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:

baby

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, Caryn Johansen, and Jordan Snyder 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.

References:

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. https://doi.org/10.1177/0898264316661390

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. https://doi.org/10.1097/GME.0000000000000795

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. https://doi.org/10.1016/j.mrrev.2015.08.001

Harley, C. B., Futcher, A. B., & Greider, C. W. (1990). Telomeres shorten during ageing of human fibroblasts. Nature, 345(6274), 458–460. https://doi.org/10.1038/345458a0

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. https://doi.org/10.1111/ggi.12772

Introducing: Science Says!

The former SPCG is now “Science Says”!! According to news headlines, science says a lot of things, but what do we really learn from scientific studies, and how do these findings impact our daily lives?

Wading through science-related news can be difficult, but science isn’t an elite league of geniuses or a collection of hard facts. Science is a process of gathering evidence from carefully controlled tests to gain understanding of the natural world. Our goal is to empower everyone to investigate how scientific findings impact their daily lives. We’re cultivating a community of science communicators to demystify the scientific process and challenge misconceptions. So what does science really say?

Science Distilled: March Preview

This past Wednesday, March 15 we heard from Dr. Lauren Camp of UC Davis Entomology & Nematology and Hung Doan of UC Davis Plant Pathology. They both spoke about parasite diversity, the many different hosts parasites attack, and the way parasites can hide. Here’s a quick interview for you to meet the people behind the science!

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What inspired you to study science?

Hung: Curiosity. As a child I was always curious about how things work. At first I wanted to study medicine, but it turned out I was afraid of blood, and didn’t like harming rats for research. Plants don’t get hurt so I realized I could enjoy research on plants.

Lauren: When I was a kid I realized it was something that I liked. It was also something that I was good at. I would look at my hair, fingers, and toys under a microscope. And my dad is a scientist. While it wasn’t a path he pushed me toward, my siblings and I would go to the lab with him during the summers. I started with an interest in human research and medicine, then realized I didn’t quite fit in with the premed crowd. I took an invertebrate biology class and was so excited by it. You look at animals and think they are all just fuzzy things with spines- but there is so much interesting variation in animals beyond that. And then I started to study parasites and I was done. They were so fascinating evolutionarily, in terms of what they can do and how common they are.

Do you have any affection for your study organism?

Lauren: It’s hard to have affection for something that is harming people and animals, and plants that we depend on for food. My study organism is a parasite that does relatively little to hurt raccoons, but can get into the brains of humans. I do find them fascinating though. A parasitologist once told me, saying you like parasites is kind of inappropriate, because they are harming people all over the world. I do experience excitement when talking to other people about it.

Hung: The pathogens I study just harm plants. Whether I see it in the field or in the lab, I get excited when I recognize the diseases. During my masters’ degree I worked with a plant disease called Fusarium, which lives in the soil indefinitely. When a farmer tells you they spotted it in the field, it’s exciting. Because you can then breed resistance to the disease, and the crops can overcome the disease. I definitely have pictures of Fusarium around- it’s kind of my research baby.

When someone approaches you as a scientific expert, how do you react?

Hung: When you speak with people who don’t have training in science, so many things can surprise them. Just the idea that plants can get disease can be surprising. I grew up in San Jose, where there is lots of biotech, but a disconnect in the way people don’t really know where their food comes from. Plenty of people I know studied a little biology in school, but sort of missed the big picture. It’s also good to have an outlet of friends and family where you don’t have to talk about science all the time.

Lauren: My dad has a PhD, and also studies parasites. So I didn’t have to be the scientist of the family- my dad already had that covered. And it often seemed like he knew about everything, how things work in the world. And that can be intimidating to hear! Now that I have my PhD as well, I’m taking that role a little more with my family. My grandfather and my mom have actually attended some of my formal science talks at meetings, and it helps me think about how I communicate my work. I make sure at the meeting that my mom can understand my science presentation, because she’s actually in the room. Among friends, if someone brings up raccoons I might talk about it. But we have lots of other interests in common- and I have non-scientist friends.

What do you like to do while you’re not doing science?

Hung: I have too many hobbies! I’m starting to scale them down. I enjoy mushroom foraging, hiking, fishing, painting. It varies by day, and I’m pretty spontaneous.

Lauren: I’m building my hobbies back up, after I had scaled them down to finish my PhD. I’m feeling motivated to start running again. I play D&D and love that. I’m reading a lot of books and listening to podcasts. Puzzles can be calming. I also really enjoy spending time talking with small groups of friends.

When people approach you as an expert due to your science background, how do you respond?

 Hung: I run a plant diagnostic lab, so this happens often with farmers. I start with a caveat that I don’t always know the answers. I can guess what the disease is, but usually have to get a sample into the lab to confirm it. Often, it’s not even a pathogen problem in plants, it’s some kind of non-biological stress from over-babying the plants. Overwatering and too much salt can look a lot like pathogens to the untrained eye. Sometimes we get plants from the bonsai industry, where a $10k plant comes in sick. 30 years of careful cultivation, and the plant looks sick because the grower has spoiled it! People can get very worried about their plants, and will text and call me for updates. I also have to be careful in how I state my conclusions – based on what I found in the lab, here is what I’m confident to tell you. But you are always free to get a second opinion. 100% certainty is rare in science.

Lauren: There’s a condition called “delusional parasitosis” in which people are convinced they have a parasite, despite all medical evidence. It’s hard to tell someone that they are  wrong about that. When I do outreach talks, sometimes people have strange ideas about parasites. I respond compassionately, but it’s important to be clear about what makes biological sense. Sometimes friends assume that all humans have parasites. We all have lots of bacteria living within us, but they are not parasites. They are “commensal”, meaning that the bacteria have no negative effect on us. Except when something really bad happens to your immune system, then the bacteria can overgrow and start to act like a pathogen,  like a parasite. But you can’t call these bacteria parasites of humans- because the vast majority of the time, they aren’t! We’re not riddled with worms or protozoans. There are parasites that are possible to get in the United States. But with sanitation and water filtration, we avoid most parasite threats. It’s more of a problem in other parts of the world.

Why is science communication important to you?

Hung: The general public needs to be aware that plants do get disease, and where their food comes from. It affects us personally, and affects politics. If people know that some areas are still under active research- then when it’s time to vote, people are more likely to really look into the issues, read about them, and come to a clear understanding. The plant disease clinic is a big outreach effort. We go to the farmers, to grower meetings. People need to know that science is not so complicated. Anyone can grasp a basic understanding of science! And if people realize that, they’ll be more supportive of research.

Lauren: We need people to understand that science isn’t so complicated. There are bits of science, some of the techniques, that are complex and difficult. But any scientist can talk to people about the basic ideas. I like to do outreach with a range of ages, from young kids up to adults. It’s personally fulfilling and lots of fun. I really enjoy how easy it is to gross people out with parasites! It’s funny to push those buttons just a little bit. I also like to break down the stereotypes, like the idea that someone who has a parasite infection is somehow “dirty”. Parasites are super common in the world. About half of ALL organisms are parasites. It’s also important that people realize when to be concerned about parasites. I also like just telling people about nematodes, which I study. Not all of those are parasites, but they are everywhere too.

Interview by Nicole Soltis of Science Says

Photography by Bobby Castagna of Sac Science Distilled

Science Distilled: HIV research recap

February’s Sac Science Distilled at Old Ironsides featured two HIV researchers from UC Davis: Dr. Lauren Hirao and Brenna Kiniry. You can learn a little more about them and their lives as scientists in our preview post here. Talking to Lauren and Brenna, they both have similar views of what it takes to communicate about hot topics like HIV. They find it important to talk to people as equals and understand where they are coming from. Without taking the time to build a background, it can be hard to bridge gaps in knowledge.

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The event kicked off with the scientists sharing some FAQ about their experiences in talking about science. On the whole, the public cares a lot about HIV/AIDS, but sometimes unclear information can lead to inaccurate beliefs. By sharing these preconceptions the speakers ensured the room, full of people from myriad backgrounds, could start the talk on the same page. They also made sure the audience understood the fundamentals of the virus and its global distribution before moving onto sharing research.

Brenna began by teaching the audience about how far treatment and education have come since the virus was first identified in the 1980s. The main concept here is the “cascade of care”. This means that for HIV-positive patients to lead healthy lives, it is essential for them to: be properly diagnosed, receive consultation and care, receive ongoing care, and have continued access to antiretroviral drugs. At any of these stages, patients can lose control of the infection and progress to AIDS. So, effective treatment must take a holistic view of the process; a great anti-HIV drug isn’t going to help much if the people who need it are not getting diagnosed or entering care programs. In fact, Brenna said it is estimated that 1 in 8 HIV-positive people are not aware of their infection. She talked about how important education is in improving that number, and how historical records of infections and mortality show that education really does have a tremendous impact on saving lives from this disease.

We learned about how a perfect cure—one that is safe, effective, and affordable—has not yet been achieved, but that 16 FDA trials are currently underway to test better and better treatments. There was a lot of excitement about how new developments with CRISPR technology could even lead to patients’ own immune cells being modified to help eradicate the virus from their bodies. It’s not going to be showing up in doctor’s offices tomorrow, but it is an exciting possibility.

After Brenna’s segment, the Powerhouse Science Center led us all in an activity to meet our neighbors and see firsthand how quickly an “infection” can travel through a crowd. While we were fortunate enough to have our “infection” be a cup of slightly alkaline water, the exercise still got all the 40-odd participants up, talking, and mixing our cups. Once everyone had figured out who got infected by the original 3 carriers (most people after only 3 exchanges!), Dr. Lauren Hirao took the stage to speak about HIV vaccines.

Lauren did her PhD research on vaccines, specifically ones containing DNA that could be active against HIV, and gave us an overview of the field. Since, “science education is better when it’s anthropomorphized,” she started out with some great cartoons to illustrate the normal immune response to an infection, and how that differs for HIV. She explained a lot of the different challenges, both in biology and in financing, that researchers like her face. Although a prominent HIV researcher claimed in 1984 he believed there would be a vaccine by 1986, Lauren told us about why that has not yet happened and why they have not lost hope.

Research has uncovered more and more complexity over the years, and each new discovery leads to more potential targets. While many of these targets deserve careful study, bringing a vaccine through trials can be prohibitively expensive. Combined with the fact HIV is a rapidly-evolving virus, making a good vaccine becomes quite difficult. It means you must consider the diversity of the target, its evasion from your immune system, and the opportunity your body has to create the right response to the vaccine. Many vaccine trials have taken place over the years, and Lauren told us about some of the more noteworthy ones. While many have had little impact on people’s infection rates in the real world, new ideas are being developed and studied constantly. One class of vaccines that seems to do well across a wide diversity of HIV varieties is broadly neutralizing antibodies. These, as well as other types of vaccines like the DNA ones Lauren studied, are showing promise for the future.

Lauren closed by telling us that there was recently another claim made about the time to an effective HIV vaccine. This time it was Bill Gates suggesting it could be achieved by 2030. While it will still take a tremendous amount of hard work, the discoveries and enthusiasm shared by our speakers made it seem like an important, achievable goal.

Mark your calendars for the next talks on March 15, when we’ll hear from two UCD researchers about the hidden world of parasites in plants and animals- and check out our new location at Streets Pub and Grub!

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About the author:

Eric Walters is a PhD student at the University of California in Davis. For more content from the UC Davis science communcation group “Science Says“, follow us on twitter @SciSays

Meeting #2: Chapters 2 and 3

In chapters 2 and 3 we continue working our way through the food chain from farmer to consumer.  We start by examining the farmer. In these chapters, Patel walks us through different scenarios involving farmers in countries Patel calls the “global south”. We are introduced to the plight of the rural farmer in India, Mexico and Korea as examples of the widespread failure to protect and uplift our growers around the world. Particular emphasis (and criticism) is placed on the trade and economic connections between these countries and the economic powers-that-be like the World Bank.

We began the discussion with farmers, the vice of globalization and government inattentiveness that squeezes them.  While capitalism and the pursuit of profit can send many into poverty traps, Patel notes how governments often share the blame in creating them.  Particularly, when governments manipulate statistics (which the Indian government did and does to, as Utsa Patinik says, abolish the poor when convenient) to give the illusion of prosperity or fails to shield losers in the game of international trade, the government becomes complicit in the plight of its most helpless people. This is a point that Patel drives home repeatedly with examples from all over the globe.

NAFTA proved a particularly good example of a government failing its people in the eyes of Patel. Patel (and perhaps more notably prominent members of the current political climate…ahem, Trump) harshly criticizes NAFTA, saying that it pits “the livelihood of Mexico’s poorest against the most productive and highly subsidized agricultural sectors in the world” (that of its northern neighbor). Because of the heavy corn subsidies in the US, Mexican corn farmers are unable to compete in the now shared market. This is a problem that was exacerbated by Mexico’s decision to devalue the peso soon after NAFTA took effect. The combination tore through Mexican society and sent a surge of Mexicans from a now bankrupt countryside into cities and into the United States.

In this mode of trade agreements, the consumer benefits while the producer suffers as the price of goods fall. Patel argues that this is particularly problematic in agriculture where most of the producers are poorer than their customers. The overall effect of these trade agreements and without any protection of poor, rural farmers against shifting markets, is increased inequality around the world.

In addition to economic perils, Patel addresses the shifting diets of populations in the global south stemming from globalization and trade. In particular, he discussed the effect of Walmart spreading south of the border into Mexico and the bulging waistbands that came with the move. Patel argues that with Walmart came more processed food, which in turn altered the diet of Mexicans for the worse causing a surge in obesity and other health issues, especially for those living near the US border.

Our main take-away from these two chapters is mostly how little we all know about economics and the intricacies within. Every “fix” seems to create new issues with unforeseen consequences (exactly how unforeseen they are is something about which Patel might argue with us). It helps to take a broad view of the roles things like trade has in agriculture. Patel also urges us to recognize that social issues play an important role in economics and trade at the same time that they are shaped by economics.

In the next two chapters we will explore more deeply how international trade in agriculture has shaped cultures around the world and how food was (and is, Patel would argue) used as a tool by those in political power.

Science Distilled: February Preview

Meet the Scientist, February 9 2017

We’d like you to get to know a bit about our Science Distilled speakers before the monthly talks. We’ll post short profiles to give you a glimpse of the personality and background of our featured scientists!

hirao_lauren_024brenna-kiniry-casual-pic_Left: Lauren Hirao, Right: Brenna Kiniry

 

We sat down with our two speakers for February’s Science Distilled: Dr. Lauren Hirao, a postdoctoral scholar in the Medical Microbiology and Immunology department, and Brenna Kiniry, a Ph.D. candidate in Microbiology. Both scientists are working on HIV research at UC Davis.

What inspired you to study science?

Brenna – I grew up on a farm and was given a microscope kit while I was in elementary school.  I would take gum, saliva, water from our llama pond, put them on slides and look at them under the microscope. The first time I saw little creatures under the slide I thought “oh my god!”  I would often talk with my father, a doctor, about science and it instilled in me from a young age just how cool science was.

Lauren – In 6th grade we had a science fair project and I got the highest grade in the class. I thought to myself “I must be kind of good at this!” In middle school I also happened to be the best in my science class, and that kept me going and interested in science. From there the rest is history.

How does audience change the way you communicate your science?

Brenna – Kids are much more open to listening to what you have to say. They get excited about something new immediately. If you can hook them in with something fascinating, you have their attention. Adults come with preconceived notions of how they think the world works. Personal beliefs can even hinder adults’ ability to look at the scientific data, or accept the findings.

Lauren – When I speak with friends who aren’t in biology, I try using the public health approach. I relate the science back to them. The politics of our science can be interesting, behind the scenes of the paper. Which means being skeptical. For example, if a press release is tied to a science conference rather than a published article, take it with a huge grain of salt.

How do you set your science workday off to a good start?

Brenna – Music is a big motivator, though the genre depends on how well my experiments are going! I also like to give myself a list of tasks I’m going to concentrate on that day, and try my best.

Lauren – On our floor we have a European style morning routine. We always start our day with coffee and chatting together.

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How do you spend your time when you’re not busy working in the lab?

Brenna – I try to play an active role in science-based medicine and skepticism. If a friend brings me some new story about a new miracle food, I’ll turn them back to look critically at the data. Besides that, I fill up my time with science communication- and I love to exercise.

Lauren – I’m always searching for the next novel thing. So if it’s not in the lab, it’s outside it. Falconry, flying trapeze, or traveling. The weirder the activity the more likely I’ll do it. I like to take my nephews on fun adventures. We always do something they’ve never done before, but now the bar is set really high! Parasailing, swimming with sharks, just a few examples of trying to broaden their worldview.

Interview by Nicole Soltis and Bobby Castagna of Sac Science Distilled

Bookclub Meeting #1: Introductions

As we went around the table introducing ourselves we noted a major theme arising in our motivation to join the bookclub. We all joined to learn more about the entire food system, and how our college major or thesis work or personal background fits in. We are all students at UC Davis. Some of us are in graduate school, a couple of us are undergraduate students. We are studying things like global disease, animal science, cell biology, biochemistry, plant biology and plant breeding (with a minor in Spanish!). All subjects pertinent to the conversation of food on some level.

Following introductions and after establishing expectations of our discussions of Raj Patel’s Stuffed and Starved, we went to chapter 1: Introduction.

Chapter one lays the framework for the main issue Patel aims to breakdown in the remainder of the book: Why in a world where so many people (entire populations in fact) are overfed to the point of obesity are there people in other areas dying from starvation? Clearly there is a something wrong with the food system causing this discrepancy, right? At the very least something (or most likely, several things) is not working like it should. And how do we fix it?

Patel lays out the situation in terms that will bring you to tears, anger and frustrate you and, for me at least, make you feel tiny and insignificant in solving the apparent myriad of problems in our food system. You cannot read the first chapter without feeling something. Whether or not you agree with his verdicts and accusations against the causes of such food inequality, the first chapter reminds you that feeding people involves an intricate web of many industries, resources and people. But understanding is the first step in forming a solid game plan to solve a problem, even one as complicated and expansive as making sure everyone on Earth can get a nutritious meal.

It’s no coincidence that Patel chooses the coffee grower as his first example of a failing food system. Coffee is one of the most consumed beverages in the world. I was drinking a corporate cup as I read this chapter (gasp). He chooses an evocative example of a food system issue, to which many of us can connect, in order to give us pause in examining how our role as consumer might be contributing to the problem. He wants this to be personal. And it is. We all need nutritious food to survive and lead long, healthy lives. And with scary statistics about farmer suicide rates, correlations between marketing strategies and increasing health concerns, rising undernourished populations in developing countries with climbing obesity percentages in developed nations, it’s difficult to ignore the possibility that the way in which we get our food might be causing harm to those who grow it.

With the stage set, Patel aims to explore and dissect the forces that shape the food system in order to get at the causes behind its major failings and offer potential ways out. He will take us from the farm to the distributor to the processing plant to the market and eventually to our plates.

As a bookclub, we will follow Patel through his logic, criticize his points, discuss our thoughts on his conclusions and report back here.

Next up, chapters 2 and 3…farmer suicides, NAFTA and California. It wouldn’t hurt to brush up on your knowledge of economics…

 

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.

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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.

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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.

Acknowledgements

 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.

References

KJ Mukamal, EB Rimm. Alcohol’s effects on the risk for coronary heart disease. Alcohol Res Health 25, 255-61 (2001).

Charles W. Bamforth. Nutritional aspects of beer–a review. Nutrition Research 22, 227–237 (2002).

Michael Roerecke, Jürgen Rehm. The cardioprotective association of average alcohol consumption and ischaemic heart disease: a systematic review and meta-analysis. Addiction 107, 1246–1260 (2012).

Sara Arranz, Gemma Chiva-Blanch, Palmira Valderas-Mart’, Alex Medina-Remón, Rosa M. Lamuela-Raventós, Ramón Estruch. Wine Beer, Alcohol and Polyphenols on Cardiovascular Disease and Cancer. Nutrients 4, 759–781 (2012).

Kaye Middleton Fillmore, Jacqueline M. Golding, Karen L Graves, Steven Kniep, E. Victor Leino, Anders Romelsjo, Carlisle Shoemaker, Catherine R. Ager, Peter Allebeck, Heidi P. Ferrer. Alcohol consumption and mortality. I. Characteristics of drinking groups. Addiction 93, 183–203 (1998).

Risk assessment, explained: Interview with Dr. Travis Bui

-By Brittany Anderton

In a few weeks, Donald Trump will be inaugurated as the 45th president of the United States. Although science wasn’t featured prominently in the lead-up to the election, science inevitably influences our daily lives, in part by informing policy decisions.

Last October, Science magazine published six “science lessons” for the next president, agnostic to exactly who that person would be. Of the issues, including brain health, gene editing, and artificial intelligence, the topic that caught my attention most was risk assessment.

It is probably not surprising that this topic most interested me. As a Chancellor’s Fellow at the University of California, Davis, I am applying my PhD training in basic biology to a new discipline: the teaching and communication of biotechnology. Despite rigorous, federally-regulated testing and a scientific consensus based on two decades of evidence indicating that genetically engineered (GE) foods pose no greater risk to human health or the environment than conventionally grown foods, a sizable proportion of the public still thinks that GE foods are worse for health than non-GE foods. GE foods remain a contentious subject for which it is clear that scientists and many members of the public evaluate risk differently.

Recent evidence suggests that individuals’ aversion to GE foods stems in part from a gut instinct that flags them as unnatural, and therefore dangerous. However, as stated in the Science article, “[people] aren’t so great at assessing risk” and “gut instinct can lead to poor policy,” especially when we let our instincts deny the use of technologies that could be beneficial.

Relying on gut instinct alone can lead us to overestimate some risks (such as flying) and underestimate others (such as driving). Scientific risk assessment, on the other hand, uses complex statistical models to make evidence-based determinations of risk. Unfortunately, it is usually performed in ivory towers or behind closed doors, which doesn’t aid public understanding of how it works.

I thought it would be helpful to have an expert explain how scientists approach and calculate risk, since this type of evaluation commonly informs policy. Luckily, I have a friend, Dr. Travis Bui, who does risk analysis for a living. I got his take on the subject by conducting an informal interview. Some of Travis’s responses have been edited for brevity.

Before we start, a requisite disclaimer so that Travis can keep his day job 🙂 – 

The views and opinions expressed in this interview are those of the interviewee and do not necessarily reflect the official policy or position of any current of former employer.

BA: Hi Travis! You have a PhD in Environmental and Occupational Health from the University of Pittsburgh. What did you study in grad school?

TB: Hi Brittany! My research primarily focused on assessing human health risks from exposure to mycotoxins – toxic substances produced by fungi, which contaminate food around the world. One of the more interesting and complicated projects was assessing climate change impacts on mycotoxin risks in US maize. We found that the mycotoxins that are currently found in the US will decrease, but the levels of aflatoxin and fumonisin will increase. This could prove to cause serious concern for corn growers as aflatoxin is one of the most potent liver carcinogens. My other work focused on assessing the impacts of mycotoxin regulations on human health. The “take home message” from this research was that regulations are often put in place to protect human health, but the positive impact of a regulation in one country could negatively impact another. For example, farmers in less developed regions who attempt to export crops to countries with strict regulatory guidelines will often be forced to export only their highest quality crops while consuming the low quality foods.

BA: What types of risk do you evaluate in your current job?

TB: Currently I am working in the agriculture industry assessing aggregate human health risks to pesticides and genetically modified (GM) foods [Note: the terms genetically engineered (GE) and genetically modified (GM) are used interchangeably throughout this post]. Aggregate risk means that I look at exposure from ALL sources. This includes exposure from food, drinking water, residential exposure, as well as to professional applicators. I take into account all routes of exposure including dermal, inhalation, oral and dietary. The risks are assessed based on a variety of age groups and even gender! The overall process is very in-depth and time consuming. The largest effort goes into the collection of data. Without accurate data, the risk assessments won’t be accurate and the risk could be over- or under-estimated.

BA: How would you describe the scientific approach to risk assessment? Think of telling it to your grandma or great-uncle, for example.

TB: The most important thing to remember in risk assessment is that risk is a function of hazard and exposure. Even the most hazardous substance poses no risk if you are never exposed to it and something you are exposed to daily isn’t a risk if there is little or no hazard. We’d all agree that a hurricane is very dangerous (hazardous), but if you are living in Iowa, you don’t have any exposure and, therefore, have little to no risk from it. Without hazard AND exposure, there is no risk.

The scientific approach to risk assessment seeks to incorporate real world (or as close to real world as possible) data for both hazard and exposure. For example, to determine how hazardous a chemical is, a scientist might look in the literature, compare it to a similar chemical, or conduct a study. Exposure may be estimated from a survey, a database, or another study. From here, the data is combined in various statistical and mathematical models to predict risk. These models range in complexity and vary based on the data you have. Assuming you have GOOD data, the more model inputs you have, the more complex the assessment, but the benefit is an increase in accuracy of the assessment. It’s a very dynamic process and there isn’t a “one-size-fits-all” approach to this science, but the approach is similar in all instances.

BA: Whew! Sounds complicated! So the take-home message is that risk is a function of hazard AND exposure. Can you tell us how the results of risk analyses are interpreted?

TB: Often times, risk assessments may be conducted using a tiered approach. This means that the first pass of a risk assessment could be very simple with limited inputs, but the model is HIGHLY conservative. If the risk is over-estimated and still is acceptable [ie, wouldn’t likely harm most people], your work is done! If the assessment isn’t acceptable [ie, you get inconclusive results], more data may need to be collected and analyzed in order to more accurately predict the risk.

Determining the acceptable level of risk is a whole other issue and varies based on the topic you are working with. In some cases, there is no benefit that will outweigh the risk, but there are many instances when some risk is acceptable because the benefit is worth it. For example, the pharmaceutical industry balances this constantly as you’ll see in commercials all the time – benefits of the drug vs. the side effects.

BA: To summarize, it sounds like the process of risk evaluation is iterative and relies on the best available data. Let’s switch gears to public perception of risk. Can you name a common misperception regarding risk you have encountered outside of work?

TB: Public misperception of risk is increasingly more common and there are a number of examples that I see on almost a daily basis. One very important thing to keep in mind with regard to risk misperception is social media. Social media is a very powerful tool and is probably one of the biggest culprits in spreading risk misperception. I cannot stress this enough because many of the examples I come across occur on Facebook or Twitter when people begin re-posting information from a celebrity or someone with little or no scientific background on the topic.

With that being said, some of the most common encounters I have with risk misperception are the idea that “organic” food is safer than conventionally grown and/or GM-food. There are many other examples like the anti-vaccine movement, but working in agriculture over the past few years, I have become very familiar with the “organic” movement. Fortunately, this has allowed me to spend a great deal of time reviewing literature on both sides of the argument.

BA: How do you typically address misperception of risk regarding GM (or GE) food?

TB: When someone tells me they prefer GMO-free, I always start by asking “why”. The majority of the time, the response I get is that “because it is safer” and the conversation abruptly ends. In the few instances that the conversation progresses beyond that interaction, I often find that someone read something on the internet or a celebrity tweeted something indicating that organic made them feel better or GM products made them “sick”. Ultimately, it is their choice to spend the money, time and effort to eat organic, but I still encourage them to research the topic and understand their decision. The most important thing that I push for as a risk assessor is an educated decision! On the flip side, as a risk assessor, we need to continue to push for better risk communication and have a louder voice. Even a basic understanding of risk-benefits would allow consumers to make more educated decisions.

It’s important to think back to the risk paradigm – hazard and exposure. Obviously exposure is high since GM proteins are in much of what we eat, but what about the hazard? Fortunately, this topic has been widely studied and thousands of scientific, peer-reviewed literature points out that the toxicity of GM-foods is no more than conventionally produced foods. Ultimately, this means the toxicity component of the risk paradigm is minimal; therefore risk is minimal. The benefits of GM technology far outweigh any possible risks and the peer-reviewed, scientific evidence behind this is increasingly apparent.

This argument is much more complex than a short paragraph, but it is important to think about risk as a function of hazard and exposure. As a risk assessor, I hope to encourage people who feel strongly one way or the other to do some research beyond what you read online or see on TV. Consider the source of information, think critically and don’t be afraid to ask questions!

BA: I agree that empowering people to critically evaluate the sources of their information is an important step towards addressing risk misperceptions. Okay, last question. Is there a risk-related topic that you think the public should be more aware of? Why?

TB: Many of the risk-related issues the public will face over the next few years are known, but the data needed to properly assess the risk is still being determined. Emerging infectious diseases are always something the public needs to be aware of and the landscape is constantly evolving. A few years ago we dealt with the Ebola virus outbreak and now we are dealing with viruses like Zika and chikungunya. With Ebola, many people survived the virus, which historically had a case fatality rate of nearly 50%. What will the long-term impacts be to survivors? Do they pose future risk as carriers of the virus?

Zika is another major concern that the public is aware of, but the actual risk is still undetermined. With the lack of data on both hazard and exposure, this is a topic that requires close monitoring. Obviously, we know the short-term impacts of the Zika virus, but what will the long-term effects be?

A huge thank-you to Dr. Travis Bui for taking the time to participate in this interview. If you’d like to follow up on any of the topics discussed here, please email Brittany at bnanderton@ucdavis.edu

Science Distilled: Geological Adventures Recap

On Wednesday, November 16, Sac Science Distilled hosted another pair of engaging public science talks at Old Ironsides. November’s themes were adventure and geology, as professors Dr. Steven Skinner and Dr. Amy Wagner (both of Sac State’s geology department) regaled a packed house with tales of swashbuckling, deep sea diving, and the science behind it all.
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Steven Skinner studies paleomagnetism, which is the long-time history of Earth’s magnetic field. This may sound odd, since we think of Earth’s magentic field as constant – it’s the reason magnetic compasses work. But through studying the magnetic properties of certain volcanic rocks, and rocks in sea floor spreading zones, geologists have determined that the Earth’s magnetic field has actually flipped direction many times over the course of the planet’s history. This knowledge enables researchers to figure out how land masses have moved through history, by measuring signatures of the magnetic field that were left in rocks at the time they were formed.
If that wasn’t cool enough, Steven’s research calls him to one of the most extreme environments on earth: Antarctica. In between slides depicting magnetic fields and moving tectonic plates, Steven showed pictures and video of ice-breaking ships pounding through heavy seas, snow-covered landscapes, and steep Antarctic cliff faces. It was clear from his animated demeanor that Steven loves every part of his job, from the lab to the field and back again.
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After a short demo from the Powerhouse Science Center on retracing geological history by looking at patterns in rock, we heard from Amy Wagner, whose research focuses on the ocean as it relates to climate. A key piece in understanding what’s happening to our climate right now, and how human activity impacts it, is understanding how it worked in the past. As Amy very eloquently explained, the atmosphere can have a big impact on ocean circulation via changing temperature and salinity, and ocean circulation in turn has a major effect on the atmosphere – it’s why, for instance, the UK has a temperate climate while being north of the Canadian border in latitude.
Amy’s research also takes her on fantastic adventures. To get a sense of the history of ocean circulation, Amy studies the growth behavior of deep-sea corals. These aren’t exactly the brightly colored corals that you can snorkel to off the coast of Australia – rather, they are typically much more plain-looking, smaller, and extremely slow growing. Their slow growth is the key that lets Amy see signatures of the conditions they were growing in for decades into the past.
The most impressive expedition Amy described was diving a kilometer and a half below the sea surface inside the Alvin submersible – the same vessel which discovered the wreckage of the Titanic! In addition to the fascinating technical details of the vessel and its scientific equipment, Amy showcased the human side of diving in Alvin. As with many long-standing human endeavors, diving in Alvin has its traditions – including being doused with buckets of icy water after your first dive. It was clear from the buoyancy of Amy’s account that any hypothermia has been long forgotten.
To look at the crowd, you might think you were at a standup comedy show – cheerful, attentive faces, and full glasses all around. Mark your calendars for the next talks on January 18, when we’ll hear from a pair of UCD chemists about how chemicals can be seen as tinker toys to build useful  compounds- but be sure to get there early if you want a seat!

About the Author

Jordan Snyder is a PhD student at the University of California in Davis. For more content from the UC Davis science communcation group “Science Says“, follow us on twitter @SciSays