Moving science communication into the public sphere–how?

Mike and David Dobbs both have great posts up discussing “whither rewards for scientists who communicate to the public?” This ended up being one of the themes of my recent SciencePub talk in Columbus–what are the incentives–and disincentives–to scientists for bringing their work to the public at large, rather than simply publishing in journals?
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Twittering in the classroom

Readers may be interested in participating in this, from Dave Wessner at Davidson College:

Building on a project I piloted last fall, I will explore the potential role of Twitter more intentionally this fall in a course I teach on HIV/AIDS at Davidson College. I invite you to join me in this exploration.

Here are a few details:
Basically, I am interested in extending the class conversation outside the classroom walls and beyond the appointed class hours. I want the students to begin thinking on their own about what aspects of the subject (HIV/AIDS, in this case) truly interest them. I want to move away from the professor as purveyor of all information model. I want students to improve their ability to critically analyze information from disparate sources.

With Twitter, students can gather information from a wide variety of sources, some very reliable, some less reliable. They also can post information/questions/thoughts and get feedback from a wide variety of sources – again, some reliable and some not. Finally, Twitter provides a platform that they can easily access in their dorm room, the student union, or the local coffee shop (at any time of the day or night). And accessing Twitter, I hope, will not seem as overtly class-related to the students as accessing, for instance, course material via Blackboard.

This fall, I am requiring the students in my seminar to have a Twitter account. Students will post items on a regular basis, using the hashtag #BIO361. We also will devote some time on a regular basis to discussing items or responses from Twitter. Our first post probably will be on the first day of classes – Tuesday, August 24, 2010.

For this project to work most effectively, we need a critical mass of people outside of our class to participate. If you, your students, friends, or colleagues would like to join us, please do. We will appreciate any new comments, retweets, or responses. I’m looking forward to an engaging discussion throughout the semester.

This is up and running now, so keep an eye on #BIO361 and @dawessner.

Getting the whole story- attempting to make sense of disease through evolutionary medicine

Student guest post by Anne Dressler

The idea of evolutionary medicine is new to me and my understanding is quite shallow but it has piqued my interest. Currently, the book “Why We Get Sick” by Randolph M. Nesse and George C. Williams has been satisfying my curiosity during the 15 minutes of intellectual thought I have left at the end of the day while reading before bed. From what I’ve read, I’m finding how useful it can be to consider disease in light of evolution and I’m left wondering how I haven’t heard of it before. I’m guessing I’m not the only one interested, so let’s talk evolutionary medicine, starting with some of the basics and finishing with why I find this particularly interesting for the nexus between infectious and chronic disease.

If basic biology and traditional medicine make up the plot of our disease “stories”, evolutionary medicine would be somewhat like the moral. My roommate is a medical student and when asked, she can tell you how just about anything in the human body works and what is happening when things go wrong. When asked why things go wrong, her answer will refer to a proximate cause, such as certain foods leading to plaque build up which can lead to heart disease. If the question of why is rephrased, as in why does the disease even exist at all, then she’s stumped. This is the question considered by evolutionary medicine. Why aren’t our bodies able to repair clogged arteries? Why are we prone to infections? Why are our bodies so good at some things but so inept at others? At first I found theses questions strange- after studying epidemiology’s risk factors for the past year, I had started viewing them as the sole reason for the existence of disease. And that kind of makes sense…if you completely ignore evolution. Enter famous and ubiquitous Dobzhansky quote:

“Nothing in biology makes sense except in the light of evolution.”
-Theodosius Dobzhansky

It is through the perspective of evolution that one can consider why a disease exists beyond the obvious.

In their book, Nesse and Williams propose six categories for evolutionary explanations of disease: infection, novel environments, genes, design compromises, evolutionary legacies, and defenses. The basis for all these explanations is evolution through natural selection thus I think it is wise to keep in mind some key points. First, natural selection occurs when survival and reproduction are affected by genetic variation among individuals. Genes are only passed on by the organisms that survive to reproduce. Note, surviving to reproduce doesn’t necessarily have anything to do with health or survival later in life nor does it necessarily mean good health before reproduction either.

“If tendencies to anxiety, heart failure, nearsightedness, gout, and cancer are somehow associated with increased reproductive success, they will be selected for and we will suffer even as we ‘succeed,’ in the purely evolutionary sense.”
-Randolph M. Nesse and George C. Williams, Why We Get Sick

Also, think Richard Dawkins and “selfish genes”- selection doesn’t consider populations, but rather benefits genes. With this in mind, let’s go over one of the proposed categories for explaining disease- infection (even if it is just skimming the surface).

Infectious agents have long been a cause of human disease. As we have evolved means to avoid infection, pathogens have evolved means to counter us leaving us prone to infection. Due to their relatively rapid reproduction, pathogens can evolve much more quickly than we can. One way we attempt to make up for this deficiency is by using antibiotics. Interestingly, by using antibiotics we are essentially taking advantage of the evolutionary advantages of another organisms. Toxins produced by fungi and bacteria are a result of millions of years of selection to combat pathogens and competitors. Dangerously, many believed that with antibiotics we would finally be in control of infections. Unfortunately, that was an underestimation of evolutionary forces and while almost all staphylococcal strains were susceptible to penicillin in 1941, today nearly all are resistant. This pattern is standard for most newly introduced antibiotics

The concept seems simple enough, but it’s not the only thing we’ve misunderstood about the evolution of pathogens. A common misperception is that a pathogen will evolve from being virulent to being more and more benign in order for the host to live long enough for the pathogen to pass on offspring to new hosts. This makes sense, yet doesn’t fully take into account the need to pass on offspring. Being able to disperse offspring to new hosts may mean it is most beneficial to the pathogen for the host to be sneezing, coughing, or laying prostrate. Another force behind pathogens evolving increased virulence is within-host selection. Simply, if there is more than one strain of a pathogen within a host, the one that uses the host’s resources most effectively will be the one to disperse the most offspring.

So if infections are one evolutionary explanation for disease, what’s an example? I recently came across an interesting article about infection and it’s relation to premenstrual syndrome. In the article Premenstrual Syndrome: an evolutionary perspective on its causes and treatment, Doyle et al. propose premenstrual syndrome is due to an exacerbation of a set of infectious diseases during cyclic changes of immunosuppression by estrogen and progesterone. While genetics and non-infectious environmental influences have been examined and found largely unable to explain PMS, infectious causes have been overlooked. However, it is know how immune function varies throughout the menstrual cycle in such a way that there could be less effective control of fungi, viruses, and intracellular bacteria, so making the leap to a persistent infection contributing to PMS doesn’t seem too difficult. Supporting this hypothesis is a long list of chronic diseases with suspected infectious causes that are exacerbated premenstrually including Crohn’s disease with Mycobacterium avium and juvenile onset OCD with Streptococcus pyogenes.

I think the most important point to take from this article is that there may be many other chronic diseases we don’t yet fully understand that are caused by infectious agents.

Yet even while the who, what, when, and where of some diseases may already be understood, the why of a disease is usually ignored. With an evolutionary perspective, we can try to answer the question of why diseases arise and persist under the forces of selection. These insights could help answer some old questions, such as those regarding unknown causes of chronic diseases, and ask some new ones, such as how could PMS be treated if it’s cause really is infectious. Finally, while guiding health care practices to improve health is the ultimate goal, at the very least evolutionary medicine reminds us to keep thinking about things in new ways.


Doyle, C., H. A. Ewald, and P. W. Ewald. “Premenstrual Syndrome: An Evolutionary Perspective on its Causes and Treatment.” Perspectives in biology and medicine 50.2 (2007): 181-202.

Gammelgaard, A. “Evolutionary Biology and the Concept of Disease.” Medicine, health care, and philosophy 3.2 (2000): 109-16.

Nesse, Randolph M., and George C. Williams. Why we Get Sick. New York: Vintage Books, 1994.

Nesse, R. M. “How is Darwinian Medicine Useful?” The Western journal of medicine 174.5 (2001): 358-60.

Stearns, S. C., and D. Ebert. “Evolution in Health and Disease: Work in Progress.” The Quarterly review of biology 76.4 (2001): 417-32.

Williams, G. C., and R. M. Nesse. “The Dawn of Darwinian Medicine.” The Quarterly review of biology 66.1 (1991): 1-22.

Student guest posts: infectious causes of chronic disease

It’s that time again. I teach a class in even years on infectious causes of chronic disease, looking at the role various infections play in cancer, autoimmune disease, mental illness, and other chronic conditions. When I last taught the course in 2008, the students were assigned two writing assignments–to be posted here on the blog. Since this turned out pretty well last time, I decided to repeat the assignment this year; so over the next week or so, I will be putting up guest posts authored by students on various topics under the broad umbrella of infection and chronic disease.

Constructive comments on their posts are appreciated, but keep in mind that they’re students doing this as an assignment and still learning. Finally, these posts are the students’ own; I’m formatting them for publication here, but beyond that their words (and opinions!) are their own.

Post listing:

What is the hygiene hypothesis?

What might have caused my cousin’s nasopharyngeal carcinoma

Post-polio syndrome week: no presidential proclamation required

Cytomegalovirus and heart disease

A look into obesity and gut flora

A rule worth keeping?

Autism and the link to infectious disease

Getting the whole story–attempting to make sense of disease through evolutionary medicine

Parvovirus and Rheumatoid Arthritis–how are they related?

Reviewing the big P…Prions!

Enteroviruses and Type I Diabetes Mellitus

The role of beta-HPVs in skin cancer development

C-sections, allergies, and probiotics

HIV/AIDS prevention; time for change

Misc. links

Back to the grind this week unfortunately, but the swine flu/H1N1 story is still developing and still fascinating. The most recent numbers show 286 confirmed US cases in 36 states.

There are many remaining questions on the evolution and epidemiology of this strain–and many pundits sure they know what’s going to happen next. Mike takes one of them downWendy Orent, who I’ve blogged about previously. Orent is claiming (based on a black/white version of the evolution of virulence in pathogens) that the spread of this strain is attenuating the virus, and that future outbreaks will be milder. Mike nicely explains why that may, or may not, happen–and why it’s folly to predict with certainty either scenario at this point.

Unrelated to influenza, an editor at the Guardian is angry at anti-vaxers, after his young daughter (11 months old, too young for the MMR vaccine) has developed measles:

According to the Health ­Protection Agency there were 1,348 cases of ­measles last year, compared with 56 in 1998. In 2006 a 14-year-old boy died of ­measles – the first fatal case for 14 years. The reduction in herd immunity is ­causing unnecessary suffering.

The decision by many of my neighbours not to vaccinate their children is on a par with the drunk who decides to get into his car to drive home. It is a personally reckless action that also endangers the lives of everyone else on the road. Society should view the MMR refuseniks with the same degree of scorn.

Finally, the winners of the 2009 Alliance for Science Essay contest have been announced (H/T Panda’s Thumb and Evil Monkey).

Help Isis help undergrads

Dr. Isis has a sweet announcement today. In conjunction with the American Physiological Society, she’s funding an award for undergraduate researchers. She’s donating her monthly Scienceblogs payment to the cause, and APS is providing matching funds, up to $500. Help her out by clicking over to check out her blog; her post describing the award is here for more information.

Anti-evolution bill in Iowa

I am so incredibly tardy with this information that Arizonian John Lynch and the lovely folks at Uncommon Descent have already blogged this, but recently an “academic freedom” bill was introduced in Iowa. For those who may be unfamiliar, in addition to “teach the controversy,” these “academic freedom” bills are one of the new tactics for creationists who want to introduce creationism into science classrooms via the back door by claiming that teachers need the protection to teach “the full range of scientific views” when it comes to evolution (in other words, to teach creationism/ID). The bill states that:
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The science fair: what’s a parent to do (or not to do?)

This started out in the comments to Janet’s conundrum about what to do regarding her child’s upcoming science fair:

I’m very committed to the idea that a science fair project is the kind of thing a kid should control, from start to finish — conceiving the project, formulating some clear questions and some promising strategies for answering them, doing the experiments and making the observations, adjusting the strategies as necessary, setting up more experiments, looking at the results, figuring out what they might mean, flagging the questions that remain unanswered, and then figuring out how to communicate it all to kids (and teachers) who weren’t right there with you doing all the research.

If a parent does this stuff (or acts as PI to the kid’s lab tech), I think the parent may learn a lot, but the kid will not get the same experience.

Having attended many science fairs over the past few years (from elementary to high school level), I absolutely agree. It’s all too obvious when the parent has carried out the project, and the kid has taken a backseat (or in the worst cases, just ends up being a spokesperson for the parents’ project.) My experience with my own child below…
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Field work 101…a crash course for my summer students

As I’ve mentioned, this has been a busy year. In the span of 3 months, 3 small grants were funded; enough to keep me busy for the next year. Though my training prior to arriving here was almost exclusively in bench microbiology (mostly molecular microbiology/molecular epidemiology), I knew when I took my current job that I wanted to expand that and go beyond just examining whatever samples someone else had on hand, and set up my own studies. Being Iowa, a big focus of our work is rural health and agriculture, so this has taken me out to cattle and pig farms–previously with a technician who worked for me, and a large animal veterinarian who we work with. This summer so far it’s been just me, my grad student, and our summer interns (including some who’d never been on a farm before)–pictures included after the jump.
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