Obesogens Are Making Us Fat, Not Fast Food

Stewart Lonky, M.D.

The other day, I was sitting with a group of friends when one started griping about fast food marketing campaigns targeted at children, particularly minority kids where the obesity and related- illness rates are much higher than the general population. Despite recent national data showing that childhood obesity rates have stabilized at 17 percent, and are even declining among 2- to 5-year-olds, childhood obesity is still at epidemic levels.

Right now, between 12-13 million U.S. children are obese — that’s one out of every six children — and millions more are overweight, with the CDC estimating that more than 30% of children 2−19 years old fall into this category. Obese children have an increased risk of high blood pressure, high cholesterol, sleep apnea, bone and joint problems, as well as asthma and type 2 diabetes. They’re at increased risk of bullying and even mental illnesses like depression. It’s a shame that more than 200,000 American children have type 2 diabetes.

But here’s where things get more complicated. Obesity isn’t a simple matter of calories in versus calories out. It never has been. Our weight woes were never about the dinosaur energy balance model of eating less and exercising more, or too much television or too much access to inexpensive, high-calorie fast food. The knowledge of what to eat and what not to eat for weight loss has been known for 50 years. We all know that French fries aren’t a diet food.

Despite all we know about the underlying causes of extreme weight gain, many scientists remain unconvinced, even ignoring other critical factors affecting the nation's obesity spike. I’m still surprised how few scientists, and physicians, pay attention to, or even know about the most significant factor underlying extreme weight gain: A class of natural and synthetic endocrine-disrupting chemicals, which we know as obesogens. Bruce Blumberg, professor of developmental and cell biology and pharmaceutical sciences at the University of California, Irvine first coined the term “obesogen” and it is any chemical that promotes weight gain by:

  • Increasing the number of fat cells.
  • Increasing fat storage in existing fat cells.
  • Changing the metabolic rate.
  • Altering hormonal control of appetite or satiety.
  • Shifting energy balance to favor the storage of calories.

The Threat to Weight Gain That is Hidden … Yet Everywhere

Scientists have known for years that obesogens disrupt our hormonal systems’ delicate balance and functioning, altering the way our bodies store fat and regulate metabolism, leading to weight gain and its associated diseases. Not surprisingly, the increase in obesity prevalence correlates with the rise in the use and distribution of industrial chemicals. This is perhaps the biggest reason why we struggle to lose weight. Even an extreme, calorie-restricted diet won't lower your obesogen exposure. Obesogens are ubiquitous and are found in any number of sources — from hormones administered to animals, plastics in some food and drink packaging, processed foods ingredients, and pesticides sprayed on produce.

Organotins, which are also obesogens, are widely used in polyvinyl chloride plastics manufacture, crop fungicides, and pesticides, and as slimicides in industrial water systems. A “slimicide” is an anti-slime agent and an antimicrobial agent that kills slime-producing microorganisms such as bacteria, slime, fungi, and algae. Slimicides are also used in paper manufacturing. They specifically affect the body’s metabolism by changing the way it responds to calories.

Organotins

Organotins also include chemicals like tributyltin (TBT), a wood preservative and marine antifouling paint and fungicide, which is now banned, in part because of its habit of turning female snails into males. TBT’s obesogenic effects are thought to be due largely to its ability to bind with hormone receptors called PPARĪ³ (peroxisome proliferator-activated receptor gamma) receptors that play an important role in turning pre-fat cells into mature fat cells, a process known as adipogenesis. This binding to the PPARĪ³ receptor also affects fat storage and glucose metabolism. It also impacts other hormone receptors, such as retinoid X receptor (RXR), and the thyroid gland. Thus, TBT promotes obesity by increasing the number of fat cells, the storage of fat in existing fat cells, changing the metabolic rate, altering hormonal control of appetite or satiety, or shifting energy balance to calorie storage, meaning it can either directly or indirectly lead to increased fat accumulation and weight gain. In one study, animals exposed to tributyltin and triphenyltin developed more and bigger fat cells. The animals treated with these chemicals didn’t eat a different diet than the ones that didn’t get fat. They ate the same diet, but still got fatter.

The Negative Impact Beyond Weight Gain

Obesogens’ effects are not strictly limited to fat metabolism and weight gain. They also affect fertility, particularly in males, increase the risk of genital malformation, reduce male birth rates, trigger precocious puberty, impair immune function, and increase the risk of miscarriage, behavior problems, brain abnormalities, various cancers, and cardiovascular disease. Most significantly, obesogens damage the unborn and newborn, who are vulnerable to epigenetic changes via their mother. Prenatal obesogen exposure has been shown to tilt a type of stem cell in the body in the direction of fat cell development at the expense of other cell types (bone or muscle as examples). Thus, in utero and early postnatal obesogen exposure predisposes a child to obesity by influencing all aspects of adipose tissue growth, starting from multipotential stem cells and ending with mature adipocytes. Some evidence suggests that the intrauterine environment has a significant and lasting effect on the long-term health of the growing fetus and the development of metabolic disease in later life. Metabolic diseases have been associated with epigenetic changes that occur without changes in the DNA sequence, such as cytosine methylation of DNA (these epigenetic modifications can be reversed by the addition of methyl donors, such as dietary folic acid, which I explain in greater detail at the end of this article).

It’s clear to me that we can’t continue to frame the obesity discussion simply in terms of calories in and calories out, or by only examining the nutritional content of food. Given the proliferation of industrial pollutants, a paradigm shift in thinking is needed. A heightened understanding of the effects of these endocrine-disrupting chemicals is key to freeing ourselves from weight gain. Without it, we remain stuck in the insidious cycle of weight loss and weight gain.

How Can We Protect Ourselves from Obesogens?

Below are a few common sense and easy-to-follow recommendations for reducing the effects of obesogen exposure.

Buy less plastic.

We really don't know yet if the BPA in computer casings, car dashboards, and other things we contact every day makes its way into our bodies. But it seems likely that anything that's plastic and ends up in a landfill could break down and contaminate groundwater. Try only purchasing plastic items you really need, which may help keep BPA out of your house dust and off your skin, not to mention help eliminate it from our waterways. I never put plastic in the oven or the microwave. Heat damages plastic and increases leaching. Avoiding plastic-wrapped meat is also a good idea since most varieties contain mostly PVC (the plastic wrap most folks use at home is increasingly made from polyethylene). PVC contains phthalates that, according to animal studies, may lower testosterone levels. In humans, lower testosterone leads to weight gain as well as a decrease in muscle mass and sex drive. Go to a butcher who uses paper instead.

Consume a diet high in folic acid.

There are now a number of studies that show that consuming a diet high in folic acid (dark leafy greens, asparagus, broccoli, citrus fruits, beans, peas, lentils, seeds and nuts, just to name a few) can actually reverse in utero-induced epigenetic changes in adult animals. When attempting to lose weight, these items are a definite “plus” in the diet and should help with overcoming some obesogen-induced disadvantages. If necessary, you can also add a high-quality folic acid supplement. But please be sure to check the manufacturer. Not all brands have equal bioavailability.

Keep protein intake high when dieting.

One of the reasons why high protein, low carbohydrate diets are so successful is that they may reverse some in-utero epigenetic changes. This may be one of the reasons why people who try Atkins, Paleo, and other high-protein, low-carb diets have early success.

Try to maintain a diet with adequate L-methionine.

Once again, animal data show that adults with previous epigenetic changes can reverse these changes by supplementing with methionine, an amino acid that favors DNA methylation. Foods high in this amino acid include eggs, lean beef, lamb, Brazil nuts, parmesan cheese, and soybeans (even if roasted).

These are just a few of my recommendations for taking control of some of the changes resulting from our constant obesogen exposure, as well as the exposures that caused changes in previous generations. You see, some of these changes are generational; they are passed down from one generation to the next. But, we can take control and change course by following a modified diet and limiting exposure to obesogens.

About: Stewart Lonky, M.D., is a physician, toxicologist, and biomedical engineer. He is board certified in internal medicine, pulmonology and critical care medicine, and a recognized expert in the related fields of preventive medicine and environmental toxicology and its associated diseases. Dr. Lonky is known for his cutting edge research into the causes, treatment and prevention of toxic chemical exposures and heralded for his in-depth knowledge of obesity's biological, environmental, and social influences, which is the subject of his forthcoming book. Dr. Lonky resides and practices in Los Angeles, California. www.stewartlonky.com

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