Let’s Talk About Sex, Baby!: The Effect of Red Wine Consumption on Sperm Performance

(As an aside: how many of you now have that song stuck in your head after reading the title?…ahhhhh high school memories….).

The lights are turned down low, the Barry White is softly pumping through the stereo, and you’ve got yourself a nice big glass of red wine and your lover by your side…OK, without starting to making this sound too much like a bad porno movie, I’ll let your mind wander however you’d like with that and shift into a more scientific mode…

Quite some time ago, I covered an article discussing the relationship between alcohol consumption and the success rate of in vitro fertilization. This study found that increased levels of alcohol consumption negatively affects fertilization success when consumed by either men and women, though they only considered more heavy consumption (at least 4 drinks) and did not differentiate between the different types of alcohol.

Very basically, in order to have successful fertilization, a sperm must be able to penetrate the exterior wall of the egg by producing and releasing a specific type of enzyme to break down that wall. This can either happen naturally by copulation (wah wah wee wah…) or by in vitro methods outside of the body.

See page for author [Public domain], via Wikimedia Commons

See page for author [Public domain], via Wikimedia Commons

Studies have found that estrogens in both male and female reproductive systems play a critical role in fertilization success. Specifically, estrogens elicit biochemical changes in the sperm that result in the activation of the little swimmers by allowing them to bind to the zona pellucida (“wall”) of the egg and go through acrosome reactions to break down that wall and fertilize the egg. Without this activation, the sperm are just bumbling around like drunken idiots looking for a good score they’re never going to get.

In addition to estrogens, studies have also found many compounds present in the environment that possess similar sperm activation activities and capabilities. Specifically, genistein, quercetin, and 8-prenylnaringenin; all classified as phytoestrogens; have been shown to have these estrogen-like activities. Genistein is found in soy and legumes, quercetin is found in parsley and red wine, and 8-prenylnaringenin is found in hops and beer. Though these compounds may behave similarly to estrogen in terms of the ability to activate sperm for fertilization, some research has indicated that “too much” of these compounds can instead have an inhibitory effect and negatively affect fertilization success.

Myricetin is another compound very similar to quercetin, which is found in very high levels in berries, tea, and red wine. According to the study presented today, very few studies have examined the effects of these estrogen-like compounds in male human reproduction, and in particular no studies have examined Myricetin. In other studies not related to human reproduction, the effects of Myricetin have been mixed: some studies have found it has antioxidative properties, while other studies have found just the opposite. Similarly, some studies have shown Myricetin has anti-carcinogen properties, while other studies have found the compound promotes tumor growth. What about the effects of Myricetin in male human reproduction? Is it helpful? Or detrimental? To date, no studies have examined this topic.

By Gilberto Santa Rosa from Rio de Janeiro, Brazil. (be_sperm.) [CC-BY-2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

By Gilberto Santa Rosa from Rio de Janeiro, Brazil. (be_sperm.) [CC-BY-2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

The study presented today aimed to evaluate the effects of Myricetin in red wine on sperm biology and potential reproductive success, with potential applications for “putting it into practice”.


To collect sperm samples, donors made sweet love to a plastic cup after 3 days of abstaining from any sexual activities. Those sperm with normal volume, count, motility, vitality and morphology were pooled together and processed.

Pooled sperm samples were separated into different treatments: 10nM Myricetin; 100nM Myricetin; 1μM Myricetin; 100nM Myricetin with 1μM ICl, AbERα, AbERβ, or 10μM LY. Positive (capacitated sperm) and negative (incapacitated sperm) controls were used. Sperm were exposed to the treatments for a 30 minute period.

The following were measured after treatment exposures: sperm protein, sperm mobility and viability, cholesterol levels in sperm, acrosin activity, glucose-6-phosphate dehydrogenase activity, and Acyl-CoA dehydrogenase activity.


• Stimulation with 10nM and 100nM of Myricetin resulted in a 25% and 50% increase in sperm motility, respectively.
o The 100nM result was the same as the positive control.
• Stimulation with the greatest level of Myricetin (1μM) resulted in a decrease in sperm motility compared with the control and other Myricetin treatments.
• Stimulation with 10nM and 100nM of Myricetin resulted in a 20% and 30% increase in sperm viability, respectively.
o The 100nM result was the same as the positive control.
• All Myricetin treatments resulted in significant increases of cholesterol in sperm.
o The 100nM result was similar to the positive control and the 1μM treatment was less effective than the 10nM and 100nM treatments.
• Treating the sperm samples with combinations of Myricetin and either ICl, AbERα, AbERβ, or LY resulted in the reversal of this trend and effectively rendered the sperm incapacitated.
o This suggests that Myricetin may play an important role in the activation of sperm samples at certain concentrations.
• For the 10nM and 100nM Myricetin treatments, there was a significant increase in acrosin activity compared with the controls, with the 100nM treatment showing a greater increase than the 10nM treatment.
o The 100nM treatment showed a 70% increase in acrosin activity compared with the negative controls, which was almost equal to the result for the positive control.
• The highest concentrations of phosphorylated AKT were found in the 100nM Myricetin treatment samples, which was about 5 times greater than the untreated negative control.
• 100nM and 1μM Myricetin treatments showed greater increases in glucose-6-phosphate dehydrogenase activity than the 10nM treatment, with the 100nM Myricetin treatment being the most effective.
• Stimulation with 10nM and 100nM of Myricetin resulted in a 10% and 40% increase in acyl-CoA dehydrogenase activity compared with the untreated negative control, with the 100nM treatment being the most effective.


The results of this study generally showed that exposure of sperm to lower doses of Myricetin improved their mobility and viability/survival, while the higher doses of Myricetin were not as effective.

In order for a sperm to fertilize an egg, it must first become “capacitated”, which allows it to produce the enzymes necessary to penetrate the hard exterior shell of the egg and increase success of fertilization. To be successfully capacitated, cholesterol levels in sperm must increase, as well as the induction of phosphorylation of specific proteins. The results of this study showed that Myricetin, when exposed to sperm at lower doses and for a short period of time, is effective in capacitating the sperm and increasing their capacity to produce the enzymes necessary to successfully fertilize an egg by inducing these same responses in sperm samples.

While the results of this in vitro (in the lab/petri dish) study are fascinating, I’m not convinced we’d see the same thing in vivo (i.e. in the body). First, this study does not take into consideration the effect of the body’s surrounding environment on this mechanism. What I mean is that when the sperm are swimming around in the female reproductive tract, they are exposed to a lot of compounds and hormones that weren’t examined in this study. How do these female hormones and compounds influence the efficacy of Myricetin on sperm performance?

Recall: Myricetin is a compound with estrogen-like characteristics. Also recall: Myricetin at the highest doses was not as effective (and sometime inhibitory) as the lower doses in sperm performance. So, think about it: what happens when you have your sperm exposed to a small dose of Myricetin but then placed in the presence of the estrogen compounds in the female reproductive tract? Wouldn’t this result in increased estrogen-like compound concentrations and ultimately reduce the effectiveness of the Myricetin? I’m not sure, but I think a study somehow incorporating a more natural environment as found in the female reproductive tract is necessary to determine how sperm performance will be altered in “real life”.

Even if Myricetin actually does perform as similarly in vivo as it does in vitro, how much wine would a man need to drink in order to beef up his sperm performance? Studies have shown that myricetin and quercetin make up 20-50% of the flavonol component of red wine, ranging from 53 to 200mg/L.

By Meister des Rasikapriyâ-Manuskripts [Public domain], via Wikimedia Commons

By Meister des Rasikapriyâ-Manuskripts [Public domain], via Wikimedia Commons

According to the authors of this study, one would only need to consume 1-2 glasses of red wine a day in order to achieve the Myricetin levels tested in this study. However, if the extra estrogen in the female reproductive tract interacts in an inhibitory or toxic manner with the levels of Myricetin in the red wine, sperm performance, mobility, and viability may be significantly decreased instead of increased as we saw with Myricetin alone.

I would certainly take these results with a grain of salt if I were you. It’s very possible that the interaction between the Myricetin in the red wine and the estrogen in the female reproductive tract result in a inhibitory or toxic effect on the sperm, which is something that should really be studied before any real conclusions can be made here. I do wonder if when in in vitro fertilization scenarios, a man drinking a glass or two of red wine prior to donating sperm and the fertilization of the egg outside of the female body (i.e. thus without the excess estrogen) would be as beneficial as we saw in the results of this study.

Of course, a lot more research needs to be done in this field, so certainly talk with your doctor about your alcohol consumption habits if you are trying to conceive. Maybe we’ll learn more about the interaction of red wine and sperm performance in the female reproductive tract in subsequent experiments; however this study does give some indication that red wine or at the very least Myricetin supplements could play an important role in human reproductive success (or failure).

What do you all think of this study? Please share your thoughts!

Source: Aquila, S., Santoro, M., De Amicis, F., Guido, C., Bonofiglo, D., Lanzino, M., Cesario, M.G., Perrotta, I., Sisci, D., and Morelli, C. 2013. Red Wine Consumption May Affect Sperm Biology: The Effects of Different Concentrations of Phytoestrogen Myricetin on Human Male Gamete Function. Molecular Reproduction and Development 80: 155-165.

4 comments for “Let’s Talk About Sex, Baby!: The Effect of Red Wine Consumption on Sperm Performance

  1. WineKnurd
    May 21, 2013 at 9:44 pm

    Late to the post party, but we just found out that Mrs. Knurd is expecting a baby girl in October. Let’s just say that red wine definitely had a role in things 😉

    • Becca
      May 21, 2013 at 9:45 pm

      Oh my goodness!!! I’m so happy for the Knurd family! hehehe. Is this your first? Congratulations! I’m certain all that red wine made you good and fertile 😉

  2. WineKnurd
    May 21, 2013 at 10:13 pm

    Yep this is our first! We are both very excited!! Mrs. Knurd eschewed Brunello and Albarino as names, so we will go with something a bit more traditional 🙂

    • Becca
      May 21, 2013 at 10:15 pm

      Awwww that’s so great! Congratulations again! ….and yes, please don’t give your children wine names. They’ll be made fun of on the school yard forever! hehehe.

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