Beer Phytoestrogens

Why do alcoholic men develop so-called man boobs and other feminine traits? We know estrogens produce feminization, and our liver clears estrogens from the body. As such, the original theory was that alcohol-induced liver damage led to the retention of excess estrogens. The problem was that when researchers measured estrogen levels, they weren’t elevated. What’s more, even those with cirrhosis of the liver appeared to clear estrogens from the body normally, and men’s testicles started shrinking even before serious liver disease developed.

So, alternative explanations were considered. If it’s not due to estrogens produced endogenously, meaning within the body, maybe alcoholics are being exposed to “exogenous estrogenic substances from dietary sources”—perhaps from phytoestrogens in the plants that alcoholic beverages are made from. The discovery that plants could contain hormonal compounds was made back in 1951 by two Australian chemists charged with finding out the cause of an “epidemic of infertility in sheep that was ravaging their nation’s wool industry.” It took them ten years, but they finally figured out the cause: a compound called genistein, present in a type of clover, and the same phytoestrogen found in soybeans.

You can read about the dreaded clover disease on scare-mongering websites, but you’ll note they never talk about the difference in dose. To get as much as the sheep were getting from clover, you’d have to drink more than 1,000 cartons of soymilk a day or eat more than 8,000 soy burgers or about 800 pounds of tofu a day.

This is not to say you can’t overdo it. There are two case reports in the medical literature that describe feminizing effects associated with eating as few as 14 to 20 servings of soy foods a day. But at reasonable doses, or even considerably higher than the one or two servings a day Asian men eat, soy phytoestrogens do not exert feminizing effects on men.

So, back in 1951, we realized plant compounds could be estrogenic. Two German researchers realized that perhaps that’s why women who handle hops start menstruating, and, indeed, they found estrogenic activity in hops, which is the bittering agent used to make beer. They found trace amounts of the soy phytoestrogens, but in such tiny quantities that beer would not be expected to have an estrogenic effect. In 1999, however, a potent phytoestrogen called 8-prenylnaringenin was discovered in hops, which I discuss in my video The Most Potent Phytoestrogen Is in Beer. In fact, it’s the most potent phytoestrogen found to date, fifty times more potent than the genistein in soy, “provid[ing] an obvious explanation for the menstrual disturbances in female hop workers in the past.” Today, we have machines to pick our hops, so our only exposure is likely via beer consumption, but the levels in beer were found to be so low that they shouldn’t cause any concern.

Then in 2001, a study on a hops-containing “dietary supplement for breast enhancement” raised the concern that another phytoestrogen in hops called isoxanthohumol might be biotransformed by our liver into the more potent 8-PN, which would greatly augment the estrogenic effect of hops. This study was conducted on mice, though. Thankfully, a study using human estrogen receptors found no such liver transformation, so all seemed fine…until 2005. “[T] he liver is not the only transformation site inside the human body.” The human colon contains trillions of microorganisms with enormous metabolic potential. It’s like a whole separate organ within our body, with a hundred livers’ worth of metabolizing power. So, let’s effectively mix some beer with some poop and see what happens.

Indeed, up to a 90 percent conversion was achieved. Up to then, “the concentration of 8-PN in beer was considered too low to affect human health. However, these results show that the activity of the intestinal microbial community could more than 10-fold increase the exposure concentration.” This can explain why you can detect 8-PN in the urine of beer-drinkers for days: Their gut bacteria keep churning it out. Obviously, the amount of straight 8-PN in beer is not the only source of estrogen effects given this conversion. So, a decade ago, the question remained: Might drinking too much beer cause estrogenic effects and feminize men? See my video What Are the Effects of the Hops Phytoestrogen in Beer? for the update.


Other videos on phytoestrogen include:

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

For menstrual health videos, 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:

Reversing Massive Obesity With Diet

Dr. Walter Kempner introduced the first comprehensive dietary program to treat chronic kidney disease and, in doing so, also revolutionized the treatment of other disorders, including obesity. Kempner was Professor Emeritus of Medicine at Duke, where he came up with the so-called rice diet, which basically consisted of rice, sugar, fruit, and fruit juices, was extremely low in sodium and fat, and included no animal fat, no cholesterol, and no animal protein. The sugar was added as a source of calories so people wouldn’t lose too much weight. But some people need to lose weight, so he started treating obese patients with a lower calorie version of the diet, which I discuss in my Can Morbid Obesity Be Reversed Through Diet? video.

He published an analysis of 106 patients who each lost at least 100 pounds. Why 106? Kempner simply picked the last 100 people who lost more than 100 pounds, and, by the time he finished reviewing their charts, 6 more had joined the so-called century club. Average weight loss among them was 141 pounds. “This study demonstrates that massively obese persons can achieve marked weight reduction, even normalization of weight, without hospitalization, surgery, or pharmacologic intervention…[O]ne important fact to be gained from this study is that, despite the misconception to the contrary, massive obesity is not an uncorrectable malady. Weight loss can be achieved, massive obesity can be corrected, and it can be done without drastic intervention.”

Well, Kempner’s rice diet is pretty drastic, so definitely don’t try this at home. In fact, the rice diet is dangerous. It’s so restrictive that it may cause serious electrolyte imbalances, unless the patient is carefully medically supervised with frequent blood and urine lab testing. Dangerous? Says who? Said the world’s number-one advocate for the rice diet: Dr. Kempner himself.

The best, safe approximation of the diet, meaning low in sodium and without fat, protein, or cholesterol from animals, would be a vitamin B12-fortified diet centered around whole, unprocessed plant foods. However, even a medically supervised rice diet could be considered un-drastic compared to procedures like getting one’s internal organs stapled or rearranged, wiring someone’s jaws shut, or even undergoing brain surgery.

Attempts have been made to destroy the parts of the brain associated with the sensation of hunger, by irradiation or going in through the skull and burning them out. “It shows how ineffective most simpler forms of treatment are that anyone should think it reasonable to produce irreversible intracranial lesions in very obese patients.” The surgeons defended these procedures, however, explaining that their “justification in attempting the operation is, of course, the very poor results of conventional therapy in gross obesity, and the dark prognosis, mental and physical, of the uncorrected condition.” In reply, a critic countered, “Such strong feelings [about how dark the prognosis is] run the risk of being conveyed to the patient, to the effect of masking the operative dangers and steam-rolling the patient’s approval.” The surgeon replied, “If any ‘steamrolling’ is taking place, it comes rather from obese patients who sometimes threaten suicide unless they are accepted for experimental surgical treatment.”

As of 2013, the American Medical Association officially declared obesity a disease, by identifying the enormous humanitarian impact of obesity as requiring the medical care and attention of other diseases. Yet the way we treat diseases these days involves drugs and surgery. Anti-obesity drugs have been pulled from the market again and again after they started killing people—an unrelenting fall of the pharmacological treatment of obesity.

The same has happened with obesity surgeries. The procedure Kempner wrote about was discontinued because of the complication of causing irreversible cirrhosis of the liver. Current procedures include various reconfigurations of the digestive tract. Complications of surgery appear to occur in about 20 percent of patients, and nearly one in ten of which may be death. In one of the largest studies, 1.9 percent of patients died within a month of the surgery. “Even if surgery proves sustainably effective, the need to rely on the rearrangement of [our] anatomy as an alternative to better use of feet and forks [that is, diet and exercise] seems a societal travesty.”


For more on Kempner and his rice diet, see my videos:

Learn more on the surgical approach in Reversing Diabetes with Surgery and Stomach Stapling Kids.

And, for more on weight, 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 Avoid Fatty Liver Disease

In the documentary Supersize Me, Morgan Spurlock eats exclusively at McDonald’s for a month and predictably his weight, blood pressure, and cholesterol go up, but so do his liver enzymes, a sign his liver cells are dying and spilling their contents into the bloodstream. His one-man experiment was actually formally replicated. A group of men and women agreed to eat two fast food meals a day for a month. Most of their liver values started out normal, but, within just one week, most were out of whack, a profound pathological elevation in liver damage.

What’s happening is non-alcoholic fatty liver disease (NAFLD), the next global epidemic, as I discuss in my video How to Prevent Non-Alcoholic Fatty Liver Disease. Fatty deposits in the liver result in a disease spectrum from asymptomatic fat buildup to non-alcoholic steatohepatitis (NASH), which can lead to liver scarring and cirrhosis, and may result in liver cancer, liver failure, and death.

NAFLD is now the most common cause of chronic liver disease in the United States, affecting 70 million Americans, nearly one in three adults. Fast food consumption is a great way to bring it on, since it’s associated with the intake of soft drinks and meat. Drinking one can of soda a day may raise the odds of NAFLD by 45 percent, and those eating the equivalent of 14 chicken nuggets’ worth of meat a day have nearly triple the rates of fatty liver compared to those eating 7 nuggets or less.

It’s been characterized as a tale of fat and sugar, but evidently not all types of fat are culpable. Those with fatty hepatitis were found to have eaten more animal fat and cholesterol, and less plant fat, fiber, and antioxidants. This may explain why adherence to a Mediterranean-style diet, characterized by high consumption of foods such as fruits, vegetables, whole grains, and beans, is associated with less severe non-alcoholic fatty liver disease. It could also be related to the presence of specific phytonutrients, like the purple, red, and blue anthocyanin pigments found in berries, grapes, plums, red cabbage, red onions, and radicchio. These anthocyanin-rich foods may be promising for the prevention of fatty liver, but that’s mostly based on petri dish experiments. There was one clinical trial that found that drinking a purple sweet potato beverage seemed to successfully dampen liver inflammation.

A more plant-based diet may also improve our microbiome, the good bacteria in our gut. “‘We are what we eat’ is the old adage but the modern version might be ‘we are what our bacteria eat.’” When we eat fat, we may facilitate the growth of bad bacteria, which can release inflammatory molecules that increase the leakiness of our gut and contribute to fatty liver disease.

Fatty liver disease can also be caused by cholesterol overload. The thought is that dietary cholesterol found in eggs, meat, and dairy oxidizes and then upregulates liver X receptor alpha, which can upregulate something else called SREBP, which can increase the level of fat in the liver. Cholesterol crystals alone cause human white blood cells to spill out inflammatory compounds, just like uric acid crystals in gout. That’s what may be triggering the progression of fatty liver into serious hepatitis: “the accumulation of sufficient concentrations of free cholesterol within steatotic hepatocytes [fatty liver cells] to cause crystallization of the cholesterol.” This is one of several recent lines of evidence suggesting that dietary cholesterol plays an important role in the development of fatty hepatitis—that is, fatty liver inflammation.

In a study of 9,000 American adults followed for 13 years, researchers found a strong association between dietary cholesterol intake and hospitalization and death from cirrhosis and liver cancer, as dietary cholesterol can oxidize and cause toxic and carcinogenic effects. To limit the toxicity of excess cholesterol derived from the diet, the liver tries to rid itself of cholesterol by dumping it into the bloodstream. So, by measuring the non-HDL cholesterol in the blood, one can predict the onset of fatty liver disease. If we subtract HDL from total cholesterol, none of the hundreds of subjects followed with a value under 130 developed the disease. Drug companies view non-alcoholic fatty liver disease as a bonanza, “as is the case of any disease of affluence…considering its already high and rising prevalence and…[its] needing continuous pharmacologic treatment,” but maybe avoiding it is as easy as changing our diet, avoiding sugary and cholesterol-laden foods.

“The unpalatable truth is that NAFLD could almost be considered the human equivalent of foie gras (loosely translated from French as ‘fat liver’). As we overeat and ‘force-feed’ ourselves foods that can result in serious health implications, however, having such a buttery texture in human livers is not a delicacy to be enjoyed by hepatologists [liver doctors] in clinical practice!”


Like my video Preventing Gout Attacks with Diet, How to Prevent Non-Alcoholic Fatty Liver Disease covers an important topic worth the extensive coverage the video provides.

For more on how bad added sugars are for us, see:

For more on how bad cholesterol can be, 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: