It is very hard, and very weird to try to get a handle on how human health has changed between the 19th century and today. Obviously, the way we live has changed dramatically. But understanding how that impacts health (or doesn't) is complicated by the fact that healthcare, science, and public health research changed dramatically during those years, as well.

And all that science hasn't happened in a vacuum. The names we give various disorders change. Whether or not we consider something to be a disorder, at all, might change. And our cultural understanding changes, too—especially when it comes to mental illness.

At the Mind Hacks blog, Vaughn Bell has an excellent breakdown of two recent studies that try to put the modern diagnosis of post-traumatic stress disorder (PTSD) into a cultural and historical context. Many people assume that PTSD is just a new name for something that has always existed—look at shell shock, which made it onto Downton Abbey last season. But these new papers suggest that the distinction between what soldiers experienced in the past and what they experience today might go deeper than naming conventions.

The diagnosis of PTSD involves having a traumatic experience and then being affected by a month of symptoms of three main groups: intrusive memories, hyper-arousal, and avoidance of reminders or emotional numbing ... there has been a popular belief that PTSD has been experienced throughout history but simply wasn’t properly recognised. Previous labels, it is claimed, like ‘shell shock’ or ‘combat fatigue’, were just early descriptions of the same universal reaction.

But until now, few studies have systematically looked for PTSD or post-trauma reactions in the older historical record. Two recent studies have done exactly this, however, and found no evidence for a historical syndrome equivalent to PTSD.

A study just published in the Journal of Anxiety Disorders looked at the extensive medical records for soldiers in the American Civil War, whose mortality rate was about 50-80 greater than modern soldiers fighting in Iraq and Afghanistan. In other words, there would have been many more having terrifying experiences but despite the higher rates of trauma and mentions of other mental problems, there is virtually no mention of anything like the intrusive thoughts or flashbacks of PTSD.

Read the rest at Mind Hacks

David Dobbs adds some more context to Bell's post at the Neuron Culture blog.

About 20 years ago, the United States and a few other countries started using a different pertussis vaccine than had been used previously. The change was in response to public fear about some very rare neurological disorders that may or may not have had a relationship to that older vaccine (it couldn't ever be proven one way or the other).

The vaccine we use today was created to get around any possible mechanism for those disorders and, along the way, ended up having lower rates of the less-troubling (and far, far more common) sort of side effects, as well. Think short-term redness, swelling, or pain at the site of injection.

The downside, reports Maryn McKenna, is that this new vaccine might not be as effective as the old one. In fact, scientists at the Centers for Disease Control, Kaiser Permanente Medical Center in San Rafael, Calif., and Australia's University of Queensland’s Children’s Medical Research Unit, are raising the possibility that a less effective vaccine could be part of why we're now seeing a big increase in pertussis outbreaks.

In the most recent research, a letter published Tuesday night in JAMA, researchers in Queensland, Australia examined the incidence of whooping cough in children who were born in 1998, the year in which that province began phasing out whole-cell pertussis vaccine (known as there as DTwP) in favor of less-reactive acellular vaccine (known as DTaP). Children who were born in that year and received a complete series of infant pertussis shots (at 2, 4 and 6 months) might have received all-whole cell, all-acellular, or a mix — and because of the excellent record-keeping of the state-based healthcare system, researchers were able to confirm which children received which shots.

The researchers were prompted to investigate because, like the US, Australia is enduring a ferocious pertussis epidemic. When they examined the disease history for 40,694 children whose vaccine history could be verified, they found 267 pertussis cases between 1999 and 2011. They said:

"Children who received a 3-dose DTaP primary course had higher rates of pertussis than those who received a 3-dose DTwP primary course in the preepidemic and outbreak periods. Among those who received mixed courses, rates in the current epidemic were highest for children receiving DTaP as their first dose. This pattern remained when looking at subgroups with 1 or 2 DTwP doses in the first year of life, although it did not reach statistical significance. Children who received a mixed course with DTwP as the initial dose had incidence rates that were between rates for the pure course DTwP and DTaP cohorts."

You can read the rest of the story at Maryn's Superbug blog

A key thing to remember: This is a nuanced theory that may or may not turn out to be right. But, if it does turn out that this vaccine isn't as effective as we want it to be, that's not a dark mark against vaccines, in general. Sometimes, medicine doesn't work as well as intended. It's a risk of medicine. And the fact that it's major research institutions pointing this possibility out, should give people some comfort in the scientific process. If doctors and organizations who promote childhood vaccination are all in the pockets of an evil conspiracy then there would be no reason why they'd ever do research like this, or talk about it publicly.

All this week, The Chicago Tribune is posting a multi-part investigative report about the fire-retardant chemicals that turn up in everything from the foam in our couch cushions, to the plastic casings on our television sets. Turns out, research shows these chemicals don't actually prevent fire deaths and injuries. Worse, research does show that these chemicals are dangerous to human health—especially in the quantities to which we are exposed. Dose makes the poison, but we're not talking about small doses here. As the Tribune so succinctly puts it: This isn't something where we measure exposure in parts per million, it's measured in pounds.

The Tribune has also done a very good job of documenting both the existence and history of a pattern of corporate lies and manipulation that has made sure these chemicals remained a mandated part of our lives even as science shows they aren't helping us.

The lies are infuriating, but the history part is particularly fascinating. After all, it's easy to understand why chemical companies would lie and manipulate politics in order to maintain a lucrative market for their products. But why does that market exist, to begin with? Behind the scenes, our continued exposure to these chemicals comes down to two key issues: One poorly designed product safety test that encouraged heavy use of flame-retardants in foam instead of small doses of safer chemicals in fabric, and a 1970s-era attempt to deflect negative press away from cigarettes.

The problem facing cigarette manufacturers decades ago involved tragic deaths and bad publicity, but it had nothing to do with cancer. It had to do with house fires.

Smoldering cigarettes were sparking fires and killing people. And tobacco executives didn't care for one obvious solution: create a "fire-safe" cigarette, one less likely to start a blaze. The industry insisted it couldn't make a fire-safe cigarette that would still appeal to smokers and instead promoted flame retardant furniture — shifting attention to the couches and chairs that were going up in flames.

But executives realized they lacked credibility, especially when burn victims and firefighters were pushing for changes to cigarettes. So Big Tobacco launched an aggressive and cunning campaign to "neutralize" firefighting organizations and persuade these far more trusted groups to adopt tobacco's cause as their own. The industry poured millions of dollars into the effort, doling out grants to fire groups and hiring consultants to court them.

Playing With Fire: The entire four-part series updated all this week.

So far, parts 1 and 2 have been published.

H5N1, the famous bird flu, is deadly to humans. Of the 566 people who have contracted this form of influenza, 332 have died. But, so far, the people who have caught bird flu don't seem to have contracted the disease from other humans, or passed it on. Instead, they got it from birds, often farm animals with whom the victims were living in close contact. H5N1 was first identified 14 years ago, and there's never been a documented case of it being passed from person to person.

But that doesn't mean such a leap is impossible.

That's because of how the influenza virus works. Influenza is made up of eight pieces of RNA, containing 10 genes, and they all replicate independently of one another and there's no system for error correction*. That means you have more opportunity for mutations to arise that change what the virus does and who it can infect. Think of it like dice. Genetic replication is like putting a die in a jar, shaking it up and seeing what you get. Everybody does that. But influenza has eight die, not one. So it accumulates mutations faster. As a bonus, influenza viruses that infect the same host can share genes—essentially creating a baby virus that carries traits from different parents.

That's why, despite 14 years of relatively low-risk behavior, scientists are still concerned about what H5N1 might do in the future. All it would take, theoretically, is the right roll of the dice, and suddenly you have a flu virus with a 60% kill rate that can pass from person to person.

At least, theoretically. Could that actually happen? And, if so, how likely is it that the "right" bad combination of genes will come up? You can see why these are important questions to ask, and that brings us to the controversy.

Studying the genetics of H5N1 is nothing new. Its genome has been sequenced since 2004, for instance. But, until 2011, nobody had ever tested out a pretty fundamental idea in the control and management of H5N1: The theory that its genetics prevented it from simultaneously being both super deadly and passed from person to person.

That theory hinged on what we know about one of the proteins in H5N1. Specifically, the protein designated H5. Here's the LA Times:

Strains carrying the H5 type of a key influenza protein that helps the virus bind to cells in a host had never evolved to travel through the air from person to person. Even if H5N1 did evolve such an ability, some researchers reasoned that it might do so at the expense of its ability to take hold deep in the lung. And that would make it less lethal.

As one scientist described it to the LA Times, this theory was, basically, "We've not seen this happen before so it can't happen." But that's not a particularly strong basis on which to pin all your fears about a global pandemic.

That's why researchers in Europe and the U.S. decided to try something risky—see whether they could prompt existing H5N1 viruses to mutate into the very thing everybody's been dreading. Nobody knows a lot about this research, but, at Slate.com, Carl Zimmer explains what is known:

They’ve carried out their experiments on ferrets, which respond to flu viruses much like humans do. What few details we know of the unpublished research comes from a talk Dutch virologist Ron Fouchier gave in August at a virology conference, along with subsequent news reports. Fouchier began the experiment by altering the H5N1 virus’s genes in two spots. Then he passed the virus from one ferret to another, allowing the virus to mutate and evolve on its own inside the animals. After several rounds, Fouchier ended up with an H5N1 virus that could spread through the air from one ferret to the other. If unleashed—and if proven capable of spreading from human to human with the same high mortality rate—it could make the deadly 1918 pandemic look like a pesky cold.

So that's one part of the controversy. Was this a responsible thing to do?

On the one hand, zomgwe'reallgonnadierunhide, right? On the other, this research has already taught us something really, really important. Not only can H5N1 make the leap to mammal-to-mammal transmission, but it did so faster and easier than the researchers had guessed. Knowing that matters, because it could help public health officials make better plans for where to use limited resources, and it could help other scientists figure out a way to fight a human transmissible H5N1 pandemic if it did happen in nature. But, if I may flip the waffle back over again, there are some legitimate scientists who don't think the benefits outweigh the risks of creating this thing. Carl Zimmer again:

Ian Lipkin, the director of the Center for Infection and Immunity at Columbia University, believes there’s no reason to assume that the mutations that arose in Fouchier’s experiments would be the ones that would arise out in the real world. “On the other hand,” Lipkin says, “publishing this information would give people a roadmap to creating Frankenstein viruses.”

And that brings us to the other part of the controversy: What to do with Fouchier's research.

This is where the government gets involved. These studies were funded by the National Institutes for Health. When NIH got the papers, they passed them on to the National Science Advisory Board for Biosecurity. On December 20, the NSABB recommended that Fouchier's study, and a similar one conducted by the University of Wisconsin's Yoshihiro Kawaoka, only be published once key data and details are removed, effectively rendering the studies un-reproducible.

The board can't technically force this. But the board is also a big deal and so Science, Nature, the NIH, and the paper's authors are all listening. That's why the papers haven't actually been published yet. The people involved are still figuring out how to handle them.

This matters a lot. Reproducibility—being able to read another scientist's research paper and independently test out their conclusions—is a key part of how science works. Remove that element, and it becomes harder to verify claims like this, not to mention much harder to actually get the benefits out of this risky research. The people involved are trying to work out a system under which qualified scientists could have access to the full data, but others say that isn't good enough. Especially considering the fact that H5N1 wouldn't make the best bioterrorism tool, anyway. Peter Christian Hall writing for Reuters:

[No one in the history of biological weapons] ever tried to weaponize a flu strain—for good reason.

Influenza in general is an equal-opportunity menace, particularly dangerous when a strain is so unfamiliar that humanity lacks immunity to it. This would put at great risk anyone trying to assemble a pandemic H5N1 to launch at “target” populations. Indeed, such an attack would unleash global contagion that would swiftly and inevitably incapacitate an aggressor’s own people. Influenza doesn’t respect borders.

Even arguably irrational terrorists like Aum Shinrikyo never got into anything near as notoriously unpredictable and uncontrollable as the flu, Hall writes. Of course, his argument is pretty similar to the one scientists used to use to reassure themselves that H5N1 couldn't be both deadly and human transmissible: We've not seen this happen before, so it won't.

Of course, it's also worth pointing out that these experiments were a lot more technologically complex than the short description here makes them sound. This isn't just about taking a bunch of ferrets and making them sick. It required some serious lab equipment that not just anybody has access to.

Moreover, this isn't the first time scientists have made a deadly flu virus in the lab. Back in 2005, a team reverse-engineered the 1918 pandemic flu. After a lot of debate, their research was eventually published in full, reproducible form. Peter Palese was one of the scientists on that team, and he's written an essay on Nature about his experience, as part of a plea to publish the H5N1 research in full, too.

He makes a case both for the importance of risky research, and for why all science (even kind of scary science) needs to remain open source.

During our discussions with members of the NSABB, we explained the importance of bringing such a deadly pathogen back to life. Although these experiments may seem dangerously foolhardy, they are actually the exact opposite. They gave us the opportunity to make the world safer, allowing us to learn what makes the virus dangerous and how it can be disabled. Thankfully, the discussions were largely constructive — within a week, the NSABB recommended that we continue to study the virus under biocontainment conditions, and publish the results so that other scientists could participate in the research. After we published our full paper in 2005, researchers poured into the field who probably would not otherwise have done, leading to hundreds of papers about the 1918 virus. As a result, we now know that the virus is sensitive to the seasonal flu vaccine, as well as to the common flu drugs amantadine (Symmetrel) and oseltamivir (Tamiflu). Had we not reconstructed the virus and shared our results with the community, we would still be in fear that a nefarious scientist would recreate the Spanish flu and release it on an unprotected world. We now know such a worst-case scenario is no longer possible.

I make the same argument today that we made in 2005 — publishing those experiments without the details is akin to censorship, and counter to science, progress and public health. ... Giving the full details to vetted scientists is neither practical nor sufficient. Once 20–30 laboratories with postdoctoral fellows and students have such information available, it will be impossible to keep the details secret. Even more troublesome, however, is the question of who should decide which scientists are allowed to have the information. We need more people to study this potentially dangerous pathogen, but who will want to enter a field in which you can't publish your most scientifically interesting results?

This really fascinating image comes from a Scientific American guest blog post about the appendix. What does the appendix have to do with cholera? Turns out, the more we study the appendix, the more it appears that this organ—once thought to be useless—is actually a storage system that allows your gut to repopulate itself with beneficial bacteria following a bout with a dramatic, gut-wrenching such as cholera.

This theory makes a lot of sense, but it hasn't been proven yet. The blog post, written by Rob Dunn, tells the story of a couple of studies that seem to add further support to the theory. In one, 11% of people with an appendix had a recurrence of Clostridium difficile infection, while 48% of those without an appendix had a recurrence.

Grendell’s results do not prove Parker is right. Science does not work that way. More tests, even true experiments, need to be done. Maybe there was something else that differed between individuals with and without their appendixes. Maybe the result only applies to the mostly white population Winthrop hospital serves. Maybe the immune system plays a more important or different role than Parker envisions. These “maybes” are part of what make science beautiful — the idea that each question, each test, and each day, lead to more questions. Every good question is a road that goes on forever, diverging and bounding forward, sometimes quickly, other times more slowly, as new paths emerge and some of the old ones run straight into brick walls.

Where does this leave us? In your body is an organ that appears to be/may be/could be helping out the bacteria in your life so they can, in turn, help keep you alive. If you do not have your appendix anymore, you may be at an increased risk of recurrence and even death when confronted with a pathogen like C. diff., cholera or any of a wild kingdom of other pathogens. This possibility raises the question of what to do if your appendix (or your child’s appendix) becomes inflamed. First things first, you should seek medical attention. As for what the treatment should be, while appendicitis can be deadly, recent studies suggest some, but not the majority, of cases of appendicitis can be resolved using antibiotics, though the topic is an active area of research and little is known about the prognosis for individuals treated with antibiotics for appendicitis later in life7. Might there, some day, be solutions other than surgery and antibiotics, solutions that aim at restoring the sanctuary of the appendix? Maybe. Until then, doctors keep cutting infected appendixes out. When they do, when they hold them up, they hold up a symbol — a somewhat gross, pinky-finger-sized symbol –both of our complex relationship with other species and of how little we know.

UPDATE: Hey guys, I screwed up on this one. NPR points out that the story I wrote about here is pretty heavily biased, produced by a website that's run by a law firm specializing in food poisoning cases. And the claims made here don't line up with evidence. Apologies. I normally manage to avoid being suckered in by stuff like this, but we all have bad days. Thanks to those in the comments who pointed out the flaws.

Honey that comes from large grocery stores, big-box chains, and individual packet servings in restaurants may not be honey you can trust. That's because the vast majority of this honey has had all the pollen filtered out of it, effectively preventing regulators from knowing where the honey came from.

Food Safety News purchased honey in 10 states, and the District of Columbia, and had it independently tested by scientists at the University of Texas. Roughly 76% of the honey from grocery stores and big box stores was lacking pollen. 100% of the honey purchased at drugstores and distributed at restaurants in single-serving packets lacked pollen. Only the samples that came from farmer's markets, co-ops, and smaller niche stores like Trader Joe's and PCC all contained all of the pollen they were supposed to.

Why do you care? This really isn't about the pollen, itself. Instead, it's about what the pollen (or lack thereof) represents. There aren't a lot of reasons someone would want to filter honey so aggressively that they remove the pollen. It adds costs to production, lowers the quality of the honey, and doesn't produce much of a benefit for businesses. In fact, according to research by Food Safety News, there's really only one benefit you could get from filtering out the pollen: Without the pollen, nobody can tell where the honey came from.

This is the part you should care about. A desire to hide the origins of honey is a pretty big red flag that the honey might be coming from places with potentially dangerous production practices. Honey from China, for instance, can be contaminated with animal antibiotics that are illegal in the the U.S. and Europe because they are fatal to a small percentage of people. Honey from India has turned up laced with heavy metals. Without pollen, there's no way to verify that the honey you're getting is safe. It might well be. But no one can tell. And if it does hurt you, there's no way to connect it to other honey from the same source, which makes it harder to recall all the dangerous honey.

In fact, before pap smears became commonplace, cervical cancer killed more American women than any other sort of cancer. But in places where the pap smear isn't practical, this new technique can help. From the New York Times:

Nurses using the new procedure, developed by experts at the Johns Hopkins medical school in the 1990s and endorsed last year by the World Health Organization, brush vinegar on a woman’s cervix. It makes precancerous spots turn white. They can then be immediately frozen off with a metal probe cooled by a tank of carbon dioxide, available from any Coca-Cola bottling plant.

... Dr. Bandit Chumworathayi, a gynecologist at Khon Kaen University who helped run the first Thai study of VIA/cryo, explains that vinegar highlights the tumors because they have more DNA, and thus more protein and less water, than other tissue.

It reveals pre-tumors with more accuracy than a typical Pap smear. But it also has more false positives — spots that turn pale but are not malignant. As a result, some women get unnecessary cryotherapy. But freezing is about 90 percent effective, and the main side effect is a burning sensation that fades in a day or two. By contrast, biopsies, the old method, can cause bleeding.

This image comes from “Microbiological laboratory hazard of bearded men," a peer-reviewed research paper concerning the risk bearded scientists who work with bacteria and viruses might pose to their families. Published in 1967, the study tested whether bearded men were more likely to accidentally "carry" microbes home with them.

You can read the whole study online. And thank God for that. Because it's full of more great out-of-context quotes than I have time to cut and paste today.

Conclusion: Dirty hippie scientists shouldn't normally be a threat to family and friends. However, accidental beard-based contamination is possible, if the bearded scientist in question does a lot of repetitive, close-contact work with microbes. (Read: Grad students) In which case, those scientists should really wash their beards before they leave the lab.

Thanks, David Ng!

If a centenarian jumped off a bridge while eating a bag of jelly donuts and chain-smoking, would you do it, too?

That's basically the message in a new column by LiveScience's Christopher Wanjek, which looks at why the people who live the longest should not necessarily be health role models for the rest of us.

It seems that longevity goes hand-in-hand with some funny yesbuts. What you eat and how active you are doesn't seem to matter ... if you're one of the very, very lucky folks with a genetic predisposition toward surviving into extreme old age. For everybody else, there's pretty good evidence that healthy habits actually do extend your lifespan. Part of what fascinates me about the studies that show that is that they often compare Seventh Day Adventists to the general population. Why? Because Seventh Day Adventists generally don't eat meat (the first time I ever saw lentil loaf, it came from SDA cookbook), and are discouraged from booze, cigarettes, drugs, and caffeine. It also doesn't hurt that they run a massive, and well-respected, healthcare system, centered around Loma Linda University. Makes 'em easier to study like that.

For the general population, there is a preponderance of evidence that diet and exercise can postpone or ward off chronic disease and extend life. Many studies on Seventh Day Adventists — with their limited consumption of alcohol, tobacco and meat — attribute upward of 10 extra years of life as a result of lifestyle choices.

Irradiating food doesn't make it radioactive, and it does kill dangerous bacteria, like the E.coli that killed many Europeans this summer. But it's also not a panacea against food poisoning and it's definitely not the most popular idea ever thought up. In a column in the New York Times, Mark Bittman examines the evidence behind irradiation, and how that evidence does and doesn't get considered in the choices we make about food.

When it comes to irradiation, you might need a primer. (I did.) Simply put, irradiation — first approved by the FDA in 1963 to control insects in wheat and flour — kills pathogens in food by passing radiation through it. It doesn’t make the food radioactive any more than passing X-rays through your body makes you radioactive; it just causes changes in the food. Proponents say those changes are beneficial: like killing E. coli or salmonella bacteria. Opponents say they’re harmful: like destroying nutrients or creating damaging free radicals.

Many people are virulently for or against. Michael Osterholm, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, says that irradiation “could do for food what pasteurization has done for milk.” (The main difference between irradiation and pasteurization is the source of the energy used to kill microbes.) Wenonah Hauter, the executive director of Food & Water Watch — which calls irradiation “a gross failure” — told me it was “expensive and impractical, a band-aid on the real problems with our food system.”

There are a few people in the middle. Former assistant secretary of the Department of Agriculture (USDA) Carol Tucker-Foreman is mostly anti-, but said that if she ran a nursing home or a children’s hospital — a place where people with weaker-than-average immune systems were cared for — it “might be something I wanted to do.” Marion Nestle, a New York University nutrition professor and the author of “Safe Food: The Politics of Food Safety” (and a food-movement icon), allows that “the bottom line is that it works pretty well if done right, and I’m not aware of any credible evidence that it does any worse harm to foods than cooking. But it isn’t always done right, and foods can become re-contaminated after irradiation.”

Heat and high doses combine in dangerous ways for a couple of reasons:

First, stimulants themselves raise body temperature, which is not what you want during a heat wave. They also interfere with the body's ability to regulate temperature to cool itself down. The high body temperatures that result are one way that stimulant overdose kills—so extra heat makes matters worse.

Secondly, chemical reactions that injure or kill brain cells can occur when high doses of these drugs are taken. These may be more toxic when the temperature is higher. High doses of stimulants cause excess release of dopamine and glutamate— if these levels get high enough, the resulting chemical reactions can be deadly to cells. That process may increase overdose risk as well as contributing to long-term harm in those who survive.