The Difference Between Alpha and Beta Receptors Explain Soy’s Benefits

“[S]oyfoods have become controversial in recent years…even among health professionals…exacerbated by misinformation found on the Internet.” Chief among the misconceptions is that soy foods promote breast cancer because they contain a class of phytoestrogen compounds called isoflavones, as I explore in my video, Is Soy Healthy for Breast Cancer Survivors? Since estrogens can promote breast cancer growth, it is natural to assume that phytoestrogens might, too, but most people do not realize there are two different types of estrogen receptors in the body, alpha and beta. Unlike actual estrogen, soy phytoestrogens “preferentially bind to and activate ERβ,” estrogen receptor beta. “This distinction is important because the [two types of receptors] have different tissue distributions within the body and often function differently, and sometimes in opposite ways. This appears to be the case in the breast,” where beta activation has an anti-estrogenic effect, inhibiting the growth-promoting effects of actual estrogen—something we’ve known for more than ten years.

The effects of estradiol, the primary human estrogen, on breast cells are “completely opposite” to those of soy phytoestrogens, which have “antiproliferative effects on breast cancer cells…even at [the] low concentrations” we get in our bloodstream after eating just a few servings of soy. This makes sense, given that after eating a cup of soybeans, the levels in our blood cause significant beta receptor activation, as you can see at 1:27 in my video.

Where did this outdated notion that soy could increase breast cancer risk come from? The concern was based largely on research that showed that the main soy phytoestrogen, genistein, stimulates the growth of mammary tumors in a type of mouse—but, it turns out, we’re not mice. We metabolize soy isoflavones very differently from rodents. As you can see at 2:00 in my video, the same soy phytoestrogens led to 20 to 150 times higher levels in the bloodstream of rodents. The breast cancer mouse in question had 58 times higher levels. What does this mean for us? If we ate 58 cups of soybeans a day, we could get some significant alpha activation, too, but, thankfully, we’re not hairless athymic ovariectomized mice and we don’t tend to eat 58 cups of soybeans a day.

At just a few servings of soy a day, with the excess beta activation, we would assume soy would actively help prevent breast cancer. And, indeed, “[s]oy intake during childhood, adolescence, and adult life were each associated with a decreased risk of breast cancer.” Those women who ate the most soy in their youth appeared to grow up to have less than half the risk. This may help explain why breast cancer rates are so much higher in the United States than in Asia, where soy foods are more commonly consumed. Yet, when Asians come to the United States and start eating and living like Americans, their breast cancer risk shoots right up. Women in their 50s living in Connecticut, for example, are way at the top of the breast cancer risk heap, as you can see at 3:00 in my video, and have approximately ten times more breast cancer than women in their 50s living in Japan. It isn’t genetic, however. When Japanese women move to the United States, their breast cancer rates go up generation after generation as they assimilate into American culture.

Are the anti-estrogenic effects of soy foods enough to actually change the course of the disease? We didn’t know until the first human study on soy food intake and breast cancer survival was published in 2009 in the Journal of the American Medical Association, suggesting that “[a]mong women with breast cancer, soy food consumption was significantly associated with decreased risk of death and [breast cancer] recurrence.” That study was followed by another study, and then another, each with similar findings. That was enough for the American Cancer Society, which brought together a wide range of cancer experts to offer nutrition guidelines for cancer survivors, concluding that, if anything, soy foods should be beneficial. Since then, two additional studies have been published for a total of five—five out of five studies that tracked more than 10,000 breast cancer patients—and they all point in the same direction.

Pooling all of the results, soy food intake after breast cancer diagnosis was associated with both reduced mortality and reduced recurrence—that is, a longer lifespan and less likelihood that the cancer comes back. This improved survival was for women with estrogen receptor negative tumors and estrogen receptor positive tumors, and for both younger women and for older women.

Pass the edamame.


Flaxseeds are protective for likely the same reasons. For more on this, see my videos Flaxseeds and Breast Cancer Survival: Epidemiological Evidence and Flaxseeds and Breast Cancer Survival: Clinical Evidence.

What about women who carry breast cancer genes? I touched on that in BRCA Breast Cancer Genes and Soy and Should Women at High Risk for Breast Cancer Avoid Soy?.

What about genetically modified soy? See GMO Soy and Breast Cancer.

Who Shouldn’t Eat Soy? An excellent question I answer in that video.

For even more information on soy, see:

Not all phytoestrogens may be protective, though. See The Most Potent Phytoestrogen Is in Beer and What Are the Effects of the Hops Phytoestrogen in Beer?.

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 to Boost the Fat Burning Hormone FIAF

Although recent increases in the availability of junk food and decreases “in institutionally driven physical activity” have created an obesity-permissive environment, several other factors may contribute. We know, for example, that the use of antibiotics is linked to obesity, so our gut flora may play a role. I discuss this in my video Is Obesity Infectious?.

Recently, specific bacterial species were identified. Eight species seemed protective against weight gain, and they are all producers of a short-chain fatty acid called butyrate.

Early on, we thought there might be some intestinal bacteria that were able to extract additional calories from what we eat, but the relationship between our gut flora and obesity has proven to be more complex, as you can see at 0:49 in my video. Our gut flora may affect how we metabolize fat, for example, such as through the hormone FIAF—fasting-induced adipose factor.

While we’re fasting, our body has to stop storing fat and instead start to burn it off. FIAF is one of the hormones that signals our body to do this, which could be useful for someone who is obese, and may be one way our gut flora manages our weight. Some bacteria repress this hormone, thereby increasing fat storage. In contrast, when we feed fiber to our fiber-eating bacteria, those that secrete short-chain fatty acids like butyrate are able to upregulate this hormone in all human cell lines so far tested.

“Currently, when an individual fails to lose weight…the only other option is surgery,” but “[a]s the mechanisms of the microbiota’s [gut flora’s] role in weight regulation are elucidated, one can envision transplanting intestinal contents from a thin individual into an obese individual.” Such so-called fecal transplants may suffer from “repulsive esthetics,” though. It turns out there may be easier ways to share.

We’ve known that people who live together share a greater similarity in gut bacteria than people living apart. This could be because co-habitants inadvertently swap bacteria back and forth, or possibly because they eat similar diets, living in the same house. We didn’t know…until now. Not only do co-habiting family members share bacteria with one another—they also share with their dogs, who are probably eating a different diet than they are. You may be interested in the charts at 2:22 in my video.

In fact, it’s been “suggest[ed] that homes harbor a distinct microbial fingerprint that can be predicted by their occupants.” Just by swabbing the doorknobs, you can tell which family lives in which house, as shown at 2:35 in my video. And, when a family moves into a new home, “the microbial community in the new house rapidly converged” or shifted toward that of the old house, “suggesting rapid colonization by the family’s microbiota.” Experimental evidence suggests that individuals raised in a household of lean people may be protected against obesity—no fecal transplant necessary. (Indeed, people may be sharing gut bacteria from kitchen stools instead.)

Moreover, as we know, people living together share more bacteria than those living apart, but when a dog is added to the mix, the people’s bacteria get even closer, as you can see at 3:11 in my video. Dogs can act like a bridge to pass bacteria back and forth between people. Curiously, owning cats doesn’t seem to have the same effect. Maybe cats don’t tend to drink out of the toilet bowl as much as dogs do?

Exposure to pet bacteria may actually be beneficial. It’s “intriguing to consider that who we cohabit with, including companion animals, may alter our physiological properties by influencing the consortia of microbial symbionts [or bacteria] that we harbor in and on our various body habitats.” This may be why “[r]ecent studies link early exposure to pets to decreased prevalence of allergies, respiratory conditions, and other immune disorders” as kids grow older. In my video Are Cats or Dogs More Protective for Children’s Health?, I talk about studies in which dog exposure early in life may decrease respiratory infections, especially ear infections. Children with dogs “were significantly healthier,” but we didn’t know why. Indeed, we didn’t know the mechanism until, perhaps, now—with the first study tying together the protection from respiratory disease through pet exposure to differences in gut bacteria. None of the studied infants in homes with pets suffered from wheezy bronchitis within the first two years of life, whereas 15 percent of the pet-deprived infants had. And, when comparing stool samples, this correlated with differences in gut bacteria depending on the presence of pets in the home.

There was a famous study of 12,000 people that found that a “person’s chances of becoming obese increased by 57%…if he or she had a friend who became obese,” suggesting social ties have a big effect. However, given the evidence implicating the role of gut bacteria in obesity, this “raises up the possibility that cravings and associated obesity might not just be socially contagious”—that is, because, for instance, you all go out together and eat the same fattening food—“but rather truly infectious, like a cold.”


Viruses may also play a role in obesity. How? See Infectobesity: Adenovirus 36 and Childhood Obesity. An Obesity-Causing Chicken Virus may help explain the link found between poultry consumption and weight gain, and you may also be interested in Chicken Big: Poultry and Obesity.

The important question: Can Morbid Obesity Be Reversed Through Diet? Find out in my video, and also check out Coconut Oil and Abdominal Fat.

For more on the amazing inner world in our guts, 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:

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: