Which Alcohol Has The Most Estrogen?

Results – For all the hormones and other proteins examined, the levels changed as would be expected if the congeners contained biologically active phytoestrogens (see figures 4 and ​ 5, p.225) ( Gavaler et al.1995 a ). Thus, the levels of FSH and LH decreased, with trough levels significantly lower than baseline levels.

Conversely, the levels of prolactin, HDL cholesterol, and SHBG increased during the study period and reached peak levels that were significantly higher than the baseline levels. The women’s weights did not change over the study period. In addition, following the recovery period of 1 week, the levels of all five markers returned to values that did not differ significantly from baseline levels.

No statistically significant differences existed in the estrogenic effects of the various congener concentrates. Effects of alcoholic beverage congeners on (A) follicle-stimulating hormone (FSH) and (B) luteinizing hormone (LH) levels in postmenopausal women. For 4 weeks, the women consumed congener amounts corresponding to those present in one standard drink of the beverage daily. Basal hormone levels were determined before the women began the experiment. Trough levels represent the lowest hormone levels that were detected during the 4-week administration period of alcoholic beverage congeners. Recovery levels were determined 1 week after the last ingestion of congeners. All congeners had estrogenlike effects (i.e., resulted in lower FSH and LH levels). The effects of the various congeners did not differ significantly. NOTE: The wide bars represent mean values, whereas the narrow brackets represent the standard error of the mean. A star above a bar indicates a significant difference from basal levels as determined by paired T-test ( p < 0.025). The differences in baseline levels result from variations in the mean levels of the subjects in the various groups. IU/L = International units per liter. Effects of alcoholic beverage congeners on the levels of (A) prolactin (Prl), (B) high-density lipoprotein (HDL) cholesterol, and (C) sex hormone-binding globulin (SHBG) in postmenopausal women. For 4 weeks, the women consumed congener amounts corresponding to those present in one standard drink of the beverage daily.

Basal hormone levels were determined before the women began the experiment. Peak levels represent the highest hormone levels that were detected during the 4-week administration period of alcoholic beverage congeners. Recovery levels were determined 1 week after the last ingestion of congeners. All congeners had estrogenlike effects (i.e., resulted in elevated levels of Prl, HDL cholesterol, and SHBG).

The effects of the various congeners did not differ significantly.

Does alcohol increase estrogen in me?

Alcohol, estrogen and breast cancer risk – Alcohol can change the way a woman’s body metabolizes estrogen (how estrogen works in the body). This can cause blood estrogen levels to rise. Estrogen levels are higher in women who drink alcohol than in non-drinkers, Higher estrogen levels are in turn, linked to an increased risk of breast cancer, Learn more about estrogen and breast cancer risk,

How much alcohol affects estrogen?

1) Anxiety and Mood disorders – Taking the time to rest, move your body in fun ways, and enjoy mindful moments daily are key to preventing the daily stressors of life from taking over. Women are naturally more likely to develop stress, depression, and anxiety disorders, making stress-relieving activities all the more necessary.

1. Panic attacks, phobias, generalized anxiety disorder, and even PTSD are almost twice as common in women than in men.
2. Surprisingly, alcohol can increase the amount of estrogen women produce.
3. However, since there are many other negative hormonal effects of heavy alcohol consumption, it’s not exactly beneficial.

More estrogen from alcohol does not guarantee less risk of developing issues. Anxiety, stress, and inflammation have all been shown to increase with drinking. Mindful habits restore balance The good news is that stress hormones can find their balance again as soon as you switch to healthier lifestyle habits.

Does wine produce more estrogen?

Drinking red wine in moderation may reduce one of the risk factors for breast cancer, providing a natural weapon to combat a major cause of death among U.S. women, new research from Cedars-Sinai Medical Center shows. The study, published online in the Journal of Women’s Health, challenges the widely-held belief that all types of alcohol consumption heighten the risk of developing breast cancer.

Doctors long have determined that alcohol increases the body’s estrogen levels, fostering the growth of cancer cells. But the Cedars-Sinai study found that chemicals in the skins and seeds of red grapes slightly lowered estrogen levels while elevating testosterone among premenopausal women who drank eight ounces of red wine nightly for about a month.

White wine lacked the same effect. Researchers called their findings encouraging, saying women who occasionally drink alcohol might want to reassess their choices. “If you were to have a glass of wine with dinner, you may want to consider a glass of red,” said Chrisandra Shufelt, MD, assistant director of the Women’s Heart Center at the Cedars-Sinai Heart Institute and one of the study’s co-authors.

• Switching may shift your risk.” In the Cedars-Sinai study, 36 women were randomized to drink either Cabernet Sauvignon or Chardonnay daily for almost a month, then switched to the other type of wine.
• Blood was collected twice each month to measure hormone levels.
• Researchers sought to determine whether red wine mimics the effects of aromatase inhibitors, which play a key role in managing estrogen levels.

Aromatase inhibitors are currently used to treat breast cancer. Investigators said the change in hormone patterns suggested that red wine may stem the growth of cancer cells, as has been shown in test tube studies. Co-author Glenn D. Braunstein, MD, said the results do not mean that white wine increases the risk of breast cancer but that grapes used in those varieties may lack the same protective elements found in reds.”There are chemicals in red grape skin and red grape seeds that are not found in white grapes that may decrease breast cancer risk,” said Braunstein, vice president for Clinical Innovation and the James R.

Linenberg, MD, Chair in Medicine. The study will be published in the April print edition of the Journal of Women’s Health, but Braunstein noted that large-scale studies still are needed to evaluate the safety and effectiveness of red wine to see if it specifically alters breast cancer risk. He cautioned that recent epidemiological data indicated that even moderate amounts of alcohol intake may generally increase the risk of breast cancer in women.

Until larger studies are done, he said, he would not recommend that a non-drinker begin to drink red wine. The research team also included C. Noel Bairey Merz, MD, director of the Women’s Heart Center, director of the Preventive and Rehabilitative Cardiac Center and the Women’s Guild Chair in Women’s Health, as well as researchers from the University of Southern California Keck School of Medicine and Hartford Hospital in Connecticut.

Does red wine raise estrogen levels?

Red wine sensitivity? Could be hormonal imbalance! This blog is just an observational note. There is plenty of literature going over the changes that occur as we get older regarding our ability to handle alcohol. There is also conflicting data regarding the safety of moderate alcohol consumption and whether or not moderate drinking contributes to or reduces the risk of cancer in women.

But what we do see is that women after the age of 40 have a hard time drinking red wine without consequences. Peri-menopause and menopause are defined by changes in hormone levels in women’s bodies. These changes occur variably but usually start around the age of 40. Alcohol is known to raise estrogen levels, but there is evidence that the chemicals in red grape seeds and skins may actually decrease estrogen levels.

If your peri-menopausal symptoms are caused by a drop in estrogen then red wine may make things worse! We do know that balancing our hormones thru bio-identical hormone replacement (BHRT) is best begun early to limit the side effects of hormone replacement if started years after menopause.

My website has a hormone balance that can help to see if you have been suffering from issues with estrogen balance. I am happy to talk with you about your hormone levels and I offer testing at my office. Alcohol has been both blamed for worsening and rejoiced as a cure for peri-menopausal symptoms. There are all kinds of ideas to try to mitigate the headaches from drinking red wine, including organic wines, low tannin reds and even wines grown in special regions of Italy that purport to have low histamines.

But, my bet will be that it is the rapidly changing hormone levels that make women more sensitive to red wine and that by fine tuning hormone levels, you can be free to indulge in that nectar of the gods. Cheers and save a glass for me! : Red wine sensitivity? Could be hormonal imbalance!

Is beer full of estrogen?

Does Beer Increase Estrogen? Many men ask if beer can actually increase the amount of estrogen you have in your body. Some are understandably worried that drinking too much of their favorite game day beverage can negatively impact their estrogen levels and cause unwanted side effects.

1. Here at LT Men’s Clinic, we get this question a lot, and the answer isn’t exactly black and white.
2. First, it is important to note that casually drinking a beer will not dramatically increase your estrogen levels and cause you to grow larger breasts or experience any of the side effects of low testosterone.

So, don’t worry that having a cold one will cause your entire hormone system to get out of whack. However, it can be a completely different story when it comes to alcohol abuse. If you are abusing alcohol and drinking in excess, you may be surprised to find what chemicals are used in most beers.

Beer contains phytoestrogen and prolactin. These two chemicals can increase the estrogen levels your body produces. If this happens too much, your body will react and decrease testosterone levels—which can put you at risk for low T. This is also why it is important to limit alcohol consumption when undergoing testosterone treatment.

So, why does this happen with beer? These two estrogen-increasing chemicals are typically found in hops and barley, which of course, are two of the most common ingredients in beer. But beer isn’t the only culprit. Wines and certain liquors, such as bourbon, can also contain phytoestrogen.

The more you know about alcohol and its impact on your testosterone and estrogen levels—the better off you will be at making the right choices to keep your hormones balanced. If you have more questions about the things that could impact your estrogen levels, give the experts at LT Men’s Clinic a call.

We are available to help answer your questions and talk to you about different hormone replacement therapies that may be able to help you should you have questions about hormonal imbalances. Give us a call at 817-369-3605 to schedule your appointment with us today.

Does vodka increase estrogen in males?

Alcohol’s Effects on Leydig Cells and Testosterone Metabolism – Alcohol’s adverse effects on Leydig cell function and testosterone production were demonstrated in a study of young, healthy male volunteers with normal liver function who received alcohol over a 4-week period ( Gordon et al.1976 ).

In that study, a 15-percent alcohol solution was administered every 3 hours, around the clock, together with a diet replete with protein, vitamins, folic acid, and minerals. The total daily alcohol dose was 220 grams, or approximately 3 grams per kilogram body weight. With this level of alcohol consumption, testosterone levels in the men’s blood declined as early as 5 days into the study and continued to fall over the entire study period.

The investigators attributed the decline in testosterone to a decrease in the production rate and an increase in the breakdown and removal of testosterone from the blood (i.e., an increased metabolic clearance rate). Since those initial studies were performed, numerous studies in humans and laboratory animals have confirmed the reduction in testosterone levels after both one-time (i.e., acute) and long-term (i.e., chronic) alcohol exposure.

For example, in healthy male rats a single alcohol dose resulted in a profound reduction in testosterone levels that lasted for up to 96 hours ( Steiner et al.1996 ). Alcohol’s effects on testosterone metabolism are somewhat different, however, in men with alcoholic liver disease compared with men without alcoholic liver disease.

Thus, although the production rates and blood levels of testosterone are reduced in both groups of men, the metabolic clearance of testosterone increases only in men without alcoholic liver disease. In men with alcoholic liver disease, in contrast, the metabolic clearance is decreased ( Southren et al.1973 ).

1. Another mechanism through which alcohol may lower testosterone levels is the conversion of testosterone or one of its precursors into estrogens through a process called aromatization.
2. For example, testosterone can be metabolized to an estrogen called estradiol.
3. Similarly, the immediate precursor of testosterone—androstenedione—can be converted into a less potent estrogen called estrone.

This conversion process may be enhanced in men who regularly consume alcohol. Several studies found that some people with alcoholic liver disease have increased levels of estrogens in the blood ( Van Thiel et al.1974, 1978 ; Gordon et al.1978 ). This increase does not appear to be caused by decreased estrogen breakdown and therefore must result from increased estrogen production ( Gordon et al.1978 ).

Animal studies have indicated that alcohol does not directly enhance estrogen production in the testes (which produce both testosterone and estrogen). Instead, increased aromatization of testosterone and androstenedione to estrogens occurs in other tissues, such as the liver and fat tissue ( Gordon et al.1979 ).

In those tissues, alcohol stimulates an enzyme called aromatase, which mediates the aromatization reaction ( Gordon et al.1979 ). Consequently, in addition to decreased testosterone production and metabolism, higher-than-normal percentages of testosterone and androstenedione are converted into estradiol and estrone, respectively, in heavy drinkers.

This increased conversion may account for the elevated estrogen levels and abnormal breast enlargement observed in some heavy drinkers. For example, in the study by Lloyd and Williams (1948), 42 percent of males with alcoholic cirrhosis exhibited enlarged breasts. In addition to causing breast enlargement, estrogens appear to exert a negative feedback effect on LH and FSH production and may thereby contribute to alcohol’s suppression of those key reproductive hormones (see the section “Alcohol’s Effects on the Anterior Pituitary Gland”).

Clinical studies have demonstrated that alcohol not only alters testosterone metabolism but also diminishes testosterone production (e.g., Southren et al.1973 ). To elucidate the mechanisms underlying the alcohol-induced reduction in testosterone secretion, researchers have investigated alcohol’s effects on testes studied outside the body (i.e., in vitro) or analyzed the testes independent of the rest of the body.

In those experiments, testosterone production in the isolated testes decreased, as it had in studies in intact animals (e.g., Badr et al.1977 ; Cobb et al.1978 ) These findings indicate that alcohol exerts its effect, at least in part, by acting directly on the testes (although alcohol also affects hormone production in the hypothalamus and anterior pituitary, as described in the following sections).

Researchers have proposed several mechanisms that may contribute to the alcohol-induced testosterone suppression ( Anderson et al.1983 ). For example, investigators have suggested that alcohol’s breakdown product, acetaldehyde, may be a contributing factor, because in some studies acetaldehyde was more potent than alcohol in suppressing testosterone release (e.g., Badr et al.1977 ; Cobb et al.1978 ).

Possibly, however, acetaldehyde does not itself suppress testosterone production. Instead, the enzyme that mediates the breakdown of alcohol to acetaldehyde uses certain molecules (i.e., cofactors) that are also required by enzymes involved in testosterone production, thereby preventing testosterone generation ( Ellingboe and Varanelli 1979 ; Gordon et al.1980 ).

Other studies have noted an increase in β-endorphin levels in the testicular fluid after acute alcohol exposure ( Adams and Cicero 1991 ). As described previously, testicular β-endorphin inhibits testosterone production and/or release. Researchers recently confirmed the role of β-endorphin through a study in which rats were treated with a substance that inhibits β-endorphin activity (i.e., naltrexone) ( Emanuele et al.1998 ).

In that study, naltrexone prevented the fall in testosterone after both acute and chronic (i.e., for 14 days) alcohol ingestion. Naltrexone, which is currently used in alcoholism treatment to decrease alcohol craving, therefore may potentially be used to prevent reductions in testosterone levels and the associated adverse consequences in alcoholics who are unable to discontinue drinking on their own.

Disturbances in other hormonal systems also may contribute to the alcohol-induced suppression of testosterone levels. For example, the adrenal hormones cortisol (in humans) and corticosterone (in rats) can suppress the reproductive system by inhibiting the ability of the Leydig cells to produce and release testosterone.

1. Studies in humans and animals found that alcohol exposure increases adrenal hormone levels, thereby interfering with reproductive functions ( Rivier and Vale 1988 ).
2. Finally, nitric oxide (NO), a gas found in all tissues, may contribute to alcohol’s toxic effects.
3. NO affects numerous biological processes, including widening of the blood vessels (i.e., vasodilation), the immune response, communication between cells of the nervous system, and hormone secretion.

For example, NO has been shown to decrease testosterone secretion ( McCann and Rettori 1996 ). In the testes (as well as in many other tissues), the gas is generated by an enzyme called nitric oxide synthase (NOS). Research has indicated that inhibition of the enzyme NOS by various substances can prevent the alcohol-induced decline in testosterone levels ( Adams et al.1993 ; Shi et al.1998 ).

Can alcoholism cause low estrogen?

Alcohol’s Effects on Estrogen Levels – Excessive alcohol consumption is linked to lower estrogen levels in women. This decrease in estrogen is associated with depression and anxiety and an increased risk for osteoporosis. Estrogen helps regulate blood sugar levels, so its depletion can also cause fluctuations in energy and mood.

Does alcohol increase breast size?

1. Alcohol messes with your estrogen levels. – Drinking alcohol actually increases your levels of estrogen, a hormone important to a woman’s reproductive system. Women who regularly drink alcohol show higher levels of estrogen in their bodies compared to women who don’t drink.

What wine is good for estrogen?

What does science have to say about it, and is there a difference between what type of alcohol you drink and its effect on estrogen? – Science has long held the belief that any alcohol consumption will increase estrogen levels, and related issues such as breast cancer risk.

1. However, more recent studies show that it may not be as straight forward.
2. Both what you drink, and how much of it seem to play a role (surprise!).
3. A Cedar-Sinai study published in 2012 challenged that belief.
4. This study found that chemicals in red wine (from the skins and seeds of red grapes) slightly lowered estrogen levels among premenopausal women who drank 8 ounces of red wine nightly for about a month (1).

However, in other studies no beneficial effect was found with any other alcohol consumption, though the risks may still be low at one drink per day (2). A literature review done in 2015 by researchers at the Washington University in St. Louis demonstrated that small amounts of red wine may be protective due to resveratrol, where other alcohols such as white wine did not show a beneficial effect. A controlled diet study reported that consumption of 30 g ethanol (∼2.5 drinks) per day for three menstrual cycles was associated with a 28% increase in plasma estradiol and a 21% increase in plasma estrone among women aged 21–40 years (2). Both estradiol and estrone are types of estrogen in the body, with estradiol being the most bioactive in premenopausal years.

A recent meta-analysis of eight prospective studies among postmenopausal women showed that alcohol intake is positively associated with all the sex hormones (meaning an increase in alcohol relates to an increase in hormones), with the strongest association for dehydroepiandrosterone sulfate (DHEAS), which is a precursor to both estrogens and testosterone (3).

In one study, blood estrone and DHEAS were increased by 8 and 5% in women consuming 15 g of alcohol (roughly 1.25 drinks) per day, respectively.

What vitamins increase estrogen?

2. Getting enough of the minerals and vitamins that help estrogen levels – Some vitamins and minerals help your body produce estrogen and use it more effectively. To increase your estrogen levels, consider adding:

Boron, a mineral that helps your body absorb testosterone and estrogen Vitamin B, which helps your body create and use estrogen Vitamin D, which functions as a hormone in the body and helps with estrogen production Vitamin E, because research shows vitamin E may help reduce hot flashes and insomnia.

Does red wine block estrogen?

The Effects of Red Wine and White Wine on Blood Estrogen and Progesterone Levels – Full Text View

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our for details.

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Sponsor:

Information provided by (Responsible Party):

Noel Bairey Merz, Cedars-Sinai Medical Center

Brief Summary: Healthy pre-menopausal women will be recruited in order to test the effects of red wine and white wine on blood estrogen and progesterone levels. The women will be randomized and rotated through two different treatments (red wine, white wine).

• Estrone and estradiol are hormones in the category of estrogens.
• It is known that the bodies of both men and women may convert (or aromatize) a certain amount of naturally occurring testosterone into estrogen.
• Aromatase inhibitors have been used to prevent this conversion, or aromatization, of testosterone into estrogen, in the treatment of estrogen-dependent breast cancer in women.

This inhibition leads to a marked decrease in estrogen (estradiol and estrone) levels. Naturally occurring aromatase inhibitors include grapes, grape juice, and red, but not white wine. The aromatase inhibitory effects are attributed to wine phytochemicals and not to alcohol.

Based upon this information, the investigators will monitor the estrogen levels at various phases in the menstrual cycles of women since hormone levels naturally vary throughout the menstrual cycle. Several epidemiologic studies have found that there is a correlation with moderate to high levels of alcohol consumption and breast cancer.

Therefore, study participants will be asked to drink only a eight ounces of wine which should have minimal or no risk for the development of breast cancer.

Healthy	Other: Red Wine Other: White Wine	Not Applicable

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Active Comparator: Red Wine Other: Red Wine 8 ounces of assigned beverage (red wine) each evening and abstinence from any other alcoholic beverages, grape juice, grapes, or raisins. Active Comparator: White Wine Other: White Wine 8 ounces of assigned beverage (white wine) each evening and abstinence from any other alcoholic beverages, grape juice, grapes, or raisins.

Primary Outcome Measures :

blood estrogen and progesterone levels

Inclusion Criteria:

1. female
2. pre-menopausal with regular ovulatory cycles for 12 months prior to the study
3. willingness and ability to participate in study requiring alcohol consumption
4. in general good health
5. BMI of 18.5-35
6. on regular, unrestricted diet
7. not currently, or within the past 3 months, using oral contraceptives or other hormone replacement therapy

Exclusion Criteria:

1. male
2. irregular menstrual cycles or vasomotor symptoms within the last 12 months
3. pregnant (or breast feeding)
4. any hormone therapy including phytoestrogens, oral contraceptives, SERMs (selective estrogen receptor modulators), or androgens (or precursors) for three months prior to the study
5. history of alcohol abuse
6. history of any estrogen-dependent neoplasia
7. high intake of dietary soy products
8. Minors < age 21 years

Layout table for location information

Cedars-Sinai Women’s Heart Center
Los Angeles, California, United States, 90048

Cedars-Sinai Medical Center

Layout table for investigator information

Principal Investigator:	Glenn D Braunstein, MD	Cedars Sinai Medical Cneter

Keywords provided by Noel Bairey Merz, Cedars-Sinai Medical Center: : The Effects of Red Wine and White Wine on Blood Estrogen and Progesterone Levels – Full Text View

Are red grapes high in estrogen?

Five Best Foods for Low T: – 1. Vitamin D Studies have shown that increasing certain nutrients, such as vitamin D, which also helps the body absorb calcium, can increase testosterone levels in men. Vitamin D is found naturally in seafood such as tuna, salmon and mackerel.

• It is also found in cheese, milk, wheat bran and egg yolk.
• If your diet does not contain enough vitamin D, over the counter supplements may be a good place to start.2.
• Red Grapes Red grapes are not just a tasty snack.
• As it turns out, red grapes may be just what the doctor ordered to raise testosterone levels, too.

Red grapes contain phytochemicals that help to block the absorption of estrogen – the other side of the gender hormone coin. Studies have shown that men with low T levels may have a corresponding increase in estrogen. Other estrogen fighting foods include cauliflower, broccoli, cabbage, Brussels sprouts and bok choy.3.

Coconut In recent years, the coconut has emerged as an all-around champion of good nutrition. Because coconut is an excellent source of saturated fats that are used in the body’s production of testosterone, coconut may be an ideal source for healthy fats. Also, coconut oil consists of medium chain triglycerides (MCTs), which are broken down by the body differently than other forms of fat, which can actually improve your cholesterol levels.

Coconut oil is also good for prostrate health.4. Shellfish and Organ Meat Shellfish, like organ meats such as liver, are rich in magnesium and other minerals. Magnesium is known for increasing the bioavailability of testosterone. This means that your body is able to use more of the testosterone you make.

As you age, your body is less able to use the testosterone you produce. You can also add magnesium in the form of supplements.5. Garlic Garlic is another superfood that is getting a lot of attention these days. For one thing, garlic contains a chemical known as diallylsulfide which increases testosterone while decreasing cortisol (a nasty stress hormone) levels.

Garlic goes well with many foods and can be easily consumed over the course of a day.

Do red grapes lower estrogen?

Red Grapes – In the skin of red grapes is resveratrol, a chemical that works to block estrogen production. Along with acting as an antioxidant, resveratrol helps flush excess estrogen from the body. Foods rich in resveratrol can also help reduce levels of testosterone. Recipe: Baked Brie Cheese Board 16 of 17

Does beer have more estrogen than soy?

Soy Vs Beer: Which Promotes Estrogen More? To watch video in fullscreen, hit play & then in lower right Many men cite soy’s estrogen-promoting effects as a reason not to go vegan, with concerns of lowered testosterone, gynecomastia, and hormonal imbalance.

1. But does soy really have a detrimental impact on men’s health? What we eat has a significant impact on our body’s hormonal balance of testosterone and estrogen in our bodies.
2. More than any other food, as an estrogen-boosting food, often cited by men as a reason to not go vegan.
3. On the other hand, is stereotypically associated with manliness and virility—liquid testosterone even, if we’re to believe some commercials.

But outside of the Internet hype and advertiser hyperbole, what is the true hormonal impact of what we put in our bodies? It’s no secret that what we eat affects our health, though you’d never know that from speaking with, I cannot even count the number of times I’ve heard from men that they can’t go vegan because of the estrogenic effects of soy, with the most-often offered pejorative “man boobs” being a main concern.

In this third installment of the with of Nutritionfacts.org, we’ll get to the bottom of the soy controversy and see what foods and beverages are the most beneficial or detrimental to testosterone levels. For more in depth information on and diet as well as what to eat and avoid, be sure to check out the,

Now let’s hear what Dr. Greger has to say about the hormonal impact of diet. Addressing the soy controversy and concerns men have of estrogen-promoting effects: ” 1951 Australia—that’s where it all starts. Where we have two Australian chemists who are tasked with trying to solve the mystery of why sheep in Australia were becoming infertile, devastating the wool industry in Australia.

These two chemists discovered that it was the clover—that there was clover that had a phytoestrogen called “genistein,” the same phytoestrogen found in soy. And it had these estrogenic effects and it was affecting the fertility of the sheep. And so if you go online and you read about the dangers of soy, you’ll see “the dreaded clover disease”—lots of allusions to “the dreaded clover disease.” But you’ll notice what they don’t talk about is the dosing.

To get as much of this phytoestrogen in your body as the sheep were in clover, one would have to drink—one would have to eat 8,000 soy burgers a day or 800 pounds of tofu or 1,000 cartons of a day. And only then would you get the same kind of effects that these poor sheep were getting.

• Now that’s not to say you cannot over do it.
• There have been two case reports in literature of feminizing effects in men eating as few as like 14 to 25 servings of soy a day, alright? But at any reasonable amount of soy intake—so these were men drinking gallons of soy milk a day—but if you stick to less than 14 servings a day of soy, no feminizing effects ever reported.

And in fact, have beneficial effects for prostate health etc. etc.” On what foods in are best to balance or enhance male hormonal levels: ” It will be a plant-based diet, as I talked about before. Avoiding beer actually. It’s interesting the most potent phytoestrogen in the world is not in soy—it’s in beer.

So some of these German scientists saw this work in Australia and said “Ah hah! That’s why female hop-pickers start menstruating as soon as they start touching hops.” And that’s because of this powerful estrogenic effects of “hopein,” which is the phytoestrogen found in the bittering agent in beer. And indeed, women who drink beer actually have stronger bones, less hot flashes, et cetera—and that’s because of this phytoestrogen effect.

Unfortunately, the phytoestrogen in beer attaches preferentially to alpha estrogen receptors, as opposed to beta estrogen receptors, increasing the risk of breast cancer. So the reason that you see hop extracts in so-called breast enhancement supplements is because of that phytoestrogenic effect, whereas soy phytoestrogens attach preferentially to beta receptors, unlike your own estrogens—your own endogenous estrogen.

And so actually have a breast cancer reducing effect through the same protective effect in terms of hot flashes. And so alcohol itself can decrease testosterone levels, but beer in particular. So I’d encourage people, if they’re worried about testosterone, they shouldn’t be chugging a 6-pack.” Emily: It’s kind of astonishing how there is the stereotype that for men the way to be the manliest you can possibly be is to be consuming you know a bunch of meat and drinking a lot of beer.

And it sounds like it’s kind of the worse maybe you can have for and, Dr. Greger: And life span. I hope you enjoyed hearing from Dr. Greger on the estrogenic affects of soy and—surprisingly—. The hormonal impact of what we eat reaches far beyond fears of feminization, as we saw with the cancer promoting effects of hops and cancer reducing effects of soy.

Regardless of gender, the hormones in what we consume can have life-altering and life-ending consequences. Now I know tracking nutrition can be a pain, so I wanted to let you know about, It’s a free website and app that I’ve used in several of my videos because of it’s uniquely detailed nutrition reports and ease of use.

Plus, they were awesome enough to sponsor the, to help get that vital educational info out, and have come on board for the remainder of the Men’s Health Series as well! Be sure to for your free profile! You can also find links to relevant studies and Dr.

• To support free education like this, please see the or join us in the,
• Now go live vegan, give soy a break, and I’ll see you soon.
• — Emily Moran Barwick

1. R.B. Bradbury and D.E. White, “761. The Chemistry of Subterranean Clover. Part I. Isolation of Formononetin and Genistein,” no.0 (January 1, 1951): 3447–49, doi:10.1039/JR9510003447.
2. Greger, MD, Michael, How Much Soy Is Too Much?, 10 vols., 2012, https://nutritionfacts.org/video/how-much-soy-is-too-much/.
3. Supporting Studies for How Much Soy Is Too Much: Supporting Studies for “How Much Soy Is Too Much”: Xiao Ou Shu et al., “Soy Food Intake and Breast Cancer Survival,” JAMA?: The Journal of the American Medical Association 302, no.22 (December 9, 2009): 2437–43, doi:10.1001/jama.2009.1783; Chisato Nagata et al., “Dietary Soy and Fats in Relation to Serum Insulin-like Growth Factor-1 and Insulin-like Growth Factor-Binding Protein-3 Levels in Premenopausal Japanese Women,” Nutrition and Cancer 45, no.2 (2003): 185–89, doi:10.1207/S15327914NC4502_07; Antonella Dewell et al., “Relationship of Dietary Protein and Soy Isoflavones to Serum IGF-1 and IGF Binding Proteins in the Prostate Cancer Lifestyle Trial,” Nutrition and Cancer 58, no.1 (2007): 35–42, doi:10.1080/01635580701308034; Gertraud Maskarinec et al., “Insulin-like Growth Factor-1 and Binding Protein-3 in a 2-Year Soya Intervention among Premenopausal Women,” The British Journal of Nutrition 94, no.3 (September 2005): 362–67; A.H. Wu et al., “Epidemiology of Soy Exposures and Breast Cancer Risk,” British Journal of Cancer 98, no.1 (January 15, 2008): 9–14, doi:10.1038/sj.bjc.6604145; Bahram H. Arjmandi et al., “Soy Protein Has a Greater Effect on Bone in Postmenopausal Women Not on Hormone Replacement Therapy, as Evidenced by Reducing Bone Resorption and Urinary Calcium Excretion,” The Journal of Clinical Endocrinology and Metabolism 88, no.3 (March 2003): 1048–54, doi:10.1210/jc.2002-020849.
4. Mark Messina and Virginia L. Messina, “Exploring the Soyfood Controversy:,” Nutrition Today 48, no.2 (2013): 68–75, doi:10.1097/NT.0b013e31828fff54.
5. Mark Messina, “Soybean Isoflavone Exposure Does Not Have Feminizing Effects on Men: A Critical Examination of the Clinical Evidence,” Fertility and Sterility 93, no.7 (May 1, 2010): 2095–2104, doi:10.1016/j.fertnstert.2010.03.002.
6. Michael Greger, M.D., The Most Potent Phytoestrogen Is in Beer, vol.31, 2016, https://nutritionfacts.org/video/the-most-potent-phytoestrogen-is-in-beer/.
7. Supporting Studies for The Most Potent Phytoestrogen: S.R. Milligan et al., “Identification of a Potent Phytoestrogen in Hops (Humulus Lupulus L.) and Beer,” The Journal of Clinical Endocrinology and Metabolism 84, no.6 (June 1999): 2249–52, doi:10.1210/jcem.84.6.5887; W. Chen et al., “Beer and Beer Compounds: Physiological Effects on Skin Health,” Journal of the European Academy of Dermatology and Venereology: JEADV 28, no.2 (February 2014): 142–50, doi:10.1111/jdv.12204; Sam Possemiers et al., “Activation of Proestrogens from Hops (Humulus Lupulus L.) by Intestinal Microbiota; Conversion of Isoxanthohumol into 8-Prenylnaringenin,” Journal of Agricultural and Food Chemistry 53, no.16 (August 10, 2005): 6281–88, doi:10.1021/jf0509714; Bradbury and White, “761. The Chemistry of Subterranean Clover. Part I. Isolation of Formononetin and Genistein”; E.R. Rosenblum et al., “Isolation and Identification of Phytoestrogens from Beer,” Alcoholism, Clinical and Experimental Research 16, no.5 (October 1992): 843–45; Olaf Schaefer et al., “Development of a Radioimmunoassay for the Quantitative Determination of 8-Prenylnaringenin in Biological Matrices,” Journal of Agricultural and Food Chemistry 53, no.8 (April 20, 2005): 2881–89, doi:10.1021/jf047897u; N.G. Coldham et al., “A Binary Screening Assay for pro-Oestrogens in Food: Metabolic Activation Using Hepatic Microsomes and Detection with Oestrogen Sensitive Recombinant Yeast Cells,” Food Additives and Contaminants 19, no.12 (December 2002): 1138–47, doi:10.1080/0265203021000014789; J.S. Gavaler et al., “The Phytoestrogen Congeners of Alcoholic Beverages: Current Status,” Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) 208, no.1 (January 1995): 98–102; Sam Possemiers et al., “The Intestinal Microbiome: A Separate Organ inside the Body with the Metabolic Potential to Influence the Bioactivity of Botanicals,” Fitoterapia 82, no.1 (January 2011): 53–66, doi:10.1016/j.fitote.2010.07.012; D.H. Van Thiel, “Feminization of Chronic Alcoholic Men: A Formulation,” The Yale Journal of Biology and Medicine 52, no.2 (April 1979): 219–25; A. Galvão-Teles et al., “Alterations of Testicular Morphology in Alcoholic Disease,” Alcoholism, Clinical and Experimental Research 7, no.2 (1983): 144–49; N.G. Coldham and M.J. Sauer, “Identification, Quantitation and Biological Activity of Phytoestrogens in a Dietary Supplement for Breast Enhancement,” Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research Association 39, no.12 (December 2001): 1211–24; Kenneth D.R. Setchell, Nadine M. Brown, and Eva Lydeking-Olsen, “The Clinical Importance of the Metabolite Equol-a Clue to the Effectiveness of Soy and Its Isoflavones,” The Journal of Nutrition 132, no.12 (December 2002): 3577–84.
8. Rosenblum et al., “Isolation and Identification of Phytoestrogens from Beer.”
9. Michael Greger, M.D., What Are the Effects of the Hops Phytoestrogen in Beer?, vol.31, 2016, https://nutritionfacts.org/video/what-are-the-effects-of-the-hops-phytoestrogen-in-beer/.
10. Supporting Studies For “What are the effects of the hops phytoestrogen in beer”: Larissa A. Korde et al., “Childhood Soy Intake and Breast Cancer Risk in Asian American Women,” Cancer Epidemiology, Biomarkers & Prevention: A Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology 18, no.4 (April 2009): 1050–59, doi:10.1158/1055-9965.EPI-08-0405; Mark Frederick McCarty, “Isoflavones Made Simple – Genistein’s Agonist Activity for the Beta-Type Estrogen Receptor Mediates Their Health Benefits,” Medical Hypotheses 66, no.6 (2006): 1093–1114, doi:10.1016/j.mehy.2004.11.046; Christina A. Clarke et al., “Recent Declines in Hormone Therapy Utilization and Breast Cancer Incidence: Clinical and Population-Based Evidence,” Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology 24, no.33 (November 20, 2006): e49-50, doi:10.1200/JCO.2006.08.6504; Kevin Zbuk and Sonia S. Anand, “Declining Incidence of Breast Cancer after Decreased Use of Hormone-Replacement Therapy: Magnitude and Time Lags in Different Countries,” Journal of Epidemiology and Community Health 66, no.1 (January 2012): 1–7, doi:10.1136/jech.2008.083774; Messina, “Soybean Isoflavone Exposure Does Not Have Feminizing Effects on Men”; Messina and Messina, “Exploring the Soyfood Controversy”; Kenneth D.R. Setchell, Nadine M. Brown, and Eva Lydeking-Olsen, “The Clinical Importance of the Metabolite Equol-a Clue to the Effectiveness of Soy and Its Isoflavones,” The Journal of Nutrition 132, no.12 (December 2002): 3577–84; M.G. Lê et al., “Alcoholic Beverage Consumption and Breast Cancer in a French Case-Control Study,” American Journal of Epidemiology 120, no.3 (September 1984): 350–57; S. Milligan et al., “Oestrogenic Activity of the Hop Phyto-Oestrogen, 8-Prenylnaringenin,” Reproduction (Cambridge, England) 123, no.2 (February 2002): 235–42; J.S. Gavaler, “Alcoholic Beverages as a Source of Estrogens,” Alcohol Health and Research World 22, no.3 (1998): 220–27; Vida Aghamiri et al., “The Effect of Hop (Humulus Lupulus L.) on Early Menopausal Symptoms and Hot Flashes: A Randomized Placebo-Controlled Trial,” Complementary Therapies in Clinical Practice 23 (May 2016): 130–35, doi:10.1016/j.ctcp.2015.05.001; Olaf Schaefer et al., “8-Prenyl Naringenin Is a Potent ERalpha Selective Phytoestrogen Present in Hops and Beer,” The Journal of Steroid Biochemistry and Molecular Biology 84, no.2–3 (February 2003): 359–60; Aafje Sierksma et al., “Effect of Moderate Alcohol Consumption on Plasma Dehydroepiandrosterone Sulfate, Testosterone, and Estradiol Levels in Middle-Aged Men and Postmenopausal Women: A Diet-Controlled Intervention Study,” Alcoholism, Clinical and Experimental Research 28, no.5 (May 2004): 780–85; Annekathrin M. Keiler, Oliver Zierau, and Georg Kretzschmar, “Hop Extracts and Hop Substances in Treatment of Menopausal Complaints,” Planta Medica 79, no.7 (May 2013): 576–79, doi:10.1055/s-0032-1328330; R. Erkkola et al., “A Randomized, Double-Blind, Placebo-Controlled, Cross-over Pilot Study on the Use of a Standardized Hop Extract to Alleviate Menopausal Discomforts,” Phytomedicine: International Journal of Phytotherapy and Phytopharmacology 17, no.6 (May 2010): 389–96, doi:10.1016/j.phymed.2010.01.007; L.R. Chadwick, G.F. Pauli, and N.R. Farnsworth, “The Pharmacognosy of Humulus Lupulus L. (Hops) with an Emphasis on Estrogenic Properties,” Phytomedicine: International Journal of Phytotherapy and Phytopharmacology 13, no.1–2 (January 2006): 119–31, doi:10.1016/j.phymed.2004.07.006; Arne Heyerick et al., “A First Prospective, Randomized, Double-Blind, Placebo-Controlled Study on the Use of a Standardized Hop Extract to Alleviate Menopausal Discomforts,” Maturitas 54, no.2 (May 20, 2006): 164–75, doi:10.1016/j.maturitas.2005.10.005; Adriane Fugh-Berman, “‘Bust Enhancing’ herbal Products,” Obstetrics and Gynecology 101, no.6 (June 2003): 1345–49; Juan D. Pedrera-Zamorano et al., “Effect of Beer Drinking on Ultrasound Bone Mass in Women,” Nutrition (Burbank, Los Angeles County, Calif.) 25, no.10 (October 2009): 1057–63, doi:10.1016/j.nut.2009.02.007.

Aghamiri, Vida, Mojgan Mirghafourvand, Sakineh Mohammad-Alizadeh-Charandabi, and Hossein Nazemiyeh. “The Effect of Hop (Humulus Lupulus L.) on Early Menopausal Symptoms and Hot Flashes: A Randomized Placebo-Controlled Trial.” Complementary Therapies in Clinical Practice 23 (May 2016): 130–35.

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Doi:10.1111/jdv.12204. Clarke, Christina A., Sally L. Glaser, Connie S. Uratsu, Joseph V. Selby, Larry H. Kushi, and Lisa J. Herrinton. “Recent Declines in Hormone Therapy Utilization and Breast Cancer Incidence: Clinical and Population-Based Evidence.” Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology 24, no.33 (November 20, 2006): e49-50.

doi:10.1200/JCO.2006.08.6504. Coldham, N.G., R. Horton, M.F. Byford, and M.J. Sauer. “A Binary Screening Assay for pro-Oestrogens in Food: Metabolic Activation Using Hepatic Microsomes and Detection with Oestrogen Sensitive Recombinant Yeast Cells.” Food Additives and Contaminants 19, no.12 (December 2002): 1138–47.

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doi:10.1016/j.phymed.2010.01.007. Fugh-Berman, Adriane. “‘Bust Enhancing’ herbal Products.” Obstetrics and Gynecology 101, no.6 (June 2003): 1345–49. Galvão-Teles, A., L. Gonçalves, H. Carvalho, and E. Monteiro. “Alterations of Testicular Morphology in Alcoholic Disease.” Alcoholism, Clinical and Experimental Research 7, no.2 (1983): 144–49.

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doi:10.1016/j.maturitas.2005.10.005. Keiler, Annekathrin M., Oliver Zierau, and Georg Kretzschmar. “Hop Extracts and Hop Substances in Treatment of Menopausal Complaints.” Planta Medica 79, no.7 (May 2013): 576–79. doi:10.1055/s-0032-1328330. Korde, Larissa A., Anna H.

Wu, Thomas Fears, Abraham M.Y. Nomura, Dee W. West, Laurence N. Kolonel, Malcolm C. Pike, Robert N. Hoover, and Regina G. Ziegler. “Childhood Soy Intake and Breast Cancer Risk in Asian American Women.” Cancer Epidemiology, Biomarkers & Prevention: A Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology 18, no.4 (April 2009): 1050–59.

doi:10.1158/1055-9965.EPI-08-0405. Lê, M.G., C. Hill, A. Kramar, and R. Flamanti. “Alcoholic Beverage Consumption and Breast Cancer in a French Case-Control Study.” American Journal of Epidemiology 120, no.3 (September 1984): 350–57. Maskarinec, Gertraud, Yumie Takata, Suzanne P.

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• Isoflavones Made Simple – Genistein’s Agonist Activity for the Beta-Type Estrogen Receptor Mediates Their Health Benefits.” Medical Hypotheses 66, no.6 (2006): 1093–1114.

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Messina, Mark, and Virginia L. Messina. “Exploring the Soyfood Controversy:” Nutrition Today 48, no.2 (2013): 68–75. doi:10.1097/NT.0b013e31828fff54. Milligan, S., J. Kalita, V. Pocock, A. Heyerick, L. De Cooman, H. Rong, and D. De Keukeleire. “Oestrogenic Activity of the Hop Phyto-Oestrogen, 8-Prenylnaringenin.” Reproduction (Cambridge, England) 123, no.2 (February 2002): 235–42.

Milligan, S.R., J.C. Kalita, A. Heyerick, H. Rong, L. De Cooman, and D. De Keukeleire. “Identification of a Potent Phytoestrogen in Hops (Humulus Lupulus L.) and Beer.” The Journal of Clinical Endocrinology and Metabolism 84, no.6 (June 1999): 2249–52. doi:10.1210/jcem.84.6.5887.

• Nagata, Chisato, Hiroyuki Shimizu, Rieko Takami, Makoto Hayashi, Noriyuki Takeda, and Keigo Yasuda.
• Dietary Soy and Fats in Relation to Serum Insulin-like Growth Factor-1 and Insulin-like Growth Factor-Binding Protein-3 Levels in Premenopausal Japanese Women.” Nutrition and Cancer 45, no.2 (2003): 185–89.

doi:10.1207/S15327914NC4502_07. Pedrera-Zamorano, Juan D., Jesus M. Lavado-Garcia, Raul Roncero-Martin, Julian F. Calderon-Garcia, Trinidad Rodriguez-Dominguez, and Maria L. Canal-Macias. “Effect of Beer Drinking on Ultrasound Bone Mass in Women.” Nutrition (Burbank, Los Angeles County, Calif.) 25, no.10 (October 2009): 1057–63.

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Possemiers, Sam, Arne Heyerick, Veerle Robbens, Denis De Keukeleire, and Willy Verstraete. “Activation of Proestrogens from Hops (Humulus Lupulus L.) by Intestinal Microbiota; Conversion of Isoxanthohumol into 8-Prenylnaringenin.” Journal of Agricultural and Food Chemistry 53, no.16 (August 10, 2005): 6281–88.

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“Development of a Radioimmunoassay for the Quantitative Determination of 8-Prenylnaringenin in Biological Matrices.” Journal of Agricultural and Food Chemistry 53, no.8 (April 20, 2005): 2881–89. doi:10.1021/jf047897u. Schaefer, Olaf, Michael Hümpel, Karl-Heinrich Fritzemeier, Rolf Bohlmann, and Wolf-Dieter Schleuning.

1. 8-Prenyl Naringenin Is a Potent ERalpha Selective Phytoestrogen Present in Hops and Beer.” The Journal of Steroid Biochemistry and Molecular Biology 84, no.2–3 (February 2003): 359–60.
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———. “The Clinical Importance of the Metabolite Equol-a Clue to the Effectiveness of Soy and Its Isoflavones.” The Journal of Nutrition 132, no.12 (December 2002): 3577–84. Shu, Xiao Ou, Ying Zheng, Hui Cai, Kai Gu, Zhi Chen, Wei Zheng, and Wei Lu. “Soy Food Intake and Breast Cancer Survival.” JAMA?: The Journal of the American Medical Association 302, no.22 (December 9, 2009): 2437–43.

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Pike. “Epidemiology of Soy Exposures and Breast Cancer Risk.” British Journal of Cancer 98, no.1 (January 15, 2008): 9–14. doi:10.1038/sj.bjc.6604145. Zbuk, Kevin, and Sonia S. Anand. “Declining Incidence of Breast Cancer after Decreased Use of Hormone-Replacement Therapy: Magnitude and Time Lags in Different Countries.” Journal of Epidemiology and Community Health 66, no.1 (January 2012): 1–7.

doi:10.1136/jech.2008.083774. : Soy Vs Beer: Which Promotes Estrogen More?

Can coffee increase estrogen levels?

Caffeine and Estrogen: A Complex Relationship – When it comes to hormonal balance, caffeine and estrogen have a complex relationship. In fact, if you’re trying to balance your hormones, caffeine may be a no-go. Research shows that it can increase estrogen levels. Image by Michelle Nash

Which alcohol increase testosterone?

As a result, an influx in the red wine compound quercetin leaves lab samples with a higher level of testosterone compared to those lab samples that didn’t interact with quercetin.

Does Guinness have estrogen?

Guinness may improve bone health – As well as being the hormone responsible for keeping our menstrual cycle ticking, estrogen is essential for maintaining strong, healthy bones, As our estrogen levels decline during perimenopause and beyond, our bones become more vulnerable to breaks and fractures.

1. Guinness and many other beers may help to combat this as they contain hops, which are phytoestrogens.
2. A phytoestrogen is a plant chemical that can bind to the estrogen receptors in the body.
3. It mimics the effects of our natural hormones.
4. The mildly estrogenic effects of hops were first noticed when the girls who were employed to harvest hops started menstruating earlier than similarly aged girls not working in the fields.

This may help to explain why a 2009 study has shown that moderate beer consumption can help to promote bone mineral density. Another study of 1,700 women showed that those who were considered moderate beer drinkers had the highest bone density.

Why is vodka not good for men?

Alchohol present in vodka are a major concern especially on excessive consumption. It can expose you to major diseases of multiple organs such as brain, liver, heart and pancreas. Excessive consumption may lead to faster heartbeat, elevated blood pressure and can also disrupts the immune system.

Which alcohol lowers testosterone?

The Direct Effect of Alcohol on Your Testosterone – First, studies continue to show that heavy doses of alcohol directly cause a decrease in testosterone production in men. In a review of the available research, scientists concluded that a 160-pound man would need to drink 5 or 6 glasses of beer that contains between 4.5 and 6 percent alcohol per 12-ounce glass in order to cause a direct decrease in serum testosterone levels.

1. That’s still an approximation, but it supports what we’ve known for decades: Ethanol alcohol is a testicular toxin, and these large doses reduce testosterone function, sperm count, fertility, and can even cause permanent damage to the testes.
2. Alcoholic men are known to suffer higher rates of infertility and extremely low testosterone levels.

An important side note is that no differences between adolescents and adults were identified, which means binge drinking among younger males likely has harmful effects on their hormone balance—possibly resulting in Low T symptoms despite their relatively young age.

What drinks are high in estrogen?

1. Red wine – Consuming phytoestrogen-rich foods and drinks like red wine in moderation (up to 5 ounces/148 milliliters a day for women of all ages) has been shown to reduce the risk of cardiovascular disease and breast cancer. Research has now revealed that it may be due to phytochemicals in the skins of the grapes used to make red wine.

Does alcohol affect estrogen absorption?

Abstract – Many women take supplemental estrogens after menopause, a practice called hormone replacement therapy (HRT). Moderate alcohol consumption may increase estrogen levels in women receiving HRT, potentially affecting their risk for various adverse health effects.

Two recent studies, however, provide no strong evidence for an effect of alcohol on hormones in postmenopausal women. The possible association between alcohol consumption and risk of cancer of the breast does not appear to be mediated by estrogens. Both estrogens and moderate alcohol consumption have been associated with a decreased risk for cardiovascular disease; however, alcohol’s beneficial effect on heart disease does not appear to involve hormonal mechanisms.

Additional research is needed to define the consequences of moderate drinking on hormone levels after menopause. Keywords: AODE (alcohol and other drug effects), menopause, female, sex hormones, estrogens, mammary gland, neoplastic disease, cardiovascular disorder, moderate AOD use, drug therapy, literature review Approximately 30 percent of American women are older than age 50, the average age of menopause ( Cramer and Xu 1996 ).1 Epidemiological studies suggest that approximately 50 percent of women in this age group consume at least moderate quantities of alcohol ( National Institute on Alcohol Abuse and Alcoholism 1997 ).2 Therefore, any adverse effects of alcohol among this population could have a significant effect on public health.

Menopause is characterized by greatly diminished levels 3 of a group of steroid reproductive hormones called estrogens. Estrogens (e.g., estrone and estradiol) travel through the bloodstream and exert widespread physiological effects on organ growth and development. Approximately 25 percent of postmenopausal women take supplemental estrogens to alleviate unpleasant symptoms of menopause, a practice called hormone replacement therapy (HRT) ( Ginsburg et al.1996 ).

Estrogens have various effects on the health of postmenopausal women ( Rich-Edwards and Hennekens 1996 ). For example, HRT decreases the risk of cardiovascular disease and osteoporosis 4 but may increase the risk of breast cancer ( Ginsburg et al.1996 ).

Recent experimental studies show that moderate alcohol consumption may increase estrogen levels in post-menopausal women receiving HRT ( Ginsburg et al.1996 ). This article reviews some of the basic hormonal changes associated with menopause, examines the effects of alcohol consumption on estrogen levels after menopause, and discusses the relationship of postmenopausal alcohol use to the risks of cardiovascular disease and cancer.

Although several reproductive hormones may play important roles in the menopausal transition, this article focuses on estrogens, in part because the health effects of altered estrogen levels are relatively well understood. For a discussion of alcohol’s effects on post-menopausal women with alcoholic cirrhosis, see Gavaler (1995),

How does alcohol affect estrogen metabolism?

Discussion – In this population of 1864 postmenopausal women from a nested case-control study within the WHI-OS cohort, we observed nominal associations for increasing concentrations of parent oestrogens with increasing alcohol intake among both never/former and current MHT users, consistent with prior studies.

• We also observed trends of increased 2-hydroxylation pathway oestrogen metabolites with increasing alcohol intake, although trends did not meet the FDR threshold.
• Liquor was associated with increased concentrations of circulating parent oestrogens and 2-, 4-, and 16-pathway oestrogen metabolites among never/former MHT users across frequency of use categories; oestrogen metabolite associations with liquor intake did not remain with further adjustment for parent oestrogens.

Prior randomised dietary interventions and prospective studies have supported that alcohol intake is associated with postmenopausal hormone levels. The Women’s Alcohol study, a placebo controlled 8-week crossover feeding study among 51 healthy postmenopausal women not using MHT, showed that 15–30 g per day alcohol intake increased serum oestrone sulphate by 7.5–10.7% and DHEAS by 5.1–7.5% ( Dorgan et al, 2001 ).

In a pooled meta-analysis of 13 prospective studies ( N =6291) from across the globe, sex hormone concentrations were ∼ 10–25% higher among postmenopausal women consuming ⩾ 20 g alcohol per day ( ∼ 20% women) compared with non-drinkers, including oestradiol, oestrone, androstenedione, DHEAS, and testosterone; SHBG concentrations were reduced by 10% ( Key et al, 2011 ).

Fifteen to 30 g alcohol per day approximates one to two standard drinks/day, in contrast to median intakes of ∼ 0.4 standard drinks/day among drinkers in our population. The effect sizes we observed in our analysis for parent oestrogens were consistent with these prior studies, but did not reach statistical significance, possibly due to sample size.

Few prior studies have evaluated associations of alcohol consumption with circulating sex steroid hormone metabolites, which may provide insight into alcohol’s potential role in modifying oestrogen metabolic pathways. Understanding how alcohol influences endogenous metabolic pathways is of high importance given that the biological mechanisms underlying alcohol’s strong association with breast and other cancers, which include sex steroid hormone metabolism, remain poorly defined.

Alcohol may influence oestrogen metabolism through increased aromatase activity in the liver and other tissues, stimulating conversion of androgens to oestrogens ( Rinaldi et al, 2006 ), decreased catabolism of sex hormones by the liver through accumulation of hepatic nicotinamide-adenine dinucleotide (NADH) – leading to oxidation and inhibition of oestradiol conversion to oestrone ( Ginsburg et al, 1996 ), and direct/indirect adrenal gland cell signalling promotion for DHEAS production (a precursor of oestradiol) ( Onland-Moret et al, 2005 ; Shafrir et al, 2014 ).

• How alcohol associates with different oestrogen hydroxylation pathways among postmenopausal women, however, is unknown.
• A recent analysis evaluated associations of alcohol intake with parent oestrogen/oestrogen metabolites, although women were pre-menopausal and metabolites were measured in urine ( Hartman et al, 2016 ).

Alcohol intake was only associated with oestradiol, but not other parent oestrogens/metabolites. Although menopausal status has not been shown to be a significant modifier of the alcohol-breast cancer association ( Trentham-Dietz et al, 2014 ), the majority of breast cancer cases are diagnosed after menopause, with elevated circulating oestrogens being a strong risk factor ( Key et al, 2002 ), highlighting the importance of evaluating alcohol’s effects on oestrogen metabolism in this population.

1. Evaluating ratios of unconjugated to combined oestrogens provides insight into how the pattern of metabolism might vary between never/former and current MHT users.
2. We saw that circulating oestrogen metabolites among MHT users were predominantly conjugated in comparison with non-users.
3. Relative concentration of parent to total oestrogens was also higher, suggesting a potential mechanism for enhanced breast cancer risk with alcohol intake in MHT users.

Similar to our observation of an overall alcohol association with parent oestrogens among MHT users, moderate alcohol consumption increased circulating oestradiol among postmenopausal women using MHT but not those who were not on MHT in a randomised, double-blind, placebo-controlled, crossover feeding study ( Ginsburg et al, 1996 ).

Furthermore, among postmenopausal women in a prospective cohort ( N =5035), an interaction between intake of two or more alcoholic drinks per day and MHT use was observed for risk of developing breast cancer; drinkers that also used MHT had an increased risk of breast cancer compared with non-MHT users that abstained from alcohol (HR=1.27, 95% CI=1.09–1.49 per 1 drink/day increase, p -trend=0.004 among MHT users; HR=0.98, 95% CI=0.82–1.78 per 1 drink/day increase, p -trend=0.79 among non MHT users) ( Nielsen and Gronbaek, 2008 ).

An alcohol-MHT synergistic effect on breast cancer has been supported by analyses within four other large, prospective cohorts ( Gapstur et al, 1992 ; Chen et al, 2002 ; Suzuki et al, 2005 ; Zhang et al, 2007 ). A biological rationale for these findings has been suggested, including decreased conversion of oestrogen to its metabolites, a shift in metabolism to different hydroxylation pathways ( Ginsburg et al, 1996 ), and altered rate of ethinyloestradiol clearance ( Ginsburg et al, 1995 ) among MHT users.

In our analysis, drinkers who were taking MHT consumed more total alcohol, on average, than never/former MHT users. It is also possible that dose of alcohol consumption among women in our study may have influenced the differences in magnitudes of association we observed between MHT groups. We found that highest compared with lowest category of liquor intake among drinkers was associated with 20–30% increases in both parent oestrogens and 2-, 4-, and 16-hydroxylation pathway metabolites among never/former MHT users.

In contrast to total alcohol consumption, never/former MHT users consumed more liquor, on average, than current MHT users. The liquor associations remained with further adjustment for total alcohol intake. When we additionally adjusted for parent oestrogens, the pathway associations were not retained, suggesting that they were not independent of parent oestrogens.

1. This might suggest increased oestrogen formation/reduced catabolism as opposed to hydroxylation pathway effects.
2. The ratio of unconjugated to combined oestrone was nominally reduced with higher liquor consumption, which suggests increased oestrone sulphation or glucuronidation (conversion to oestrone sulphate/glucuronide).

Sulphated oestrone is stored as an oestrogen substrate reservoir, whereas glucuronidated oestrone is excreted ( Hong and Chen, 2011 ). Few studies have evaluated associations of sex hormones by types of alcohol, in part due to limitations in sample size ( London et al, 1991 ; Hankinson et al, 1995 ; Newcomb et al, 1995 ; Hartman et al, 2016 ).

• Feeding studies have generally utilised 95% ethanol as the alcohol exposure thus have not evaluated wine or beer intake ( Dorgan et al, 2001 ; Mahabir et al, 2004 ).
• Further research on differences in sex steroid hormone metabolism by alcohol type is warranted.
• Polyphenols in red wine have been shown to be a cancer chemopreventive agent ( Scalbert et al, 2005 ).

Nonetheless, updated dose-response meta-analyses support that all alcohol types, including red wine intake, are associated with increased risk for colorectal and breast cancers ( World Cancer Research Fund/American Institute for Cancer Research, 2010 ; World Cancer Research Fund/American Institute for Cancer Research, 2017 ).

• While we did not observe an association of wine or beer intake with oestrogen metabolism, it is possible that these alcohol types increase cancer risk through other mechanisms such as formation of acetaldehyde, oxidative stress, altered carcinogen clearance, and impaired immunity.
• In the context of cancer prevention, understanding hormonal mechanisms influenced by lifestyle exposures like alcohol consumption may provide targets for cancer prevention intervention in high risk populations.

In the same population of women to the current study, parent oestrogens were found to be positively related to endometrial cancer risk (particularly unconjugated oestradiol) ( Brinton et al, 2016 ). Higher oestrone, and 2- and 4- and 16-pathway metabolites were also associated with non-serous ovarian cancer risk ( Trabert et al, 2016 ).

Our data from the current analysis support current recommendations to limit alcohol consumption for cancer prevention. Strengths of our study include the high reliability, sensitivity and specificity of the LC-MS/MS assay, comprehensive evaluation of oestrogen/oestrogen metabolites by exogenous hormone use, and the ability to evaluate associations by alcohol type.

However, several limitations exist. The median dose of alcohol consumption in our study was modest and may have been inadequate to enable us to detect associations with oestrogen metabolism. Additionally, sample size may have been limited to detect statistically significant associations, given adjustment for multiple comparisons.

• We were unable to evaluate earlier life alcohol exposure, which may have been higher than postmenopausal consumption.
• Additionally, the current analysis was cross-sectional at the time of entry into the study.
• We did not evaluate how alcohol intake changed, or how alcohol intake was associated with oestrogen metabolism over time, which may be relevant in terms of future disease risk.

Alcohol was evaluated using a self-reported questionnaire and thus misreporting could lead to alcohol usage misclassification. However, misreporting of intake is not likely to be associated with endogenous hormone concentrations, so associations would likely be attenuated.

• The analysis was cross-sectional so we were unable to make inference about causality.
• We evaluated usual (12-month) frequency of alcohol consumption, but were unable to compare acute versus chronic alcohol exposure, or alcohol exposure across the life course.
• We evaluated average weekly alcohol consumption, which may not be the relevant exposure to evaluate effects on oestrogen metabolism since the timing of last alcohol ingestion could influence oestrogen concentration due to the short half-life of oestrogens ( Ginsburg et al, 1998 ).

Women enrolled in the WHI-OS included a subset that declined participation in WHI trials, which could have introduced selection bias in terms of alcohol exposure, although participants of the WHI clinical trials ( Jackson et al, 2003 ; Ritenbaugh et al, 2003 ; Stefanick et al, 2003 ) had a similar distribution of alcohol consumption to the observational study ( Langer et al, 2003 ).

1. Future studies would also benefit from evaluating adrenal steroid precursors to oestrogens in addition to the analytes evaluated in the current study.
2. We did not have participant genotype data; evaluating gene–alcohol interaction in relation to oestrogen hormone metabolism could contribute to the literature in this area.

In conclusion, this study strengthens the evidence that alcohol consumption increases circulating oestrogen among postmenopausal women. Our observations suggest that alcohol, specifically liquor, influences parent oestrogen concentrations, potentially through increased oestrogen production, as opposed to modifying oestrogen metabolism.