The Obesogen Effect

Why We Eat Less and Exercise More but Still Struggle to Lose Weight

Contributors

By Bruce Blumberg, PhD

With Kristin Loberg

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An eye-opening account of the landmark research into the hidden chemicals that are endangering our health and keeping us fat.

Being overweight is not just the result of too many cheeseburgers or not enough exercise. According to leading-edge science, a new group of silent saboteurs in our daily lives is contributing greatly to our obesity epidemic: obesogens. These weight-inducing offenders, most of which are chemicals, disrupt our hormonal systems, altering how we create and store fat, and changing how we respond to dietary choices and caloric intake. Because they are largely unregulated, obesogens lurk all around us-in food, furniture, plastic products such as water bottles and food storage containers, and other surprising exposure points. Even worse: research has shown that the effects of some obesogens can be passed on to future generations by irreversibly interfering with the expression of our genes. The good news is we can protect ourselves by becoming more informed consumers.

In The Obesogen Effect, Dr. Bruce Blumberg explains how obesogens work, where they are found, and how we can minimize their effects. Dr. Blumberg offers a highly practical three-step solution for reducing exposures. He explains why one size does not fit all in a weight loss program, what harmful additives are in our household goods, and how we should shop for obesogen-free items we use every day-from vegetables and meats to canned soup as well as household cleaners, air fresheners, and personal care products. The Obesogen Effect, is an urgent call to action to protect your body, clean up your life, and set a straight course for better health.

Excerpt

What if everything you thought you knew about the biology of body weight is wrong?




INTRODUCTION

Fat: An Unrequited Love Story

When you think about the causes of overweight and obesity, conditions that now affect the majority of Americans, two factors likely come to mind immediately: dreadful dietary habits and lack of exercise. This is what I call the “orthodox wisdom” that we hear all the time. But what if I said you are wrong? Well, at least not 100 percent right. You’re missing a huge influence that has been driving our epidemic for the last half century, and it has nothing to do with a penchant for sitting on the couch eating potato chips and drinking regular soda. It has to do with obesogens—chemicals in our environment that promote weight gain.

No one wants to be fat, but most of us are, despite working hard to eliminate unwanted pounds. Something is wrong with this narrative. I coined the term “obesogens” in 2006 to describe chemicals that can make you fat.1 This sounded the alarm and spurred a flurry of scientific research studying the phenomenon of chemical-induced obesity. My team found that a chemical we were studying for other reasons had the ability to make mice fat. That started me thinking that there might be an alternative explanation for our irrepressible fatness other than calories in versus calories out. And I was right.

Take a moment to consider this from a purely logical standpoint: If weight were simply determined by calories eaten minus calories burned (more formally called the energy balance equation), don’t you think we would be able to easily manage our weight? Why can we balance our bank checkbooks, but not our caloric checkbooks? In arithmetic, one plus one equals two no matter what language you speak. But one plus one can equal more than two when it comes to the weight equation of the human body. I will explain how this is possible in the book.

Observational studies in humans have pointed to a strong link between exposure to certain environmental chemicals and greater body mass index (BMI).2 The BMI is a general measure that relates your weight in kilograms to your height.3 BMI is often used as an indicator of obesity on one end of the spectrum and underweight on the other. In 1997, the World Health Organization (WHO) convened for its first meeting on the rising obesity epidemic and adopted new criteria for “normal weight” (BMI of 18.5–24.9), “overweight” (BMI of 25–29.9), and “obese” (BMI of 30 or higher).4 The easiest way to measure your BMI is to use an online calculator, which will divide your weight in kilograms by the square of your height in meters to arrive at the number.

An important 2016 study showed that average BMI today is higher than it was a little more than a generation ago, even when our caloric intake and physical activity is about the same.5 Put another way, adults today find it harder to maintain the same weight than did adults twenty to thirty years ago, even at the same levels of food intake and exercise. These days people are about 10 percent heavier than people in the 1980s, even if they eat and exercise as they did back in the heyday of leg warmers and Sony Walkmans. And despite what you hear, we exercise more than we did in the 1980s—not less. There is another explanation that will unfold chapter by chapter.

The time has come to present the untold story of obesogens with the hope that you can take better control of your waistline, your health, and especially the well-being of your children and future generations. After all, nowhere is the obesity epidemic more painfully disturbing to witness and acknowledge than in our young. In January 2016, the World Health Organization released a statement declaring that the number of obese children worldwide today is “alarming.”6 I will add the words “disheartening” and “unacceptable.”

I don’t mean to minimize poor diet and physical inactivity; these remain leading causes of overweight and obesity. But we in the scientific community are increasingly finding that exposure to chemicals in our diet and environment may be an under-recognized risk factor. In the last decade, other researchers and I have identified dozens of chemicals that can increase susceptibility to becoming obese in animals and trigger cells grown in a lab (cultured cells) to become fat cells.7,8 The narrative about our obesity epidemic, which is now a severe public health crisis, continues to be stuck in the conversation about our modern lifestyles—too much food (especially the wrong kind) and not enough sweating. When doctors address patients who are overweight, they resort to the same old questions: “What are you eating? How much are you exercising?” Doctors rarely ask about what their patients may be exposed to (even unwittingly) in daily life. Indeed, many are hostile to the idea that chemical exposure may have effects on health. The quiz coming up shortly will begin to clue you in to what kinds of exposures I am talking about, many of which may surprise you because you never knew there was a connection to your weight. Losing weight is no longer only about putting down the doughnuts and hopping on a treadmill.

What is missing from the never-ending conversation about weight and how to control it is the role played by obesogens and how these little-acknowledged yet potent and deleterious substances that we encounter daily—in our food, households, workplaces, and even medicine cabinets—are severely impacting our waistlines and overall health. Obesogens contribute to obesity by disrupting the normal development and balance of fat metabolism—how your body creates and stores fat. Obesogens can reprogram stem cells in the body to develop into more fat cells. Obesogen exposure also changes how your body responds to dietary choices and handles calories. So even though you have bought into the latest trends—Paleo, low-carb, gluten-free, Zumba, or CrossFit gyms—you can still struggle mightily with weight because of what is in your environment (broadly defined).

One of the most pernicious ramifications of obesogens is that their effects can be passed on to future generations. That’s right: the effects of obesogen exposure can be heritable. The havoc that obesogens wreak on our bodies can be passed down to our biological children, grandchildren, and beyond. This is why understanding the science of obesogens and knowing how to avoid them is particularly important for women who intend to become pregnant, are already pregnant, or have young children. The developmental years are a sensitive period in one’s life, during which the body can be more vulnerable to, and affected by, chemical exposure. Our children, grandchildren, and beyond deserve to have the best possible chance to live long, healthy, and lean lives without being saddled with a predisposition to the burden of obesity and its related consequences. My hope with this book is to show you how to make it more likely that your children will succeed rather than fail to control their weight, as well as to help you reduce the impact of obesogens in your own life.

Now, before we begin the journey, I will share a little bit about me. I didn’t start my doctoral life searching for obesogens. As happens with so many discoveries in science, I stumbled upon them while exploring other areas in biology. When I arrived at UCLA as a new PhD student in 1982, I wanted to study developmental biology—how organisms grow and develop from a single cell into complex, multicellular organisms such as humans. At that time, all of the developmental biologists at UCLA were exploring the genetics and development of the fruit fly, Drosophila, which I didn’t find particularly appealing. Instead, I ended up studying the biochemistry of the extracellular matrix—the connective tissue that helps hold the body together. When I became a postdoctoral fellow at UCLA, I finally studied vertebrate developmental biology, looking for embryonic inducers—molecules that play critical roles in directing embryonic cells to form new tissues and tell the developing embryo where the head, arms, legs, and so on should go. Most everyone else in the field was studying peptide growth factors (proteins that stimulate cell growth) as embryonic patterning molecules, but my background with the extracellular matrix led me to look for small, fat-soluble molecules that could move freely through the sticky matrix around cells, whereas growth factors cannot. Small, fat-soluble molecules such as steroid hormones are ideal candidates for such molecules and were already known to be important for development. As you will soon learn, hormone levels can control how you behave and how your body develops and functions, even including your metabolism and risk for obesity. The receptors that these hormones bind to are powerful molecular switches that control the activity of many other genes. Since quite a few apparent receptors were then known for which no hormones had been identified (these are called “orphan receptors”), I set out to find new receptor-hormone combinations.

Later, I moved to the Salk Institute for Biological Studies in the Gene Expression Laboratory of Dr. Ron Evans, the world leader in hormone receptor research, to improve my chances of identifying new hormones. In 1996, while I was busily developing methods to identify new hormone-receptor combinations, I got a call from my colleague Dave Gardiner at the University of California–Irvine about deformed frogs that were being found in Minnesota. Dave and a few other scientists thought that the cause could be a retinoid (a chemical related to vitamin A) in the water and wanted to know how difficult it would be to test their hypothesis. I applied the same methods we developed to identify new hormones to find chemicals in the water that might be activating retinoid receptors to cause the types of deformities observed in the Minnesota frogs. That got me started on the path toward looking for environmental chemicals that disrupt hormonal signaling and thereby alter development (so-called endocrine disrupting chemicals, or EDCs). The rest is history that I will share in the book.

Fasten your seat belt. What you are about to learn will stun you on one level but inspire you on another (and make you feel a little better about yourself if you have struggled with your weight). You are not alone when it comes to matters of weight and the emotional toll of being on a seemingly endless diet to achieve and maintain weight loss. It is an uphill battle. You are also not alone if you answer “yes” to any of the questions coming up in the first chapter that will help you to grasp how many things in your environment could be making you fat—and keeping you fat despite your best efforts. Together we can identify the hidden factors that are sabotaging your health and weight loss efforts. Let’s begin.




PART I

In the Fatlands: The New Science of Obesity




CHAPTER 1

Why Are We So Fat Despite Our Best Efforts?

The Hidden Factor No One Is Talking About

If we could give every individual the right amount of nourishment and exercise, not too little and not too much, we would have found the safest way to health.

—Hippocrates, the father of medicine (460–370 BCE)

If you could go back in time to an era when people believed the earth was flat, how difficult do you think it would be to convince someone that it was, in fact, round? What argument would you use to prove your point? And no, you cannot time travel with a globe in your pocket or images taken from the moon. Without any evidence of a round earth on hand, chances are you would have a tough time convincing anyone that you were right. After all, it is difficult to see the curvature of the earth from its surface—we see straight horizons, not curves. The idea of a spherical shape first appeared in Greek philosophy, credited to Pythagoras in the sixth century BCE. Aristotle provided evidence for it on empirical grounds by around 330 BCE, but it would take centuries for universal acceptance of a round earth that revolved around the sun. Even today, at least four U.S. professional basketball players claim to believe the earth is flat, so you cannot convince everyone, no matter how strong the data are!

When I speak before large professional audiences about obesogens and their impact on the obesity epidemic, I used to feel like that hapless individual trying to persuade the Flat Earth Society that the planet is indeed spherical. Old theories die hard, especially ones that people have clung to for a long time or when the reality seems to defy logic. This is absolutely true when it comes to our ideas about how and why we are so fat today. Laymen and doctors alike continue to believe that body weight is exclusively determined by the number of calories consumed compared with those burned—simple as that. Just look at the website of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), where it states definitively: “Overweight and obesity result from an energy imbalance.”9 If only this were the case. You might be surprised to learn that the number of health clubs has doubled over the same period that obesity has doubled. Clearly people are trying hard not to be obese. If only the solution revolved around diet and exercise alone.

Though most everyone has a clear picture of what obesity looks like, obesity is primarily defined by the body mass index (BMI). According to the WHO and American Medical Association, you are considered to be “underweight” if your BMI is less than 18.5, “normal weight” if your BMI is between 18.5 and 24.9, “overweight” if your BMI is between 25 and 29.9, and “obese” if your BMI is 30 or higher. A BMI beyond 40 is considered to be morbidly obese and indicative of a serious health problem. The BMI is a calculation based on height and weight but does not distinguish muscle from fat and bone in the body. I often show a slide comparing three people with identical BMIs of 32. One has extensive subcutaneous (below-the-skin) fat, which is not really problematic for health; another has abundant visceral fat deep inside and around the organs, which, as we will describe later, confers many of the health risks associated with obesity. The third picture is of the “Governator,” Arnold Schwarzenegger, at the pinnacle of his bodybuilding career. Despite having a BMI of 32, he was not remotely obese or even overweight. Thus, BMI is not a perfect indicator of whether or not you are obese. However, it is easy to calculate and a convenient generalization.

Let’s do one more imaginary time-travel experiment: Think about what it would be like for a family of Stone Age hunter-gatherers to experience the modern world (think The Flintstones meets My 600-lb Life). I picture stunned looks on the faces of our ancestors as they take in our modern conveniences—cars, cell phones, computers, electricity, and even supermarkets. And they are also taken aback by our body size. Given our twenty-first-century bulk, would they recognize us as members of their own species? Unlike us, they worked hard for every morsel and probably rarely had much leisure time to sit around eating unhealthy food. There were no fast-food restaurants or processed meals.

Hippocrates was right to stress the importance of moderation in diet and exercise as well as the value of food; diet was considered to be one of the most important interventions in Hippocratic medicine. This was certainly true in his time, but it misses a key part of the equation today. Hippocrates could not have known about endocrine disruptors or the effects they can have on our health and weight. And he, too, would probably be scratching his head in bewilderment at the obese masses at the dawn of the twenty-first century—a mere twenty-four hundred years after he lived.

Inexorably, we have grown accustomed to seeing a world of fat around us. The obesity facts are played over and over again in the media, so much so that they no longer surprise us. Overweight and obese individuals are the norm in most areas of the country instead of an anomaly. But fifty years ago you would have been hard-pressed to find many such people on the planet, let alone in one geographic location. As recently as 1990, obese adults in the United States comprised less than 15 percent of the population in most states. By 2010, thirty-six states had obesity rates of 25 percent or higher, and twelve of those had rates of 30 percent or higher.10 Obesity has increased threefold over the past forty years and has doubled worldwide in the last twenty years; in the last thirty years, obesity has more than doubled in children and quadrupled in teens. Today there are more overweight and obese adults aged twenty years and older in the United States (70.7 percent) than those of normal, healthy weight and underweight.11-13 More than one-third of U.S. adults are obese, and a whopping 86 percent of us are expected to be overweight by 2020. A full 20.6 percent of adolescents aged twelve to nineteen years are obese; 17.4 percent of children aged six to eleven years are obese; and almost 10 percent of kids only two to five years old are already saddled with obesity.11,13 Individuals who had previously enjoyed life in the slim lane at the lower end of the body mass index are now gaining weight, too, and entering the “overweight” and “obese” categories. It becomes difficult to even see the problem because when everyone around you is overweight, it turns into the expected.

But this is not normal. Could it be that we really lack the willpower to control our waistlines through classic diet and exercise because we live in an age of abundance? That it is all about lack of self-control? I don’t think so. Let’s not forget that there is also an obesity epidemic among infants of six months of age and younger, an age group where food choices and limited physical activity cannot explain this phenomenon; infants move as little or as much as they want and eat until they are full. The obesity epidemic is not limited to humans, either—it is also affecting animals living with us, including domestic dogs and cats, feral rats living in cities, and, crucially, primates and rodents living in research colonies where diets are carefully controlled.14 Are these animals also suffering from a lack of willpower? Highly doubtful.

The seminal 2016 study on our increased average BMI that I mentioned in the introduction was among the first to really call out the new facts.5 The researchers in this particular study mined dietary data from 36,377 U.S. adults from the National Health and Nutrition Examination Survey (NHANES) between 1971 and 2008 and showed that we are 2.3 points higher on the body mass index today than we were just a generation ago—even after correcting for how much we eat and exercise. The published conclusion spoke volumes: “Factors other than diet and physical activity may be contributing to the increase in BMI over time.” Granted, as I mentioned, BMI itself is not the best measure of obesity because it does not differentiate between fat mass and muscle mass or even where the fat is located, an important factor we will explore later. Yet despite the shortcomings of BMI as a metric, it does offer a reasonable reference point to use in evaluating body composition in the population.

So what is the most compelling explanation for these new facts? Something has changed in our environment—something that occurs where humans live, work, and eat.

HOW EXPOSED ARE YOU?

Take a look around you and think about a typical day, including that of your young children if you have them. In what ways can your environment impact your biology—and especially that of your children who are still developing, which makes them uniquely vulnerable? Here is a brief quiz that can help clue you in to the kinds of exposures that can cause a human body to create more fat. Many of these exposures could have happened long ago.

Do you regularly drink from plastic beverage containers, including soda bottles, juice, and so forth?

Do you have trouble sleeping well on a regular basis? (And yes, sleep deprivation can be considered an “exposure”; see chapters 5 and 9.)

Do you live in an urban environment with air pollution or in a loud setting such as near a busy highway or airport?

Do you feel that you have a lot of stress and/or don’t respond well to stress?

Do you buy a lot of prepackaged foods/meals rather than whole foods and fresh ingredients from which to create meals?

Do you eat conventionally grown fruits and vegetables?

Do you drink tap water?

Are you taking drugs that list weight gain as a potential side effect?

Do you clean your home with commercial, non-green products?

Are you exposed to herbicides, pesticides, and fungicides around your home or neighborhood?

Do you use air fresheners or scented products (including cosmetics that list “fragrance” in their ingredients)?

Do you spend most of your days being inside, in a car, in an office?

Do you sit more than three hours per day?

As a child, did you drink a lot of juice, soda (regular or diet), and flavored milk or eat a lot of processed foods?

Did your mom smoke when she was pregnant, or were you exposed to secondhand smoke as a child?

Was your mom overweight or obese while she was pregnant with you?

Was your dad obese before you were conceived?

Don’t panic if you answered “yes” to any of these questions. Knowledge is power, and I will equip you with the information you need to take better charge of your waistline and health. In this chapter, we will take a tour of the obesity epidemic so you have a solid foundation to understand what I am calling “the new science of fat.” It will help you begin to see why some people gain weight faster and lose it more slowly than others, irrespective of diet and exercise.

THEN AND NOW: THE MYSTERY OF OUR MODERN SCOURGE

The image below shows two different individuals.

Back in our hunter-gatherer days more than ten thousand years ago, when we had to forage for our food by collecting wild plants, fishing, and pursuing wild animals, most of us resembled the individual on the left. Modern hunter-gatherers in Africa and elsewhere who continue to live this way still look like the woman on the left. However, many of us come closer to looking like the person on the right.

Some would argue that one of the reasons it is so easy to turn into the person on the right is that we evolved when food was much harder to find. We were programmed for survival in a world where food was scarce and periods of famine were frequent. But today we live in a calorie-rich environment 365 days a year. Food is abundant, and unhealthy foods tend to be the most affordable, available options. Many of these unhealthy foods are engineered to act on our brain’s pleasure centers to keep us addicted and coming back for more, similar to how drug addicts on heroin or crack cannot easily quit.15 While the theories around whether obesity-causing genes are widespread, or whether there is an obesity-favoring metabolic program, the idea that we have been molded by evolution to use calories sparingly makes some sense and is worth considering.

The “thrifty gene” hypothesis suggests that the two images here reflect an obvious mismatch between our Stone Age genes and space age circumstances. Having access to ample calories allowed the body to build fat stores quickly when food was available so it could endure long stretches of food shortages, which were inevitable and common throughout much of human evolution. Perhaps we retain essential components of this hunter-gatherer genome—after all, a small percentage of each of our genomes is derived from our Neanderthal and Denisovan cousins.16 These genes helped us store fat during times of abundance so that this fat could be used during those regular periods of scarcity, and thus they lead to energy being spent sparingly. The end of famine in developed countries means that accumulated changes in genes that were once favorable for storing fat instead could cause widespread obesity. In other words, “famine genes” that were once advantageous for survival became liabilities that could threaten health and longevity in the land of plenty.

Geneticist James Neel first described the “thrifty gene” hypothesis in 1962 to help explain why diabetes has such a strong genetic basis yet results in such negative effects.17 According to the theory, the genes that predispose someone to diabetes—the “thrifty genes”—were advantageous long ago. But once modern society changed and we developed agriculture, our access to food changed, too. Our bodies no longer needed those thrifty genes, but they were still active. Today they continue to prepare us for a famine that will not arrive. Our thrifty genes are partially responsible for the obesity epidemic, which is closely tied to the development of diabetes.

If there are such things as “thrifty genes,” then it must be possible to identify them with the advent of modern, affordable DNA-sequencing methods. This is where the thrifty gene hypothesis has run into some critics. If these thrifty genes have been around for the two hundred thousand years or so that we Homo sapiens have existed, and agriculture began only around twelve thousand years ago, then pretty much everyone should carry the majority of the thrifty genes that have ever existed. Dr. John Speakman, a prominent challenger of the thrifty gene hypothesis, showed in a 2016 paper that none of the common obesity-related genes that had been identified conferred any properties or traits that could be considered to have provided an adaptive advantage.18 On the other hand, perhaps there are bona fide thrifty genes that have yet to be identified, so the case is not yet closed. As we will discuss in chapter 5, it is clear that there is a “thrifty phenotype.” That is, in both human and animal studies, it is possible to identify individuals that store more of the calories they consume as fat, whereas others burn more calories or eliminate more in their feces. If thrifty genes are not responsible, then what is?

Genre:

  • "Why do we get hungry, feel tired, and gain weight? A likely culprit is our fat cells. THE OBESOGEN EFFECT, written by the researcher who literally defined this new field, explains how our diet and other exposures can program the body for weight gain-beyond calories in, calories out-and what you can do about it!"—David Ludwig, MD, PhD, author of the #1 New York Times bestseller Always Hungry?
  • "If you think obesity is about couch potatoes and gluttony, or calories in vs. calories out, you must think again. Or better yet, read this book. It tells a complex scientific story with vivid, accessible clarity about the role that obesogens-chemical contaminants that can alter our metabolism, appetite and more-play into making us fat. The bad news is that obesogens are all too common and hard to avoid if you aren't paying attention. The book's good news is that there are many simple, practical steps you can take that will protect you and your family."
    John Peterson Myers, PhD, Chief Scientist, Carnegie Mellon University
  • "Every wonder why it is so easy to gain weight and hard to lose it? This simple to read, scientifically factual book can change your life-it is a must read."—Jerry Heindel, Commonweal
  • "You probably agree that cigarettes cause cancer, even knowing that not everyone who gets cancer smokes cigarettes and not everyone who smokes cigarettes gets cancer. Bruce Blumberg makes the case clearly that industrial chemicals cause obesity in a similar way. Bruce is an eminent researcher who, through his discoveries, has changed the way we think about body weight regulation-both in a fundamental way, as well as by providing insight into the role of industrial chemicals. This readable book, with its solid scientific base, will change the way you think about the obesity epidemic-and what we can do about it."—R. Thomas Zoeller, PhD, Professor of Biology

On Sale
Mar 20, 2018
Page Count
320 pages
ISBN-13
9781478970644

Bruce Blumberg, PhD

About the Author

Bruce Blumberg, PhD, has been conducting pioneering research in endocrinology and developmental biology for more than thirty years. He is professor in the Departments of Developmental and Cell Biology, Pharmaceutical Sciences, and Biomedical Engineering at the University of California, Irvine (UCI). At UCI, his laboratory studies the biology of nuclear hormone receptors in development, physiology, and disease with a particular emphasis on how these are affected by hormonally active compounds in the diet and environment. In 2012, he was elected as a fellow of the prestigious American Association for the Advancement of Science.

Learn more about this author