What Happens When Pregnant Women Eat More Animal Protein

Are high-protein diets during pregnancy healthful or harmful? That question was answered about 40 years ago in the infamous Harlem Trial of 1976: a “randomized controlled trial of nutritional supplementation pregnancy, in a poor black urban population in the United States.” The study, which I discuss in my video The Effect of Animal Protein on Stress Hormones, Testosterone, and Pregnancy, “was begun when protein was commonly assumed to be deficient in the diet of the poor.” Had researchers actually analyzed their diets before they started, they would have realized that this wasn’t true, but why let facts get in the way of assumptions? So, the researchers split poor black pregnant women into three groups, each receiving one of the following treatments: (1) an extra 40 grams of animal protein a day, which is essentially a couple cans of Ensure, (2) an extra 6 grams of animal protein, or (3) no extra protein. Then they sat back and watched what happened. The high-protein group suffered “an excess of very early premature births and associated neonatal [infant] deaths, and there was significant growth retardation” in the babies who survived. More protein meant more prematurity, more deaths, and more growth retardation, which you can see reflected in the chart at 1:00 in my video.

What’s more, animal protein intake during pregnancy has been associated with children becoming overweight later in life and getting high blood pressure. The “offspring of mothers who reported eating more meat and fish had higher systolic blood pressure” in adulthood. This was part of another failed dietary intervention trial in which mothers were advised to eat a pound of meat a day. The increased weight gain and high blood pressure may be due to the obesity-causing chemical pollutants in the meat supply, as I’ve discussed in my video Animal Protein, Pregnancy, and Childhood Obesity, or the animal protein-induced rise in the growth hormone IGF-1. Or, it could be due to a steroid stress hormone called cortisol.

As you can see in the chart at 2:01 in my video, a single meal high in animal protein can nearly double the level of the stress hormone in the blood within a half hour of consumption, much more than a meal closer to the recommended level of protein. When subjects are given a meal of crab, tuna fish, and cottage cheese, the stress hormone level shoots up. If they’re instead given some barley soup and a vegetable stir-fry on rice, the stress hormone level goes down after the meal, as you can see at 2:27 in my video. Imagine eating meat-fish-dairy meals day after day. Doing so “may chronically stimulate” our stress response axis “and increase the release of vasoactive hormones” that could increase our blood pressure. And, all that extra cortisol release has been linked to increased risk for elevated blood levels of insulin, triglycerides, and cholesterol.

When men on a high-protein diet, “such as meat, fish, poultry, egg white,” were switched to a high-carb diet of bread, vegetables, fruit, and sugary junk, their cortisol levels dropped about a quarter within 10 days. At the same time, their testosterone levels shot up by about the same amount, as you can see at 3:09 in my video. High-protein diets suppress testosterone. That is why, if men eating plant-based diets begin to eat meat every day, their testosterone levels go down and some estrogens actually go up, and that’s why bodybuilders can get such low testosterone levels. It’s not the steroids they’re taking. If you look at natural bodybuilders who don’t use steroids, there is a 75 percent drop in testosterone levels in the months leading up to a competition. Testosterone levels were cut by more than half, which is enough to drop a guy into an abnormally low range, as you can see at 3:47 in my video. It’s ironic that they’re eating protein to look manly on the outside, but it can make them less and less manly on the inside. And, from an obesity standpoint, in general, a drop in testosterone levels may increase the risk of gaining weight and body fat. What does cortisol have to do with weight?

There’s actually a disease caused by having too much cortisol, called Cushing’s syndrome, which can increase abdominal obesity. Even in normal women, though, chronic stress and chronic high cortisol levels can contribute to obesity. What’s more, if they’re pregnant, high-meat and low-carb diets may increase cortisol levels in the moms, which can lead to inappropriate fetal exposure to cortisol, which, in turn, can affect the developing fetus, resetting her or his whole stress response thermostat and leading to higher cortisol levels in later adult life. This can have serious, life-long health consequences. Every maternal daily portion of meat and fish was associated with 5 percent higher cortisol levels in their children as much as 30 years later, though green vegetable consumption was found to be protective. Higher meat consumption, such as three servings a day compared to one or two, was associated with significantly higher cortisol levels, but eating greens every day appeared to blunt some of that excess stress response, as you can see at 5:12 in my video.

As well, the adult children of mothers who ate a lot of meat during pregnancy don’t only have higher stress hormone levels, they also appear to react more negatively to whatever life throws at them. Researchers put them through the Trier Test, which involves public speaking in front of a panel of judges, following by a live math exercise. You can see in my video at 5:36 a chart comparing the stress hormone responses in those whose moms ate less than two servings of meat per day, about two servings a day, or about two to three servings a day. Note that before the test started, the cortisol levels of the two groups eating less meat started out about the same, but their exaggerated cortisol response was laid bare when exposed to a stressful situation. The real-world effects of this are that after that sort of test, when people are given their own private snack buffet with fruits and veggies versus fatty, sugary, comfort foods like chocolate cake, guess who may eat less of the fruits and veggies? Those who have high chronic stress levels. “Cortisol has been implicated as a factor in motivating food intake” even when we aren’t really hungry.

It’s no surprise then that a woman’s animal protein intake during pregnancy may lead to larger weight gain for her children later in life—and maybe even for her grandchildren. “Remarkably, recent evidence suggests that the long-term consequences of adverse conditions during early development may not be limited to one generation, but may lead to poor health in the generations to follow, even if these individuals develop in normal conditions themselves.” Indeed, the diet of a pregnant mother may affect the development and disease risk of her children and even her grandchildren. Ultimately, these findings may shed light on our rapidly expanding epidemics of diabetes, obesity, and heart disease.


Whoa, there was a lot to unpack! Rather than break it up, since so much of it was tied together, as you could see, I compiled everything into this one, heftier piece. You may want to read this a second time and watch the video to absorb it all.

For more on how a woman’s diet during pregnancy can affect her children, see Maternal Diet May Affect Stress Responses in Children and Animal Protein, Pregnancy, and Childhood Obesity.

Protein is such a misunderstood nutrient. For more information, check out:

In health,
Michael Greger, M.D.

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

Proof that Lifelong Cholesterol Reduction Prevents Heart Disease

“It is well accepted that coronary atherosclerosis is a chronic progressive disease that begins early in life and slowly progresses over several decades” before symptoms arise. However, the average age in cholesterol-lowering drug trials is 63; therefore, people have already been exposed to a lifetime of circulating LDL cholesterol. It’s no wonder pharmaceutical therapies typically reduce cardiovascular disease risk by only 20 to 30 percent.

We know LDL, the so-called bad cholesterol, plays “a central role” in the “initiation, development, and progression” of our number-one killer. In fact, more than 100 prospective studies involving more than a million people have demonstrated that those with higher LDL levels are at higher risk.

“It seems reasonable to assume, therefore, that if lowering LCL-C [cholesterol] levels beginning later in life can slow the progression of advanced atherosclerotic plaques…then keeping LDL-C levels low, beginning much earlier in life” might prevent our arteries from getting clogged in the first place. A reasonable assumption, certainly—but let’s not just assume.

“It would be…unethical to set up a controlled clinical trial in which young adults with elevated serum cholesterol levels were treated or not treated over their lifetime”—just as we couldn’t ethically set up a study in which half the young adults are made to start smoking to see if smoking really does cause lung cancer. That’s where observational studies come in. We can follow people who already smoke and compare their disease rates to those who don’t.

It was aroud 40 years ago when the president of the American Heart Association tried to argue we should all stop smoking even though there were no randomized controlled trials. You can see a copy of the “Presidential Address” entitled “The Case for Prevention of Coronary Heart Disease” to the AHA’s 47th Scientific Sessions at 1:34 in my video. Those who smoke have a higher risk of heart attack, and the more we smoke the higher the risk. After we stop smoking, our risk drops. The same can be said for high cholesterol.

Young men 18 through 39 years of age were followed for up to 34 years, and their cholesterol levels, even when they were young, predicted long-term risk of heart disease and death. Men in their 20s and 30s who have a total cholesterol just under 200 have a “substantially longer estimated life expectancy”—around 4 to 9 years longer—than those with levels over 240.

“Evidence from observational studies, however, [is] vulnerable to confounding” factors. Eating a diet that is plant-based enough to lower cholesterol below average, for example, may add years to our lives regardless of what our cholesterol actually is. Ideally, we’d have a long-term, randomized, controlled trial.

Nature may have actually set one up for us. Each of us, at conception, gets a random assortment of genes from our mother and our father, and some of those genes may affect our cholesterol levels. Just like there are rare genetic mutations that result in unusually high cholesterol levels, there are rare genetic mutations that lead to unusually low cholesterol levels, “provid[ing] an ideal system in which to assess the consequences of low LDL cholesterol levels independently of other factors that may modify disease progression,” such as confounding diet and lifestyle factors.

Starting at 3:14 in my video, you can see what I mean. About 1 in 40 African Americans have a mutation that drops their LDL cholesterol from around 130 down toward more optimal levels. Now, this group didn’t eat healthy to get achieve that drop. It’s just in their genes. More than half had high blood pressure and there were a lot of smokers and diabetics in the group, yet those with genetically low LDL levels still had a significant reduction in the incidence of coronary heart disease even in the presence of all those other risk factors. How significant? How much less heart disease? A remarkable 88 percent of heart disease was simply gone.

The astounding finding was that the risk of heart disease in these individuals was reduced by more than 80 percent, whereas the same 20- to 40-point decrease in LDL from drugs only reduces risk around 30 percent. Makes sense, though, because the folks with the mutation had low levels their entire life. They didn’t simply start taking a pill when they were 60.

“The magnitude of the effect of long-term exposure to lower LDL-C [cholesterol] concentrations observed in each of these studies represents a threefold greater reduction in the risk of CHD,” or coronary heart disease, compared to drug treatment started later in life. (As an aside, for all of my fellow research nerds, check out that p value shown in my video at the 4:30 mark. You’d have to do arourd a quintillion studies to get that kind of result by chance!)

“Therefore, a primary prevention strategy that promotes keeping LDL [cholesterol] levels as low as possible, beginning as early in life as possible, and sustaining those low levels of LDL [cholesterol] throughout the whole of one’s lifetime has the potential to dramatically reduce the risk of CHD,” coronary heart disease.


If you don’t know your cholesterol level, you should get it checked—maybe even starting in childhood. See my video Should All Children Have Their Cholesterol Checked? to learn more.

What if you do get tested and your doctor tells you not to worry because your cholesterol’s “normal”? Having a “normal” cholesterol level in the society where it’s normal to drop dead of a heart attack (the number-one killer of men and women) is not really such a good thing. See my video When Low-Risk Means High-Risk.

Check out Optimal Cholesterol Level and What’s the Optimal Cholesterol Level? to find out where you should be.

What if your doctor tells you your LDL is large and fluffy? See my video Does Cholesterol Size Matter?.

In health,
Michael Greger, M.D.

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

How the Egg Industry Tried to Bury the TMAO Risk

“Metabolomics is a term used to describe the measurement of multiple small-molecule metabolites in biological specimens, including bodily fluids,” with the goal of “[i]dentifying the molecular signatures.” For example, if we compared the metabolic profile of those with severe heart disease to those with clean arteries, we might be able to come up with a cheap, simple, and noninvasive way to screen people. If heart patients happened to have something in their blood that healthy people didn’t, we could test for that. What’s more, perhaps it would even help us understand the mechanisms of disease. “To refer to metabolomics as a new field is injustice to ancient doctors who used ants to diagnose the patients of diabetes” (because the ants could detect the sugar in the diabetics’ urine).

The first modern foray discovered hundreds of substances in a single breath, thanks to the development of computer technology that made it possible to handle large amounts of information—and that was in 1971, when a computer took up nearly an entire room. “[N]ew metabolomics technologies [have] allowed researchers to measure hundreds or even thousands of metabolites at a time,” which is good since more than 25,000 compounds may be entering our body through our diet alone.

Researchers can use computers to turn metabolic data into maps that allow them to try to piece together connections. You can see sample data and a map at 1:28 in my video Egg Industry Response to Choline and TMAO. Metabolomics is where the story of TMAO started. “Everyone knows that a ‘bad diet’ can lead to heart disease. But which dietary components are the most harmful?” Researchers at the Cleveland Clinic “screened blood from patients who had experienced a heart attack or stroke and compared the results with those from blood of people who had not.”

Using an array of different technology, the researchers identified a compound called TMAO, which stands for trimethylamine N-oxide. The more TMAO people had in their blood, the greater the odds they had heart disease and the worse their heart disease was.

Where does TMAO come from? At 2:19 in my video, you can see a graphic showing that our liver turns TMA into TMAO—but where does TMA come from? Certain bacteria in our gut turn the choline in our diet into TMA. Where is the highest concentration of choline found? Eggs, milk, and meats, including poultry and fish. So, when we eat these foods, our gut bacteria may make TMA, which is absorbed into our system and oxidized by our liver into TMAO, which may then increase our risk of heart attack, stroke, and death.

However, simply because people with heart disease tend to have higher TMAO levels at a snapshot in time doesn’t mean having high TMAO levels necessarily leads to bad outcomes. We’d really want to follow people over time, which is what researchers did next. Four thousand people were followed for three years, and, as you can see in the graph at 3:10 in my video, those with the highest TMAO levels went on to have significantly more heart attacks, strokes, or death.

Let’s back up for a moment. If high TMAO levels come from eating lots of meat, dairy, and eggs, then maybe the only reason people with high TMAO levels have lots of heart attacks is that they’re eating lots of meat, dairy, and eggs. Perhaps having high TMAO levels is just a marker of a diet high in “red meat, eggs, milk, and chicken”—a diet that’s killing people by raising cholesterol levels, for example, and has nothing to do with TMAO at all. Conversely, the reason a low TMAO level seems so protective may just be that it’s indicative of a more plant-based diet.

One reason we think TMAO is directly responsible is that TMAO levels predict the risk of heart attacks, strokes, or death “independently of traditional cardiovascular risk factors.” Put another way, regardless of whether or not you had high cholesterol or low cholesterol, or high blood pressure or low blood pressure, having high TMAO levels appeared to be bad news. This has since been replicated in other studies. Participants were found to have up to nine times the odds of heart disease at high TMAO blood levels even after “controll[ing] for meat, fish, and cholesterol (surrogate for egg) intake.”

What about the rest of the sequence, though? How can we be certain that our gut bacteria can take the choline we eat and turn it into trimethylamine in the first place? It’s easy. Just administer a simple dietary choline challenge by giving participants some eggs.

Within about an hour of eating two hard-boiled eggs, there is a bump of TMAO in the blood, as you can see at 4:51 in my video. What if the subjects are then given antibiotics to wipe out their gut flora? After the antibiotics, nothing happens after they eat more eggs. In fact, their TMAO levels are down at zero. This shows that our gut bacteria play a critical role. But, if we wait a month and give their guts some time to recover from the antibiotics, TMAO levels creep back up.

These findings did not thrill the egg industry. Imagine working for the American Egg Board and being tasked with designing a study to show there is no effect of eating nearly an egg a day. How could a study be rigged to show no difference? If we look at the effect of an egg meal (see 5:32 in my video), we see it gives a bump in TMAO levels. However, our kidneys are so good at getting rid of TMAO, by hours four, six, and eight, we’re back to baseline. So, the way to rig the study is just make sure the subjects hadn’t eaten those eggs in the last 12 hours. Then, you can show “no effect,” get your study published in the Journal of the Academy of Nutrition and Dietetics, and collect your paycheck.


Unfortunately, this appears to be part for the course for the egg industry. For more on their suspect activities, see:

For more on the TMAO story, 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 presentations: