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

Next level science communication: humanize, normalize, illuminate

Easton White, UC Davis PhD student, population biology

Typically, Science Communication seminars or workshops spend a lot of time convincing participants why science communication is important. I am beyond this point. And, furthermore, I think we as a scientific community are beyond this point. We know the importance of science communication for science literacy, scientific funding, and science policy. Scientists will either get on board or be left behind.

How do we move to the next level? I think small, focused workshops are one potential avenue. Recently, I attended a science communication workshop at the University of California, Davis. The workshop was hosted by two groups: The People’s Science and Science Says. Stephanie Fine Sasse, the Executive Director of The People’s Science, led the event. Stephanie and the workshop organizers executed a great workshop on several dimensions.

First, the workshop was limited to 30 people and the room was small, which made the time more intimate and focused. Second, organizers asked participants to prepare a lay summary of a recent paper prior to the workshop. This facilitated discussions about our summaries during the workshop. Third, the workshop was three hours in length, providing enough time to dive into specific issues. Lastly, Stephanie did a great job of discussing specific tactics scientists can implement moving forward. She illustrated her points through a number of good examples and participant exercises.

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Moving beyond the workshop setup, what did participants actually learn? To begin the workshop, Stephanie presented a brief history of science literacy and science communication. This set the stage for current challenges science communicators face. She argued that now scientists have to reach out to the public and science itself has to be more connected to society. She also pointed to solutions which work to engage the public in science, like citizen science projects. There were three major takeaways I took from Stephanie’s presentation.

1) We (scientists) need to humanize scientific research.

Here, Stephanie stressed the importance of including the scientist, and their story, when communicating science. This builds trust between the science and the public. It is important for people to understand scientists are people too, not just some expert in an ivory tower. Further, telling a scientist’s story creates a more interesting story for the public.

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2) We need to normalize science communication.

A lot of scientists worry about participating in science communication. They fear that colleagues may perceive them in a negative light. It will be important to create a culture within science where science communication is not only typical, but also incentivized. Tangible incentives for science communication would allow researchers more time to communicate their science. For instance, science communication could be part of a broader impacts statement in a grant or during the tenure process.

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3) We need to illuminate the scientific process.

Yes, it is important to explain the latest and coolest scientific findings to the public. However, it is equally important—if not more so—to discuss the scientific process itself. Again, the storytelling of science is important. Describing the process that led to the discovery has at least two benefits. First, describing the process helps people understand how science works. For instance, describing the way a drug is brought into development would hopefully make people feel more at ease about the process. In addition, learning about the process of science enables people to think critically themselves.

What practical, tangible steps can scientists take? First, scientists must carve out time for science communication. As we all know too well, if you do not plan something in your schedule, you will never get to it. Once an individual wants to engage in science communication, there are a number of questions one should ask themselves:

-What audience do you want to reach? This will determine the appropriate medium for communicating science.

-Are there groups that you can collaborate with to communicate your science? A number of universities now have groups focused on science communication, either informally through clubs or through a media communications department.

After answering these questions, the next step would be to develop the material for presentation.

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Moving forward it will be important to offer small and focused workshops. A small group enables a richer dialogue between participants and instructors. Focused workshops are important to get into the nitty gritty details of how to actually engage with science communication. Lastly, a small and focused workshop allows participants to test their ideas on a willing audience. The workshop can serve as a laboratory for experiments with new analogies, active learning exercises, or pieces of writing.

You can find more information here:

8 bee experts weigh in on pollinator decline & Cheerios’ bid to save them

We’ve been hearing a lot about declining bee populations. As scientists, we’re concerned about our pollinator friends. So we interviewed 8 entomologists, bee-keepers, and other pollinator experts to cut through the buzz about bees.

The Gist

Honeybees are okay, but wild pollinators are at risk. The biggest threat is habitat loss, but climate change, insecticides, and diseases also spell trouble. Certain agricultural practices can help, and we can all do our part by planting flowers instead of keeping grassy lawns and encouraging city planners to do the same. If you got one of those wildflower packages from Cheerios, consider ditching those seeds for native ones instead.

To bee or not to bee

We asked the experts whether or not bees are in trouble. The overwhelming response: WHICH bees?

Honey bees are commercially managed by beekeepers and trucked around to pollinate crops from almonds to zucchinis. The “beepocalypse” first gained attention in 2006 when honey bees in the US were dropping like flies, especially during winter months. The varroa destructor, a nasty mite, is likely the main perpetrator along with diseases it spreads. Insecticides and fungicides could also factor in, but it’s unclear how big of a role they actually play in the field.  

But honey bees are not even native to the US, and they’re managed like livestock. So bees died, beekeepers upped their numbers, and now honey bee populations are stable, maybe even increasing. But honey bees aren’t the only bees – far from it – and they aren’t the only insects that pollinate food crops and other plants, which whole ecosystems depend on. What’s worse, when beekeepers cart honeybees across the nation, they carry parasites and pathogens that can spread to wild populations.

Some wild bees ARE at risk, particularly solitary bees, some species of bumble bees, and other non-bee pollinators. The rusty-patch bumble bee is considered an endangered species in the US, and many other species are on the red list in Europe. While there are over 20,000 species of bees in the world and 4,000 in the US alone, we only have population data on a few. More research (and more funding) could identify at-risk pollinators.

People vs Pollinators

Pollinators face many perils, but most experts agree food and habitat loss dominate. For pollinators, food means flowers/plants and habitats mean undisturbed places for nests/hives/colonies/larvae. We actually compete with bees for homes and food. If a prairie is plowed to plant acres upon acres of soybeans, pollinators in that field lose their livelihood. If a forest is cleared for a housing development or a golf course, the flowers wild bees depend on go too. If you weed and mow your own yard, you too are contributing to pollinator decline.

While we could probably live without golf courses and lawns, we do need homes and food. Planning developments, gardens, and farms with pollinators in mind can make a big difference. That means leaving ditches, parks, lots, and lawns in their natural weedy state whenever possible. If the weeds really must be cleared, plant flowers in their place instead of grass– Preferably local flowers that vary in shape and color and flower at different times.

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Screenshot from httpp://

Apiaries in Agriculture

Farmers have an extra challenge. They need to ensure their crops have ample room to grow and don’t get choked out by competing plants, but plowing or spraying stubborn weeds destroys habitats. Pollinator habitats can be managed within and around farms by planting cover crops, practicing crop rotations, or managing less-fertile land as refuges for insects. Technologies that help increase yield per acre may also help prevent more prairies, forests, or wetlands from being converted into farms.

Insecticides that stop hungry bugs from mowing down crops can also mean bad news for pollinators. It’s tough to study the specific role of insecticides, because any given bee might be exposed to multiple compounds at varying levels. These factors interact with other threats like poor nutrition and disease, so it’s nearly impossible to identify a single, direct cause.

The bottom line: anything designed to kill insects — from commercial insecticides to organic alternatives to home remedies — certainly can’t help. On the other hand, banning specific pesticides may not be the best approach. Farmers have to control pests somehow, and alternatives might not prove any friendlier to pollinators or farmworkers.

Scientists are working to develop pest control methods that are more specific, and plants that produce their own defenses, so sprays aren’t necessary. In the meantime, integrative pest management approaches that “balance the good guys against the bad guys” can help protect beneficial insects like bees.

The end all bee all

In short, there are many threats to pollinators, and we don’t really have a good understanding of exactly which bugs are threatened. Such a multifaceted problem calls for a multifaceted solution, and no silver bullet is going to do the trick. But we know that habitat loss is a big concern, and we can all help by remembering pollinators when we make land-management choices. That’s why Cheerios distributed 1.5 billion wildflower seeds for free. The idea is awesome, but experts worry the execution is not.

Trouble is, no pack of wildflower seeds can possibly be native to every region in the United States. While Cheerios did their homework to ensure that none of the seeds spawn from known invasive species, scientists are still concerned. Some of the flowers included are considered noxious weeds and could prove problematic for farmers. These foreign flowers may also compete for pollination with native species, giving the invaders an edge, and potentially harming pollinators with a specific taste for native plants.

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All our experts agreed that planting wildflowers is a great idea, but you should really try to plant flowers native to your home region. The Xerces society can be very helpful in that department, as can the Lady Bird Johnson Wildflower Center and the Missouri Botanical Garden Plant Finder.

That said, General Mills has really done some great things to help pollinators. As have other corporations including Bayer, Haagen-Daz, Monsanto, and more. Their efforts should be applauded.

Want to know more?

-Expert Q & A

-Reader-friendly & expert-recommended sources

Scientific literature backing these claims

A BIG THANK YOU to these great eight bee buffs:



Dalton Ludwick is a doctoral candidate in Plant, Insect and Microbial Sciences at the University of Missouri. His research focuses on the management of western corn rootworm, a serious pest of corn, with Bt proteins.

Rea Manderino is a PhD student at SUNY – College of Environmental Science and Forestry in Syracuse, NY.  Her research has focused on the impact of gypsy moth presence in North America, and this has included examining the far-reaching influences of non-native organisms in our native ecosystems. Rea is also co-moderator of ‘Relax, I’m an Entomologist’ on Facebook.

Val Giddings is a geneticist, an outdoor enthusiast, an amateur beekeeper, and a policy nerd. Like some folks have a wine cellar with varieties from around the world, Val has a honey cellar.

Dr Manu Saunders is an ecologist based at the University of New England, Australia. Her research focuses on beneficial insects that provide ecosystem services in crop systems, particularly pollinators and natural enemies of pest insects. She writes about pollinators, ecology and agriculture at


Jerry Hayes is the Honey Bee Health lead for Monsanto’s newly formed BioDirect business unit.  Before joining Monsanto he was the Chief of the Apiary Section for the Florida Department of Agriculture and Consumer Services. In that role he was responsible for the regulatory health of the 350,000 colonies in the State of Florida, a State highly dependent on Honey Bee pollination for agricultural success.  For the past 30 years Jerry has written a monthly column in the American Bee Journal called The Classroom and a book by the same name.  Jerry is a founding member of the Colony Collapse Working Group, a science advisory board member for Project Apis mellifera (PAm) , the Bee Informed Partnership, and he serves on the Steering Committee of the Honey Bee Health Coalition.  He has been author and co-author on multiple research papers that delve into how to understand and preserve honey bee health. In Jerry’s 35 plus years in the Apiculture Industry his overarching desire has been to create sustainable honey bee management practices while partnering with other segments of agriculture.  The cornerstone of his career has been to educate others that honey bees are the key pollinators and the critical role they play in agriculture; while in parallel encouraging the development of multi dimensional landscapes for the benefit of honey bees and all pollinators.

Rachael E. Bonoan is a Ph.D. Candidate who studies honey bee nutritional ecology in the Starks Lab at Tufts University. She is interested in how seasonal changes in the distribution and abundance of flowers (i.e. honey bee food!) affect honey bee health and behavior. Rachael is also the President of the Boston Area Beekeepers Association and enjoys communicating her research and the importance of pollinator health to scientists, beekeepers, garden clubs, and the general public. More info on bees via Rachael’s website or twitter @RachaelEBee

Kelsey Graham is a pollinator conservation specialist. Her graduate work has focused on invasive species and their impact on native pollinators and plants. She has used an interdisciplinary approach to provide a comprehensive assessment of an invasive species, the European wool-carder bee (Anthidium manicatum), within their invaded ecosystem. She will be defending her PhD in April 2017, and beginning a post-doctoral research position at Michigan State University in Dr. Rufus Isaacs lab, where she will study how landscape features impact the local bee community.

Dr. Maj Rundlöf is an ecologist and environmental scientist at Lund University in Sweden, currently visiting UC Davis as an international career grant fellow to work with bumble bees in Neal Williams lab. Her most recent research focuses on impacts of land use change and pesticides, particularly the disputed neonicotinoids, on bees and the pollination services they provide to crops and wild plants. A large part of her research is in the interface between conservation biology and agricultural production, aiming at exploring how we can support biodiversity while also facilitating food production. She has, for example, studied how farming practices influence plants, butterflies, bumble bees and birds as well as how created habitats influence crop yields and ecosystem services like pollination and biological control by pest’s natural enemies. The bumble bee, one of these pollinating insects, is her favorite study organism.


About the Author: Jenna E Gallegos is a 5th year plant biology PhD student at the University of California, Davis. Science Says is a science communication and outreach group composed of UC Davis graduate students and postdocs.


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.

WTF Wednesday – Why Hate on Coffee?

Coffee seems to be one of those misunderstood foods. One day it’s great for us and the Starbucks sales boom, the next day it’s awful and everyone’s swearing off coffee.


There is some truth to this, so for this week’s WTF Wednesday we’re going to dive into the mixed results from coffee research.

Adults in America drink a whole lot of coffee; it’s the second most consumed beverage (water is #1, hollaaa). Coffee doesn’t just have caffeine, it has hundreds of biologically active compounds and we haven’t even identified all of their functions yet! Due to its popularity, research has been dedicated to exploring the effects of consuming this beverage. Is it good? Is it bad? So far the evidence shows coffee can have a wide range of health effects.

Some potential benefits: 

  • may lower risk of type II diabetes
  • can help with weight loss/management
  • reduce depression
  • brightens up the morning!

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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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