How a dating podcast made me question sperm’s epigenetic integrity

by Nichole Holm


I recently heard one of my favorite journalists, Mona Chalabi, discuss one of my least favorite subjects: how men are often encouraged to date younger women.

It’s true—the effect of age on women’s reproductive success is widely known. We’ve all heard of the “biological clock ticking” metaphor, and there’s over a century of data to correlate advanced maternal age with increased risk of genetic abnormalities in children.

However, Chalabi points out that this same encyclopedia of information does not exist for men. In fact, it’s only in the last few decades that any paternal characteristics were considered in fertility studies. Of course, this neglects a significant source of potential research, particularly given how many questions still exist in health and development, such as the causes of infertility, autism, cancer, and many other diseases.

There are a few known facts: respectively, men and women date, marry, and have children at very different ages. The average age for a woman to have her first child is 26 years old, while the average age for a man is 31 years old.

This disparity made me wonder if researchers are considering the father when studying the parental relationships between children and developmental risks. And naturally, because I am a genetics PhD candidate and self-proclaimed nerd, I became curious about the sperm—specifically, whether anyone has noted differences in sperm for men of different lifestyles, which could indicate transmitting different genetics to their children.

Such differences would be seen in the sperm’s epigenetic material. Epigenetics is a field of genetics, which studies the environment around our DNA that controls how genes are expressed.

If we think about our DNA as an instruction manual, it would have all the instructions to grow and keep a human alive. But epigenetic markers on top of our genes act like highlighters and sharpies, marking up the manual to highlight the areas that are important and redacting areas that don’t need to be read, effectively turning genes on and off.

Most of these epigenetic markers develop while we are still a developing embryo—which is why research suggests the maternal environment is crucial for the future health of a baby. Everything from maternal stress, pollution, smoking, and nutrition has been linked to significantly different epigenetic marks on their babies.

But one key difference in the epigenetics of males and females is how their sperm and eggs develop; females develop all of their eggs before they are even born, and release them one at a time once they hit puberty. According to Dr. Janine LaSalle at UC Davis, this means that the epigenetic marks on each egg are likely set in the time that an egg is released, so approximately within a 30-day window before fertilization.

Males, however, do not even produce sperm until they begin puberty, and that sperm is constantly created afterwards.

It was recently revealed that sperm epigenetics are not as stable as we once thought, leaving each newly created sperm susceptible to changes in its epigenetic marks. Recent studies looking into this have confirmed that the lifestyle and exposures of men significantly alters their own sperm’s epigenetics.

Smoking, cocaine, stress, obesity, and even exercise before conception can change not only the epigenetics of sperm, but also increase the risk of their children developing psychiatric and metabolic disorders. This means men’s experiences can change how their genes are expressed in their sperm, and possibly transmit to future children.

Since sperm are constantly generated throughout a man’s lifetime, they are also susceptible to new changes in their genes, called mutations. As men age, they can accumulate more mutations over time, and lead to what is called the Paternal Age Effect (PAE).

A number of syndromes such as Apert Syndrome, Achondroplasisa (also known as dwarfism), thanatophoric dysplasia, and Costello Syndrome are all associated with PAE. In addition, children are at an increased risk of developing some cancers, schizophrenia, and bipolar disorder as paternal age increases.

Even still, not enough research has been done to determine the age at which PAE becomes a concern. Sperm banks limit the age of donors to 40 years old, but it is not nearly as well characterized in men as it is for women. And in spite of the data to support increased risks with paternal ages and exposures, paternal factors are still rarely discussed or considered as much as maternal age.

Overall, the script we have heard and probably repeated to ourselves is based on a great deal of one-sided data.

A mother’s contribution to a child’s health and epigenetics is clear, but data on how the father contributes is not as well known. This field is new, and could hold many of the keys scientists and families have been looking for as to why adverse birth events happen.

Ultimately, equal research into paternal genetics as well as maternal genetics is necessary to understand all components of development and disease. Reducing gender bias in research needs to go in both directions, ensuring the male and female characteristics are understood to better advance the field as a whole.

While men may be selective in a woman’s age, should women be equally as selective in a man’s lifestyle or age? With regards to the data skew highlighted by Chalabi, could further research into paternal epigenetics advance more than just science, but also society?

Time and research will tell.




Thank you to Dr. Janine LaSalle and Dr. Tom Glaser for sharing your time and expertise on maternal and developmental epigenetics, which enabled clarity on this report.

***Do you want to know a more advanced concept in prenatal epigenetics?

After an egg and sperm fuse [to form a fertilized zygote], most of the epigenetic marks are erased. Some are maintained, and the rest are reset according to the needs of the zygote throughout development. The amount to which these differently marked genes in sperm and eggs are remembered (without being erased) is still unknown, but definitely worth more research to understand.


Nevertheless, foreign DNA persisted


A few months ago, an article surfaced and claimed that a woman contains DNA from every sexual partner she’s ever had. Surely unprotected sex can have legitimate consequences, such as unexpected pregnancies and/or risking numerous sexually transmitted infections. But, should females also fear their partners’ DNA persisting inside of them for the rest of their lives? Science says not really…

(Contraceptives can mitigate almost all of these risks.)

We tracked down the original scientific publication that inspired this claim and spoke with the head researcher, Dr. J. Lee Nelson, a member of Fred Hutch Cancer Research Center and Professor of Medicine at the University of Washington. The study, titled “Male microchimerism in women without sons: Quantitative assessment and correlation with pregnancy history,” aimed to assess how frequently microchimerism occurs and whether or not a woman’s pregnancy history can influence her likelihood of being a microchimera.

But what even is a microchimera? And what does it have to do with sex?

A chimera is an organism (ex. human, cat, etc.) that is made from cells that have different DNA, or genetic code. Usually, in organisms that have a lot of cells, all of the cells contain the same DNA. However, in chimeras, this is not true. Chimerism happens when two genetically distinct organisms merge—like a fetus absorbing its twin in the womb. Chimerism can lead to some interesting drama, such as “How a Man’s Unborn Twin Fathered His Child”. By definition, a microchimera is a little bit (“micro”) of a chimera. Indeed, microchimeras contain only a small amount of foreign DNA.

Note: a Chimera is a hybrid fire-breathing monster that comes from Greek mythology.


Microchimeras are real and definitely not monsters.

To be a microchimera, you don’t need to absorb your twin! If you have ever received a blood transfusion or a bone marrow transplant, you were a microchimera for at least a moment in time. If you have ever donated blood, your DNA may be coursing through someone else’s veins, saving another person’s life and giving them the privileged title of “microchimera.”

Females can become microchimeras through pregnancy. In pregnant females, fetal material can cross the placenta and circulate through the mother. Interestingly, this form of microchimerism can last (even decades!) after the pregnancy has ended. This is where the confusion about having your partner’s DNA in you forever originated.

In this study, a team of scientists tested for male DNA in the blood of 120 women—some with rheumatoid arthritis (RA) and some healthy. RA is an autoimmune disorder in which the immune system of a person with RA mistakenly assumes the person’s joint lining is a foreign invader and launches an attack against it. The researchers kept track of the women’s pregnancy histories, including whether they had ever been pregnant, had an abortion, had a miscarriage, or given birth. Researchers found that pregnancies can have a beneficial effect on RA: women who have given birth are less likely to develop RA, and arthritis symptoms can subside in pregnant women with RA. Researchers think this may occur because fetal cells and/or fetal DNA circulating in the mother’s bloodstream could temporarily trick the immune system into working properly again. It is a compelling hypothesis (with more work to be done) that will hopefully help those suffering from RA.

Dr. Lee and her colleagues did not find a difference between women with and without RA in terms of how often male DNA was found in their blood. They did find male DNA in 21% of women who had never given birth to a son. This means that a successful birth is not a requirement to becoming a microchimera.  Pregnancy history matters though—women who had elected abortions in their first trimester were the most likely group to have male DNA floating around in their blood, even when compared to women who had spontaneous abortions.

However, all scientific studies have limitations. In this study, there are two main limitations: 1) small sample size and 2) looking for male DNA, not foreign cells.

The study only looked at 120 participants to determine how common male microchimerism is in women. This number may sound like a lot of people, but in terms of making conclusions about the general population, it is fairly small. To make bold claims about the frequency of something in the population, you must look at thousands of people with a wide variety of age, ethnicity, medical history, and more. That does not mean this study drew irrelevant conclusions, it just means that more studies need to be done to support their work if claims are to be made about the entire human population.

Secondly, the study used a technique called PCR, or polymerase chain reaction, to test whether male DNA was present in the blood. PCR works by finding a specific gene or gene segment, and then making millions of copies of that segment. PCR is useful for figuring out how much of a certain gene is present. In this study, Dr. Lee’s team amplified a male gene (Y chromosome) with PCR to see how much of it was present in female blood.

Their PCR experiment could not find foreign female DNA. If women in the study were ever pregnant with a girl, this form of microchimerism was not detected. Looking for a male gene is a lot easier than looking for a foreign female gene, so most microchimerism studies focus on finding male microchimerism.

Additionally, this means that the study did not look for foreign cells, but only for foreign DNA. The idea that male DNA could be free-floating in the bloodstream cannot be excluded, meaning that fetal cells are not the only potential source of male DNA.

In their conclusions, Dr. Lee and her team explain that male microchimerism is not rare in women without sons. Some of the reasons for this include unrecognized spontaneous abortion, vanished male twin, and DNA of mother’s older brother transferred from the maternal circulation during her own fetal life. Dr. Lee explains that her team lists sexual intercourse as a potential cause for microchimerism because they are “just acknowledging a possibility brought up by others that there could be transient male DNA following intercourse…the thinking is simply that there is male DNA in sperm and that it may take a while to clear this.” To their knowledge, sexual intercourse has never been shown to be a cause of microchimerism.

Male DNA can actually circulate in female blood! Microchimerism can be linked to pregnancy, and thus intercourse. Although microchimerism has not been proven to result from recreational sexual intercourse, scientists will not rule this hypothesis out until they can accurately test it. And if it is proven true that DNA from your sexual partners may circulate in you, should we be scared? I don’t think so.

Copulation, the type of sexual reproduction humans and many other animals engage in, has been around for hundreds of thousands of years. The threat of male DNA in females, presumably, has not changed much since the dawn of homo sapiens. And there is no need to start worrying about it now.

So, why did these scientists even study male microchimerism? Well, before this paper, most microchimerism work only studied women who had given birth to a son. Dr. Lee and her group have shown that a successful birth is not a requirement to be a microchimera. Indeed, they found that male DNA was more likely to be found in a female’s blood if the pregnancy didn’t go to term, because of elected or spontaneous abortion. They also wanted to know if women with RA were different than healthy women in terms of microchimerism but found no difference.

New ways of becoming a microchimera are being discovered, too. A French group found male cells in female livers from fetal life to adulthood (Guettier). Guettier’s team indicated that alternative sources of male DNA in a female can be from a vanished twin, an older male sibling, or a prior miscarriage. In reference to this study, Dr. Lee notes that “there are obviously a number of different ways male cells can be acquired by a female.”

In my humble opinion, microchimerism is flat-out fascinating. It is not that rare for a woman to be a microchimera. And to my knowledge, there are no negative health consequences associated with it. Instead, it is being studied because of its potential to alleviate symptoms of rheumatoid arthritis and other autoimmune disorders. So could retaining foreign DNA in your circulation potentially be an asset or just a simple process of evolution? Hopefully future studies on microchimerism will unravel its purpose.



Guettier C, Sebagh M, Buard J, et al. Male cell microchimerism in normal and diseased female livers from fetal life to adulthood. Hepatology. 2005;42(1):35-43. doi:10.1002/hep.20761.

Landy H, Keith L. The vanishing twin: a review. Human Reproduction Update. 1998;4(2):177-183. doi:10.1093/humupd/4.2.177.

Utter GH, Reed WF, Lee T-H, Busch MP. Transfusion-associated microchimerism. Vox Sanguinis. 2007;93(3):188-195. doi:10.1111/j.1423-0410.2007.00954.x.

Yan Z, Lambert NC, Guthrie KA, et al. Male microchimerism in women without sons: Quantitative assessment and correlation with pregnancy history. The American Journal of Medicine. 2005;118(8):899-906. doi:10.1016/j.amjmed.2005.03.037.



Lead author and expert contact: Sam Tucci

Background research: Maria Paz Prada

There’s a lot going on in your baby’s brain–and diaper


Invisible to the naked eye, trillions of microbes are in, on, and around your body. By the numbers, the amount of individual bacteria on you is nearly equal to the number of  cells that make up your body. These bacteria populations– termed your ‘microbiome’– and the impacts they have on their human hosts fascinate microbiologists, and rightfully so. Studies correlating bacterial species A to human trait Z are frequent, but their popularity on social media tends to be more affected by the click-a-bility of the headline than the soundness of their science.

One such paper generated considerable buzz this past summer, stating that bacteria in an infant’s poop can predict the child’s cognitive development. If there’s one thing I love more than poop jokes, it’s vague assurances that one weird trick can make kids smarter. Internet audiences appear to feel the same. The original paper stands as the most downloaded paper ever from the journal Biological Psychiatry, and coverage from myriad sources drew sizable attention. The IFLScience article alone racked up over 7,100 shares, the title unabashedly stating “The Poop Of Babies Reveals How Smart They’ll Be.” How valid are these claims? How robust was the study? We felt that it was our duty to find answers.

Looking at the study itself, the researchers used well-established methods in their sample collection, bacterial identification, and statistical analysis. Eighty-nine fecal samples, each from a different 1-year-old, were collected, frozen, and checked for bacterial contents through DNA sequencing. The diversity of the fecal bacteria (meaning the number of species observed) between and within samples was calculated and compiled alongside other traits, such as family income, delivery method, maternal and paternal ethnicity, breastfeeding, antibiotic use during pregnancy, and more. The children were also examined over a period of three years with a set of cognitive tests and brain scans. The outcomes of these cognitive tests were then compared to the different variables collected by the researchers. The study found that multiple variables were associated with the bacterial content of the baby poop, and the bacterial content of the poop was associated with cognitive development. While correlations between traits like family income and cognitive development were observed, the researchers primarily reported on the link between bacterial diversity and cognitive abilities.

In a press release, Dr. Rebecca Knickmeyer, the lead professor associated with the study, stated “the big story here is that we’ve got one group of kids with a particular community of bacteria that’s performing better on these cognitive tests…This is the first time an association between microbial communities and cognitive development has been demonstrated in humans.”  It’s particularly important to understand that this is only an association. However, the rest of the press release, and most the media coverage, were quick to suggest a stronger relationship. Were the media outlets accurately reporting what the science says?

Fortunately, Dr. Jonathan Eisen, an accomplished microbiology professor here at UC Davis, has been asking these kinds of questions of published microbiome studies for years. Dr. Eisen says that studies like these are often valid, but get oversold somewhere along the translation from the research bench to the general public. Regarding our questions on this study, he said, “many papers report correlations between microbiomes and some health or disease state. But then the press release or the scientist quoted claims a causal connection. It seems so simple, but so many people seem to butcher the ‘correlation does not equal causation’ concept.” When asked to put the study’s conclusions into his own words, Dr. Eisen responded, “the microbiome ​of baby’s poop is correlated to some aspects of their cognitive development and, as of yet, we have absolutely no idea why this is.”

This was not the first, and will certainly not be the last, study that finds interesting associations between aspects of the human microbiome and health. While these works build important foundations upon which further studies can elaborate, news media can be quick to overstate the connection. So, the next time you see a headline making a bold claim about your microbiome (or poop!):

  1. Ask yourself if they’re equating correlation and causation.
  2. Check if the claims are supported by the evidence.
  3. And, when in doubt, check if Dr. Eisen has given it his “Overselling the Microbiome Award.


Lead Author: Eric Walters

Literature Review: Caryn Johansen

Expert Contact: Sam Tucci

Your Guide to Post-Traumatic Osteoarthritis

Bone and Joint Research Blog

Have you ever injured your ACL or sprained an ankle? If so, you, along with millions of others, may be at risk of developing post-traumatic osteoarthritis (PTOA). PTOA is huge problem worldwide, affecting about 5.6 million people in the US alone, and representing an annual cost of about $3 billion [1]. The incidence of PTOA is also expected to rise with rates of obesity and sports injuries [2,3]. However, few people truly understand what PTOA is, despite the sheer number of people affected by the disorder.

So what exactly is post-traumatic osteoarthritis?

Post-traumatic osteoarthritis is a degenerative joint disease that can lead to significant pain and loss of mobility. PTOA affects diarthrodial joints, which are your most movable joints. Diarthrodial joints include knees, shoulders, and fingers. Traumatic injuries to these joints that lead to sprains (overstretching or tearing of soft tissue) or bony fractures can eventually…

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Talking to your dog does not mean you are smart

Let’s talk about your pet. Specifically, about talking to your pet. Talking to a pet has received some media attention recently. A few articles cited scientific theories as proof that talking to a pet indicates higher than average intelligence. Baby-talk to your pit bull? Don’t worry, one article croons, it means you’re “one smart cookie.” Another article reassures you that talking to your dog makes you “smart AF.” Yet another article, talking to your pet means that you are both smart and creative. Congratulations!

Unfortunately for pet owners, talking to your pet does not indicate either higher than average intelligence or creativity.

What it does signify is that you are human, and you are expressing an ancient human behavioral trait – the ability of humans to project human emotions and intentions onto non-humans.

You have likely heard the term before – anthropomorphism. It was coined in the 6th century BCE by Xenophanes, a Greek philosopher and critic while observing that religious devotees often depicted deities as looking similar to themselves. Anthropomorphization is prevalent in art, religion, writing, language, and other expressions, from prehistory to contemporary times.

The oldest archeological example of transferring human traits to animals is referred to as the Lowenmensch figurine. Dated to about 40,000 years ago, this human figure has a lion head.

Humans also have a history of anthropomorphizing the environment and climate to help explain events: when a deity is angry and wrathful, disaster strikes.

An interesting scientific question is why do humans anthropomorphize? What is the psychology behind it and what is its role in society, if it has one?

Nicholas Epley, a professor of behavioral science at the University of Chicago, researches the psychology behind anthropomorphism to answer these questions. His 2014 book Mindwise: How We Understand What Others Think, Believe, Feel, and Want, argues that humans are constantly using personal interpretations of events to understand the actions and behaviors of other people and objects. He says the ability to recognize another human mind “involves the same psychological processes as recognizing a mind in other animals, a god, or even a gadget,” whether that mind exists or not.

In one experiment, Epley and collaborators imaged research subjects’ brains in an fMRI to test the hypothesis that strong anthropomorphization results in brain activity in the region of the brain associated with awareness of other humans. They found that anthropomorphism activated the region associated with self-projection and theory of mind, or our perception that others are separate from ourselves.

However, Dr. Cristina Moya, a professor of anthropology at UC Davis, noted:”Just because a brain region lights up during a given activity, it doesn’t mean that when that region lights up the person is engaging in that activity. That is, there could be multiple activities and thought processes that could produce a similar fMRI pattern. The argument commits the same fallacy as saying all Davis residents live in California, therefore if one lives in California one lives in Davis.”

Epley argues that there are basically three psychological reasons for anthropomorphism. First, it’s entirely reasonable for humans to interpret the world through their personal perceptions, as this is their foundational knowledge of the world. Second, humans anthropomorphize because they desire to explain things and to understand the world around them. Ascribing human explanations for the world helps make sense of chaos around us. And third, humans anthropomorphize for human connections when we are lonely.

So, a person might assign a human characteristic to explain why her dog is barking and try to reason with her dog to stop, especially when she feels lonely, but that doesn’t mean she’s smarter than average.

Dr. Alexandra Horowitz, an adjunct associate professor in the Department of Psychology at Barnard College, also pointed out that we don’t know whether other species anthropomorphize. “We don’t know that other animals don’t think of and explain the world around them using extrapolations from how their own species works,” she said in an email. There is evidence that zoomorphism does occur and that the barking dog may be making canine-based assumptions about her owner. Anthropomorphism therefore does not even mark the intelligence of the human species, much less an individual’s intelligence.

Epley did not cover this in his report on anthropomorphism. Instead, anthropomorphism was reported as distinctly human. While it’s true that anthropomorphism is human-specific, the biological process underlying anthropomorphism is probably not. In other words, a dog could be engaging in “caninomorphism” when she projects dog-interpretation onto the actions of her owner.

Epley and others have made the case that anthropomorphism is a process similar to projecting personal interpretation of the world onto other humans and that this process plays a role in contemporary society. Unfortunately, although this does point to higher cognition in humans, it is not an indicator of individual intelligence.

Talking to your pet does not indicate that you are especially smart or creative. The articles that reported this seemed to have misinterpreted the phrase “human intelligence” to mean personal intelligence, rather than intelligence in an evolutionary context. In addition, there’s no evidence that the process behind anthropomorphism is human-specific. Nonetheless, anthropomorphising your pet reflects a pretty interesting human trait that may have been evolutionarily beneficial and may still play an important role in contemporary society.

About the Authors

Caryn Johansen, Eric Walters, and Taylor Reiter are graduate students at the University of California in Davis. This post was written as part of a project called “Science REALLY says” which seeks to ensure scientific data is accurately represented by the media. For more content from the UC Davis science communication group “Science Says“, follow us on twitter @SciSays and like us on facebook.



We thank Dr. Alexandra Horowitz (adjunct associate professor in the Department of Psychology at Barnard College) and Dr. Cristina Moya (assistant professor of anthropology at the University of California in Davis) for helpful comments.



Epley, N. (2014). Mindwise: How We Understand What Others Think. Believe, Feel, and Want.

Epley, N., Waytz, A., & Cacioppo, J. T. (2007). On seeing human: a three-factor theory of anthropomorphism. Psychological review, 114(4), 864.

Waytz, A., Morewedge, C. K., Epley, N., Monteleone, G., Gao, J. H., & Cacioppo, J. T. (2010). Making sense by making sentient: effectance motivation increases anthropomorphism. Journal of personality and social psychology, 99(3), 410.


No, your baby is not racist.

Babies are terrible at a lot of things. They’re terrible at walking, they puke all over, cry at the worst times, and stare at people in the grocery store. No social etiquette whatsoever. But, contrary to recent media claims, they are not racist.


Saying that a baby can be racist misunderstands racism and child development. So, what’s with the headlines dogging on the youngest members of our society? We have this fascination (exhibit A, exhibit B) with attributing adult motivations and personality traits to babies. But babies aren’t just miniature adults.



The science behind these racist babies headlines is much less terrible and much more interesting. Two recent studies from a group of child development researchers led by Dr. Lee Kang at the University of Toronto looked at how babies view race.


In the first, Dr. Kang’s group tested whether babies preferentially follow the gaze of a same-race woman or a different-race woman in a game of animal picture pop-up. The researchers began with a “learning phase” (see the figure below). During this learning phase, the woman always, never, or only sometimes looked at the animal picture. This would “teach” a baby whether the actress was reliable.


After going through the learning phase, the babies were given a test trial (the actual experiment). This is when the researchers watched whether or not the baby followed the gaze of the woman before the animal popped up.


The results are what you might expect: the babies followed the gaze of the familiar/similar looking woman (of the same race) more often than a different-race woman. But this was only the case when the women-gazers were only somewhat reliable. If the gaze of either woman predicted the location of the animal 100% of the time, the baby would follow the women’s eyeline equally as often regardless of race. Conversely, when each woman’s gaze was completely unreliable in indicating the location of the animal on the screen, the baby would follow neither.


This showed a couple things. First, babies weigh reliability by picking up patterns from which they then make decisions. In this case, these initial patterns are in the learning phase. The babies in this experiment were able to pick up on whether or not the women were reliable in predicting the animal pop-up and then decide to follow or not follow their gaze in the test trial. Second, the experiment showed that babies discern differences in facial characteristics. The more familiar a baby is with certain facial characteristics the more likely they will follow cues from those people in uncertain situations.


“babies discern differences

in facial characteristics”


In the second experiment, Dr. Kang and colleagues recorded how long each baby looked at pictures of different and similar-race adult faces as they listened to either happy or sad music. One of the most interesting findings of this experiment was the difference in response depending on the baby’s age. Older infants (9 months old versus 3-6 months old) were more likely to gaze at same race faces when paired with happy music and different race faces with the sad music.


The results of these studies point to a tendency of babies of a certain age to have preference for same-race faces, indicative of racial bias. Dr. Kang however, clarified that by saying that infants are racially biased “we mean that infants show a tendency to favor the individuals of one race over those of another emotionally or behaviorally, just like their strong preference for female adults over male adults, attractive adults over unattractive adults, adults speaking the native language over adults speaking non-native language, or even familiar adults over strangers.”


It would be interesting in the future to study the preferences of babies adopted by different-race families. This would allow scientists to determine if adopted babies prefer faces similar to their families or faces of their own ethnicity. This also raises interesting questions about when in developmental time babies start to conceptualize their own ethnicity by recognizing and comparing physical characteristics of other people.




What is immediately clear is that babies integrate multiple types of information from their environment (the faces they see, the voices they hear, the genders they interact with, etc.). In scientific terms, preference for one race over another is “racial bias.” However, it’s important to make the distinction between racial bias in the scientific sense, and racism.


Babies notice physical traits in others and test the patterns they create. This racial bias can be clearly contrasted with what we think of as racism, which Dr. Kang explains as when “an individual displays overtly negative attitudes towards people from another race group, subscribes overt stereotypes about them, and most importantly, discriminates against them in action.”


So what does it mean if your baby is racially biased? This shouldn’t be a cause for alarm…just yet. Of course, as Dr. Kang mentions, the most important question is whether “such early bias will grow into the overt form of racism in adulthood.” We don’t know the full answer to this question since more work needs to be done to make these direct connections, but it’s something Dr. Kang and his colleagues are actively interested in and aim to explore in the future.


“exposure to a diversity of

races reduces implicit bias”


What we can say is that these results lend a lot of weight to the role of environment on a child’s social development. A baby’s world during the first year of life is typically populated with same-race individuals. There is genuine concern that biases based on unfamiliarity, however innocent, could develop into unfair stereotypes. Dr. Kang suggests that parents “consider introducing their infants and children to books, people, and TV programs that depict other-race individuals as individuals, not as a group.” The impact of diversity on a child’s social development has been explored by Kang as well as other research groups, all of which conclude that exposure to a diversity of races reduces implicit bias in children and improves their ability to distinguish personal characteristics in other race individuals.


So, babies aren’t racist—they just act based on the familiar. And in a world so big and confusing for a baby, can you blame them? While it must’ve been tempting to write headlines calling babies “bigots” (maybe it’s the alliteration), that’s not what the studies aimed to test nor what they concluded. What the “racist babies” articles meant to say was that babies show preference for faces that look like theirs. And while it’s alarming to imagine that a fully-formed, socially present (and utterly shameless) person is sizing us up from the crib, babies are probably too busy trying to figure out the world around them to judge you based on your ethnicity.


About the Authors

Destiny Davis (author) and Sam Tucci (editor) are graduate students at the University of California in Davis. This post was written as part of a project called “Science REALLY says” which seeks to ensure scientific data is accurately represented by the media. For more content from the UC Davis science communication group “Science Says“, follow us on twitter @SciSays and like us on facebook.



 We thank Dr. Lee Kang (Professor of Applied Psychology and Human Development at the University of Toronto) for helpful comments.


References (*main studies discussed)


*Xiao, N.G., Wu, R., Quinn, P.C., Liu, S., Tummeltshammer, K.S., Kirkham, N.Z., Ge, L., Pascalis, O., Lee, K. (2017). Infants Rely More on Gaze Cues From Own-Race Than Other-Race Adults for Learning Under Uncertainty. Child Development.


*Xiao, N.G., Quinn, P.C., Liu, S., Ge, L., Pascalis, O., Lee, K. (2017). Older but not younger infants associate own-race faces with happy music and other-race faces with sad music. Developmental Science.


Xiao, W.S., Fu, G., Quinn, P.C>, Qin, J., Tanaka, J.W., Pascalis, O., Lee, K.(2015). Individuation training with other-race faces reduces preschoolers’ implicit racial bias: a link between perceptual and social representation of faces in children. Developmental Science.


Anzures, G., Quinn, P.C., Pascalis, O., Slater, A.M., Lee, K. (2010). Categorization, categorial perception, and asymmetry in infants’ representation of face race. Developmental Science.


Anzures, G., Wheeler, A., Quinn, P.C., Pascalis, O., Slater, A.M., Heron-Delaney, M., Tanaka, J.W., Lee, K. (2012). Brief daily exposures to Asian females reverses perceptual narrowing for Asian faces in Caucasian infants. Journal of Experimental Child Psychology.


Bar-Haim, Y., Ziv, T., Lamy, D., Hodes, R.M. (2006) Nature and Nurture in Own-Race Face Processing. Psychological Science.


Heron-Delaney, M., Anzures, G., Herbert, J.S., Quinn, P.C., Slater, A.M., Tanaka, J.W., Lee, K., Pascalis, O. (2011). Perceptual Training Prevents the Emergence of the Other Race Effect during Infancy. PLoS One.


Kelly, D.J., Quinn, P.C., Slater, A.M., Lee, K., Gibson, A., Smith, M., Ge, L., Pascalis, O. (2005). Three-month-olds, but not newborns, prefer own-race faces. Developmental Science.




Wine won’t make you smarter, but your brain plays a big role in tasting

You might have noticed this headline circulating on the Internet:

“Drinking wine makes you smarter!”

As graduate students, we wish! These claims stem from an interview with Yale neuroscientist Dr. Gordon Shepherd on his new book, Neuroenology: How the Brain Creates the Taste of Wine. Unfortunately for wine lovers, these articles ran away with Dr. Shepherd’s take on the complex nature of taste.

The claim with the most mileage is that tasting wine is better for your brain than doing math problems or listening to music. Dr. Shepherd mentions these activities as reference points to demonstrate the complexity of tasting. But in an interview with us, he stressed that whether or not tasting is more engaging than math or listening is solely speculation. Indeed, the book makes no claims about the superiority of drinking wine over other activities. Dr. Shepherd’s writings are based on a series of peer-reviewed studies about the intricate science of tasting. Here’s what the experts agree on:

1) Flavor isn’t intrinsic to food; the brain is what creates the perception of flavor. This is similar to pain. A hot object is not inherently a painful item, but if you touch something hot, your body detects a potential source of harm and activates a set of neural pathways, which create the sensation of pain. Likewise, when you taste something, your brain is responsible for processing and synthesizing all of the sensory inputs into a “flavor” that you perceive.

“flavor is different from taste”

To sensory scientists, flavor is different from taste. Taste strictly refers to the sensations of sweet, sour, salty, bitter, or umami (savory). On the other hand, flavor results from a combination of tastes, aromas, and other senses. Even feel, sight, sound, and memory can contribute! For example, artificially changing the color of white wine to red makes us perceive the flavor differently. Flavor requires the integration of all of our senses, each with its own mechanisms and pathways, why is partly the reason so many regions of the brain are activated during tasting.

2) Eating is a surprisingly complex physiological process, and most of it happens unconsciously. For instance, mechanically manipulating and swallowing food requires fine motor control of muscles from the face, tongue, and throat, which the brain must coordinate with breathing and multiple sensory inputs. Smell alone is more complicated than “first meets the nose.” When most of us think about smelling our food, we imagine sniffing our meal as it lies in front of us; this type of smelling is called orthonasal However, a huge part is played by retronasal smell, which occurs when we breathe out and bring the air in our mouth to our nose. This brings volatiles, (i.e. airborne particles) from the food we’re eating to our olfactory receptors, which recognize the volatiles and integrate them into our flavor perception.

“like wiggling your hand around to find an object”

Since the brain must synthesize these many inputs to create the sensation of flavor, the tasting of food and wine is considered an active process. This makes tasting less like feeling a touch on your hand, and more like wiggling your hand around to find an object. Dr. Shepherd notes, “As a physiologist, to me that is the fascinating part.”

3) Neuroenology focuses specifically on the motor activity of manipulating wine, like the swishing of liquid with the tongue. But these same principles apply to the tasting of any food. So, does this mean that eating or drinking literally anything will make us “smarter”? Unfortunately, no. All this really means is that the act of tasting is a very rich sensory experience that involves many areas of the brain.

Keep in mind that heightened brain activity is not always a good thing! Dr. Shepherd writes that “there is evidence that in rodents fed on a high-sugar diet, brain cells are activated in areas such as the insula and the OFC, which are also activated by an addiction to cocaine.” We can all probably agree that binging on sugar and cocaine to become “smarter” won’t work out.

“The very concept of ‘intelligence’ is controversial”

That said, a study on master sommeliers did find that the regions of their brains involved in smelling were denser compared to non-experts. Master sommeliers also exhibited increased levels of brain activity during non-wine related smelling tests. So, it’s true that developing an expertise can cause actual physiological changes to the brain. As an expert in a particular field, your brain structure could become specialized in a similar way, but this does not necessarily equate to intelligence. The very concept of “intelligence” is controversial and difficult to measure or quantify.

“There is no magic food or drink

that will make you smarter.”

Furthermore, master sommeliers are extremely skilled at what they do. There are only 236 master sommeliers in the world, and this dearth isn’t due to a lack of interest. Master sommeliers must pass a series of notoriously difficult tests, including blind wine tastings, in which they’re required to accurately identify everything from the kind of grapes used, where the grapes came from, aromas present, alcohol and acidity levels, and more. We shouldn’t conflate their years of dedication and active training with our everyday wine tasting; their brains exhibit these qualities due to their rigorous training and preparation, not due to exposure to wine. We also caution that the authors consider this a “pilot study” on a small group of people who were not age-matched, and they recommend more studies to follow up on these findings. (For more, check out the studies on musicians, perfumers, or London taxi drivers)

“working on flavor is a wonderful way

to exercise your brain.”

So what’s the takeaway? There is no magic food or drink that will make you smarter. Rather, hard work and repetition will cause certain functional areas of your brain to develop in ways that can enhance specific skills. However, refining your tasting abilities can be an enjoyable way to develop greater sensory-cognitive skills. As Dr. Shepherd suggests, “working on flavor is a wonderful way to exercise your brain.”



About the Authors

Lynn Ly, Debbie Fetter, and Colin Shew are graduate students at the University of California in Davis. This post was written as part of a project called “Science REALLY says” which seeks to ensure scientific data is accurately represented by the media. For more content from the UC Davis science communication group “Science Says“, follow us on twitter @SciSays and like us on facebook.



 We thank Dr. Gordon Shepherd (professor of neuroscience at Yale and author of Neuroenology: How the Brain Creates the Taste of Wine) for helpful comments.



Shepherd, G. M. (2015). Neuroenology: how the brain creates the taste of wine. Flavour, 4(1), 19.

Small, D. M. (2012). Flavor is in the brain. Physiology and Behavior, 107(4), 540–552.

Spence, C. (2013). Multisensory flavour perception. Current Biology, 23(9), R365–R369.

Muñoz-González, C., Rodríguez-Bencomo, J. J., Moreno-Arribas, M. V., & Pozo-Bayón, M. Á. (2011). Beyond the characterization of wine aroma compounds: Looking for analytical approaches in trying to understand aroma perception during wine consumption. Analytical and Bioanalytical Chemistry, 401(5), 1501–1516.

Silva Teixeira, C. S., Cerqueira, N. M. F. S. A., & Silva Ferreira, A. C. (2016). Unravelling the olfactory sense: From the Gene to Odor Perception. Chemical Senses, 41(2), 105–121.

Banks, S. J., Sreenivasan, K. R., Weintraub, D. M., Baldock, D., Noback, M., Pierce, M. E., … Leger, G. C. (2016). Structural and Functional MRI Differences in Master Sommeliers: A Pilot Study on Expertise in the Brain. Frontiers in Human Neuroscience, 10(August), 1–12.

Shepherd, G. M. (2017). Neuroenology: How the Brain Creates the Taste of Wine. NEW YORK: Columbia University Press. Retrieved from

Gluten probably won’t kill you and a gluten-free diet probably won’t either

Gluten-free diets are all the rage. I mean, if your yogurt label says ‘gluten-free’ then gluten must be bad right? But wait, what about those recent headlines claiming there’s arsenic in gluten-free foods? Is it safe to eat literally anything?

If you feel this way trying to navigate nutrition advice, you’re not alone. According to headlines practically anything can either kill you or cure you. This might leave you feeling like science is wishy washy, and maybe you should turn to your pastor or yoga instructor for nutrition advice instead. The truth is, food science is nuanced and headlines are not. In this post, we’ll guide you through the gluten gamut and share some general tips for navigating nutrition science news.

First, unless you’re one of the less than 2% of people with Celiacs disease or a wheat allergy, you probably don’t need to worry about gluten. Gluten is a protein found in wheat that helps to give bread that nice gooey texture. Contrary to some claims that gluten is a byproduct of modern “genetic tinkering”,  we’ve been eating gluten since the dawn of wheat domestication about 10,000 years ago. We’ve only been digesting gluten-related news hysteria for about the last 6 years thanks to a book called “Wheat Belly”.

“Wheat Belly” was written by Dr. William Davis after he noticed that the health and weight of many of his patients improved when they stopped eating wheat. He attributes this difference to gluten and inflammation. In the science world, we call this kind of evidence “anecdotal” because it comes from casual observations not carefully controlled studies.  Scientists have tested Davis’s theory by administering controlled tests where (for example) people with self-reported gluten sensitivities consumed either wheat or whey proteins. So far, the evidence doesn’t match the anecdote.  

But reports of celiac disease and other wheat-related allergies ARE on the rise. There are several possible explanations for this. Our attention to the diagnosis of these conditions and the sensitivity of the tests required to confirm them has increased. Additionally allergies and autoimmune diseases like celiac are on the rise in general. We don’t yet know why this is, but one intriguing possibility is the hygiene hypothesis–basically, in our increasingly urbanized and sterile environment, children are exposed to less immune challenges, causing their immune system to mistake friend for foe. There is some evidence to support this hypothesis. For example, children who grow up on dairies or in close contact with pets are less likely to develop asthma and allergies.

That still doesn’t explain why some people feel better when they cut wheat out of their diets. Wheat has changed over the ages with breeding, so it’s possible that modern wheat could cause irritation, but it is difficult to say, because cutting wheat out of your diet means cutting a whole lot of other stuff too. Obviously if you give up beer, pizza, and cookies your health will improve. By eliminating wheat, you’d probably eat less processed foods which tend to be high in sugars, calories, salts, etc.

The promise of a gluten-free diet has lead 1 in 3 Americans to consider the switch, expanding a niche market into an advertiser’s dream. You can now buy gluten-free chicken nuggets, brownies, and even beer. What luck! Now we can go gluten-free and still have all the junk that typically hides in wheat-based processed foods. But headlines are now claiming that these foods may come with a side of heavy metals and arsenic.

In a study published recently by the University of Illinois, scientists found 50% more arsenic and 60% more lead in the urine of people on a self-reported gluten-free diet. Before you set fire to your pantry, food toxicologist Dr. Carl Winter noted that these “estimates are all below levels of concern identified by the US EPA,” but by less of a margin of safety than is typically allowed for compounds such as pesticides which are carefully monitored and highly scrutinized.

To put these amounts into perspective, Arsenic has an LD50 of 15mg/kg. That means if you fed a bunch of 1kg rats 15mg of straight arsenic, half of them would die. But rats are pretty small. It would take 900 mg of Arsenic in one serving to kill a Gwyneth Paltrow-sized rat. That’s about 5000 times more arsenic that you’d find in a typical 1 pound bag of rice. In urine, the limit considered safe for arsenic is 100ug/L which is still way more than the 12ug/L found from those on a Gluten-free diet (for comparison, those who eat gluten still peed 8ug/L of arsenic).

What’s more, the specific source of the arsenic in gluten-free diets is important. Although they didn’t directly test for it, the researchers speculate that these elevated levels of arsenic come from an increased consumption of rice. Many gluten-free products contain rice flour as a substitute for wheat flour, and according to UC Davis rice extension specialist Dr. Bruce Linquist, “arsenic is higher in rice than many other cereal crops due to the anaerobic soil conditions rice is grown under”. Other studies have found arsenic in rice-based gluten-free foods but not in gluten-free foods lacking rice. This doesn’t mean you should throw away all the rice in your cabinet either. As toxicologists like to say, the dose makes the poison. One study indicated that Asian households living in the US are only exposed to about 2.8 ug of arsenic per day from eating rice. There’s more arsenic than that in our tap water. 

So what’s the takeaway? Gluten probably won’t kill you and a gluten-free diet probably won’t either. Neither will rice or tap water. On the other hand, too much of absolutely anything can kill you. A small number of celiac patients have faced arsenic poisoning because they were unknowingly eating rice-based products 3 meals a day. For anyone, especially children, the FDA recommends a varied diet to decrease the risk of exposure to arsenic. The same strategy can be applied to many dietary concerns. Variety is good, homogeneity is bad. So although it’s cliche, a good rule of thumb is everything in moderation–even arsenic.

About the Authors

Jenna E Gallegos, Lynn Ly, and Eric Walters are graduate students at the University of California in Davis. This post was written as part of a project called “Science REALLY says” which seeks to ensure scientific data is accurately represented by the media. For more content from the UC Davis science communication group “Science Says“, follow us on twitter @SciSays and like us on facebook.


 We thank Dr. Carl Winter (food toxicology extension specialist, UC Davis) and Dr. Bruce Linquist (sustainable management of rice systems extension specialist, UC Davis) for helpful comments.


Bulka, C. M., Davis, M. A., Karagas, M. R., Ahsan, H., & Argos, M. (2017). The Unintended Consequences of a Gluten-Free Diet. Epidemiology (Cambridge, Mass.), 1–7.

Kim, H., Patel, K. G., Orosz, E., Kothari, N., Demyen, M. F., Pyrsopoulos, N., … C, C. (2016). Time Trends in the Prevalence of Celiac Disease and Gluten-Free Diet in the US Population: Results From the National Health and Nutrition Examination Surveys 2009-2014. JAMA Internal Medicine, 108(5), 818–824.

Mantha, M., Yeary, E., Trent, J., Creed, P. A., Kubachka, K., Hanley, T., … Creed, J. T. (2016). Estimating Inorganic Arsenic Exposure from U.S. Rice and Total Water Intakes. Environmental Health Perspectives, (August).

Pietzak, M. (2012). Celiac disease, wheat allergy, and gluten sensitivity: when gluten free is not a fad. JPEN. Journal of Parenteral and Enteral Nutrition, 36(1 Suppl), 68S–75S.

Jara, E. a, & Winter, C. K. (2014). Dietary exposure to total and inorganic arsenic in the United States, 2006–2008. International Journal of Food Contamination, 1(1), 3.

Vierk, K. A., Koehler, K. M., Fein, S. B., & Street, D. A. (2007). Prevalence of self-reported food allergy in American adults and use of food labels. Journal of Allergy and Clinical Immunology, 119(6), 1504–1510.

Munera-Picazo, S., Burló, F., & Carbonell-Barrachina, A. A. (2014). Arsenic speciation in rice-based food for adults with celiac disease. Food Additives & Contaminants. Part A, Chemistry, Analysis, Control, Exposure & Risk Assessment, 31(8), 1358–66.

Agency for Toxic Substances and Disease Registry (ATSDR). 2007. Toxicological Profile for Arsenic. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Services.

US Food and Drug Administration. (2016) Arsenic in Rice and Rice Products.

Darren Seifer. (2012) Is Gluten-Free Eating a Trend Worth Noting? Report from The NPD Group.

Fertility and fraying tips: What does your DNA say about when to have kids?

Having kids in your 30s has an amazing effect on your DNA…” “Want to live longer? Give birth in your 30s…” The headlines are seductive. I immediately wanted to print them out for my grandchild-less mom.

Too bad they’re not true. After looking at the study these articles are citing, here’s what the science really says.

First, aging is complicated. There are literally a lifetime of variables that compound, interact, and eventually contribute to our age of death. There are entire fields of research dedicated to studying how to live healthier for longer periods of time (like medicine!).

The 2009 Nobel prize in medicine was awarded to scientists who cleared up a major question in aging research. How does DNA protect itself during cell division? The answer is telomeres. Telomeres are repetitive bits of DNA that protect the ends of tightly wound strands of DNA called chromosomes. Each new round of cell divisions shortens the length of the telomere.

To understand why, it might help to imagine the vast rounds of division the cells in your body undergo throughout your lifetime. Your stomach cells divide and completely replace older cells in just a couple of days. Your liver cells turnover every 10 to 20 days (thank goodness). In fact, the majority of your cells are in constant flux. Dividing and growing, dividing and growing every second. Each time one of your cells divides, it has to copy its DNA. Given how often this happens it makes sense that the ends of the DNA strands might start to fray.

A telomere is to a chromosome what an aglet is to a shoelace. Over time chromosomes, like shoelaces, can fray and splinter. Chew a little bit and maybe nothing happens. Chew too much and problems arise. Telomeres don’t include important genes so you can gnaw more of them and the cell still runs okay. Like our own version of tree rings, short telomeres are an indicator of old age.

Researchers studying telomere length and longevity noticed telomeres fray less in some individuals who live long healthy lives. Indeed, some centenarians (people of 100+ years in age) have similar telomere lengths to those in younger generations.

The researchers of the study mentioned in those catchy headlines were curious to see if there was an association between telomere length and fertility. They found that mothers who gave birth at older ages were more likely to have longer telomeres than younger mothers. In fact, the oldest mothers had the longest telomeres.

I want to stress the words “more likely” in the above paragraph. There is an association between long telomeres and the age at which one gives birth, not a direct link. I’ll invoke the famous “correlation does not equal causation” phrase here, which means just because two things are observed together does not mean that one causes the other. Wearing a raincoat might be correlated to more car wrecks but wearing a raincoat doesn’t cause car wrecks and car wrecks aren’t why you put on a raincoat. The headlines suggest waiting to have children will make you live longer. More likely, women already apt to live longer remain fertile later in life.

As the scientists are careful to admit, there are several limitations to this study. First, their measure of prolonged fertility is the age at which the mother had her last child. But of course, not having a child does not mean that the mother is infertile. The study did not include other types of pregnancies that may not have resulted in a surviving child (ie. miscarriages, still-births, etc). The age at which a woman decides to give birth is also varied, personal, and influenced by a myriad of things. The researchers mention environmental and social factors such as economic status and familial relationships that factor into the decision. Finally, the participants of the study were all non-Hispanic white women, but populations differ in the length and stability of their telomeres.

Given what we know about telomeres and their impact on aging (long telomeres=more likely to live longer) and the conclusions from this study (prolonged fertility=more likely to have long telomeres) we can cautiously conclude that prolonged fertility might be a good indicator that the mother will live longer. Here’s a diagram to help:


The significant association between maternal age and telomere length is interesting because it means there might be a genetic basis behind fertility and longevity. Because of the genetic component, you can see similar effects in blood relatives. So keep an eye on your siblings.

All in all, having good DNA (or long telomeres) could be the key to living longer. Having good DNA could mean that you stay fertile for longer too, but deciding to have kids later in life won’t make you live longer. The headline should read, “Good DNA has an amazing effect on your fertility.” But as any good scientific research study usually ends, more research is needed.

…A last word of advice, use protection when replicating.

About the Authors

Destiny Davis (author), Caryn Johansen (editor), and Jordan Snyder (editor) are PhD students at the University of California in Davis. This post was written as part of a project called “Science REALLY says” which seeks to ensure scientific data is accurately represented by the media. For more content from the UC Davis science communication group “Science Says“, follow us on twitter @SciSays and like us on facebook.


Aubert, G., & Lansdorp, P. M. (2008). Telomeres and Aging. Physiological Reviews, 88(2).

Brown, L., Needham, B., & Ailshire, J. (2016). Telomere Length Among Older U.S. Adults: Differences by Race/Ethnicity, Gender, and Age. Journal of Aging and Health.

Fagan, E., Sun, F., Bae, H., Elo, I., Andersen, S. L., Lee, J., … Schupf, N. (n.d.). Telomere length is longer in women with late maternal age. CE.

Franzke, B., Neubauer, O., & Wagner, K.-H. (2015). Super DNAging—New insights into DNA integrity, genome stability and telomeres in the oldest old. Mutation Research/Reviews in Mutation Research, 766, 48–57.

Harley, C. B., Futcher, A. B., & Greider, C. W. (1990). Telomeres shorten during ageing of human fibroblasts. Nature, 345(6274), 458–460.

Ishikawa, N., Nakamura, K.-I., Izumiyama-Shimomura, N., Aida, J., Matsuda, Y., Arai, T., & Takubo, K. (2016). Changes of telomere status with aging: An update. Geriatrics & Gerontology International, 16, 30–42.

A beer a day keeps the doctor away? Here’s the science behind the headlines

Just in time for holiday gatherings, news outlets reported that drinking a beer a day could prevent heart disease and stroke:

Time-“The Truth About What Alcohol Does to Your Heart” (Nov 13, 2016)

Huffington Post UK-“Drinking One Beer A Day Can Prevent Stroke And Heart Disease, Study Suggests” (Nov 14, 2016)

Daily Mail- “Regular Drinking Preserves ‘Good Cholesterol’ Levels” (Nov 14, 2016)

These articles missed some major points about alcohol and health. The original study was conducted by PhD candidate Shue Huang at Pennslyvania State University. Huang followed 80,000 healthy Chinese adults for six years and monitored how their drinking habits affected cholesterol levels. Adults who drank moderately maintained more good cholesterol as they aged. Importantly, these are preliminary results presented at the American Heart Association’s Scientific Sessions, 2016. Often, the point of presenting such results at conferences and sessions is to receive feedback from others in the field. News media outlets failed to mention that these results have not been peer-reviewed. In the peer review process , experts in the field ensure the credibility of published research by critiquing the study design, analysis, results, and conclusions prior to publication. We contacted Huang for details about her study, but she was uncomfortable giving any more details until it had finished undergoing the peer-review process.

So, what are the facts? Beer is packed with polyphenols and other compounds that have complex, not-well-studied, potentially beneficial effects on our bodies. It is likely that some of these compounds improve HDL cholesterol levels. However, beer contains alcohol…a substance that is unduly bad for health. Alcohol leads to weight gain and liver disease, causes poor sleep, and is associated with reckless decision-making.

Although some of these trends have been established, teasing out cause and effect is difficult with alcohol, especially with beer and wine. Several studies have found correlations between beer or wine and good health, but it is unclear whether it is the alcohol itself or other compounds unique to beer or wine specifically that have an effect. And as one study pointed out, “moderate drinkers tend to be younger, leaner, more physical active, of higher socioeconomic status, and more likely to be married compared with people who abstain or drink rarely.” Each of these confounding factors—age, weight, physical activity, income, and marriage status—can also effect health, and knowing which factor is contributing in what way is difficult determine.

We reached out to Kenneth J. Mukamal, MD, MPH, an expert in cardiovascular health and alcohol consumption. He commented that, “drinking alcohol (probably any kind) tends to raise HDL-cholesterol levels…that fact is very well established in the literature…The DailyMail piece certainly goes well beyond that – they reference risk of stroke, but that’s not directly addressed in the original abstract, and decisions about how much alcohol to drink have relatively little to do with whether alcohol raises levels of this biomarker…”

Essentially, Huang’s study reaffirmed that alcohol increases HDL cholesterol levels. However, this does not necessarily translate to increased health per se, especially due to other negative effects of alcohol consumption. There are far better ways to increase HDL levels, like eating a well-balanced diet, exercising, or taking niacin.

Although many studies suggest health benefits from moderate drinking in some circumstances, there have been no long-term, randomized, double-blind control trials —the gold standard in clinical research—to determine if beer can reduce heart attacks or stroke while increasing general healthfulness.

Why does study design matter? Epidemiological studies survey populations, collecting data on things like eating and drinking habits, socioeconomic status, and health outcomes over time. They are powerful for detecting trends in massive populations, and they can assess associations on a far larger scale (and at a much lower cost) than randomized control trials (RCT). However, epidemiological studies can only draw correlations, not determine causation. This is best illustrated by an example. The image below is from the New England Journal of Medicine, and depicts a strong correlation between the amount of chocolate a country consumes and the number of Nobel laureates from that country. However, this correlation is likely illegitimate—the amount of chocolate consumed in a country likely has no effect on the number of Nobel laureates from that country. In a RCT, people would be fed either chocolate or a placebo with all other lifestyle and diet factors kept the same. After time, the number of Nobel laureates in each group would be compared. This fictitious trial would be very difficult and expensive to conduct, as chocolate would have to be fed to people starting at infancy, and a large number of people would have to be fed chocolate in order to have enough Nobel laureates to give the results statistical significance.


Figure from: Messerli, F. H. (2012). “Chocolate Consumption, Cognitive Function, and Nobel Laureates.” New England Journal of Medicine 367(16):1562-1564

To relate this back to the beer study at hand, although there is a connection between alcohol consumption and increases in or maintenance of HDL cholesterol levels, the cause of this correlation is unknown. Although drinking beer in moderation is likely okay, there is no direct evidence that drinking beer reduces disease.

About the Authors

Taylor Reiter, Zane Moore, and Lynn Ly are PhD students at the University of California in Davis. This post was written as part of a project called “Science REALLY says” which seeks to ensure scientific data is accurately represented by the media. For more content from the UC Davis science communication group “Science Says“, follow us on twitter @SciSays and like us on facebook.


 We thank Dr. Kenneth J. Mukamal (clinical investigator of cardiovascular health, epidemiology, and alcohol consumption at Harvard Medical School Teaching Hospital and Beth Israel Deaconess Medical Center) for helpful comments.


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