and a lot of the effects are lagging given that some of them are epigenetic and some of them take years to develop. What I thought was a really interesting concept that was brought up in the paper as well, is that some of these effects aren’t immediate. You’re not going to see the next day that this obesogen is affecting you. And so that’s where sometimes having that more closed-loop biofeedback can be so helpful.

Well, thank you so much, Rob, for chatting about all of this and it’s such a fascinating topic. This paper is, I think, going to do a lot to just totally change the world as all your work does. And we really look forward to spreading the message and helping get this information out there. So thank you so much.

Dr. Lustig: I just want to say that this is the work of 44 separate scientists and they all deserve an enormous amount of credit. And I particularly want to thank Jerry Heindel who basically was the taskmaster to keep this 44 herd of cats herded and got this done. And he deserves a lot of credit. And Jerry, if you’re listening, hats off to you.