Can we “catch” breast cancer?

Third of five student guest posts by Dana Lowry

In 1911, Peyton Rous first discovered viruses can cause cancer.  A chicken with a lump in her breast had been brought to Rous by a farmer.  Rous prepared an extract that eliminated bacteria and tumor cells and injected this extract into other chickens—tumors grew.  Rous suggested “a minute parasitic organism” was causing the tumor growth, which is now known to be a virus.  However, Rous’ discovery remained very controversial, and it wasn’t until 1966 that he was awarded a Nobel Prize for his discovery.  Since Rous’s discovery, researchers have found an estimated 15 percent of all cancers worldwide are associated with viruses.  Some common virus and cancer associations are: human papilloma virus (HPV) and cervical cancer, hepatitis B and liver cancer and human T lymphotropic virus type 1 (HTLV-1) and T-cell leukemia.

Epstein-Barr virus (EBV), a member of the herpesvirus family, is one of the most common viruses worldwide.  Among 35 to 40 year olds in the U.S., up to 95% have been infected with EBV.  Oftentimes, children infected with EBV have no clinical signs or symptoms; however, 30% to 50% of adolescents and young adults exposed to EBV for the first time will develop infectious mononucleosis, commonly known as mono.  In the U.S., individuals are usually exposed to EBV in adolescence or young adulthood compared to developing countries, where oftentimes individuals are exposed as infants or young children.  EBV usually remains dormant in the body throughout an individual’s lifetime, similar to the varicella-zoster virus, the virus responsible for the chicken pox.  EBV is known to play a role in Burkitt ’s lymphoma (cancer of the immune cells), nasopharyngeal cancer (cancer of the upper throat) and Hodgkin’s lymphoma (cancer of the lymphatic system), but can EBV also play a role in breast cancer?

In 2010, James Lawson and Benjamin Heng reviewed 27 papers concerning EBV and breast cancer associations. EBV infections are universal in high and low risk breast cancer groups, making it unlikely that EBV is the sole contributor to forms of breast cancer [1].  However, the age at which EBV is contracted seems to play a role in the risk of developing breast cancer. Women in Western countries are at higher risk of developing breast cancer and tend to be infected with EBV during adolescence or young adulthood, whereas women from non-Western countries have a lower risk for developing breast cancer and tend be infected during infancy or early childhood.  Hodgkin’s lymphoma shares a similar correlation with higher rates in Western countries [2].  Although there seems to be a relationship between age of EBV infections and risk of breast cancer, potential confounders need to be considered.  Women in developing countries tend to have more children, have children at a younger age and breastfeed their children for longer periods of time.  Breastfeeding, having more children and having children earlier in life all seem to be protective factors against breast cancer.

Beyond epidemiological evidence, lies biological evidence.  Twenty two of the studies Lawson and Heng reviewed were based on polymerase chain reaction (PCR) techniques. Issues have been found with standard PCR procedures, but it is becoming widely accepted that EBV can be identified in breast cancer tissue through specific PCR techniques [1].  EBV genes have been found in breast cancers through polymerase chain reaction (PCR) analyses.  EBV has not only been shown to shed in human breast milk [3], but it has also been shown to stimulate growth of human breast-milk cells [4]. The mechanism by which EBV actually causes cell alterations is not known, but it is thought to be different from the mechanisms used in lymphomas and nasopharyngeal cancer [1].

It is unlikely that we can actually “catch” breast cancer, as EBV doesn’t seem to be the sole cause of breast cancer.  EBV may contribute to breast cancer by altering genes in the breast cells which eventually leads the uncontrolled cell division, known as cancer.  More importantly, it seems the age an individual is infected with EBV may play an even bigger role in the outcome of disease.  An EBV vaccination is in the works that will hopefully prevent infectious mononucleosis and EBV-associated cancers.  However, the vaccination may not prevent the EBV infection itself; it is targeted towards the most abundant protein on the virus and on virus-infected cells.  If the vaccination proves to be successful, it will be interesting to see if a reduction in breast cancer rates will follow, along with the known cancers associated with EBV. Only time will tell.

 

References:

  1. Lawson, J. and Heng, B. (2010). Viruses and Breast Cancer. Cancers 2010, 2(2), 752-772; doi: 10.3390/cancers2020752.

 

  1. Yasui et al. (2001). Breast cancer risk and “delayed” primary Epstein-Barr virus infection. Cancer Epidemiology, Biomarkers & Prevention, 10:9-16. http://cebp.aacrjournals.org/content/ 10/1/9.long.

 

  1. Junker et al. Epstein-Barr virus shedding in breast milk. (1991). The American Journal of the Medical Sciences, 302: 220–223. http://www.ncbi.nlm.nih.gov/pubmed/1656752.

 

  1. Xue et al. (2003). Epstein-Barr virus gene expression in human breast cancer: protagonist or passenger?. British Journal of Cancer, 89:113–119. http://www.nature.com/bjc/journal/ v89/n1/full/6601027a.html

 

 

The impact of HIV on Drug-Resistant Tuberculosis

Second of five student guest posts by Nai-Chung N. Chang

Tuberculosis (TB) is a major disease burden in many areas of the world. As such, it was declared a global public health emergency in 1993 by the World Health Organization (WHO). It is a bacterial disease that is transmitted through the air when an infected individual coughs, sneezes, speaks, or sings. However, not all individuals who contract the disease will display symptoms. This separates the infected into two categories, latent and active. Latent individuals are non-infectious and will not transmit the disease, whereas active individuals are able to transmit the disease.

TB is a significant concern in patients diagnosed with HIV, since individuals diagnosed with HIV and latent forms of TB infection is more likely to develop the disease, then the HIV negative individuals. In addition, in people living with HIV, TB is one of the leading causes of death. (CDC, 2012) The fact that latent forms of the disease are capable of becoming fully active forms given the right stimulus represents a high risk to individuals living in poor conditions, which is widely present in developing nations. It is of even greater concern to individuals who have immune system diseases, such as HIV. Individuals with latent TB infection depend on robust immune system responses to prevent the infection from going into active form. HIV and similar diseases targets and weakens immune systems so that the response to infections becomes weaker, providing increased risk of TB infections and the activation of latent forms.

TB is a major concern not only because of its status as a global epidemic. While there are many forms of prevention and treatment for the disease, such as antibiotics and vaccine, these treatments are not overly effective in combating and controlling the spread of the disease. TB is widespread and has a high chance of becoming resistant to any treatment that it is exposed to, especially antibiotics and other chemotherapeutic drugs such as isoniazid. Several of these strains already exist and each has varying levels of resistance, including Multidrug-Resistant (MDR) and Extensively Drug-Resistant (XDR). MDR is a strain that is resistant to two of the most often used and potent TB drugs, isoniazid and rifampin; whereas XDR is MDR strains that have developed resistance to any fluoroquinolone and at least one of three second-line drugs such as kanamycin or capreomycin. Also, the vaccine that has been developed for preventing TB is not overly protective, and sometimes fails to protect against infection. (CDC, 2012) The vaccine is not designed to prevent the infection of TB; instead, it is aimed towards boosting and speeding up the immune system response to any new infection so that the infected individual remains in latent forms. (Russell, et al., 2010)

The increasing trends in the resistance of TB to various treatments is a serious concern as it have major impacts in controlling the spread of the disease in many regions. This condition worsens with MDR and XDR TB. With regular, normal strains of TB, latent and early infections could be combated and controlled by a successful chemotherapeutic treatment even in patients with immune system diseases. However, with MDR and XDR TB, the strains are able to fully develop in an individual with weakened immune system, as evident in areas where incidence of TB and HIV is high, such as South Africa. (O’Donnell, et al., 2013) For cases with MDR and XDR strains, the weakened immune systems are not potent enough to prevent infections or keep them in latent form. Additionally, the active forms of these strains are resistant to common, and in some cases, advanced treatments.

With the increasing development of drug-resistant TB, the most effective way to combat TB is not only through vaccines and treatments. Instead, strict public health policy is needed to properly maintain control and combat the spread of TB. With a well-structured public health system, we can ensure that the long treatment of TB is complete, since most of the increase in the resistance to treatment often results from issues during treatment. Events such as patient non-compliance to the treatment and inadequate health-care supervision can all result in the development of new strains of the bacteria that have developed resistance to the treatments that was used. (Russell, et al., 2010) Also, a well-structured public health system can maintain better supply and quality of drugs throughout the treatment process, as well as the prevention and detection of possible new drug resistant strains. More importantly, it can maintain better surveillance and ensure patient compliance during the treatment process, which would help in reducing the development of drug resistant strains. The surveillance systems can also target comorbid diseases such as HIV to reduce risk factors for activating latent forms of the disease in patients with HIV and similar diseases.

References:
CDC, 2012. Tuberculosis (TB). [Online]
Available at: http://www.cdc.gov/tb/topic/basics/default.htm
[Accessed 13 2 2013].
O’Donnell, M. R. et al., 2013. Treatment Outcomes for Extensively Drug-Resistant Tuberculosis and HIV Co-infection. Emerging Infectious Disease [Internet], 19(3).
Russell, D. G., Barry 3rd, C. E. & Flynn, J. L., 2010. Tuberculosis: What We Don’t Know Can, and Does, Hurt Us. Science, 328(5980), pp. 852-856.

Treatment of Chronic Otitis Media: Guidelines versus Practice

First of five student guest posts by Kristen Coleman

Every morning as I prepare for class, I go through the same internal dialogue, “to wear or not to wear my hearing aide.” I am forced to do this because when I was a child I, like most American children (about 80% by age 3 as estimated by the American Academy of Family Practitioners, AAFP), suffered from otitis media and my treatment resulted in hearing loss. The treatment I underwent was called tympanostomy with ventilation tube insertion, which has rapidly become the most common reason for general anesthesia in children in the United States. However, the AAFP reports that meta-analysis of studies exploring the effectiveness of this procedure indicate that benefit is only marginal at best. So why is it that our children are being exposed to this potentially quality of life altering procedure, if there is little benefit? In order to explore the reasons, we must delve further into the disease in question.

Previously, it had been commonly thought that chronic otitis media was characterized by a virus-laden sterile effusion behind the ear drum; meaning that bacteria were not thought to be present and thus, antibiotic therapy was not indicated. Now we know that chronic otitis media is most commonly due to infection of the middle ear by Streptococcus pneumoniae, Haemophilus influenza, Moraxella catarrhalis, (all of which are bacteria) or respiratory viruses. The organisms contribute to the buildup of fluid and pus behind the ear drum that is characteristic of this disease. Dr. Kim Stol and collaborators have reported findings that demonstrate that immune inflammatory response, measured through the presence of immune mediators called cytokines, may play a role in the damage to the ear during bacterial infection that commonly results in hearing loss or diminishment. As demonstrated by the research of Dr. Lusk of the University of Iowa, this immune-mediated damage can persist even after surgical intervention if bacteria persist in the middle ear, making medical management of the bacteria through antibiotic therapy even more essential.

Due to this evidence, the AAFP and other leading organizations that publish guidelines for treatment recommend antibiotic therapy as the gold standard of care for children suffering from chronic otitis media. These guidelines indicate rigorous treatment with high doses of antibiotics such as amoxicillin/clavulanate, cephalosporins and macrolides. If these antibiotics do not offer relief, clindamycin and tympanocentesis (removal of fluid from behind the ear drum with a needle) are then warranted. It is only when all of these medical treatments fail that tympanostomy tubes may be an appropriate option. However, it has been reported by researchers at Mount Sinai School of Medicine in New York City that of the 682 children who received tympanostomy tubes as treatment for chronic otitis media in their study in 2002, only 7.5% did so in accordance to the guidelines set forth by these organizations, and that most of these operations occurred before adequate attempts at antibiotic management of the disease could be utilized. In the study performed by Dr. Stol, it was reported that of the 116 participants in the study who were suffering from chronic otitis media, only 6.9% had received a recent antibiotic prescription, despite the fact that 53% of these patients were suffering from a bacterial form of the disease that may have responded favorably to antibiotic therapy.

As for me and my story, I had an initial round of ventilation tubes places in my ear drums when I was 6 years old, along with an adenoidectomy which was thought to help diminish my ear infections. My family was told that my disease was due to a virus and I was not prescribed any antibiotics prior to my surgical procedure. These tubes fell out the next year, and my chronic otitis media still had not resolved. More permanent tubes were placed in my ears at age 8 and these became lodged in my ear drums until college, all the while I suffered from chronic fluid and pain in my ears. When I had the tubes removed at age 19, my ear drums were permanently scarred and I had to undergo a bilateral tympanoplasty in which a surgeon tried to patch the holes in my ear drums, to no avail. All of this resulted in me having to wear a hearing aide in order to hear adequately at the age of 28.

As the report from Mount Sinai Medical School indicates, the discrepancy between practice and guidelines, as well as the overuse of surgical management in lieu of less-invasive medical management cannot be in the best interest of the children suffering from this disease, and steps need to be taken in order to educate physicians and families alike as to the most appropriate steps for treatment of this chronic disease in order to save our children from having stories like mine.

References:

1. Stol, Kim et al. Inflammation in the Middle Ear of Children with Recurrent or Chronic Otitis Media is Associated with Bacterial Load. The Pediatric Infectious Disease Journal. Volume 31, Number 11, pages 1128-1134. November 2012.

2. Lusk, Rodney P. et al. Medical Management of Chronic Suppurative Otitis Media Without Cholesteatoma in Children. Layngoscope: February 1986.

3. Keyhani, et al. Overuse of tympanostomy tubes in New York metropolitan area: evidence from five hospital cohort. Mount Sinai Medical School. BMJ: 2008.

4. American Association of Family Practitioners. www.aafp.org/afp/2007/1201/p1650.html

Student guest posts: infectious causes of chronic disease

It’s that time again. I teach a class every other year on infectious causes of chronic disease, looking at the role various infections play in cancer, autoimmune disease, mental illness, and other chronic conditions. Each year, the students are assigned two writing assignments-–to be posted here on the blog. 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 please 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 theirs.

Second Annual Great Plains Emerging Infectious Diseases Conference

For those of you in the general vicinity, the University of Iowa Department of Epidemiology will be once again sponsoring the Great Plains Emerging Infectious Diseases Conference on April 19-20 in Iowa City. This year’s keynote speaker will be Dr. Peter Daszak, President of the EcoHealth Alliance:

Dr. Peter Daszak, president of EcoHealth Alliance, is a leader in the field of conservation medicine and a respected disease ecologist. EcoHealth Alliance is a global organization dedicated to innovative conservation science linking ecology and the health of humans and wildlife. EcoHealth Alliance’s mission is to provide scientists and educators with support for grassroots conservation efforts in 20 high-biodiversity countries in North America, Asia, Africa, and Latin America.

As Executive Vice President of Health at EcoHealth Alliance, Dr. Daszak directed a program of collaborative research, education, and conservation policy. The program examined the role of wildlife trade in disease introduction; the emergence of novel zoonotic viruses lethal to humans such as Nipah, Hendra, SARS, and Avian Influenza; the role of diseases in the global decline of amphibian populations; and the ecology and impact of West Nile virus in the U.S. Dr. Daszak holds adjunct positions at three U.S. and two U.K. universities and serves on the National Research Council’s committee on the future of veterinary research in the U.S.

Like last year, we will also be having breakout sessions in an “unconference” format–loosely moderated by discussion leaders. If you’re thinking of attending the conference and would like to suggest or lead a session, please leave a comment or drop me a line (tara dash smith at uiowa dot edu). Looking forward to seeing some readers here in April!

Plague in Victorian San Francisco–lessons for public health communication

I have a post up today at the Scientific American Guest blog, discussing how an earthquake and denial led to prairie dog plague. It details an outbreak of plague in Victorian San Francisco–the first time plague hit the United States–and the many downstream consequences of that outbreak (which began in 1900 and wasn’t really contained until 1908). While the story is over at SciAm, here I wanted to talk more about why the outbreak became such a public health disaster.

The outbreak was first recognized by Dr. Joseph Kinyoun, a bacteriologist who had been, until his transfer to San Francisco, heading up the United States Hygienic Lab, the precursor to the National Institutes of Health. Charged with inspecting incoming ships, Kinyoun had the power to quarantine ships and their crew in harbor, in an effort to keep plague out (which was already circulating in port cities of Honolulu, Sydney, and Tokyo, amongst others). When Kinyoun first suspected a case of plague, San Francisco merchants quickly banded together to deny any such pestilence in their city. What followed was a mess of ineffective quarantines, fights over scientific data, accusations of “spiking” corpses with plague samples Kinyoun had brought with him from Washington, D.C., and an eventual call for Kinyoun’s execution.

History shows that Kinyoun was right–San Francisco had plague cases, and the plague would continue to smolder for almost a decade. As I note in the post, it still lingers today in squirrels and rodents from the Pacific Ocean inland to the Great Plains. So what went wrong, if Kinyoun clearly had the facts on his side?

Like many scientific issues today, it wasn’t the facts that ended Kinyoun’s career in San Francisco, but his messaging. Admittedly, he was acting without all the knowledge of plague transmission that we have today–it wasn’t confirmed in 1900 that rat fleas were the main vector of the disease from rodents to person, and so Kinyoun couldn’t have been sure his attempts to quarantine Chinatown would be ineffective. Furthermore, in some cases, he was merely obeying orders from his superiors. His boss, Surgeon General Walter Wyman, had recently published a monograph on plague, endorsing the idea that plague selectively targeted Asians due to their particular diets and their poverty.

Still, the way Kinyoun went about attacking those most affected in the initial outbreak–the Chinese immigrants–only served to terrify them and drive plague cases underground. Indeed, when public health officers went door-to-door searching for plague cases, one anecdote notes that a game of dominoes was set up in a home, and all the men stayed perfectly still with dominoes in their hands while officers searched the home for anyone with plague symptoms. Little did they know that a plague corpse was sitting at the card table, “Weekend at Bernie’s” style (1). Other Chinese fled Chinatown, bunking with friends and relatives elsewhere when possible. Threats were made to burn Chinatown (as had recently happened in Honolulu); Kinyoun tried to bar travel by any “Asiatics” on trains or boats leaving the city, clearly a race-based order. Furthermore, even when cases of plague were identified in Chinatown, the very practice of carrying out autopsies was offensive to the Chinese, giving them even more reason to hide their sick and dead rather than cooperate with Kinyoun and other public health authorities.

Kinyoun left the city in 1901, and eventually Rupert Blue was brought in to control the outbreak. Taking lessons from those who’d been there prior (and were unsuccessful), Blue took a much more diplomatic tack. He secured the assistance of a Chinese translator, Wong Chung, and worked within the Chinese community to gain their support. He often downplayed the outbreak–never suggesting it wasn’t happening or wasn’t important, but trying to differentiate hype from supported fact. He worked to clean up Chinatown, both in its housing and in rat infestations, rather than to quarantine infected areas. He noted that plague could occur in many different races, and avoided scapegoating one particular ethnic class. He also reached out to businessmen to educate them, and show how important cleaning up the city was for their bottom lines. He worked with the facts as Kinyoun did, but he recognized the importance of grassroots support in his campaign, and targeted reasons why various factions should support his various anti-plague measures.

In the end, while Kinyoun was practically run out of town on a rail, Blue was given banquets and numerous accolades. He served as the Surgeon General from 1912-1920, and his methods for cleaning up the city led to a decrease not only in plague, but in many infectious diseases. While Kinyoun’s science was sound, Blue managed to break down barriers and work with those who could help him spread his message, and take ownership of the work that needed to be done. He framed* the threat in terms that meant something to the populations he was working with: businessmen and threat to their incomes; immigrants’ threat to health, with promises to respect their culture and help them make their homes cleaner places to live; city and state government, noting the threat to the very reputation of California and San Francisco in the US and around the world. His tactics served him well in 1902-08, and should serve as a reminder to science communicators today as well.

(*I know that term is somewhat tainted in some circles, but bear with me…)

Further reading and references

Chase, “The Barbary Plague”.

Echenberg, “Plague Ports: The Global Urban Impact of Bubonic Plague, 1894-1901.”

Matt Damon: no poo for you

Readers may be familiar with Matt Damon’s charity work with water.org, an organization he co-founded. Water.org seeks to raise awareness of the lack of clean water by almost a billion people on earth, and lack of toilets by almost 2.5 billion–and more importantly, they work to remedy that situation by providing sustainable, local solutions. His new video brings awareness in a rather unorthodox manner: he’s refusing to go to the bathroom until everyone on earth has access to clean water and toilets.

So God created advertising

I didn’t grow up on a farm, but my dad did. He was the youngest of 13 kids, several of them who grew up to own farms of their own. As a kid, my family had almost an acre in the country, but the only animals we kept on it were stray cats and the occasional opossum (the latter, not on purpose). Still, the school I attended was definitely in a rural, farming community, and I frequently spent time at my Grandma’s farm. She’d downsized since her kids were young and working the farm, but even when I was a kid and she was in her early 80s, she still kept chickens for eggs, cows for milk and meat, and sheep for wool. Some of my favorite childhood memories are of being at her house, gathering eggs, helping my uncle shear sheep, or just playing in the hay loft.

Her farm was small, with a big white barn and a little white house. This is what most people picture when they think of “family farm,” and what the recent “So God Made a Farmer” ad exploits. This makes us feel cozy. We admire the work ethic and values of farmers, as my friend and high school classmate Matt Reese notes, and the ad painted farmers in a very positive light–a stark contrast to the other Superbowl commercials selling their products on sex appeal with half-naked models. I grew up listening to Paul Harvey and “the rest of the story,” and honestly love this speech. It reminds me of home. However, Harvey passed away almost 3 years ago, and his speech was from 1978–I was 2 years old, and farming was much different then than it is now.

Today, while small, family farms of the type romanticized in the Dodge commercial certainly still exist, more and more are becoming industrialized–more land, more animals, and all of the issues that come with those. Contrary to the white men portrayed in the commercial, approximately half of the hired workers on farms today are Hispanic, and are paid roughly $10 per hour for their work. Many of these are undocumented, making it difficult for them to raise their voices when safety or health violations have occurred, or even to receive treatment should they be injured on the farm. Farms employing less than 10 people (the majority of all farms today) are exempt from OSHA inspections, so corners may be cut regarding safety. I won’t go into all the details; others have covered modern-day farming and even made a revised video featuring Latinos. “Funny or Die” also got in on the act, swinging the pendulum about as far from the original Dodge commercial as one could go.

No matter large or small, farming is an important and incredibly difficult job. For many, it is a calling rather than just a job, and some incredible people are out there working to feed all of us. However, changes in farming over the past several decades are killing off the family farms that we (and Dodge) still idealize. As David Hinckley noted, “As it ran, it felt a little like erecting a beautiful statue to a species we are hunting into extinction.” Indeed.

Skeptical science and medical reporting (#Scio13 wrap-up)

Ivan Oransky and I moderated a session last week at ScienceOnline, the yearly conference covering all things at the intersection of science and the internets. We discussed the topic ““How to make sure you’re being appropriately skeptical when covering scientific and medical studies.”

We started out discussing some of the resources we’d put up at the Wiki link. Ivan teaches medical journalism at NYU, and noted that he recommends these criteria when evaluating medical studies. I noted I use similar guidelines, and as a scientist, think about papers in a journal club format before I cover them on the blog, considering their strengths and weaknesses (especially in study design and analysis). Ivan also mentioned the need sometimes to consult a real statistician if you don’t understand some of the analyses–suggesting to “keep a biostatistician in your backpocket” or, failing that, to reach out to those at you local university, as “they tend to be lonely people anyway.” (Just kidding, biostats friends and colleagues!) A number of stats references for journalists were also mentioned (see the Storify for specific links). From here, we handed the discussion over to the audience.

One of the first topics we reviewed was just what is meant by being “appropriately skeptical,” which was a theme of the session that we kept coming back to. How does one do that without being an asshole? The importance of criticizing the study’s limitations and weaknesses–and not necessarily being a jerk to the authors–was noted. No study is going to be perfect, after all. It was also pointed out that anyone reporting on the study should go beyond the press release, and not to do so is in fact “journalistic malpractice.” Bora also started an interesting tangent–are medical studies more likely to be fake (or more deserving of skepticism about results) than more basic science reports? Also, is it worth reporting on bad studies? Sometimes this can help to point out the bad science (like that recent mouse-GMO study, which was reported on–negatively–in many venues). This recent study on “out” versus “closeted” homosexuals in Montreal was also brought up by Annalee Newitz–a small study that was widely reported, but was it designed and powered correctly to examine the questions it supposedly answered? (I haven’t read it, but just looking over the article, looks like “no”.)

Audience members also asked how to find sources to comment on studies. Ivan has previously written a post on this, and others in the audience recommended looking at other references in the story itself, or looking at reviews or meta-analyses on the topic to see who else may have expertise in these particular areas. However, SciCurious also noted that you need to be somewhat skeptical of those as well, and examine if the authors of these reviews or analyses have their own biases that may skew the information being presented.

The idea of “Glamour Mags” was also introduced. How should those reporting on a story know whether the results were published in a “good” journal or not? Several pointed out that just because a study is in a lower impact-factor journal doesn’t necessarily mean it’s not to be trusted. Eli elaborated, noting that fraud is actually higher in the big, fancy journals, and that many studies that end up in lower-tier journals actually go through *more* peer review in some cases, as they have been rejected from higher impact publications.

Unfortunately as I was moderating, I wasn’t taking notes, and I can’t recall what we ended the session on (but it was a great comment and general agreement that it nicely tied things up). I’ve also tried to Storify the session based on the #medskep hashtag, but I’m new to Storify and it doesn’t want to embed for me. If you were there, please feel free to add to the discussion in the comments below.