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:

Is the Risk of Skin Cancer From Sun Exposure Overblown?

By the turn of the 20th century, rickets, the vitamin D deficiency disease, was rampant, thanks to city life with the shade of buildings and coal soot in the air. The dairy industry jumped at the opportunity to fortify milk with vitamin D, and so did the beer industry. According to one print ad: “Beer is good for you—but Schlitz, with Sunshine Vitamin D, is extra good for you…[so] drink Schlitz regularly—every day.” There are, of course, healthier fortified options, like vitamin D-fortified orange juice, but to reach recommended intake levels, it could take 15 to 20 cups of fortified milk, beer, and/or juice a day. As I discuss in my video The Risks and Benefits of Sensible Sun Exposure, to get those kinds of doses, it really comes down to sun or supplements.

Sunlight supplies 90 to 95 percent of vitamin D for most people. The threat of skin cancer is real, however it’s mostly from chronic excessive sun exposure and sunburns. “There is little evidence that minimal sensible exposure to sunlight will considerably increase the risk of skin cancer”—though why accept any risk when we can get our vitamin D just from supplements?

For the sake of argument, what if there were no supplements available? What if we were just trying to balance the positive and negative effects of sun exposure? On one side, we have entities like the American Academy of Dermatology that recommend that “no one should ever be exposed to direct sunlight without sun protection.” After all, the UV rays in sun are proven carcinogens, responsible for more than half of all Caucasian malignancies, blaming the tanning industry for downplaying the risk.

Even those who accept research dollars from the tanning industry acknowledge that excessive sun exposure can increase skin cancer risk, but argue for moderation, advocating for “sensible sun exposure” and blaming the sunscreen industry for overinflating the risk. However, it’s harder to impugn the motives of the dermatologists, who are essentially arguing against their financial interest since skin cancer is their bread and butter. The concern raised by UV advocates is that “sunphobic propaganda” may do more harm than good, pointing to studies such as this one from Sweden that found that those diagnosed with skin cancer tended to live longer and have less heart attacks and hip fractures. Not surprisingly, the media loved this and ran headlines like “Sunbathers live longer.” Only natural UV exposure was associated with reduced mortality, however; artificial UV exposure, like from tanning beds, was associated with increased mortality. This probably has nothing to do with vitamin D, then. Why then would those who run around outside enough to get skin cancer live longer? Maybe it’s because they’re running around outside. More exercise may explain why they live longer. And here in the United States, more UV exposure was associated with a shorter, not longer, lifespan.

There are modeling studies that suggest that at least 50,000 American cancer deaths may be attributable to low vitamin D levels that could be avoidable with more sunlight exposure that would kill at most 12,000 Americans from skin cancer. So, on balance, the benefits would outweigh the risks—but, again, why accept any risk at all when we can get all the vitamin D we need from supplements? In fact, where did they get those estimates about vitamin D preventing internal cancers? From intervention studies involving giving people vitamin D supplements, not exposing them to UV rays. So, it’s not much of a controversy after all. “In essence, the issue is framed as needing to choose between the lesser of two evils: skin cancer…versus cancer of various internal organs and/or the long list of other ailments” from vitamin D deficiency. The framework ignores the fact that there’s a third way. When we were evolving, we didn’t live long enough to worry about skin cancer, and vitamin “D was not available at the corner store.”

If we just want to look more attractive, how about eating more fruits and vegetables? When high kale models were pitted against high UV models, the golden glow from carotenoid phytonutrients won out, and the same result has been found in Caucasian, Asian, and African American faces. So, may I suggest the produce aisle to get a good healthy tan…gerine?


That’s the gist of what the last 15,950 studies on vitamin D have added to our understanding. Unless something particularly groundbreaking comes out, you can expect the next update in 2021. If you missed the first five videos in this series, see:

I also explore vitamin D as it relates to specific diseases:

The physical attractiveness is from carotenoid deposition in the skin. For more on this, see:

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 Make Your Own CoQ10

Chlorophyll is the green pigment that makes green leaves green. If you search for chlorophyll in the medical literature, a lot of what you find is about fecal fluorescence, a way to detect the contamination of carcasses in the slaughterhouse with feces to reduce the risk of food poisoning from pathogens harbored within animal feces. Fecal matter gets on meat either “with knife entry through the hide into the carcass, and also splash back and aerosol [airborne] deposition of fecal matter during hide removal”—that is, when they’re peeling off the skin. If, however, the animals have been eating grass, you can pick up the poo with a black light. As you can see in my video How to Regenerate Coenzyme Q10 (CoQ10) Naturally, a solution of chlorophyll is green, but, under a UV light, it lights up as red. So, if you have a black light in a chicken slaughter plant, you can get a drop on the droppings. The problem is most chickens aren’t outside anymore. They’re no longer pecking at grass so there’s less fecal fluorescence. We could let them run around outside or we could save money by just adding a chlorophyll supplement to their feed so we can better “identify areas of gut-spill contamination” on the meat.

The reason I was looking up chlorophyll was to follow-up on the data I presented in my Eating Green to Prevent Cancer video, which suggests that chlorophyll may be able to block carcinogens. I found a few in vitro studies on the potential anti-inflammatory effects of chlorophyll. After all, green leaves have long been used to treat inflammation, so anti-inflammatory properties of chlorophyll and their break-down products after digestion were put to the test. And, indeed, they may represent “valuable and abundantly available anti-inflammatory agents.” Maybe that’s one reason why cruciferous vegetables, like kale and collard greens, are associated with decreased markers of inflammation.

In a petri dish, for example, if you lay down a layer of arterial lining cells, more inflammatory immune cells stick to them after you stimulate them with a toxic substance. We can bring down that inflammation with the anti-inflammatory drug aspirin or, even more so, by just dripping on some chlorophyll. Perhaps that’s one of the reasons kale consumers appear to live longer lives.

As interesting as I found that study to be, this next study blew my mind. The most abundant energy source on this planet is sunlight. However, only plants are able to use it directly—or so we thought. After eating plants, animals have chlorophyll in them, too, so might we also be able to derive energy directly from sunlight? Well, first of all, light can’t get through our skin, right? Wrong. This was demonstrated by century-old science—and every kid who’s ever shined a flashlight through her or his fingers, showing that the red wavelengths do get through. In fact, if you step outside on a sunny day, there’s enough light penetrating your skull and going through to your brain that you could read a book in there. Okay, so our internal organs are bathed in sunlight, and when we eat green leafy vegetables, the absorbed chlorophyll in our body does actually appear to produce cellular energy. But, unless we eat so many greens we turn green ourselves, the energy produced is probably negligible.

However, light-activated chlorophyll inside our body may help regenerate Coenzyme Q10. CoQ10 is an antioxidant our body basically makes from scratch using the same enzyme we use to make cholesterol—that is, the same enzyme that’s blocked by cholesterol-lowering statin drugs. So, if CoQ10 production gets caught in the crossfire, then maybe that explains why statins increase our risk of diabetes—namely, by accidently also reducing CoQ10 levels in a friendly-fire type of event. Maybe that’s why statins can lead to muscle breakdown. Given that, should statin users take CoQ10 supplements? No, they should sufficiently improve their diets to stop taking drugs that muck with their biochemistry! By doing so—by eating more plant-based chlorophyll-rich diets—you may best maintain your levels of active CoQ10, also known as ubiquinol. “However, when ubiquinol is used as an antioxidant, it is oxidized to ubiquinone. To act as an effective antioxidant, the body must regenerate ubiquinol from ubiquinone,” perhaps by using dietary chlorophyll metabolites and light.

Researchers exposed some ubiquinone and chlorophyll metabolites to the kind of light that makes it into our bloodstream. Poof! CoQ10 was reborn. But, without the chlorophyll or the light, nothing happened. By going outside we get light and, if we’re eating our veggies, chlorophyll, so maybe that’s how we maintain such high levels of CoQ10 in our bloodstream. Perhaps this explains why dark green leafy vegetables are so good for us. We know sun exposure can be good for us and that eating greens can be good for us. “These benefits are commonly attributed to an increase in vitamin D from sunlight exposure and consumption of antioxidants from green vegetables”—but is it possible that these explanations might be incomplete?


This blog post has it all: a mind-blowing mechanism, practical applicability, and poop. What more could you want?

Interested in learning more about the potential downsides of cholesterol-lowering statin drugs? I’ve produced other videos on the topic, including Statin Cholesterol Drugs and Invasive Breast Cancer and The Actual Benefit of Diet vs. Drugs.

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: