How Can Animal Protein Intake Increase Childhood Obesity Risk?

If pregnant crickets are exposed to a predatory wolf spider, their babies will hatch, exhibiting increased antipredator behavior and, as a consequence, improved survival from wolf spider attack. The mother cricket appears to be able to forewarn her babies about the threat when they are still inside her, so they would be pre-adapted to their external environment. This even happens in plants. If you grow two genetically identical plants—one in the sun, one in the shade—the sun-grown plant will produce seeds that grow better in the sun, and the shaded plant will produce seeds that grow better in the shade—even though they’re genetically identical.

What’s happening is called epigenetics, external factors changing gene expression.

Vole pups born in the winter come out growing thicker coats. Vole mothers are able to communicate the season to their babies in utero and tell them to put a coat on even before they’re born. We’re no different. You know how some people have different temperature tolerances, resulting in “battles of the bedroom”? Do you turn the AC on or off? Open the windows? It’s not just genetics. Whether we’re born in the tropics or in a cold environment determines how many active sweat glands we have in our skin.

What does this have to do with diet? As I discuss in my video Animal Protein, Pregnancy, and Childhood Obesity, can what a pregnant woman eats—or doesn’t eat—permanently alter the biology of her children in terms of what genes are turned on or off throughout life?

What happened to the children born during the 1944 – 1945 Dutch famine imposed by the Nazis? They had higher rates of obesity 50 years later. The baby’s DNA gene expression was reprogrammed before birth to expect to be born into a world of famine and conserve calories at all cost. But when the war ended, this propensity to store fat became a disadvantage. What pregnant women eat and don’t eat doesn’t just help determine the birth weight of the child, but the future adult weight of the child.

For example, maternal protein intake during pregnancy may play a role in the obesity epidemic—but not just protein in general. “Protein from animal sources, primarily meat products, consumed during pregnancy may increase risk of overweight in offspring…” Originally, researchers thought it might be the IGF-1, a growth hormone boosted by animal product consumption, that may increase the production of fatty tissue, but weight gain was tied more to meat intake than dairy. Every daily portion of meat intake during the third trimester of pregnancy resulted in about an extra 1 percent of body fat mass in their children by their 16th birthday, potentially increasing their risk of becoming obese later in life, independent of how many calories they ate or how much they exercised.  But no such link was found with cow’s milk intake, which would presumably boost IGF-1 levels just as high.

Given that, perhaps instead of IGF-1, it’s the obesogens in meat, chemicals that stimulate the growth of fatty tissue. “[E]merging evidence demonstrates that environmental factors can predispose exposed individuals to gain weight, irrespective of diet and exercise.” After all, even our infants are fatter, and we can’t blame that on diet and exercise. Animals are fatter, too, and not just our pampered pets—even rats in laboratories and subways are bigger. “The likelihood of 24 animal populations from eight different species all showing a positive trend in weight over the past few decades by chance was estimated at about 1 in 10 million” so it appears something else is going on—something like obesogenic chemicals.

One such candidate is polycyclic aromatic hydrocarbons (PAHs), which are found in cigarette smoke, vehicle exhaust, and grilled meat. A nationwide study of thousands found that the more children were exposed to PAHs, the fatter they tended to be. The researchers could measure the level of these chemicals right out of their urine. Exposure can start in the womb. Indeed, prenatal exposure to these chemicals may cause increased fat mass gained during childhood and a higher risk of childhood obesity.

If these pollutants sound familiar, I’ve covered them before in relation to increasing breast cancer risk in the Long Island Breast Cancer Study Project. So, perhaps they aren’t just obesogens, but carcinogens, as well, which may help explain the 47 percent increase in breast cancer risk among older women in relation to a lifetime average of grilled and smoked foods.

If we look at one of the most common of these toxins, smokers get about half from food and half from cigarettes. For nonsmokers, however, 99 percent comes from diet. The highest levels of PAHs are found in meat, with pork apparently worse than beef. Even dark green leafies like kale can get contaminated by pollutants in the air, though, so don’t forage for dandelion greens next to the highway and make sure to wash your greens under running water.

These are fat-soluble pollutants, so they need lots of fat to be absorbed. It’s possible that even heavily contaminated plant-based sources may be safer, unless you pour lots of oil on your food, in which case the toxins would presumably become as readily absorbed as the toxins in meat.

The good news is they don’t build up in our body. As I show in my video, if we expose people to barbecued chicken, they get a big spike in these chemicals—up to a hundred-fold increase—but our body can get rid of them within about 20 hours. The problem, of course, is that people who eat these kinds of foods every day could be constantly exposing themselves, which may not only affect their health and their children’s health, but maybe even their grandchildren’s health.

Being pregnant during the Dutch famine of the mid-1940s didn’t just lead to an increase in diseases among their kids, but even apparently their grandkids. What a pregnant woman eats now may affect future generations. “The issue of generation-spanning effects of poor conditions during [pregnancy]…may shed light on the epidemic of diabetes, obesity and cardiovascular disease,” which is associated with the transition towards Western lifestyles.


Epigenetics is the science of altering the expression of our genes. No matter our family history, some genes can be effectively turned on and off by the lifestyle choices we make. See, for example:

For more on “obesogenic” chemicals, see:

I previously touched on PAHs in Meat Fumes: Dietary Secondhand Smoke.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

How to Avoid BPA

The purported link between obesity and hormone-disrupting plastics chemicals like bisphenol A (BPA) was initially based in part on observations that the rise in chemical exposure seemed to coincide with the rise of the obesity epidemic, but that may only be a coincidence. Many other changes over the last half century, like an increase in fast-food consumption and watching TV, would seem to be simpler explanations. But why are our pets getting fatter, too? Fido isn’t drinking more fries or drinking more soda. Of course, the more we watch Seinfeld reruns, the less we may walk the dog, but what about our cats? They’re also getting fatter. Are we giving both them and our kids a few too many treats? That would seem to be an easier explanation than some pervasive obesity-causing chemical in the environment building up in the pet and person food chains.

How then do we explain the results of a study of more than 20,000 animals from 24 populations, showing they are all getting fatter? The odds that this could happen just by chance is about 1 in 10 million. The study’s “findings reveal that large and sustained population increases in body weight” are occurring across the board, even in those without access to vending machines or getting less physical education in schools. Perhaps some environmental pollutant is involved. I discuss this in my video How to Avoid the Obesity-Related Plastic Chemical BPA.

We’re exposed to a whole cocktail of new chemicals besides BPA, but the reason researchers have zeroed in on it is because of experiments showing that BPA can accelerate the production of new fat cells, at least in a petri dish. This was at more than a thousand times the concentration found in most people’s bloodstream, though. We didn’t know if the same thing happened at typical levels…until now. Most people have between 1 and 20 nanomoles of BPA in their blood, but even 1 nanomole may significantly boost human fat cell production. So, even low levels may be a problem, but that’s in a petri dish. What about in people?

Why not just measure the body weights of a population exposed to the chemical compared to a population not exposed to the chemical? There is virtually no unexposed population: BPA is everywhere. In that case, how about those with higher levels compared to those with lower levels? This is what researchers at New York University did, and the amount of BPA flowing through the bodies of children and adolescents “was significantly associated with obesity.” However, since it was a cross-sectional study, a snapshot in time, we don’t know which came first. Maybe instead of the high BPA levels leading to obesity, the obesity led to high BPA levels, since the chemical is stored in fat. Or, perhaps BPA is a marker for the same kinds of processed foods that can make you fat. What we need are prospective studies that measure exposure and then follow people over time. We never had anything like that…until now! And indeed, researchers found that higher levels of BPA and some other plastics chemicals were significantly associated with faster weight gain over the subsequent decade. So, how can we stay away from the stuff?

Though we inhale some from dust and get some through our skin touching BPA-laden receipts, 90 percent of exposure is from our diet. How can we tell? When we have people fast and drink water only out of glass bottles for a few days, their BPA levels drop as much as tenfold.

Fasting isn’t very sustainable, though.

What happens with a three-day fresh foods intervention, where families switch away from canned and packaged foods for a few days? A significant drop in BPA exposure. If we do the experiment the other way, adding a serving of canned soup to people’s daily diet, we see a thousand percent rise in BPA levels in their urine compared to a serving of soup prepared with fresh ingredients. That study used a ready-to-serve canned soup, which, in the largest survey of North American canned foods, was found to have about 85 percent less BPA than condensed soups, but the worst was canned tuna.


I previously touched upon bisphenol A in BPA Plastic and Male Sexual Dysfunction. Some companies make canned foods without BPA, for example, Eden Foods. (See Do Eden Beans Have Too Much Iodine? for more information.) You can also buy aseptic packaged beans or boil your own. Personally, I like pressure-cooking them.

For more on BPA, see:

Phthalates are another concerning class of plastics chemicals. I covered those in Avoiding Adult Exposure to Phthalates and What Diet Best Lowers Phthalate Exposure?.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Foods to Avoid to Help Prevent Diabetes

We’ve known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption––especially consumption of processed meat, particularly poultry. But why? There’s a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat—particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers––tumor necrosis factor, C-reactive protein, and vascular adhesion molecules––shot up. “Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury.” The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, “may greatly reduce the already heavy burden of these toxins in the diabetic patient.” These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast’s worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents––such as viruses––present in fresh cuts of meat, including poultry.

A “crucial factor underlying the diabetes epidemic” may be the overstimulation of the aging enzyme TOR pathway by excess food consumption––but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it’s not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, “[i]n general, lower leucine levels are only reached by restriction of animal proteins.” To reach the leucine intake provided by dairy or meat, we’d have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what’s happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They’re now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but “most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats.”


For more on the information mentioned here, see the following videos that take a closer look at these major topics:  

AGEs: Glycotoxins, Avoiding a Sugary Grave, and Reducing Glycotoxin Intake to Prevent Alzheimer’s.

TOR: Why Do We Age?, Caloric Restriction vs. Animal Protein Restriction, Prevent Cancer From Going on TOR, and Saving Lives By Treating Acne With Diet

Viruses: Infectobesity: Adenovirus 36 and Childhood Obesity

Poultry workers: Poultry Exposure and Neurological Disease, Poultry Exposure Tied to Liver and Pancreatic Cancer, and Eating Outside Our Kingdom

Industrial pollutants: Obesity-Causing Pollutants in Food, Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat

The link between meat and diabetes may also be due to a lack of sufficient protective components of plants in the diet, which is discussed in my videos How May Plants Protect Against Diabetes?, Plant-Based Diets for DiabetesPlant-Based Diets and Diabetes, and How Not to Die from Diabetes.

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations: